Week Objectives

Neurology and Psychiatry

By: Onion (2014)

FAKULTAS KEDOKTERAN

UNIVERSITAS PELITA HARAPAN

TANGERANG

2016
Table of Contents
Development of the Nervous System ................................................................................................... 4
Histological Features of Neuron and Neuroglia .................................................................................... 5
Organization and Function of Major Components of the Nervous System in Human .......................... 8
Component of CNS (Hemisphere, Cerebellum, Brain Stem, Spinal Cord) ........................................... 10
Major Parts of the Brain and the Lobes of the Cerebral Cortex and Functions for Each Structure ..... 15
Embryology, Anatomy of the Brain Ventricles and CSF Circulation System Including Embryology of
Sub-Arachnoid Space .......................................................................................................................... 19
Production, Circulation and Absorption of CSF ................................................................................... 20
Congenital Anomalies of the CNS ....................................................................................................... 21
Unconsciousness Definition and the Anatomy and Physiology of Brainstem, Thalamic and Higher
Cortical Structures Involved in Consciousness .................................................................................... 27
Neural Basis of the Examination of the Consciousness Patient with Emphasis on Level of the
Consciousness, Brainstem Reflexes .................................................................................................... 28
Aetiology and Pathophysiology of Various Causes of Unconsciousness ............................................. 32
Components of Intracranial Volume (Brain, CSF, Circulating Blood) and Relationship between Volume
and ICP ................................................................................................................................................ 34
Intracranial Compartments and the Anatomical Basis, Pathology and Pathophysiology of Cerebral
Herniation that Occur with Raised ICP ................................................................................................ 37
Definition, Aetiology, Pathophysiology and Classification of Seizure.................................................. 37
Pharmacology of Anticonvulsant Drugs and Their Role in the Pathophysiology of Seizure ................ 39
The Role of Neurotransmitter in the Brain ......................................................................................... 40
The Role of BBB and Different Type of Brain Oedema ........................................................................ 40
Normal Blood Supply to and the Venous Drainage of the Head, Neck, Cerebral Cortex, Hemispheric
White Matter and Deep Gray Structures and Physiological Control of the Cerebral Blood Flow........ 43
Pathogenesis and Pathophysiology of Haemorrhagic Stroke and the Clinical Picture with Specific
Location .............................................................................................................................................. 45
Pathogenesis and Pathophysiology of Occlusive Stroke and the Clinical Picture with Specific Vessel
Occlusion ............................................................................................................................................ 45
Temporal (Time) Development of Pathogenesis of Acute Stroke and Early Management ................. 46
Rehabilitation Planning for Patients with Completed Stroke .............................................................. 46
Risk Factor, Prevention, and Management of CV Disease .................................................................. 47
Clinical Differences between UMN and LMN Lesion ........................................................................... 47
Neuroanatomy of the Brainstem Including Major Tracts and 12 Cranial Nerves Which Arise from
Brainstem and Cerebellum ................................................................................................................. 48
Location of Nuclei of Cranial Nerves on Brainstem and Function of Each 12 Cranial Nerves .............. 57
Clinical Findings with Specific Lesions in the Brainstem ...................................................................... 61

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Anatomy and Physiology of the Vestibular Component of Cranial Nerve VIII, with Emphasis on the
Role of the Vestibular System in Eye Movement and Equilibrium ...................................................... 65
Pathophysiology of Vertigo and Disequilibrium .................................................................................. 66
Anatomy of Cerebellum and Its Role on Equilibrium and Coordination ............................................. 68
Role of Myelin on Signal Transmission................................................................................................ 69
Pathophysiology of Acute Demyelinating Process and Late Pathologic Changes and the Imaging
Findings with Acute Demyelination .................................................................................................... 69
The Diagnostic Criteria for Diagnosis of Multiple Sclerosis ................................................................. 71
Action for Management and Prevention of Multiple Sclerosis ........................................................... 71
Anatomy of the Vertebral Column and Spinal Cord (External Anatomy) ............................................ 73
The 31 Pairs of Spinal Nerves from Spinal Cord as Components of PNS ............................................. 75
Internal Anatomy of the Spinal Cord with Emphasis on the Clinically Relevant Regions of Grey Matter
and the Major Ascending and Descending White Matter Tracts ........................................................ 76
Blood Supply to the Spinal Cord.......................................................................................................... 77
Clinical Findings related to Disruptions in the Ascending and Descending Pathways ......................... 78
Possible Sign caused by Disturbances in UMN Circuit and Disturbances in LMN Circuit .................... 79
Function of the Major Excitatory and Inhibitory Neurotransmitters Involved in Spinal Cord Function
(Glutamate, Lysine, GABA) and their Role in Normal Spinal Reflexes and the Maintenance of Muscle
Tone. The Changes that Underlie Spasticity in UMN Lesions .............................................................. 80
Anatomy and Physiology of Acute Pain .............................................................................................. 82
Pharmacology of the Major Analgesic Drugs used in Acute Pain (Acetaminophen, Acetylsalicyclic
Acid, NSAIDs and Opioids) and Chronic Pain ....................................................................................... 84
Pathophysiological Basis of the Physical Findings Seen in Spinal Cord Disorders ............................... 89
Autonomic Nervous System ................................................................................................................ 90
Role of the Limbic System and Temporal Lobe Structures in Memory, and their Relationships with
Cortical Association Areas ................................................................................................................... 94
Neuropsychological Changes with Functional Localization of Specific Regions of the Cortex that are
Involved in Learning and Memory ...................................................................................................... 95
Anatomical Correlates to Cognitive Capacities ................................................................................... 98
Changes in Behaviour Associated with Dementias and those of Normal Aging .................................. 98
Common Etiologies, Pathophysiologies and Genetics of Dementia .................................................. 101
Neuropathological and Neurotransmitter Changes Found in Alzheimer Disease ............................. 103
Most Common Differential Diagnosis for Patients with Cognitive Impairment and Acute Confusional
States and Factors Which Support the Diagnosis.............................................................................. 104
Changes of Sleep Pattern in Normal Aging, and in Dementing Disorders and How Environmental
Factors Influence the Sleep-Wake Cycle ........................................................................................... 105
Common Etiologies and Pathophysiologies of Insomnia and Other Sleep Disorders ........................ 106
Pharmacological and Non-Pharmacological Management Available for Alzheimer’s Dementia ...... 107

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The Pharmacology of Sedative/Hypnotic Drugs and How Aging Influences their CNS Effects .......... 108
Role of Community and Social Resources for Dementing Patients and Caregivers........................... 109
Anatomy and function of hypothalamus .......................................................................................... 110
Mental illness and social effect of mental illness .............................................................................. 110
Clinical picture signs and symptoms of psychopathology ................................................................. 111
Schizophrenia and other psychotic disease (Schizoaffective, Acute Psychotic Disorder, Delusional
Disorder) ........................................................................................................................................... 116
Pharmacology and Clinical Treatment of Antipsychotic.................................................................... 124
Dopamine Pathway of Schizophrenia and Presynaps & Postsynapse of action Central
Neurotransmitter .............................................................................................................................. 127
Substance Abuse and Psychological Aspect, Law Aspect and the Antidote ...................................... 130
Emergency Psychiatry ....................................................................................................................... 131
Classification and Evaluation Multiaxial Psychiatry .......................................................................... 132

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 Central Nervous System Development and
Malformation

Development of the Nervous System

Pembentukan otak berlangsung terus dan salah satu organ awal yang berkembang.
Pertama kali pada minggu ke-3 dari
ectoderm akan membentuk neural plate
yang seperti sandal tepi nya akan meneku
ke medial bernama plica neuralis sampai
membentuk tabung (neural tube). Bagian
anterior neuropore pada hari ke-25 akan
elongasi karena cephalocaudal folding
demikian juga posterior akan memanjang dan menyempit membentukmedulla spinalis dan
menutup pada hari ke-27.

Pada minggu ke-4 terbentuk

vesicular encephalii. Pada
awalnya terdapat 3:

1. Prosencephalon
 Telencephalon
 Diencephalon
2. Mesencephalon
3. Rhombencephalon
 Metencephalon
 Myelencephalon

Lamina terminalis akan membentuk belahan yang lanjut ke caudal. Telencephalon tumbuh
ke dorsal dan menutupi diencephalon karena di ventral ada pembentukan jantung dan
sebagainya.

Pada sel-sel di otak, mereka akan bergerak ke perifer sehingga membentuk rongga dan
pada bulan ke-4 telencephalon bentuk 2 ruangan (ventriculi laterals); diencephalon
membentuk rongga ke-3; mesencephalon membentuk saluran kecil (aqueductus sylvii).
Pada rhombencephalon terdapat ventriculus quartus.

Formation of meninges merupakan derivate mesenchyme di sekitar tubulus neuralis. Jika

dikatakan meningitis = di dura mater; leptomeningitis = di arachnoid dan pia mater. Subdural

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space adalah rongga potensial yang dapat diisi LOS. Subdural space ada bridging veins
yaitu antara pembuluh darah intra dan extra cranial.

Histological Features of Neuron and Neuroglia

Most neurons have three parts: (1) cell body, (2) dendrites, and (3) an axon. Neuronal cell
bodies also contain free ribosomes and prominent clusters of rough endoplasmic reticulum,
termed Nissl bodies to repair damaged axon in the PNS. The cytoskeleton includes both
neurofibrils and microtubules. Single axon propagates nerve impulses toward another
neuron, a muscle fiber, or a gland cell that often joins to the cell body at a cone-shaped
elevation called the axon hillock. Part closest to the axon hillock is the initial segment.
Nerve impulses arise at the junction of the axon hillock and the initial segment, an area
called the trigger zone, from which travel along the axon to their destination. Axon contains
mitochondria, microtubules and neurofibrils. Cytoplasm of an axon, called axoplasm, is
surrounded by a plasma membrane knows as axolemma.

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Site of communication between two neurons or between a neuron and an effector cell is
called a synapse. Tips of some axon terminals swell into bulb-shaped structures called
synaptic end bulbs; others exhibit a string of swollen bumps called varicositites. Both
contain membrane-enclosed sacs called synaptic vesicles that contain neurotransmitter.

Found in: brain, spinal cord, Found in: retina, inner ear Found in: sensory receptors
and all motor neurons , and the olfactory area (touch, pressure, pain, thermal)

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Astrocytes

Star shaped cells and are the largest and most numerous of the neuroglia. There are two
types: (1) protoplasmic astrocytes (short branched fibers) found in gray matter, (2) fibrous
astrocytes (long unbranched fibers) found in white matter. They make contact with blood
capillaries, neurons, and the pia mater.

Functions of Astrocytes:

1. Support neurons due to their microfilaments,

2. Create blood-brain barrier which restricts the movement of substances between the
blood and interstitial fluid of the CNS,
3. In the embryo, astrocytes secrete chemicals that appear to regulate the growth,
migration, and interconnection among neurons in the brain,
4. Help to maintain appropriate chemical environment for the generation of nerve
impulses,
5. Play a role in learning and memory by influencing the formation of neural synapses.

Oligodendrocytes

Resemble astrocytes but are smaller and contain fewer processes and responsible for
forming and maintaining the myelin sheath around the CNS axons.

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Microglia

Small cells with slender processes that give off numerous spinelike projections and function
as phagocytes (remove cellular debris formed during normal development of the nervous
system and phagocytize microbes and damaged nervous tissue).

Ependymal Cells

Cuboidal to columnar cells arranged in a single layer that possess microvilli and cilia. They
line in the ventricles and central canal to produce, possibly monitor and assist in the
circulation of CSF and also form the blood-cerebrospinal fluid barrier.

Organization and Function of Major Components of the Nervous System

in Human
Nervous system divided into two major components: (1) central nervous system and (2)
peripheral nervous system.

The central nervous system is composed of:

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 1. Brain : responsible for integrating most sensory information and coordinating
body function, both consciously and unconsciously.
2. Spinal cord : conduit for signals between the brain and the rest of the body. It also
controls simple musculoskeletal reflexes without input from the brain.
3. Medulla oblongata : conduit for fibers running between the spinal cord and higher
regions of the brain, it contains control centers for involuntary functions such as blood
pressure, breathing, swallowing and vomiting.
4. Pons : relays information between higher regions of the brain and the
cerebellum, which processes sensory information and helps coordinate movement.
5. Midbrain : primarily responsible for eye movement.
6. Diencephalon composed of two major parts:
a. Thalamus : processes and integrates all sensory information going to the
higher regions of the brain.
b. Hypothalamus : critical for homeostasis, the maintenance of the body's
internal environment. It influences nervous control of all internal organs and
also serves as the master regulator of endocrine function by its control over
the pituitary gland.
7. Cerebellum : coordinates voluntary movements such as posture, balance,
coordination, and speech, resulting in smooth and balanced muscular activity.
8. Cerebrum : responsible for conscious sensation and voluntary movement, as
well as advanced functions such as thinking, learning and emotion.

The peripheral nervous system is composed of:

1. Somatic nervous system includes:

a. Sensory nerves : from the receptor to the central nervous system
b. Motor nerves : from the central nervous system to the effector
2. Autonomic nervous system includes:
a. Sympathetic : fight or flight
b. Parasympathetic : rest and digest

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Component of CNS (Hemisphere, Cerebellum, Brain Stem, Spinal Cord)

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Major Parts of the Brain and the Lobes of the Cerebral Cortex and
Functions for Each Structure

Sensory areas:

 Primary somatosensory area (areas 1, 2, and 3)

 Primary visual area (area 17)
 Primary auditory area (areas 41 and 42)
 Primary gustatory area (area 43)
 Primary olfactory area (area 28)

Motor areas:

 Primary motor area (area 4)

 Broca’s speech area (areas 44 and 45)

Association areas:

 Somatosensory area (areas 5 and 7)

 Visual association area (areas 18 and 19)
 Facial recognition area (areas 20, 21, and 37)
 Auditory association area (area 22)
 Orbitofrontal cortex (area 11)
 Wernicke’s area (area 22, and possibly areas 39, and 40)
 Common integrative area (areas 5, 7, 39, and 40)

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  Frontal association area (areas 9, 10, 11 and 12 which is not illustrated since it can
be seen only in a medial view)
 Premotor area (area 6)
 Frontal eye field area (area 8)

Frontal Lobe

The frontal lobes are anterior to the central sulcus. They are essential for planning and
executing learned and purposeful behaviors; they are also the site of many inhibitory
functions. There are several functionally distinct areas in the frontal lobes:

 The primary motor cortex is the most posterior part of the precentral gyrus. The
primary motor cortex on one side controls all moving parts on the contralateral side of
the body; 90% of motor fibers from each hemisphere cross the midline in the brain
stem. Thus, damage to the motor cortex of one hemisphere causes weakness or
paralysis mainly on the contralateral side of the body.

 The medial frontal cortex (sometimes called the medial prefrontal area) is important
in arousal and motivation. If lesions in this area are large and extend to the most
anterior part of the cortex (frontal pole), patients sometimes become abulic
(apathetic, inattentive, and markedly slow to respond).

 The orbital frontal cortex (sometimes called the orbital prefrontal area) helps
modulate social behaviors. Patients with orbital frontal lesions can become
emotionally labile, indifferent to the implications of their actions, or both. They may be
alternately euphoric, facetious, vulgar, and indifferent to social nuances. Bilateral
acute trauma to this area may make patients boisterously talkative, restless, and
socially intrusive. The disinhibition and abnormal behaviors that can occur with aging

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 and in many types of dementia probably result from degeneration of the frontal lobe,
particularly the orbital frontal cortex.

 The left posteroinferior frontal cortex (sometimes called the Broca area or
posteroinferior prefrontal area) controls expressive language function. Lesions in this
area cause expressive aphasia (impaired expression of words).

 The dorsolateral frontal cortex (sometimes called the dorsolateral prefrontal area)
manipulates very recently acquired information—a function called working memory.
Lesions in this area can impair the ability to retain information and process it in real
time (eg, to spell words backwards or to alternate between letters and numbers
sequentially).

Parietal Lobe

Several areas in the parietal lobes have specific functions.

 The primary somatosensory cortex, located in the postrolandic area (postcentral

gyrus) in the anterior parietal lobes, integrates somesthetic stimuli for recognition and
recall of form, texture, and weight. The primary somatosensory cortex on one side
receives all somatosensory input from the contralateral side of the body. Lesions of
the anterior parietal lobe can cause difficulty recognizing objects by touch
(astereognosis).

 Areas posterolateral to the postcentral gyrus generate visual-spatial relationships

and integrate these perceptions with other sensations to create awareness of

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 trajectories of moving objects. These areas also mediate proprioception (awareness
of the position of body parts in space).

 Parts of the midparietal lobe of the dominant hemisphere are involved in abilities
such as calculation, writing, left-right orientation, and finger recognition. Lesions in
the angular gyrus can cause deficits in writing, calculating, left-right disorientation,
and finger-naming (Gerstmann syndrome).

 The nondominant parietal lobe integrates the contralateral side of the body with its
environment, enabling people to be aware of this environmental space, and is
important for abilities such as drawing. Acute injury to the nondominant parietal lobe
may cause neglect of the contralateral side (usually the left), resulting in decreased
awareness of that part of the body, its environment, and any associated injury to that
side (anosognosia). For example, patients with large right parietal lesions may deny
the existence of left-sided paralysis. Patients with smaller lesions may lose the ability
to do learned motor tasks (eg, dressing, other well-learned activities)—a spatial-
manual deficit called apraxia.

Temporal Lobes

The temporal lobes are integral to auditory perception, receptive components of language,
visual memory, declarative (factual) memory, and emotion. Patients with right temporal lobe
lesions commonly lose the ability to interpret nonverbal auditory stimuli (eg, music). Left
temporal lobe lesions interfere greatly with the recognition, memory, and formation of
language.

Patients with epileptogenic foci in the medial limbic-emotional parts of the temporal lobe
commonly have complex partial seizures, characterized by uncontrollable feelings and
autonomic, cognitive, or emotional dysfunction. Occasionally, such patients have personality
changes, characterized by humorlessness, philosophic religiosity, and obsessiveness.
Patients may have olfactory hallucinations and hypergraphia (an overwhelming urge to
write).

Occipital Lobes

The occipital lobes contain

 The primary visual cortex

 Visual association areas

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Lesions in the primary visual cortex lead to a form of central blindness called Anton
syndrome; patients become unable to recognize objects by sight and are generally unaware
of their deficits, often confabulating descriptions of what they see.

Seizures involving the occipital lobe can cause visual hallucinations, often consisting of lines
or meshes of color superimposed on the contralateral visual field.

Insula Lobes

The insula integrates sensory and autonomic information from the viscera. It plays a role in
certain language functions, as evidenced by aphasia in patients with some insular lesions.
The insula processes aspects of pain and temperature sensation and possibly taste.

Embryology, Anatomy of the Brain Ventricles and CSF Circulation

System Including Embryology of Sub-Arachnoid Space

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Production, Circulation and Absorption of CSF
CSF is formed in the choroid plexuses of each lateral ventricle flows into the third ventricle
through two narrow, oval openings, the interventricular foramina. More CSF is added by the
choroid plexus in the roof of the third ventricle. The fluid then flows through the aqueduct of
the midbrain, into the fourth ventricle. The choroid plexus of the fourth ventricle contributes
more fluid. CSF enters the subarachnoid space through three opening in the roof of the
fourth ventricle: a single median aperture and paired lateral apertures, one on each side.
CSF then circulates in the central canal of the spinal cord and in the subarachnoid space
around the surface of the brain and spinal cord.

CSF is gradually reabsorbed into the blood through arachnoid villi, fingerlike extensions of
the dural venous sinuses, especially the superior sagittal sinus. Normally, CSF is reabsorbed
as rapidly as it is formed by the choroid plexus, at a rate of about 20 mL/hr (480 mL/day).
Because the rates of formation and reabsorption are the same, the pressure of CSF
normally is constant. For the same reason, the volume of CSF remains constant.

Stimulation of adrenergic system decrease CSF production, excitation of the cholinergic

nerves increase production.

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Congenital Anomalies of the CNS
Neural tube defects (dysraphism)

Result from failure of the neural tube to close spontaneously. Etiology is unknown and many
factors affecting these anomalies such as radiation, drugs, malnutrition, environmental
(chemicals), and genetic.

Major neural tube defects:

 Spina bifida occulta

o No abnormality of the meninges, spinal cord, or nerve roots. Mostly
asymptomatic and lack neurologic signs
o Roentgenogram shows defect in closure of the posterior vertebral arches and
laminae involving L5 and S1

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 Meningocele
o Meninges herniate through a defect in the posterior vertebral arches.
o Asymptomatic children with normal neurologic findings and full-thickness skin
covering the meningocele may have surgery delated, but with thin covering
should undergo immediate surgical treatment to prevent meningitis.
o CT-scan of the head is recommended to evaluate hydrocephalus
 Myelomeningocele
o Low sacral region: bowel and bladder incontinence associated with
anesthesia in the perineal area but with no impairment of motor function
o Midlumbar region: LMN signs due to abnormalities and disruption of the
conus medullaris
o Flaccid paralysis of lower extremities, absence of deep tendon reflexes, lack
of response to touch and pain, and high incidence of postural abnormalities of
the lower extremities (including clubfeet and subluxation of the hips).
Constant urinary dribbling and a relaxed anal sphincter may be evident.
o Extends higher into the thoracic region means more extend of neurologic
deficit.
o Folic acid supplementation before conception and continued until at least
the 12th week of gestation when neurulation is complete decrease the
incidence of neural tube defects by 50%.
o Drugs that antagonize folic acid increase the risk of myelomeningocele 
trimethoprim, anticonvulsants carbamazepine, phenytoin, phenobarbital, and
primidone.

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 o Management  surgery and shunting for hydrocephalus; clubfeet may
require casting, and dislocated hips may require operative procedures.
o Long term  neurogenic bladder training, fecal incontinence training,
functional ambulation.
o Prognosis  learning problem and seizure are common; require follow-up
from multidisciplinary
 Encephaocele
o Cranium bifidum
o Cranial meningocele: CSF-filled meningeal sacs only
o Cranial encephalocele: sac plus cerebral cortex, cerebellum, or portions of
the brainstem
o Etiology similar to that for anecncephaly and myelomeningocele
o Infants with cranial encephalocele at increased risk for developing
hydrocephalus to to aqueduct stenosis, chiari malformation, or the dandy-
walker syndrome
o Diagnosis: plain x-ray, ultrasound, CT-scan; in utero by determination of AFP
levels and USG measurement of the biparietal diameter.
o Risk for visual problems, microcephaly, mental retardation and seizures

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  Anencephaly
o Failure of closure of the rostral neuropore
o Cererbral hemispheres and cerebellum absent
o 50% cases are associated with polyhydramnios

Syringonyelia

 Tubular cavitation within the spinal cord

 Associated with chiari type I or II malformation
 Etiology unknown and some cases are post-traumatic and 20% associated with
tumour
 Diagnosis do not symptomatic until adult, lesions involve the cervival cord affect the
upper extremities preferentially.

Hydrocephalus

 Results from impaired circulation and absorption of CSF or increased production

(caused bby choroid plexus papilloma)
 Obstructive / noncommunicating hydrocephalus
o Obstruction in ventricular system
o Common causes: aqueduct abnormality (stenosis) or a lesion in 4 th ventricle
o Etiology:
 Neonatal meningitis or SAH in premature infant
 Intrauterine viral infections
 Sex-linked recessive trait (rare)
 Lesions or malformations of the posterior fossa: posterior fossa brain
tumors, chiari malformation, dandy-walker syndrome
 Nonobstructive / communicating hydrocephalus
o Obliteration of subarachnoid cisterns or malfunction of arachnoid villi

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 o Etiology:
 SAH  blood in subarachnoid spaces may cause obliteration of the
cisterns or arachnoid villi and obstruction of CSF flow
 Pneumococcal and tuberculous meningitis  obstruct the basal
cisterns
 Intrauterine infections
 Leukemic infiltrates
 Clinical manifestation
o Infant
 Accelerated rate of enlargement of the head
 Brisk tendon reflexes, spasticity, clonus, Babinski sign
o Older child
 Subtler hydrocephalus
 Headache
 Change in personality
 Decrease in academic productivity
o Both age groups
 Irritability
 Lethargy
 Poor appetite
 Vomiting
o Broad forehead
o Dilated scalp veins
o Open and bulging anterior fontanel
o Percussion of the skull may produce a “cracked-pot” or Macewen sign
indicating separation of the sutures
o Setting-sun eye sign
 Treatment
o Medical management: (1) acetazolamide and (2) furosemide to temporary
relief by decreasing the CSF production
o Extracranial shunts  ventriculoperitoneal shunt or ventriculostomy
o Complication  bacterial infection of shunts
 Prognosis
o Increase risk for developmental disabilities
o Decrease mean IQ
o Abnormalities in memory function

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 o Visual problems
o Aggressive and delinquent behaviour
o Accelerated pubertal development

Dandy-walker malformation

 Characterized by a triad of:

o Complete/partial agenesis of the cerebellar vermis
o Cystic dilatation of the 4th ventricle
o Enlarged posterior fossa with upward displacement of the transverse sinuses,
tentorium, and torcular
 Other associated anomalies:
o Agenesis of the corpus callosum
o Aqueductal stenosis
o Occipital encephalocele
o Polymicrogyrya
o Syringomyelia
o Heterotopias
o Facial angiomas
o Midline cleft palate
o Cardiovascular malformations
o Polycystic kineys
 No firm imaging criteria
 Hydrocephalus not present at birth; appears by 3 months of age in 75% if infants; in
some cases, remain asymptomatic

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 Unconsciousness and Seizure

Unconsciousness Definition and the Anatomy and Physiology of

Brainstem, Thalamic and Higher Cortical Structures Involved in
Consciousness
Unconsciousness / syncope  loss of consciousness due to reduced blood flow to both
cerebral hemisphere or the brainstem. It can result from pancerebral hypoperfusion caused
by vasovagal reflexes, orthostatic hypotension, decreased cardiac output, or from selective
hypoperfusion of the brainstem resulting from vertebrobasilar ischemia.

Anatomy of brainstem, thalamic, and higher cortical structures:

Centre of awareness lies from the 2/3 upper part of the pons, midbrain, and 1/3 lower part of
the thalamus.

Physiology of consciousness:

Consciousnes refers to subjective awareness of the external worlds and self, including
awareness of the private inner world of one’s mind- that is, awareness of thoughts,
perceptions, dreams, and so on. Final level of awareness resides in the cerebral cortex and

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a crude sense of awareness is detected by the thalamus, conscious experience depends
on the intergrated functioning of many parts of the nervous system.

Global workspace theory  conscious experience depends on the brain functioning as a

“brainweb” in which some of the separate bits of subconscious information that are being
processed locally at the same time are momentarily broadcast throughout the brain (that is,
to a global workspace). This highly coordinated, widespread information exchange among
much of the cortex gives rise to subjective experience of the information. Thus information
received through specialized channels (such as sensory information) is distributed to much
of the cortex, creating a unity of mind.

Normal states of consciousness are wakefulness and sleep (sleep-wake cycle). In the
waking state people are alert and aware of their surroundings and consciously engage in
coherent thoughts and actions. Wakefulness depends on attention-getting sensory input that
“energizes” the RAS and subsequently the activity level of arousal but varies from maximum
alertness to drowsiness, depending on the extent of interaction between peripheral stimuli
and the brain. Different arousal and activity states are characterized by different brain wave
activity as recorded on an electroencephalogram.

Neural Basis of the Examination of the Consciousness Patient with

Emphasis on Level of the Consciousness, Brainstem Reflexes
Glasgow-Coma Scale:

The GCS measures the following functions:

Eye Opening (E)

 4 = spontaneous

 3 = to voice

 2 = to pain

 1 = none

Verbal Response (V)

 5 = normal conversation

 4 = disoriented conversation

 3 = words, but not coherent

 2 = no words, only sounds

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  1 = none

Motor Response (M)

 6 = normal

 5 = localized to pain

 4 = withdraws to pain

 3 = decorticate posture (an abnormal posture that can include rigidity, clenched fists,
legs held straight out, and arms bent inward toward the body with the wrists and
fingers bend and held on the chest)

 2 = decerebrate (an abnormal posture that can include rigidity, arms and legs held
straight out, toes pointed downward, head and neck arched backwards)

 1 = none

Clinicians use this scale to rate the best eye opening response, the best verbal response,
and the best motor response an individual makes. The final GCS score or grade is the sum
of these numbers.

Using the Glasgow Coma Scale

Every brain injury is different, but generally, brain injury is classified as:

 Severe: GCS 3-8 (You cannot score lower than a 3.)

 Moderate: GCS 9-12

 Mild: GCS 13-15

Mild brain injuries can result in temporary or permanent neurological symptoms and a neuro-
imaging tests such as CT scan or MRI may or may not show evidence of any damage.

Moderate and severe brain injuries often result in long-term impairments in cognition
(thinking skills), physical skills, and/or emotional/behavioural functioning.

Apnea Test

Absence of a Respiratory Drive.

Absence of a breathing drive is tested with a CO2 challenge. Documentation of an increase
in PaCO2 above normal levels is typical practice. It requires preparation before the test.

Prerequisites:

1. normotension

29
 2. normothermia

3. euvolemia

4. eucapnia (PaCO2 35–45 mm Hg)

5. absence of hypoxia

6. no prior evidence of CO2 retention (i.e., chronic obstructive pulmonary disease,

severe obesity).

Procedure:

1. Adjust vasopressors to a systolic blood pressure _100 mm Hg.

2. Preoxygenate for at least 10 minutes with 100% oxygen to a PaO2 _200 mm Hg.

3. Reduce ventilation frequency to 10 breaths per minute to eucapnia.

4. Reduce positive end-expiratory pressure (PEEP) to 5 cm H2O (oxygen desaturation

with decreasing PEEP may suggest difficulty with apnea testing).

5. If pulse oximetry oxygen saturation remains_95%, obtain a baseline blood gas

(PaO2, PaCO2, pH, bicarbonate, base excess).

6. Disconnect the patient from the ventilator.

7. Preserve oxygenation (e.g., place an insufflations catheter through the endotracheal

tube and close to the level of the carina and deliver 100% O2 at 6 L/min).

8. Look closely for respiratory movements for 8–10 minutes. Respiration is defined as
abdominal or chest excursions and may include a brief gasp.

9. Abort if systolic blood pressure decreases to _90 mm Hg.

10. Abort if oxygen saturation measured by pulse oximetry is _85% for _30 seconds.
Retry procedure with T-piece, CPAP 10 cm H2O, and 100% O2 12 L/min.

11. If no respiratory drive is observed, repeat blood gas (PaO2, PaCO2, pH, bicarbonate,
base excess) after approximately 8 minutes.

12. If respiratory movements are absent and arterial PCO2 is _60 mm Hg (or 20 mm Hg
increase in arterial PCO2 over a baseline normal arterial PCO2), the apnea test
result is positive (i.e., sports the clinical diagnosis of brain death).

30
If the test is inconclusive but the patient is hemodynamically stable during the procedure, it
may be repeated for a longer period of time (10–15 minutes) after the patient is again
adequately pre-oxygenated.

Brainstem reflexes:

Motor function test

5 = normal strength (normal strength, able to maintain the muscle contraction against
examiner resistance)
4 = mild weakness ( weakly or briefly able to overcome examiner resistance)
3 = able to support the limb against resistance but unable to overcome examiner resistance
2 = can move the limb, but unable to lift against gravity
1 = flicker but no movement
0 = no movement

31
Aetiology and Pathophysiology of Various Causes of Unconsciousness

Intracranial causes:

 Supratentorial lesions: SDH, EDH, contusion, ICH, abscess, infarct / stroke, tumour
 Subtentorial lesions: pontine haemorrhage, cerebellar haemorrhage, posterior fossa
SDH and EDH

Extracranial causes

 Intoxication – alcohol, opiate, anticholinergic

 Hypoglycaemia
 Hypotension
 Heat stroke

Causes of syncope:

 Vasovagal syncope (simple faints)

vagally mediated decreases in arterial blood pressure and heart rate combine to

32
 produce CNS hypoperfusion and subsequent syncope. Prodrome lasting 30 to 60
seconds usually precedes syncope and can include lassitude, yawning, light-
headedness, nausea, pallor, diaphoresis, salivation, blurred vision, and tachycardia.
Then loses consciousness and recovers very rapidly (20-30 seconds), with patient is
pale and diaphoretic and has dilated pupils, breathing continues, eyes remain open,
bradycardia and abnormal movements may occur. It can be diagnosed by inducing
syncope during head-up-tilt-testing. Bradycardia and hypotension of syncope can be
ameliorated by the alpha-agonist midodrine (5 mg three times daily) or with SSRI
paroxetine (10 – 40 mg/d). Tilt-training may have benefit.
 Cardiovascular syncope
syncope occurs in a recumbent position, during or after physical exertion, or in a
patient with known heart disease. Such cardiac dysfunction can result from cardiac
arrest, rhythm disturbances, cardiac inflow or outflow obstruction, intracardiac right-
to-left shunts, leaking or dissecting aortic aneurysms, or acute pulmonary embolism.
 Cerebrovascular syncope
it is an uncommon cause of episodic unconsciousness. For examples:
o Basilar artery insufficiency
Basilar artery TIA with symptoms: complex of diplopia, vertigo, dysphagia,
dysarthria, various sensory or motor symptoms, drop attacks, and occipital
headaches suggests diffuse brainstem ischemia.
o Subclavian steal syndrome
results from subclavian or innominate artery stenosis that causes retrograde
blood flow in the vertebral artery, diverting flow from brainstem and producing
hypoperfusion. Arteriography and revascularization procedures may be
considered.
o Migraine
o Takayasu disease (pulseless arteritis)
o Carotid sinus syncope
 Orthostatic hypotension
the classic diagnosis: decline in blood pressure of at least 20 mmHg systolic or 10
mmHg diastolic within 3 minutes of the patient standing from a lying position. Severe
orthostatic intolerance associated with heart rate increases (>120/min) without
significant hypotension or syncope is termed POTS (postural orthostatic tachycardia
syndrome)
 Misc causes of syncope
o Cough syncope

33
 o Micturition syncope
o Glossopharyngeal neuralgia
o Psychogenic syncope

Components of Intracranial Volume (Brain, CSF, Circulating Blood) and

Relationship between Volume and ICP
Cushing described what is now widely known as the "Cushing Triad" as a clinical tool for
recognizing the presence of elevated ICP. The triad consists of a widening pulse pressure
(rising systolic, declining diastolic), irregular respirations, and bradycardia. Cushing
quantified the Monro-Kelly doctrine, writing that the sum of the volume of the brain plus the
CSF volume plus the intracranial blood volume is constant. Therefore, an increase in one
should reduce one or both of the others.

Physiology

The most important role of the circulatory system, aside from transporting blood into all parts
of the body, is to maintain optimal CPP (cerebral perfusion pressure). The formula for
calculating CPP is below.

CPP = mean arterial blood pressure (MAP) - mean intracranial pressure (MIC)

CPP is the pressure gradient acting across the cerebrovascular bed and, therefore, a major
factor in determining cerebral blood flow (CBF). CBF is kept constant in spite of wide
variation in CPP and MAP by autoregulation.

Autoregulation is a process of adjustment on the part of the brain’s arterioles that keeps
cerebrovascular resistance constant over a range of CPP. Increased CPP causes stretching
of the walls of the arterioles, which compensate by dilating and relieving this pressure.
Likewise, in the setting of decreased pressure, the arterioles constrict to maintain CPP. This
autoregulation prevents transient pressure increases from being transmitted to smaller distal
vessels. When the MAP is less than 65 mm Hg or greater than 150 mm Hg, the arterioles
are unable to autoregulate, and blood flow becomes entirely dependent on the blood
pressure, a situation defined as "pressure-passive flow." The CBF is no longer constant but
is dependent on and proportional to the CPP.

Thus, when the MAP falls below 65 mm Hg, the cerebral arterioles are maximally dilated and
the brain is at risk for ischemia because of insufficient blood flow to meet its needs. Likewise,
at a MAP greater than 150 mm Hg, the cerebral arterioles are maximally constricted and any
further increases in pressure cause excess CBF that may result in increased ICP.

34
Note that, while autoregulation works well in the normal brain, it is impaired in the injured
brain. As a result, pressure-passive flow occurs within and around injured areas and,
perhaps, globally in the injured brain. Ideally, the goal is to maintain the CPP more than 60
mm Hg, and this can be done by either decreasing the ICP or increasing the systolic blood
pressure using vasopressors. Caution should be used to use only vasopressors that do not
increase ICP.

The volume of the skull contains approximately 85% brain tissue and extracellular fluid,
10% blood, and 5% CSF. If brain volume increases, for example in the setting of cancer,
there is a compensatory displacement of CSF into the thecal sac of the spine followed by a
reduction in intracranial blood volume by vasoconstriction and extracranial drainage. If these
mechanisms are successful, ICP remains unchanged. Once these mechanisms are
exhausted, further changes in intracranial volume can lead to dramatic increases in ICP.

The time course of a change in the brain has significance for how ICP responds. A slow-
growing tumor, for example, is often present with normal or minimally elevated ICP, as the
brain has had time to accommodate. On the other hand, a sudden small intracranial bleed
can produce a dramatic rise in ICP. Eventually, whether acute or insidious in progression,
compensatory mechanisms are exhausted, and elevated ICP follows.

The relationship between ICP and intracranial volume is described by a sigmoidal pressure-
volume curve. Volume expansion of up to 30 cm 3 usually results in insignificant changes in
ICP because it can be compensated by extrusion of CSF from the intracranial cavity into the
thecal sac of the spine and, to a lesser extent, by extrusion of venous blood from the
cranium. When these compensatory mechanisms have been exhausted, ICP rises rapidly
with further increases in volume until it reaches the level comparable with the pressure
inside of cerebral arterioles (which depends on MAP and cerebrovascular resistance but
normally measures between 50 and 60 mm Hg). At this point, the rise of ICP is halted as
cerebral arterioles begin to collapse and the blood flow completely ceases.

The relationship between ICP and CBF and functional effects was described thoroughly by
Symon and colleagues, as follows:

 CBF of 50 mL/100 g/min: Normal

 CBF of 25 mL/100 g/min: Electroencephalogram slowing

 CBF of 15 mL/100 g/min: Isoelectric electroencephalogram

 CBF of 6 to 15 mL/100 g/min: Ischemic penumbra

 CBF of less than 6 mL/100 g/min: Neuronal death

35
Normal intracranial pressure

ICP is generally measured in mm Hg to allow for comparison with MAP and to enable quick
calculation of CPP. It is normally 7-15 mm Hg in adults who are supine, with pressures over
20 mm Hg considered pathological and pressures over 15 mm Hg considered abnormal.

Note that ICP is positional, with elevation of the head resulting in lower values. A standing
adult generally has an ICP of -10 mm Hg but never less than -15 mm Hg. In supine children,
ICP is normally lower, in the range of 15 mm Hg, with infants having ICP from 5-10 mm Hg
and newborns have subatmospheric pressures regardless of position.

In adults, the choroid plexus and other locations in the CNS produce CSF at a rate of 20
mL/hour, for a total of 500 mL/day. It is reabsorbed by the arachnoid granulations into the
venous circulation. CSF volume is most commonly increased by a blockage of absorption
due to ventricular obstruction, occlusion of venous sinuses, or clogging of the arachnoid
granulations.

Causes of increased intracranial pressure

Increased ICP may result from the following:

 Space-occupying lesions: Tumor, abscess, intracranial hemorrhage (epidural

hematoma, subdural hematoma, intraparenchymal hematoma)

 CSF flow obstruction (hydrocephalus): Space-occupying lesion that obstructs normal

CSF flow, aqueductal stenosis, Chiari malformation

 Cerebral edema: Due to head injury, ischemic stroke with vasogenic edema, hypoxic
or ischemic encephalopathy, postoperative edema

 Increase in venous pressure: Due to cerebral venous sinus thrombosis, heart failure,
superior vena cava or jugular vein thrombosis/obstruction

 Metabolic disorders: Hypo-osmolality, hyponatremia, uremic encephalopathy, hepatic

encephalopathy

 Increased CSF flow production: Choroid plexus tumors (papilloma or carcinoma)

 Idiopathic intracranial hypertension

 Pseudo tumor cerebri

36
Intracranial Compartments and the Anatomical Basis, Pathology and
Pathophysiology of Cerebral Herniation that Occur with Raised ICP
 Transtentorial herniation: part of the
brain is displaced from the supratentorial
to the infratentorial compartment through
the tentorial opening.
 Uncal transtentorial herniation:
impaction of the anterior medial temporal
gyrus (the uncus) into the tentorial
opening just anterior to and adjacent to
the midbrain. The uncus compresses the
3rd nerve as it traverses the subarachnoid
space, causing enlargement of the
ipsilateral pupil. The coma that follows is
due to compression of the midbrain
against the opposite tentorial edge by the
displaced parahippocampal gyrus. Lateral displacement of the midbrain may
compress the opposite cerebral peduncle, producing Babinski’s sign and hemiparesis
contralateral to the original hemiparesis. Herniation may also compress the anterior
and posterior cerebral arteries as the pass over the tentorial reflections, with resultant
brain infarction. The distortions may also entrap portions of the ventricular system,
resulting in hydrocephalus.
 Central transtentorial herniation: symmetric downward movement of the thalamic
medial structures through the tentorial opening with compression of the upper
midbrain. Miotic pupils and drowsiness are the heralding signs. Both temporal and
central transtentorial herniations have been considered causes of progressive
compression of the brainstem, with initial damage to the midbrain, then pons, and
finally the medulla.
 Transfalcial herniation: displacement of the cingulate gyrus under the falx and across
the midline.
 Foraminal herniation: downward forcing of the cerebellar tonsils into the foramen
magnum, which causes compression of the medulla, respiratory arrest, and death.

Definition, Aetiology, Pathophysiology and Classification of Seizure

Seizure is a transient disturbance of cerebral function caused by an abnormal neuronal
discharge. Epilepsy, a group of disorders characterized by recurrent seizures, is a common

37
cause of episodic loss of consciousness. Two historic features most suggestive of a seizure
are the aura associated with seizures of focal onset and the postictal confusional state that
follows generalized tonic-clonic seizures.

Pathophysiology of seizure can be defined as increase number of glutamate and decrease in

GABA in the CNS. Once it goes above the threshold it will cause ‘spike’ in EEG which
results in an outburst of electrical signals in the brain.

Aetiology of seizure:

A. Primary Neurologic Disorders

 Benign febrile convulsions  Stroke
 Idiopathic (cryptogenic)  Mass lesions
seizures  Meningitis or encephalitis
 Head trauma  Developmental anomalies
B. Systemic Disorders
 Hypoglycaemia  Drug overdose
 Hyponatremia  Drug withdrawal
 Hyperosmolar states  Global cerebral ischemia
 Hypocalcemia  Hypertensive
 Uremia encephalopathy
 Hepatic encephalopathy  Eclampsia
 Porphyria  Hyperthermia
C. Nonepileptic Seizures

Classification of seizure

A. Generalized seizure
a. Tonic-clonic (grand mal)
b. Absence (petit mal)
c. Other types (tonic, clonic, myoclonic, atonic)
B. Partial (focal) seizures
a. Simple partial (with preservation of consciousness)
b. Complex partial (temporal lobe, psychomotor, or focal seizures with
dyscognitive features)
c. Partial seizures with secondary generalization
C. Unclassified / Psychogenic Seizures

38
Pharmacology of Anticonvulsant Drugs and Their Role in the
Pathophysiology of Seizure
Simple partial seizure:

 1st line  carbamazepine,

phenytoin
 2nd line  valproic acid,
lamotrigine, oxcarbazepine
 Gabapentine, tiagabine, topiramat

Tonic-clonic:

 1st line  valproic acid

 2nd line  lamotrigine, topiramate,
zonisamide, levetinazepam
 3rd line  phenobarbital (reduced
use due to adverse cognitive effect

Absence:

 Valproate
 Ethosuximide
 Topiramate
 Lamotrigine
 Zonisamide

Myoclonic:

 Valproate
 Zonisamide
 Clonazepam

39
Mechanism of action:

 Meningkatkan produksi GABA: benzodiazepine (diazepam, alprazolam, lorazepam,

dsb)
 Menginhibisi inaktivasi dari GABA: vigrabatin
 Memblok Cl reuptake (yang membantu fungsi GABA): tiagabine
 Blok dari Na channel (untuk depolarisasi): phenytoin, carbamazepine, topiramate,
zonisamide
 Blok dari Ca channel (untuk depolarisasi): ethosuximide dan lamotrigine
 Block di voltage gated presynapse dan postsynapse: valproate

Side effect:

 Phenytoin  ga boleh untuk ibu hamil

 Valproate dan phenobarbital  tidak disarankan untuk anak kecuali sudah >3x
episode
 Phenytoin, carbamazepine, phenobarbital  mengurangi efektivitas oral
contraceptive
 Phenytoin, carbamazepine, phenobarbital, valproate  teratogenic

Indikasi surgery : frequent, disabling seizures despite adequate trials of 2 or more

anticonvulsants.

The Role of Neurotransmitter in the Brain

 They transmit signals across a chemical synapse, such as a neuromuscular junction
from one neuron to another “target” neuron, muscle cell, or gland cell.
 Neurotransmitter are released from synaptic vesicles in synapses into the synaptic
cleft, where they are received by receptors on the target cells.
o Amino acids : glutamate, aspartate, ϒ-aminobutyric acid (GABA), glycine
o Monoamines : dopamine, cathecolamine, histamine
o Trace amines : phenethylamine, tyramine, tryptamine
o Peptides : somatostatin, opioid peptides
o Purines : ATP, adenosis
o Other : Ach, anandamide

The Role of BBB and Different Type of Brain Oedema

 A functional barrier that prevents the passage of substances
o Antibiotics
o Chemical / bacterial toxic matter

40
 From the blood to nerve tissue, so maintain constancy of the environment of the
neurons in CNS

 These neurons are very sensitive to changes in concentration of ions, e.g. K, Ca, Mg,
H and others
 The BBB results from the reduced permeability of blood capillaries of nerve tissue
 The endothelial cells do not have fenestrations
 Foot processes of astrocytes (neuroglial cells) envelop the capillaries, making it more
impermeable
 Clinical implications
o Physicians must know the degree to which drug penetrate the brain in order
to treat diseases of the CNS intelligently
o The BBB tends to break down in areas of infection / injury. Tumours develop
new blood vessels and the capillaries may be fenestrated and lack contact
with astrocytes. This helps in identifying the location of tumours eg with
radioactive iodine-labeled albumin, that penetrate normal brain tissue very
slowly, but enter tumour tissue easily.
 BBB bisa ditembus water and lipid soluble e.g. O2, CO2, alcohol, and steroid.
Glucose dan amino acid perlu transporter bersama Na
 Metronidazole, cotrimetoxazole, linezoide  menembus BBB dengan baik
 Penicillin, cephalosporin, ceftriaxone, cephotaxime, β-lactam, rifampin  menembus
dengan ok
 -mycin  ga bisa nembus BBB.

Brain edema is defined as an increase in brain volume caused by an increase in brain

volume cause by an increase in water and sodium content. It plays a major role in head
injury, stroke, and brain tumour, as well as in cerebral infections (brain abscess,
encephalitis, meningitis, etc.)

 Vasogenic oedema
increased permeability of brain capillary endothelial cells to macromolecules, such as
plasma proteins
o This increase in permeability is visualized when contrast enhancement is
observed with CT.
o Increased CSF protein levels are also indicative
o MRI shows increased signal intensity

These disorders include brain tumour, abscess, haemorrhage, infarction, and

contusion.

41
 Cellular oedema
swelling of all the cellular elements of the brain (neuron, glia, endothelial cells), with
reduction in volume of extracellular fluid space of the brain; capillary permeability not
affected; normal CSF protein; CT no contrast enhancement; and MRI normal.

 Interstitial oedema
best characterized in obstructive hydrocephalus, in which the water and sodium
content of the periventricular white matter is increased because of movement of CSF
across the ventricular ependymal surface.

42
 Cerebrovascular

Normal Blood Supply to and the Venous Drainage of the Head, Neck,
Cerebral Cortex, Hemispheric White Matter and Deep Gray Structures
and Physiological Control of the Cerebral Blood Flow

Anterior choroidal Artery Hipocampus, globus pallidus, lower internal

capsule

Anterior cerebral artery Medial frontal and parietal cortex and

subjacent white matter, anterior corpus
callosum

MCA Lateral frontal, parietal, occipital, and

temporal cortex and subjacent white matter

43
 Lenticulostriate branches Caudate nucleus, putamen, upper internal
capsule

PICA Medulla, lower cerebellum

AICA Lower and middle pons, anterior cerebellum

Superior cerebellar artery Upper pons, lower midbrain, upper

cerebellum

Posterior cerebral Upper midbrain, medial occipital and temporal

cortex and subjacent white matter, posterior
corpus calosum

Thalamoperforate branches Thalamus

Thalamogeniculate branches Thalamus

The brain receives its blood supply from the internal carotid and vertebral arteries which
drain via the cerebral veins and dural venous sinuses into the internal jugular veins. The
volume of blood in the whole brain is small and contained mainly in the venous sinuses and
pial veins. The grey matter is composed of the cell bodies of the neurons which are involved
with the complex functions of the human body and hence requires a larger proportion of the
arterial blood supply. On the other hand, the white matter is essentially composed of axons
which transmit impulses in between the neurons.

In the brain, the perfusion pressure or the CPP is affected by another pressure within the
skull [i.e. intracranial pressure (ICP) explained below]. In pathological conditions, if the ICP is
increased, the flow through the cerebral blood vessels can be restricted. In normal adults,
the CPP is variable, usually ranging between 70 and 90 mm Hg and the CBF is constant.
When the CPP decreases below 50 mm Hg, there is an increased risk of brain ischaemia
affecting the electrical activity in the brain.

The brain has the highest metabolic requirements of any organ in the body which is reflected
by its high blood flow. Because CBF is adjusted to meet the metabolic demand, oxygen by
the grey matter is approximately five times more than by the white matter.

44
Pathogenesis and Pathophysiology of Haemorrhagic Stroke and the
Clinical Picture with Specific Location
Chronic hypertension → bikin changes in walls of penetrating small cerebral arteries and
arteriole → changesnya itu termasuk fibroid necrosis sama lipohyalinosis → changes ini bisa
bikin charcot-Bouchard aneurysm → terus kalo pecah bisa bikin hemorrhagic stroke

1. Intracerebral Hemorrhage
Severe headache and depression of consciousness

2. Subarachnoid Hemorrhage
Cerebral dysfunction, vasospasm (leading to ischemia), rebleeding, extension of
blood into brain tissue (intracerebral hematoma), hydrocephalus, present with
headache

3. Subdural or Epidural Hemorrhage

Headache or altered consciousness

4. Intraventricular hemorrhage
Neurologic deficit yang tidak correspond to the contribution of any blood pressure

Pathogenesis and Pathophysiology of Occlusive Stroke and the Clinical

Picture with Specific Vessel Occlusion
DM → bikin darahnya jadi ‘thick’

Blood vessel jadinya terus terusan mompa darah yang ‘thick’ → jadinya bisa luka
(endothelial disfunction) dan biasanya di bagian yang bagian blood flownya rendah

Endothelial disfunction akan promote adhesion and subendothelial migration of circulating

monocyte and accumulation of lipid → yang akan menghasilkan inflammation

Inflammatory response seperti monocyte derived macrophage akan ‘memakan’ lipid tersebut
→ yang akan jadi foam cell dan menghasilkan → fatty streak

Growth factor sama macrophage akan menstimulasi proliferasi dari intima of smooth muscle
& beberapa dari yang tunica media pindah ke tunica intima → sel” tersebut akan
mengeluarkan extracellular matrix constituent yang bisa bikin formation of fibrous cap over
the atherosclerotic plaque

Plaque yang terbentuk dikenal dengan sitilah thrombus. Karena dalam pembuluh darah
terdapat aliran turbulensi, thrombus yang ada tersebut bisa terlepas dan mengikut aliran

45
darah. Thrombus yang mengikuti lairan darah tersebut akan menyumbah pembuluh darah
ke otak (emboli) dan lama kelamaan jadi ischemic stroke karena decreased blood flow.

Kalo ada fraktur di cap bisa terjadi plaque rupture → terus ruptured plaquenya bisa nyumbat
blood vessel → ischemic stroke → ischemic cascade

Gambaran klinis

1. Artery carotis interna

Hemiparesis/plegi kontralateral lesi

2. Anterior Cerebral artery

Hemiparesis kontralateral : tungkai > lengan

3. MCA
Pangkalnya : hemiparesis lengan = tungkai
Distal : lengan > tungkai

4. Posterior Cerebral artery

Hemiparesis kontralateral
Hemihipestesia kontralateral protopatis (nyeri, suhu)
Proprioseptif ( getar, sikap)

Temporal (Time) Development of Pathogenesis of Acute Stroke and

Early Management
A decrease in cerebral blood flow to zero cause death of brain tissue within 4 - 10 minutes;
values <16-18 mL/100g tissue per minute cause infarction within an hour; and values
<20mL/100g tissue per minute cause ischemia without infarction unless prolonged for
several hours or days.

Early management : rTPA (3-4.5 hour)

Rehabilitation Planning for Patients with Completed Stroke

Rehabilitation: early physical, occupational, and speech therapy. Educating the patient and
family about the patient’s neurologic deficit, preventing the complications of immobility, and
providing encouragement and instruction in overcoming the deficit.

46
Risk Factor, Prevention, and Management of CV Disease
Risk Factors:

 Hypertension  Smoking
 Atrial Fibrilation  Hyperlipidemia
 Diabetes  Asymptomatic carotid stenosis

Prevention:

 Physical Activity  Lifestyle

Management:

 rTPA (3 - 4,5 hour)  Anticoagulant (sesudah terjadi

 Aspirin thrombus)
 Antiplatelet (sebelum terjadi  ACEI/ARB (untuk hipertensi)
thrombus)

Clinical Differences between UMN and LMN Lesion

LMN UMN

Lesion Infranuclear Supranuclear

Tonus Flaccid Spasctic

Muscle atrophy ++ +/- (disuse)

Reflexes Hyporeflex Hyperreflex

Babinski (-) (+)

Fasciculation (+) (-)

EMG Abnormal Normal

47
 Brain Stem Cranial Nerves and Cerebellum

Neuroanatomy of the Brainstem Including Major Tracts and 12 Cranial

Nerves Which Arise from Brainstem and Cerebellum
CRANIAL NERVE 1 : Olfactory  Special Sensory

Keluar lewat : Cribiform plate of ethmoid bone

Pathway : superior part nasal cavity ada bipolar olfactory cell  mitral and tufted cell
(olfactory bulb)  Olfactory tract  lateral stria > insulae > amygdale, semilunar gyrus,
ambient gyrus (prepyriformis area) > primary olfactory area (broadmann area 28)  medial
striae  subcallosal area (dibawah genu corpus callosum) > opposite hemisphere n limbic
system > olfactory area (broadmann area 28)  medial forebrain bundle > hypothalamus >
brainstem > salivatory nuclei, vagus nerve nuclei (bikin kita ngiler kalo nyium bau makanan
enak)

Lesions:

 peripheral damage (fila olfactoria) karena rhinitis, trauma  anosmia, hyposmia

 central damage (olfactory bulb / tract)  anosmia, hyposmia
 Temporal lobe dysfunction  Kakosmia, hyperosmia

48
CRANIAL NERVE 2 : Optic  Special Sensory
Keluar lewat : Optic canal
Pathway : Retina (photoreceptors, bipolar neuron, ganglion cell) > optic nerve >
setengah dari fiber opticus decussate di optic chiasm > optic tract > superior colliculi > nuclei
in pretectal area > lateral geniculate > optic radiation > visual cortex (medial occipital lobe
broadmann area 17)

Lesions:

 Optic nerve : karena papiledema (kenaikan ICP), vasculitis (temporal arteritis),

retrobulbar lesion (multiple sclerosis)
 Optic chiasm : karena pituit tumor, craniopharyngiona, meningioma

CRANIAL NERVE 3 : Oculomotor  Motor

Lokasi nukleus : Midbrain (se level sama superior colliculi)

Keluar lewat : Superior oblique fissure

49
Lateral nuclear midbrain : superior inferior and medial rectus, inferior oblique, levator
palpebrae
superior branches : Superior rectus (lihat ke atas), levator palpebrae (menaikkan kelopak
mata)
inferior branches : medial rectus (lihat ke hidung), inferior rectus (lihat ke bawah), inferior
oblique

Medial parasympathetic nucleus (edinger-westphal nucleus) midbrain  inferior branches 

intraocular muscle (sphincter papillae muscle and ciliary muscle) = untuk mengecilkan pupil

Reflex CN 2 & 3:
Impuls yang diterima dari retina itu akan akan terbagi 2 di chiasma opticus.
Jadi, saat mata kiri diberi cahaya, impuls akan ditangkap oleh photoreceptor di retina dan
diteruskan lewat optic nerve, di chiasma opticus fiber yg menerima impuls tersebut akan
terbagi 2, satu memberi impuls ke ipsilateral (kiri), satu ke kontralateral (kanan). Selanjutnya
kedua impuls tersebut akan diteruskan ke edinger-westphal nucleus di midbrain, hal ini akan
membuat cilliary muscle berkontraksi = pupil mengecil direct dan indirect.

50
CRANIAL NERVE 4 : Trochlear  Motor

Lokasi nucleus : midbrain (selevel dengan inferior colliculi)

Keluar lewat : Superior orbital fissure

Cranial nerve paling kecil dan cranial nerve satu-satunya yang keluar dari belakang
brainstem baru ke depan.

Fungsi : Superior oblique muscle (mata lihat ke bawah)

CRANIAL NERVE 6 : Abduncens  Motor

Lokasi nucleus : Pons

Keluar lewat : Superior orbital fissure

Fungsi : Lateral rectus muscle (lihat ke lateral)

51
Lesions:

*trochlear: biasa keluhannya susah turun tangga

52
CRANIAL NERVE 5 : Trigerminal  Sensory and Motor
Lokasi nucleus : Pons

 Principal sensory nucleus (touch and discrimination)

 Spinal nucleus (pain and temperature)
 Mesencephali nucleus (proprioception)

Keluar lewat : Superior orbital fissure (V1 = Ophthalmic), Foramen rotundum (V2 =
Maxillary), Foramen ovale (V3 = Mandibular)

Pathway :

 Sensory:
pain  spinal nucleus  thalamus  post central gyrus (ipsilateral)
 Motor:
Pre central gyrus  motor nuclei  masseter, temporalis, pterygoid, anterior belly
digastrics muscle, veli palatine, tensor tympani, mylohyoid muscle (ipsilateral &
sedikit impuls ke contralateral : oleh karena itu tidak langsung kelihatan
weaknessnya jika ada defek, tapi bisa dirasain perbedaan kekuatan kontraksi antara
kiri dan kanan)

Lesions:

 common cause = vascular, MS, tumor, cerebellopontine lesion, herpes zospter

ophthalmicus.
 Peripheral Lesion of motor:
o Flaccid weakness of muscles mastication
o Sensory deficit di area persyarafan trigeminal.
o Saat buka mulut  jaw deviate to side of lesion.
o jaw jerk reflex  absent
o Corneal reflex  ipsilateral and contralateral absent.

53
CRANIAL NERVE 7 : Facial  Sensory and Motor and Special Sensory
Lokasi nucleus : Pontomedullary junction

 Main motor nuclei (Caudal pons) : motor cortex  main motor nuclei 7  otot-otot
upper face terima dari hemisphere kanan kiri, otot-otot lower face dari contralateral
hemisphere
 Superior salivatory nuclei (caudal pons) :  pterygopalatine ganglion  lacrimal
gland  submandibular ganglion  salivary gland
 Gustatory nucleus :  geniculate ganglion  2/3 anterior taste bud

Keluar dari : internal auditory meatus, stylomastoid foramen

Lesions:

 Central : stengah muka bawah kontralateral paralysis  karena stroke

 Peripheral : stengah muka atas dan bawah ipsilateral paralisis  idiopathic,
herpes, stroke brainstem
o Bell’s eye phenomenon: kornea naik ke atas saat pasien mencoba menutup
kelopak mata
o Corneal reflex: ipsilateral absent

54
CRANIAL NERVE 8 : Vestibulocochlear  Special Sensory
Lokasi nucleus : Pontomedullary junction

 Vestibular nerve : sensory dari kanal semisirkularis ; detect gerakan berputar sensory
dari utricle dan sakulus : detect gravitasi dan gerakan lurus.
Sensory dari kanal semisirkularis, utricle dan sakulus akan disampai kan lewat
vestibular nerve ke vestibular nuclei dan akan berakhir pada floculonodular lobe di
cerebellum (untuk mengatur keseimbangan).
 Cochlear nerve : Menerima impuls dari organ corti, spiral ganglion untuk proses
mendengar.
Untuk proses mendengar : cranial nerve 8  ventral posterior nucleus  parietal
cortex

Keluar dari : Internal acoustic meatus

Lesions:

 Ipsilateral deafness
 Tidak seimbang – Jatuh ke arah lesi

CRANIAL NERVE 9 : Glossopharyngeal  Sensory and Motor and Special Sensory

Lokasi nucleus : Medula oblongata

Keluar dari : Jugular foramen pars anterior

Lesions : ipsilateral loss of the gag reflex

CRANIAL NERVE 10 : Vagus  Sensory and Motor

Lokasi nucleus : Medula oblongata

 Nucleus ambiguus
o Rostral portion  glossopharyngeal nerve  stylopharyngeus muscle
o Middle portion  vagus nerve  muscle of the larynx and pharynx
o Caudal portion  intrinsic laryngeal muscle
 Dorsal motor nucleus  viscera of the thorax and abdomen

Keluar dari : Jugular foramen pars anterior

Sensory fibers

 GVA fibers  larynx, pharynx, trachea, esophagus, baroreceptors in the aortic arch,
and the viscera of the abdomen and thorax
 SVA fibers  taste buds around the epiglottis

55
  GSA fibers  posterior part of the external auditory meatus and skin behind the ear

Lesions:

 UNILATERAL:
o bilateral loss of the gag reflex
o Palate weakness: nasal regurgitation food
o Unilateral vocal cord weakness: hoarseness, hypophonia
 BILATERAL:
o paralysis of pharynx n larynx : bisa meninggal karena asfiksia

CRANIAL NERVE 11 : Accessorius  Motor

Lokasi nucleus : Medula oblongata

 Nucleus ambiguus  Cranial root fibers  intrinsic laryngeal muscles through the
recurrent laryngeal
 Spinal accessory nucleus  Spinal root fibers  sternocleidomastoid muscle and
trapezius muscle

Keluar dari : Jugular foramen pars anterior

Lesions:

 Tidak bisa menoleh ke samping, tidak bisa mengangkat bahu

 Winging scapula, Sulit menelan dan berbicara

CRANIAL NERVE 12 : Hypoglossal  Motor

Lokasi nucleus : Medula oblongata

 Hypoglossal nucleus  genioglossus, hypoglossus, and styloglossus muscles.

Keluar dari : Hypoglossal canal

Lesions:

 LMN: unilateran tongue weakness + fasciculation + atrophy + lidah deviasi

ipsilateral dgn lesi saat diminta untuk mengeluarkan lidah
 UMN: unilateran tongue weakness + lidah deviasi kontralateral dgn lesi saat diminta
untuk mengeluarkan lidah

56
Location of Nuclei of Cranial Nerves on Brainstem and Function of Each
12 Cranial Nerves

Cranial Nucleus Function of Nucleus Location

Nerves

Olfactory Anterior Olfactory

Nucleus

Opticus

Oculomotor Oculomotor Nucleus Supplies M. Medial rectus, Most lateral of the

M. Superior rectus, M. third nerve nuclei
Inferior rectus, M. inferior
oblique, M. levator
palpebrae

Trochlear Trochlear nuclei Supply GSE fibers to the Near the midline in
superior oblique muscle the anterior part of
the central gray
matter of the lower
midbrain

Trigeminal Motor (masticatory) Supplies muscle of Lateral pontine

nucleus mastication, tensor tympani, tegmentum just
mylohyoid, anterior belly of medial to main
the digastric muscle, tensor sensory nucleus of
veli palatini the trigeminal

Main sensory Aff : Convey tactile and Lateral to the motor

nucleus pressure sensation from the nucleus
face

Spinal trigeminal Aff : carry input concerning Extending from the

nucleus pain and temperature midpons to the
sensation from the face cervical cord

Mesencephalic Aff : carry proprioceptive Along the lateral

nucleus (this is the input from joints, muscle of border of the central

57
 only nucleus that mastication, extraocular gray in the upper
receives muscle, teeth, periodontium pons and midbrain
proprioceptive inputs Eff : Supply the extraocular
from musle spindles) muscle

Ophthalmic Purely sensory

division

Maxillary Purely sensory

division

Mandibular Motor and sensory

division

Abducens Abducens nucleus Supplies GSE fibers to the Located in the lower
lateral rectus muscle pons, ventral to the
floor of the fourth
ventricle near the
midline

Facial Main motor nucleus Aff : concerned with the Lateral reticular
upper face receive formation of the
corticobulbar fibers from caudal pons, just
both hemispheres above the superior
Eff : motor fibers to the olive
muscles of the facial
expression include :
Platysma
Stapedius
Orbicularis oculi
Orbicularis oris
Occipitalis
Auricular
Frontalis
Zygomaticus
Buccinator
Stylohyoid

58
 Superior salivatory Pterygopalatine ganglion Posterolateral to the
nucleus Supply the lacrimal gland motor nucleus of CN
overlying the eye as well as VII
the palatine and nasal
glands of the mouth and
nose
Submandibular ganglion
Secretory efferents to the
submandibular and
sublingual salivary glands

Gustatory nucleus

Trigeminal main Carries some cutaneous

sensory nucleus sensation from the back of
the ear and the external
auditory meatus

Vestibuloco
chlear

Vestibular Carries sensory input from

nerve the cristae ampullaris of the
semicircular canals and the
maculae of the utricle and
saccule

Cochlear Ventral cochlear Carries afferents for the

nerve nucleus and dorsal special sense of hearing
cochlear nucleus

Glossophar SVE fibers Supply stylopharyngeus Arise from the rostral

yngeal muscle nucleus ambiguus

GVA fibers Supply the baroreceptors in The fibers terminate

the carotid sinus on cells in the caudal
part of the nucleus
solitarius

59
 SVA fibers Carrying taste sensation Terminate in the
from the posterior one-third rostral portion of the
of the tongue travel to the nucleus solitarius
glossopharyngeal nerve

GSA fibers Supplies: Terminate in the

The skin behind the ear
The posterior one-third of
the tongue, eustachian tube
and posterior part of the
upper pharynx
caudal part of the
spinal trigeminal
nucleus

Vagus Main motor nucleus Rostral portion Located in the

(nucleus ambiguus) Sends motor fibers through anterior portion of
the glossopharyngeal nerve the reticular
to supply the formation and
stylopharyngeus muscle extends throughout
Middle portion the medulla
Sends motor fibers through
the vagus nerve to supply
the muscle of the larynx and
pharynx
Caudal portion
Send motors fibers in the
cranial part of the spinal CN
XI that later join the vagus
nerve and supply intrinsic
laryngeal muscle

Dorsal motor Distributed widely to Located anterior to

nucleus postganglionic neurons the floor of the fourth
supplying the viscera of the ventricle and ventral
thorax and abdomen to the sulcus limitans

Sensory fibers GVA fibers

Supply the larynx, pharynx,
trachea, esophagus,

60
 baroreceptors in the aortic
arch, and the viscera of the
abdomen and thorax
SVA fibers
Supply taste buds around
the epiglottis
GSA fibers
Supply the posterior part of
the external auditory meatus
and the skin behind the ear

Accessory

Cranial root Join the vagus nerve, and Originate from the
fibers finally reach the intrinsic caudal nucleus
laryngeal muscles through ambiguus
the recurrent laryngeal
nerve

Spinal root Supply the Originate from cells

fibers sternocleidomastoid muscle in the spinal
and trapezius muscle accessory nucleus

Hypoglossal Hypoglossal nucleus
Supplies GSE fibers to the
genioglossus, hypoglossus,
and styloglossus muscles.
Located near the
midline below the
floor of the fourth
ventricle in the
caudal medulla.

Clinical Findings with Specific Lesions in the Brainstem

No Lesion Information

Medulla

61
A Medial Medullary Syndrome (occlusion of the vertebral artery, anterior spinal artery or one
of their branches)

Corticospinal tract lesions Produce contralateral hemiparesis of the arm,

trunk, and leg (UMN lesions)

Medial lemniscus lesions Produce a contralateral deficit of proprioceptive

and tactile sensation

These lesions involve the body but spare the face

Lesions of the hypoglossal nerve Ipsilateral paralysis of half the tongue that
progresses to muscle atrophy (LMN lesions)

B Lateral Medullary Syndrome (occlusion of the posterior inferior cerebellar artery)

Spinothalamic tract lesions Produce a pain and temperature sensation deficit

to the contralateral body half

Lesions of the vestibular nuclei and Produce nystagmus, diplopia, vertigo, nausea,
pathways and vomiting

Lesions of the glossopharyngeal and Produce ipsilateral dysphagia, horseness, and

vagus nerves diminished or absent gag reflex

Lesions of descending sympathetic Produce an ipsilateral Horner syndrome (miosis,

fibers pseudoptosis, anhidrosis)

Lesions of the spinal tract and nucleus Produce an ipsilateral sensory deficit of half the
of the CN V face

Pain or parasthesia may oocur on the ipsilateral

half of the face as well as loss of cerneal reflex

C Unilateral Medullary Syndrome (due to occlusion of the vertebral artey and produce signs
and symptoms of both the medial and lateral medullary syndrome)

Pons

A Lesions of the basal pons

62
 Corticospinal tract lesions Produce a contralateral hemiparesis of the arm
and leg

Lesions of the abducens nerve Produce an internal strabismus of the ipsilateral

eye

Lesions of the facial nerve Produce an ipsilateral lower motor neuron lesion
that involves the muscle of facial expression

Facial nerve lesions produce Bell palsy, and the

facial muscle are paralyzed

B Lesions of the medial pons (occlusion of a paramedian branch of the basilar artery)

Corticospinal tract lesions Produce a contralateral hemiparesis of the arm

and leg

Corticobulbar tract lesions Produce a contralateral hemiparesis of the

muscles of facial expression that is more severe in
the lower face

Medial lemniscus lesions Produce a contraleral deficit of tactile and

proprioceptive sensation that involves half of the
body

Lesions of the abducens nucleus Produce lateral gaze paralysis in which both eys
are forcefully directed to the side contralateral to
the lesion

C Lesions of the dorsolateral pons (occlusion of the anterior inferior cerebellar artery or
superior cerebellar artery)

Spinothalamic tract lesions Produce a deficit of pain and temperature

sensation involving the contralateral body

Lesions of the vestibular nuclei and Produce nystagmus, vertigo, nausea, and
pathways vomiting

63
 Lesions of the cochlear nucleus or Produce unilateral timnitus and deafness
auditory nerve

Lesions of descending sympathetic Produce an ipsilateral Horner syndrome

fibers

Lesions of the spinal tract and nucleus Produce impaired ipsilateral facial sensation
of CN V

Lesions of the facial nucleus Produce ipsilateral facial paralysis, loss of taste
from the anterior two-third of the tongue, loss of
lacrimatation and salvation, and loss of the
corneal reflex

D Pontcerebellar angle syndrome (due to an acoustic neuroma of CN VIII. This tumor

originates from Schwann cells)

Vestibulocochlear nerve lesions Produce timnitus, hearing loss, unsteadiness, and

loss of balance, vertigo, and loss of normal
vestibular reflexes

Trigeminal nerve lesions Produce facial pain, ipsilateral sensory deficit of

half the face, and loss of the corneal reflex
ipsilaterally

Facial nerve lesions Produce ipsilateral facial weakness (usually late)

Lesions of the inferior and middle Cause failure to produce well-coordinated

cerebellar peduncles voluntary movements predominantly in the
ipsilateral extrimities

E Parimaud syndrome (usually occurs as a result of a pineal tumor. The most common sign is
paralysis of upward gaze, but an impaired downward gaze, papillary abnormalities (slightly
dilated pupil), and signs of elevated ICP)

64
Anatomy and Physiology of the Vestibular Component of Cranial Nerve
VIII, with Emphasis on the Role of the Vestibular System in Eye
Movement and Equilibrium
Canalis semisirkularis ada 3 = superior, horizontal, posterior  untuk jaga keseimbangan saat
berputar utrikle dan sakulus  untuk menjaga keseimbangan saat gerakan lurus
Endolymph = cairan seperti CSF yang membuat bend nya sel-sel rambut (kinosiliom dan stereosilia)

Jika stereosilia bengkok ke arah kinosilium, maka ion channel akan terbuka dan terjadi depolarisasi.
Di bawah ini adalah pathway saat sudah terjadi depolarisasi :
Cranial nerve 8

 vestibular nuclei superior dan lateral  flocculonodular lobe (Cerebellum)

 vestibular nuclei lateral  Medial longitudinal fasculi  CN 3,4,6
 lateral vestibulospinal tract  jaga posture tubuh
 medial vestibulospinal tract  jaga posture cervical n thoracic

Vestibuloocular reflex :
contoh: saat seseorang berputar ke arah kanan,
telinga kanan: endolymph akan bergerak ke arah kiri  menyebabkan stereosilia bend ke arah
kinosilia dan terjadi depolarisasi  impuls di sampaikan lewat nerve vestibularis menuju nucleus
vestibularis  medial longitudinal fasciculus  contralateral nucleus cranial nerve 6 (kiri) 
kontraksi lateral rectus muscle dari mata kiri. Impuls yang sampai di nucleus CN6 juga di sampaikan
ke contralateral oculomotor nuclei (kanan)  kontraksi medial rectus muscle kanan

Telinga kiri: endolymph akan bergerak ke arah kanan  menyebabkan kinosilia bend ke arah
stereosilia dan terjadi hiperpolarisasi  impuls di sampaikan lewat nerve vestibularis menuju
nucleus vestibularis  medial longitudinal fasciculus  contralateral nucleus cranial nerve 6 (kanan)
 relaksasi lateral rectus muscle dari mata kanan. Impuls yang sampai di nucleus CN6 juga di
sampaikan ke contralateral oculomotor nuclei (kiri)  relaksasi medial rectus muscle kiri

*medial longitudinal fasciculus yang menghubungkan vestibular nuclei dengan nuclei 3,4,6
(-) lesi disini = doll’s eye phenomenon

65
Pathophysiology of Vertigo and Disequilibrium
Vertigo adalah sensasi atau perasaan yang mempengaruhi orientasi ruang. Vertigo dideskripsikan
sebagai sensasi berputar.

Vertigo diklasifikasikan menjadi dua kategori berdasarkan saluran vestibular yang mengalami
kerusakan, yaitu

1. Vertigo Periferal

Vertigo periferal terjadi jika terdapat gangguan di saluran yang disebut kanalis semisirkularis, yaitu
telinga bagian tengah yang bertugas mengontrol keseimbangan. Gangguan kesehatan yang
berhubungan dengan vertigo periferal antara lain penyakit seperti benign parozysmal positional
vertigo (gangguan akibat kesalahan pengiriman pesan), penyakit meniere (gangguan keseimbangan
yang sering kali menyebabkan hilang pendengaran), vestibular neuritis (peradangan pada sel-sel
saraf keseimbangan), dan labyrinthitis (radang di bagian dalam pendengaran).

66
2. Vertigo Sentral

Saluran vestibular adalah salah satu organ bagian dalam telinga yang senantiasa mengirimkan
informasi tentang posisi tubuh ke otak untuk menjaga keseimbangan. Vertigo sentral terjadi jika ada
sesuatu yang tidak normal di dalam otak, khususnya di bagian saraf keseimbangan, yaitu daerah
percabangan otak dan serebelum (otak kecil).

Vertigo timbul jika terdapat gangguan alat keseimbangan tubuh yang mengakibatkan
ketidakcocokan antara posisi tubuh (informasi aferen) yang sebenarnya dengan apa yang dipersepsi
oleh susunan saraf pusat (pusat kesadaran). Susunan aferen yang terpenting dalam sistem ini adalah
susunan vestibuler, sistem optic (nerve 3,6) dan pro-prioseptik.

Dalam kondisi fisiologis/normal, informasi yang tiba di pusat integrasi alat keseimbangan tubuh
berasal dari reseptor vestibuler, visual dan proprioseptik kanan dan kiri akan diperbandingkan, jika
semuanya dalam keadaan sinkron dan wajar, akan diproses lebih lanjut. Respons yang muncul
berupa penyesuaian otot-otot mata dan penggerak tubuh dalam keadaan bergerak. Di samping itu
orang menyadari posisi kepala dan tubuhnya terhadap lingkungan sekitar. Jika fungsi alat
keseimbangan tubuh di perifer atau sentral dalam kondisi tidak normal/ tidak fisiologis, atau ada
rangsang gerakan yang aneh atau berlebihan, maka proses pengolahan informasi akan terganggu,
akibatnya muncul gejala vertigo dan gejala otonom. Di samping itu, respons penyesuaian otot
menjadi tidak adekuat sehingga muncul gerakan abnormal yang dapat berupa nistagmus,
unsteadiness, ataksia saat berdiri/ berjalan dan gejala lainnya

Ada beberapa teori yang berusaha menerangkan kejadian ketidakseimbangan tubuh:

1. Teori rangsang berlebihan (overstimulation)

Teori ini berdasarkan asumsi bahwa rangsang yang berlebihan menyebabkan hiperemi kanalis
semisirkularis sehingga fungsinya terganggu; akibatnya akan timbul vertigo, nistagmus, mual dan
muntah.

2. Teori konflik sensorik

Menurut teori ini terjadi ketidakcocokan masukan sensorik yang berasal dari berbagai reseptor
sensorik perifer yaitu antara mata/visus, vestibulum dan proprioseptik, atau
ketidakseimbangan/asimetri masukan sensorik dari sisi kiri dan kanan. Ketidakcocokan tersebut
menimbulkan kebingungan sensorik di sentral sehingga timbul respons yang dapat.

67
Anatomy of Cerebellum and Its Role on Equilibrium and Coordination
The cerebellum is located in the posterior fossa of the skull, dorsal to the pons and medulla from
which it is separated by the Aqueduct of Sylvius and the fourth ventricle.

Like the cerebrum, the cerebellum is covered by cortex and consists of two hemispheres, each of
which is divided into lobes. The hemispheres are separated from one another by a thin structure
called the vermis.

The anterior lobe, or paleocerebellum, is the second oldest part of the cerebellum. It receives
proprioceptive input from the spinal cord and controls the anti-gravity muscles of the body, thus
regulating posture.

The posterior lobe, or neocerebellum, is the newest part of the cerebellum. It is involved in the
coordination of muscle movement via the inhibition of involuntary movement. Inhibitory
neurotransmitters, especially GABA, are found here. This lobe plays an important role in fine motor
coordination.

The flocculonodular lobe consists of the flocculi, the most ancient part of the cerebellum, and the
nodulus, the narrowest and most inferior part of the vermis. This lobe is involved in the
maintenance of equilibrium.

Four different nuclei are located deep within each cerebellar hemisphere; the dentate nucleus, the
emboliform nucleus, the globose nucleus, and the fastigal nucleus. These deep nuclei have axons
that project to the brain stem, sending messages out to be conveyed to other parts of the central
nervous system.

The deep nuclei are regulated by radish-shaped cells located in the cerebellar cortex called Purkinje
cells. The Purkinje cells control the output of the cerebellum by inhibiting the firing of the deep
nuclei. The Purkinje cells located in the lateral cortex of the cerebellum project to the dentate nuclei,
while those in the intermediate cortex synapse with the emboliform and globose nuclei. The fastigial
nuclei receive input from Purkinje cells found in the cerebellar cortical covering of the vermis

68
Role of Myelin on Signal Transmission

bagian yang bermyelin : high K channel density

Nodus ranvier : high Na channel density

Hal ini menyebabkan energy yang dibutuhkan untuk menyalurkan impuls menjadi lebih sedikit, dan
kecepatan impuls yang di sampaikan menjadi lebih cepat dibandingkan dengan neuron yang
unmyelinated.

Nah pada gambar B kita dapat melihat kalau myelinnya rusak, action potential menjadi sulit
mencapai threshold, karena bagian high K channel nya berkurang. Kecepatan penyampaian impuls
menjadi lambat.

Pathophysiology of Acute Demyelinating Process and Late Pathologic

Changes and the Imaging Findings with Acute Demyelination
Four different damage patterns have been identified in patient's brain tissues. The original report
suggests that there may be several types of MS with different immune causes, and that MS may be a
family of several diseases. Though originally was required a biopsy to classify the lesions of a patient,
since 2012 it is possible to classify them by a blood test looking for antibodies against 7 lipids, three
of which are cholesterol derivatives

It is believed that they may correlate with differences in disease type and prognosis, and perhaps
with different responses to treatment. In any case, understanding lesion patterns can provide
information about differences in disease between individuals and enable doctors to make more
accurate treatment decisions

69
According to one of the researchers involved in the original research "Two patterns (I and II) showed
close similarities to T-cell-mediated or T-cell plus antibody-mediated autoimmune
encephalomyelitis, respectively. The other patterns (III and IV) were highly suggestive of a primary
oligodendrocyte dystrophy, reminiscent of virus- or toxin-induced demyelination rather than
autoimmunity."

The four identified patterns are:

Pattern I

The scar presents T-cells and macrophages around blood vessels, with preservation of
oligodendrocytes, but no signs of complement system activation.

Pattern II

The scar presents T-cells and macrophages around blood vessels, with preservation of
oligodendrocytes, as before, but also signs of complement system activation can be found. This
pattern has been considered similar to damage seen in NMO, though AQP4 damage does not appear
in pattern II MS lesions Nevertheless, pattern II has been reported to respond to plasmapheresis,
which points to something pathogenic into the blood serum.

The complement system infiltration in these cases convert this pattern into a candidate for research
into autoimmune connections like anti-Kir4.1, anti-Anoctamin-2 or anti-MOG mediated MS About
the last possibility, research has found antiMOG antibodies in some pattern-II MS patients.

Pattern II pathogenic T cells have already been cloned and prepared for further studies. The
functional characterization shows that T cells releasing Th2 cytokines and helping B cells dominate
the T-cell infiltrate in pattern II brain lesions.

Pattern III

The scars are diffuse with inflammation, distal oligodendrogliopathy and microglial activation. There
is also loss of myelin-associated glycoprotein (MAG). The scars do not surround the blood vessels,
and in fact, a rim of preserved myelin appears around the vessels. There is evidence of partial
remyelinization and oligodendrocyte apoptosis. For some researchers this pattern is an early stage
of the evolution of the others. For others, it represents ischaemia-like injury with a remarkable
availability of a specific biomarker in CSF

Pattern IV

70
The scar presents sharp borders and oligodendrocyte degeneration, with a rim of normal appearing
white matter. There is a lack of oligodendrocytes in the center of the scar. There is no complement
activation or MAG loss.

These differences are noticeable only in early lesions and the heterogeneity was controversial during
some time because some research groups thought that these four patterns could be consequence of
the age of the lesions. Nevertheless, after some debate among research groups, the four patterns
model is accepted and the exceptional case found by Prineas has been classified as NMO

For some investigation teams this means that MS is a heterogeneous disease. Currently antibodies
to lipids and peptides in sera, detected by microarrays, can be used as markers of the pathological
subtype given by brain biopsy.

Other developments in this area is the finding that some lesions present mitochondrial defects that
could distinguish types of lesions

The Diagnostic Criteria for Diagnosis of Multiple Sclerosis

Action for Management and Prevention of Multiple Sclerosis

Treatments for MS attacks

71
 • Corticosteroids, such as oral prednisone and intravenous methylprednisolone, are
prescribed to reduce nerve inflammation. Side effects may include insomnia, increased
blood pressure, mood swings and fluid retention.

 Plasma exchange (plasmapheresis). The liquid portion of part of your blood (plasma) is
removed and separated from your blood cells. The blood cells are then mixed with a protein
solution (albumin) and put back into your body. Plasma exchange may be used if your
symptoms are new, severe and haven't responded to steroids.

Treatment options for relapsing-remitting MS include:

• Beta interferons. These medications are among the most commonly prescribed medications
to treat MS. They are injected under the skin or into muscle and can reduce the frequency
and severity of relapses.
Side effects of beta interferons may include flu-like symptoms and
injection-site reactions.
 Liver damage is a possible side effect of interferon use. People
taking interferons may develop neutralizing antibodies that can reduce drug effectiveness.

• Glatiramer acetate (Copaxone). This medication may help block your immune system's
attack on myelin and must be injected beneath the skin. Side effects may include skin
irritation at the injection site.

• Dimethyl fumarate (Tecfidera). This twice-daily oral medication can reduce relapses. Side
effects may include flushing, diarrhea, nausea and lowered white blood cell count.

• Fingolimod (Gilenya). This once-daily oral medication reduces relapse rate.
You'll need to
have your heart rate monitored for six hours after the first dose because your heartbeat may
be slowed. Other side effects include headache, high blood pressure and blurred vision.

• Teriflunomide (Aubagio). This once-daily medication can reduce relapse rate. Teriflunomide
can cause liver damage, hair loss and other side effects. It is harmful to a developing fetus
and should not be used by women who may become pregnant and are not using appropriate
contraception, or their male partner.

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 Spinal Cord and Peripheral Nerves

Anatomy of the Vertebral Column and Spinal Cord (External Anatomy)

73
74
The 31 Pairs of Spinal Nerves from Spinal Cord as Components of PNS

75
Internal Anatomy of the Spinal Cord with Emphasis on the Clinically
Relevant Regions of Grey Matter and the Major Ascending and
Descending White Matter Tracts

76
Blood Supply to the Spinal Cord

Spinal Cord menerima supply dari : 2 posterior spinal arteries dan anterior spinal artery.

 Posterior Spinal Arteries

Direct dari vertebral arteries inside the skull or Indirectyl dari posterior inferior
cerebellar arteries.
Supply 1/3 posterior spinal cord
Pada regio upper thoracic posterior spinal arteries ini kecil, tiga pertama thoracic
segment dari spinal cord ini mudah terjadi ischemia pada segmental/ radicular
arteries.
 Anterior Spinal Artery
Terbentuk dari bersatunya 2 arteri yang berasal dari vertebral artery.
Anterior spinal artery turun pada anterior surface dari spinal cord lewat anterior
median fissure.
Cabang”nya masuk ke sunbstance of the cord dan mensuplai 2/3 anterior spinal
cord.

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 Pada segmen upper dan lower thoracic, anterior spinal artery ini bisa sangat kecil,
sehingga artery segmental/ radicular artery gampang tersumbat didaerah 4ththoracic
dan 1st lumbar.
 Segemental Spinal Arteries
Dari cabang arteri diluar vertebral column (deep cervical, intercostal, lumbar) masuk
melalui intervertebral foramina menuju vertebral canal.

Setelah masuk ke vertebral canal menjadi anterior dan posterior radicular arteries yang
menemani anterior dan psterior nerve roots ke spinal cord.

Clinical Findings related to Disruptions in the Ascending and Descending

Pathways
 Ascending

 Descending

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Possible Sign caused by Disturbances in UMN Circuit and Disturbances
in LMN Circuit
UMN LMN
Tipe Spastic Flacid
Reflex Hyperreflex Hyporeflex
Muscle Tone Hypertonus Hypotonus
Muscle Mass Disuse Athropy Wasting Athropy
Fasikulasi - +
Babinski + -
sign

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Function of the Major Excitatory and Inhibitory Neurotransmitters
Involved in Spinal Cord Function (Glutamate, Lysine, GABA) and their
Role in Normal Spinal Reflexes and the Maintenance of Muscle Tone.
The Changes that Underlie Spasticity in UMN Lesions

 Glutamate is used at the great majority of fast excitatory synapses in the brain and spinal
cord. It is also used at most synapses that are "modifiable", i.e. capable of increasing or
decreasing in strength. Modifiable synapses are thought to be the main memory-storage
elements in the brain. Excessive glutamate release can overstimulate the brain and lead
to excitotoxicity causing cell death resulting in seizures or strokes. Excitotoxicity has been
implicated in certain chronic diseases including ischemic stroke, epilepsy, Amyotrophic
lateral sclerosis, Alzheimer's disease, Huntington disease, and Parkinson's disease.

 GABA is used at the great majority of fast inhibitory synapses in virtually every part of the
brain. Many sedative/tranquilizing drugs act by enhancing the effects of GABA.
Correspondingly, glycine is the inhibitory transmitter in the spinal cord.

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81
Anatomy and Physiology of Acute Pain

Transduction  transmission  perception  modulation

 Transduction

Transduction begins when the free nerve endings (nociceptors) of C fibres and A-delta
fibres of primary afferent neurones respond to noxious stimuli. Three categories of
noxious stimuli:
 mechanical (pressure, swelling, abscess, incision, tumour growth);
 thermal (burn, scald);
 chemical (excitatory neurotransmitter, toxic substance, ischaemia, infection).

This noxious stimulation causes a release of chemical mediators from the damaged
cells including:
 prostaglandin;
 bradykinin;
 serotonin;
 substance P;
 potassium;
 histamine.

These chemical mediators activate and/or sensitise the nociceptors to the noxious
stimuli. In order for a pain impulse to be generated, an exchange of sodium and
potassium ions (de-polarisation and re-polarisation) occurs at the cell membranes. This
results in an action potential and generation of a pain impulse.

 Transmission

The transmission process occurs in three stages. The pain impulse is transmitted:
 from the site of transduction along the nociceptor fibres to the dorsal horn in the
spinal cord;

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  from the spinal cord to the brain stem;
 through connections between the thalamus, cortex and higher levels of the brain.

The pain impulse is then transmitted from the spinal cord to the brain stem and
thalamus via two main nociceptive ascending pathways. These are the spinothalamic
pathway and the spinoparabrachial pathway.

The brain does not have a discrete pain centre, so when impulses arrive in the thalamus
they are directed to multiple areas in the brain where they are processed.

 Perception

The multidimensional experience of pain has affective-motivational, sensory-

discriminative, emotional and behavioural components. When the painful stimuli are
transmitted to the brain stem and thalamus, multiple cortical areas are activated and
responses are elicited.

These areas are:

 The reticular system: This is responsible for the autonomic and motor response to
pain and for warning the individual to do something, for example, automatically
removing a hand when it touches a hot saucepan. It also has a role in the affective-
motivational response to pain such as looking at and assessing the injury to the
hand once it has been removed form the hot saucepan.
 Somatosensory cortex: This is involved with the perception and interpretation of
sensations. It identifies the intensity, type and location of the pain sensation and
relates the sensation to past experiences, memory and cognitive activities. It
identifies the nature of the stimulus before it triggers a response, for example,
where the pain is, how strong it is and what it feels like.
 Limbic system: This is responsible for the emotional and behavioural responses to
pain for example, attention, mood, and motivation, and also with processing pain
and past experiences of pain.

 Modulating

The modulation of pain involves changing or inhibiting transmission of pain impulses in

the spinal cord. The multiple, complex pathways involved in the modulation of pain are
referred to as the descending modulatory pain pathways (DMPP) and these can lead to
either an increase in the transmission of pain impulses (excitatory) or a decrease in
transmission (inhibition).

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 Descending inhibition involves the release of inhibitory neurotransmitters that block or
partially block the transmission of pain impulses, and therefore produce analgesia

Pharmacology of the Major Analgesic Drugs used in Acute Pain

(Acetaminophen, Acetylsalicyclic Acid, NSAIDs and Opioids) and
Chronic Pain
Medical management of pain (WHO Ladder):

1. Mild pain  NSAID + adjuvant

2. Moderate pain  weak narcotic + NSAID + adjuvant
3. Severe pain  strong narcotic + NSAID + adjuvant
4. Regional analgesia

Drugs intervention for pain

 Non-narcotics: simple analgetic (paracetamol/NSAIDs)

 Narcotics
 Adjuvant analgesic or coanalgesics
o Tricyclic antidepressants (amitriptyline, imipramine, clomipramine, doxepin,
nortriptyline, desipramine)
o Antiepileptics (gabapentin, pregabalin, valproate)
o Alpha-2-agonist (clonidine)
o Corticosteroids
o Bisphosphonates (osteoporotic pain)

Acetaminophen is the active metabolite of phenacetin and is responsible for its analgesic
effect. It is a weak COX-1 and COX-2 inhibitor in peripheral tissues and possesses no
significant anti-inflammatory effects.
It is administered orally for treating acute pain and fever given 325 – 500 mg 4 times daily
and proportionately less for children. Dosing in adults now recommended not to exceed 4
g/d, in most cases to prevent hepatic damage (early signs: nausea, vomiting, diarrhea, and
abdominal pain).
The drugs is useful in mild to moderate pain such as headache, myalgia, postpartum pain,
and other circumstances in which aspirin is an effective analgesic.

Acetylsalicylic acid (aspirin) is now rarely used as an anti-inflammatory medication and

will be reviewed only in terms of its antiplatelet effects (ie, doses of 81 – 325 mg once daily).
Mechanism of action: irreversibly inhibits platelet COX so that aspirin’s antiplatelet effect
lasts 8 – 10 days. In other tissue, synthesis of new COX replaces the inactivated enzyme so

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that ordinary doses have a duration of action 6 – 12 hours. Its clinical uses are TIA, UA,
coronary artery thrombosis with MI, and thrombosis after CABG.

NSAIDs anti-inflammatory activity is mediated chiefly through inhibition of prostaglandin

biosynthesis. Non-selective COX inhibitors increase the risk of GI bleeding, in the other hand
selective COX-2 inhibitor increase the incidence of edema, hypertension, and possibly
myocardial infarction. Nephrotoxicity and hepatotoxicity can occur with any NSAIDs. Types
of NSAIDs drugs: [1] proprionic acid derivative (ibuprofen), [2] pyrrolealkanoic acid derivatice
(tolmetin), [3] phenylalkanoic acid derivative (flubiprofen), [4] indole derivative
(indomethacin), [5] pyrazolone derivative (phenylbutazone), [6] phenylacetic acid derivative
(diclofenac), [7] fenamate (meclofenamic acid), [8] oxicam (piroxicam), [9] naphtylacetic acid
prodrug (nabumetone).

Selective COX-2 inhibitors:

 Celecoxib
 Meloxicam

Nonselective COX inhibitors:

 Diclofenac
 Ibuprofen
 Flurbiprofen
 Indomethacin
 Ketoprofen
 Nabumetone
 Naproxen
 Oxaprozin
 Piroxicam
 Sulindac
 Tolmetin

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Opioids is usually use to relieve severe, constant pain, whereas sharp, intermittent pain
does not appear to be as effectively controlled.
Contraindications:

1. Use of pure agonists with weak partial agonists

2. Use in patients with head injuries
3. Use during pregnancy
4. Use in patients with impaired pulmonary function
5. Use in patients with impaired hepatic or renal function
6. Use in patients with endocrine disease (addison’s disease / adrenal insufficiency and
hypothyroidism / myxedema)

Strong agonists:

 Phenanthrenes: morphine, hydromorphone, and oxymorphone useful in treating

severe pain. Heroin is potent and fast-acting, but there has been considerable
agitation to revive its use.
 Phenylheptylamines: methadone, a potent and clinically useful analgesics. It can
also block both NMDA receptors and monoaminergic reuptake transporters. These
non-opioid receptor properties may help explain its ability to relieve difficult-to-treat
pain (neuropathic, cancer pain), especially when a previous trial of morphine has
failed.
 Phenylpiperidines: fentanyl (synthetic opioids) subgroup now includes sufentanil,
alfentanil, and remifentanil.
 Morphinans: levorphanol synthetic opioid analgesic closely resembling morphine,
serotonin-norepinephrine reuptake inhibition (SNRI), and NMDA receptor antagonist
properties.

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Mild to Moderate Agonists:

 Phenanthrenes: codeine, dihydrocodeine, and hydrocodone lower binding affinity

and adverse effects that limit the maximum tolerated dose. Oxycodone is more
potent and is prescribed alone in higher doses as immediate-release or controlled-
release forms for the treatment of moderate to severe pain.
 Phenylheptylamines: propoxyphene  increasing incidence of deaths and is
ineffective  withdrawn
 Phenylpiperidines: diphenoxylate and its metabolite difenoxin not used for
analgesia but for the treatment of diarrhea. Loperamide is a phenylpiperidine
derivative used to control diarrhea.

Opioids with mixed receptor actions:

 Phenanthrenes: buprenorphine is a potent and long acting phenanthrene derivative

that is a partial µ-receptor agonist and an antagonist at the δ and κ receptors.
Buprenorphine is used as analgesic and also management of opioid dependence
and it is as effective as methadone for the management of opioid withdrawal and
detoxification in programs that include counselling, psychosocial support, and
direction by physicians qualified under the Drug Addiction Treatment Act.
Pentazocine and nalbuphine, nalbuphine is a strong κ-receptor agonist and a
partial µ-receptor antagonist.
 Morphinans: butorphanol produces analgesia equivalent to nalbuphine but produce
more sedation at equianalgesic doses.
 Benzomorphans: pentazocine subcutaneous injection is not recommended due to its
irritant properties.

Miscellaneous:

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 Tramadol: a centrally acting analgesic whose mechanism of action is predominantly
based on blockade of serotonin reuptake and has also been found to inhibit
norepinephrine transporter function. Recommended dosage is 50 – 100 mg orally 4
times daily.
 Tapentadol: analgesic with modest µ-opioid receptor affinity and significant
norepinephrine reuptake-inhibiting action.
 Both tramadol and tapentadol is contraindicated in patients with risk of seizure, and
development of serotonin syndrome.

Receptor Subtypes Location Function

delta (δ) δ1, δ2  Brain • analgesia

• Pontine nuclei • Antidepressant

effects
• amygdala
• physical dependence
• olfactory bulbs

• deep cortex

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 kappa κ1, κ2, κ3  Brain • Spinal analgesia
(κ)
• hypothalamus • Sedation

• periaqueductal • Miosis
gray
• Inhibition of ADH
• claustrum release

 spinal cord

• substantia
gelatinosa

mu (μ) μ1, μ2, μ3  brain μ1:

• Cortex  Supraspinal
(laminae III and analgesia
IV)
 physical dependence
• Thalamus
μ2:
• periaqueductal
 respiratory
gray
depression
 spinal cord
 miosis
• substantia
 euphoria
gelatinosa
 reduced GI motility

 physical dependence

Pathophysiological Basis of the Physical Findings Seen in Spinal Cord

Disorders
Central spastic paresis:

Lesion in corticospinal:

Acute phase: deep tendon reflex hypoactive and flaccid muscle weakness

Few days later reflex return hyperactive  muscle spindle responds more sensitively to
stretch than normal (particularly: upper limb and lower limb extensor)

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Hypersensitivity due  loss of descending control inhibitory control of fusimotor cells (ϒ
motor neuron) pada muscle spindle  intrafusal muscle  permanent activated
(prestretched) and respond more readily than normal to further stretching of the muscle

A disturbance of ‘regulating circuit for muscle length’ probably occur  short target length

 Spastic increased tone

 Hyperreflexia
 Pyramidal tract signs (spastic paraparesis) Babinski
 Clonus

Weakness = pyramidal

Movement disorder = extrapyramidal

Spinal cord disorders:

 Syndrome of the dorsal root ganglion

 Posterior root syndrome
 Posterior column syndrome
 Posterior horn syndrome
 Gray matter syndrome
 Syndrome of combined lesions of the posterior columns and corticospinal tracts
(funicular myelosis)
 Anterior horn syndrome
 Combined anterior horn and pyramidal tract syndrome
 Syndrome of the corticospinal tracts
 Syndrome of combined involvement of the posterior columns, spinocerebellar tracts,
and (possibly) pyramidal tracts
 Spinal cord hemisection syndrome (brown-sequard syndrome)

*see spinal cord lesions and its corresponding clinical manifestations for more info*

Autonomic Nervous System

The autonomic nervous system (ANS) regulates physiologic processes. Regulation occurs
without conscious control. The 2 major divisions:

 Sympathetic system
 Parasympathetic system

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The sympathetic and parasympathetic systems each consist of 2 sets of nerve bodies: one
set (called preganglionic) in the CNS, with connections to another set in ganglia outside the
CNS. Efferent fibers from the ganglia (postganglionic fibers) lead to effector organs.

Sympathetic nervous system

 Promotes a fight-or-flight response, corresponds with arousal and energy generation,

and inhibits digestion
 Diverts blood flow away from the gastro-intestinal (GI) tract and skin via vasoconstriction
 Blood flow to skeletal muscles and the lungs is enhanced (by as much as 1200% in the
case of skeletal muscles)
 Dilates bronchioles of the lung through circulating epinephrine, which allows for greater
alveolar oxygen exchange
 Increases heart rate and the contractility of cardiac cells (myocytes), thereby providing a
mechanism for enhanced blood flow to skeletal muscles
 Dilates pupils and relaxes the ciliary muscle to the lens, allowing more light to enter the
eye and far vision
 Provides vasodilation for the coronary vessels of the heart
 Constricts all the intestinal sphincters and the urinary sphincter
 Inhibits peristalsis
 Stimulates orgasm

Parasympathetic nervous system

 The parasympathetic nervous system has been said to promote a "rest and digest"
response, promotes calming of the nerves return to regular function, and enhancing
digestion. Functions of nerves within the parasympathetic nervous system include
 Dilating blood vessels leading to the GI tract, increasing blood flow (this is important
following the consumption of food, due to the greater metabolic demands placed on the
body by the gut)
 Constricting the bronchiolar diameter when the need for oxygen has diminished
 Dedicated cardiac branches of the vagus and thoracic spinal accessory nerves impart
parasympathetic control of the heart (myocardium)
 Constriction of the pupil and contraction of the ciliary muscles,
facilitating accommodation and allowing for closer vision
 Stimulating salivary gland secretion, and accelerates peristalsis, mediating digestion of
food and, indirectly, the absorption of nutrients

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 Sexual. Nerves of the peripheral nervous system are involved in the erection of genital
tissues via the pelvic splanchnic nerves 2–4. They are also responsible for stimulating
sexual arousal

Two major neurotransmitters in the ANS are

 Acetylcholine: Fibers that secrete acetylcholine (cholinergic fibers) include all

preganglionic fibers, all postganglionic parasympathetic fibers, and some postganglionic
sympathetic fibers (those that innervate piloerectors, sweat glands, and blood vessels).

 Norepinephrine : Fibers that secrete norepinephrine (adrenergic fibers) include most

postganglionic sympathetic fibers. Sweat glands on the palms and soles also respond to
adrenergic stimulation to some degree.

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93
 Aging of the Brain, Dementia, and Sleep

Role of the Limbic System and Temporal Lobe Structures in Memory,

and their Relationships with Cortical Association Areas
a. Limbic System: Anatomically, the limbic structures include the subcallosal, the
cingulate, and the parahippocampal gyri, the hippocampal formation, the amygdaloid
nucleus, the mammillary bodies, and the anterior thalamic nucleus (Fig.9-3).The
alveus, the fimbria, the fornix, the mammillothalamic tract, and the stria terminalis
constitute the connecting pathways of this system.

b. Temporal Lobe: The hippocampus, the elongated, medial portion of the temporal
lobe that is part of the limbic system plays a vital role in short-term memory involving
the integration of various related stimuli. It is a prominent site where LTP takes place
and is also crucial for consolidation into long-term memory. The hippocampus is
believed to store new long-term memories only temporarily and then transfer them to
other cortical sites for more permanent storage. The hippocampus and surrounding
regions play an important role in declarative memories—the “what” memories of

94
 specific people, places, objects, facts, and events that often result after one
experience and that can be declared or verbalized in a statement such as “I saw the
Statue of Liberty last summer” or conjured up in a mental image. Declarative
memories involve conscious recall. This memory type is sometimes subdivided into
semantic memories (memories of facts) and episodic memories (memories of
events in our lives).

Neuropsychological Changes with Functional Localization of Specific

Regions of the Cortex that are Involved in Learning and Memory
Learning is the acquisition of knowledge or skills as a consequence of experience, instruction,
or both. Memory is the storage of acquired knowledge for later recall. Learning and memory
form the basis by which individuals adapt their behavior to their particular external
circumstances. Without these mechanisms, it would be impossible for individuals to plan
successful interactions and intentionally avoid predictably disagreeable circumstances.
Habituation is a decreased responsiveness to repetitive presentations of an indiferent
stimulus—that is, one that is neither rewarding nor punishing. Sensitization is increased
responsiveness to mild stimuli following a strong or noxious stimulus. The snail becomes
habituated when its siphon is repeatedly touched; it learns to ignore the stimulus and no longer
withdraws its gill in response. Sensitization, a more complex form of learning, takes place in
Aplysia when it is given a hard bang on the siphon. Subsequently, the snail withdraws its gill
more vigorously in response to even mild touch. Habituation depresses this synaptic activity,
whereas sensitization enhances it.

95
96
The prefrontal association cortex are major orchestrator of the complex reasoning skills
associated with working memory. The prefrontal cortex serves as a temporary storage site
for holding relevant data and is largely responsible for executive functions involving
manipulation and integration of this information for planning, juggling competing priorities,
problem solving, and organizing activities. The prefrontal cortex carries out these complex
reasoning functions in cooperation with all the brain’s sensory regions.

Ingatan dari hippocampus

berupa shortterm memory
mengalami konsolidasi pada
temporal,
parietal association area
(ingatan sensory), temporal
association area ( ingatan
pendengaran), occipital
association area (ingatan
penglihatan), dan prefrontal
cortex dan menjadi longterm
memory

The cerebellum and relevant cortical regions play an essential role in the “how to” procedural
memories involving motor skills gained through repetitive training, such as memorizing a
particular dance routine. Procedural memories can be brought forth without conscious effort.
For example, an ice skater during a competition typically performs best by “letting the body
take over” the routine instead of thinking about exactly what needs to be done next.

97
Anatomical Correlates to Cognitive Capacities

Changes in Behaviour Associated with Dementias and those of Normal

Aging

Impairment in memory and decline in one of the following

 Ability to generate speech or understand written/spoken 
language 


98
  Ability to recognize objects 


 Ability to execute motor functions

 Ability to make judgments, plan and carry

out tasks

 Deficits cause significant impairment in

social or occupational functioning 


Cognitive Symptoms

1. Changes in memory:

a. Unable to recall day/ date/ names/ faces

b. Repeating questions/ conversations

c. Getting lost

d. Losing things

2. Changes in perception:

a. Unable to recognise objects

b. Unable to judge position / location of people / objects

c. Ignoring one side of the world (including oneself, environment)

3. Changes in executive functioning:

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 a. Difficulties with initiating task

b. Getting stuck on task / repeating actions

c. Not thinking through the consequences of actions

4. Changes in language:

a. Difficulties understanding

b. Difficulties finding word

c. Reduce vocabulary

Initial Dementia Assessment

Examination

 Physical Exam – hearing, vision, blood pressure

 Neurological Exam

 FAQ (Functional Activities Questionnaire) /IADL Instruments of Activity Daily

Living

 MMSE / Clock Drawing Test / MoCa

 Depression Asessment

Laboratory Tests

 CBC

 Glucose

 Electolytes

 Ureum, creatinin

 TSH

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Therapeutic “Diagnostic Test”

 Remove possible offending medication

 Treat depression

Common Etiologies, Pathophysiologies and Genetics of Dementia

Common cause of dementia are Alzheimer disease, vascular dementia, frontotemporal
dementia, Lewy body disease, and Parkinson disease.

1. Alzheimer disease (most common cause, affecting 60% - 70% cases)

 A progressive, degenerating disorder, which affects 15% individuals age > 65 years, and
45% individuals age > 85 years

 Pathology:

- Neuritic (senile) plaques: extracellular deposits that contain β-amyloid (Aβ) and
other proteins

- and Neurofibrillary tangles: intracellular deposits containing

hyperphosphorylated tau

 Pathogenesis:

- Genetics: in 1% of patients, results from mutation either in β-amyloid precursor

protein (APP), presenilin 1 (PS1), or presenilin 2 (PS2), onset between ages
of 30 and 60 years.

- Aβ and neuritic plaques: are deposited in cerebral and meningeal blood

vessels.

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 - Tau and neurofibrillary tangles: may involve a defect in axonal transport.

- Synaptic dysfunction: early dysfunction and later loss of synapses, prominently

affecting excitatory transmission in hippocampus and cerebral cortex.

- Neuronal loss and brain atrophy; including glutamatergic neuron in entohirnal

cortex, CA1 sector of hippocampus, cholinergic neurons in basal forebrain.

- Vascular involvement: involvement of blood vessels in amyloid pathology.

2. Vascular dementia

 Clinical findings: history of hypertension, abrupt onset of dementia, focal neurologic

symptoms or signs, pseudobulbar palsy with dysarthria, dysphagia, and pseudobulbar affect;
ataxia; gait apraxia

3. Frontotemporal dementia

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 Produces frontal and temporal lobe degeneration

 Atrophy of frontal and temporal lobes, tau inclusions

4. Lewy body disease

 Either parkinson disease with dementia or dementia with lewy bodies

 Characterized histopathologically by round, eosinophilic, intracytoplasmic neuronal

inclusions in the brainstem and cerebral cortex.

 Causes cognitive decline without prominent early memory impairment

Neuropathological and Neurotransmitter Changes Found in Alzheimer

Disease

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Most Common Differential Diagnosis for Patients with Cognitive
Impairment and Acute Confusional States and Factors Which Support
the Diagnosis

104
Changes of Sleep Pattern in Normal Aging, and in Dementing Disorders
and How Environmental Factors Influence the Sleep-Wake Cycle
Sleep-wake cycle normalnya di pengaruhi oleh:

105
Tambahan:

- adenosine  block Ach  sleep

- suasana gelap di tangkap oleh retina – suprachiasma opticus hypothalamus –

pineal gland sekresi melatonin  sleep

Environmental factors:

 Coffee : adenosine receptor antagonist  wake

 Terang : produksi melatonin berkurang  wake

 Anti histamine (diphenhydramine)  sleep

 Benzodiazepine, vigabatrin (obat-obat yang memperbanyak gaba)  sleep

Common Etiologies and Pathophysiologies of Insomnia and Other Sleep

Disorders
Primary sleep disorders may be divided into the following 2 broad categories:

• Parasomnias – These are unusual experiences or behaviors that occur during sleep;
they include sleep terror disorder and sleepwalking (which occur during stage 4
sleep) and nightmare disorder (which occurs during rapid eye movement [REM]
sleep).

• Dyssomnias – These are characterized by abnormalities in the amount, quality, or

timing of sleep; they include primary insomnia and hypersomnia, narcolepsy,
breathing-related sleep disorder (ie, sleep apnea), and circadian rhythm sleep
disorder

The suprachiasmatic nucleus, located in the hypothalamus, is thought to be the body’s

anatomic timekeeper, responsible for the release of melatonin on a 25-hour cycle. The

106
pineal gland secretes less melatonin when exposed to bright light; therefore, the level of this
chemical is lowest during the daytime hours of wakefulness.

Multiple neurotransmitters are thought to play a role in sleep. These include serotonin from
the dorsal raphe nucleus, norepinephrine contained in neurons with cell bodies in the locus
ceruleus, and acetylcholine from the pontine reticular formation. Dopamine, on the other
hand, is associated with wakefulness.

 Abnormalities in the delicate balance of all of these chemical messenger systems may
disrupt various physiologic, biologic, behavioral, and EEG parameters responsible for REM
(ie, active) sleep and NREM (slow-wave) sleep.

Pharmacological and Non-Pharmacological Management Available for

Alzheimer’s Dementia
a. Treat memory loss, gangguan berpikir, judgement, dll :

 early-moderate stage: Cholinesterase inhibitor  inhibit breakdown Ach

(Donepezil, Rivastigmine, galantamine)
(-) sideeffect: nausea, vomit, loss of appetite

 moderate-severe stage: memantine / memantine+donepezil.

(-) confusion, constipation, headache

b. Treat behavior change: (beri sesuai kebutuhan)

 Antidepressant (citolopram, fluoxetine, paroxeine, sertraline, trazodone)

 Anxiolytic (lorazepam, oxazepam)

 Antipsychotic (haloperidol, olanzapine, quetiapine, risperidone, ziprasidone)

c. Treat sleep changes (pakai jika nonpharmacological tidak bisa bikin tdur)

 Tricyclic antidepressant (nortriptyline, trazodone)

 Benzodiazepine (Lorazepam, oxazepam, temazepam)

 Sleeping pills (zolpidem, zaleplon, chloral hydrate)

 Atypical antipsikotik (Risperidone, olanzapine, quetiapine)

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Nonpharmacological

a. Sleep hygiene (tidak tidur siang, membuat environment tidur yang nyaman, mandi air
hangat sebelum tidur, olahraga pada sianghari, NO minum kopi / alkohol, jangan
terlalu kenyang maupun terlalu lapar, dll)

b. Exercise

The Pharmacology of Sedative/Hypnotic Drugs and How Aging

Influences their CNS Effects
a. Benzodiazepine  bekerja sebagai GABA agonist = memperbanyak Cl- masuk
ke dalam sel agar terjadi hiperpolarisasi.  muscle relaxation,

 anticonvulsive (diazepam, lorazepam, clonazepam, clorazepate) ,

 anxiolytic (oxazepam, clorazepate),

 antipanic (alprazolam),

 sedative-hypnotic (untuk treat insomnia = triazolam, temazepam,

flurazepam).

(-) side effect: drowsiness, ataxia, confusion, withdrawal, tolerance

b. Barbitures  depress neuronal activity (dia ini GABA agonist yang lebih kuat)

 Anticonvulsive (Phenobarbital)

 General anesthesis (Thiobarbital, methohexital)

 Mephobarbital, Pentobarbital, Secobarbital

(-) sedation, confusion, ataxia, respi depression, coma, death, tolerance,
withdrawal: anxiety, tremor, nausea, vomit, hypotension, convulsion,

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 cardiovasc collapse, rash, angioedema, dermatitis.  karena banyaknya efek
samping, jadi barbiture jarang digunakan. Biasa yang di pakai benzo

c. Other sedative-hypnotic drugs

 Buspirone  serotonin partial agonist, dopamine agonist = anxiolytic, tidur

(-) dizziness

 Zolpidem tartrate  GABA agonist lemah = untuk short term treatment

insomnia, minimal anxiolytic,minimal anticonvulsant, minimal muscle relaxant.

 Meprobamate = sedative-hypnotic drug tua (sebelum ditemukan

benzodiazepine)
(-) ataxia, hypotension, rash, NO untuk hamil

 Chloral hydrate  induce sleep in about 30minutes.

(-) epigastric distress, nausea, vomit, tolerance, addiction.

 Glutethimide  CNS depression (mirip barbiture)

(-) ataxia, sedation, epigastric pain, rash, mydriasis, constipation, xerostomia

Role of Community and Social Resources for Dementing Patients and

Caregivers

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 Psychosis

Anatomy and function of hypothalamus

Function

 Controls the release of 8 major hormones by the hypophysis, and is involved in

 Temperature regulation

 Control of food and water intake

 Sexual behavior and reproduction

 Control of daily cycles in physiological state and behavior

 Mediation of emotional responses

Mental illness and social effect of mental illness

Mental illness: A mental illness is a health problem that significantly affects how a person
feels, thinks, behaves, and interacts with other people.

Mental illness is brain dysfunction, affecting:

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a. Perception – People may experience the world with their senses (vision, smell, taste,
touch, hearing) in unusual and/or strange ways (e.g., hearing voices, seeing things that
others do not see).

b. Thinking – Thoughts may occur very quickly/slowly, may be poorly organized, confusing,
illogical, irrational, etc.

c. Mood – All human beings experience a variety of moods (e.g., depression, anxiety, mania)
and mood changes. Mental illness can emerge when symptoms cause significant distress
over time and impair one’s ability to function in daily life.

d. Behavior – People’s behavior may be quite bizarre and confusing for those who do not
understand mental illness (e.g., someone with PTSD hiding in the closet when he/she hears
helicopters; an individual with obsessive-compulsive disorder checking the stove 20 times
before leaving the house; a depressed individual lying in bed for days at a time)

Categories of mental illness

 Schizophrenia

 Major depressive disorder

 Bipolar disorder/manic-depressive disorder

 Anxiety disorders (including PTSD)

 Substance-use disorders

 Organic disorders (e.g., Alzheimer’s disease)

 Personality disorders

Clinical picture signs and symptoms of psychopathology

Psychopathology: branch of science that studies signs and symptoms of a mental disorder
Clinical pictures
1. Consciousness 6. Perception

2. Emotion 7. Memory

3. Motor Behaviour 8. Intelligence

4. Thinking 9. Insight

5. Speech 10. Judgement

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 1. Level of consciousness:
1) Compos mentis
2) Apathy
3) Somnolence
4) Stupor
5) Comma

DISTURBANCE OF CONSCIOUSNESS
 Disorientation
 Delirium
 Drowsiness
 Confusion

DISTURBANCE OF ATTENTION
 Distractibility
 Selective inattention
 Hipervigilency
 Trance

DISTURBANCE OF SUGGESTIBILTY
 Follie a deux (follie a trois)
 Hypnosis

2. Emotion a complex state of feeling with psychological, somatic, and behavioral

components.
1) Affect
 appropriate affect  blunted affect

 inappropriate affect  flat affect

 restricted/constricted  labile affect

affect

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 2) Mood:
 Disforic mood  Anhedonia

 Euthym mood  Bereavement

 Expansive mood  Aleksitimia

 Irritable mood  Suicidal idea

 Labile mood  Depression

 Elevated mood  Hipomania

 Euforia  Mania

 Ecstasy  Melankolia

3) Other Emotions:
 Anxiety  Ambivalence

 Fear  Abreaksional

 Agitation  Shame

 Tension  Guilt

 Panic  Control of impulse

 Apatis

4) Psychological disorders that accompany Mood Disorders

 Anoreksia  Decrease of libido

 Hiperfagia  Constipasi

 Insomnia  Fatigue

 Hipersomnia  Pseudosiesis

 Pica  Bulimia

3. Motor behaviour
 Hipokinesis  Abulia
 Mimikri  Anergia
 Agression  Coprophagia
 Acting out  Diskinesia

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 Muscle rigidity  Convulsion
 Twirling  Seizure
 Chorea  Distonia

4. Thinking
1) Specific Impairment in The Form/Process of Thinking
 Neologism  Irrelevant answer
 Word salad  Loosening of
 Circumstantiality associations
 Tangenciality  Derailment
 Incoherence  Flight of ideas
 Verbigeration  Clang association
 Ekolalia  Blocking

2) Specific Impairment in The Content of Thinking

 Poverty of thought

 Delutions

o Bizzare o Somatic

o Persecutory o of being Controlled

o Grandiose o of Reference

o Erotomania o thought broadcasting

o Jealous o thought insertion

o Nihilistic o Systematic

5. Speech
1) Speech Disturbance
 Logorrhea  Dysphonia

 Poverty of speech  Aphasia

 Disartria

 Stuttering

 Cluttering

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6. Perception
1) Impaired perception
 hallucinations (auditorik, visual, olfaktorious, gustatorik, tactil/haptik)
 illusion
2) Disorders Related with Cognitive and Medical Diseases
3) Disorders Related with Conversion and Dissociative
7. Memory
1) Memory impairment
 Amnesia
 Paramnesia
1. Confabulation
2. Dejavu
3. Deja entude
4. Deja pense
5. Jamais vu
2) Memory Level
 Immediate
 Recent
 Recent past
 Remote
8. Intelligence
1) Mental retardation
2) Dementia
3) Pseudodementia
4) Concrete thinking
5) Abstract thinking
9. Insight
Level:
1) Complete denial of illness
2) Slight awareness of being sick and needing help but denying it at the same
time
3) Awareness of being sick but blaming it on others, on external factors, or on
organic factors
4) Awareness that illness is due to something unknown in the patient
5) Intellectual insight

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 6) True emotional insight
10. Judgement
1) Critical judgement
2) Autonomic judgement
3) Disturbed judgement

Schizophrenia and other psychotic disease (Schizoaffective, Acute

Psychotic Disorder, Delusional Disorder)
Criteria diagnosis:

1. Harus ada sedikitnya satu gejala berikut ini yang amat jelas (dan biasanya dua gejala
atau lebih bila gejala-gejala itu kurang tajam atau kurang jelas):

a. – Thought echo = isi pikiran dirinya sendiri yang berulang atau bergema dalam kepalanya
(tidak keras) dan isi pikiran ulangan, walaupun isinya sama, namun kualitasnya berbeda,
atau

– Thought insertion or withdrawal = isi pikiran yang asing dari luar masuk kedalam
pikirannya (insertion) atau isi pikirannya diambil keluar oleh sesuatu dari luar dirinya
(Withdrawal) dan

– Thought broadcasting = isi pikirannya tersiar keluar sehingga orang lain atau
umumnya mengetahuinya.

b. – Delusion of control = waham tentang dirinya dikendalikan oleh suatu kekuatan tertentu
dari luar atau

– Delusion of influence = waham tentang dirinya dipengaruhi oleh suatu kekuatantertentu

dari luar atau

– Delusion of passivity = waham tentang dirinya tidak berdaya dan pasrah terhadap suatu
kekuatan dari luar; (tentang dirinya= secara jelas ,merujuk ke pergerakan tubuh/anggota
gerak atau kepikiran, tindakan atau penginderaan khusus).

– Delusion perception = pengalaman inderawi yang tidak wajar, yang bermakna sangat khas
bagi dirinya , biasanya bersifat mistik dan mukjizat.

c. Halusional Auditorik ;

– Suara halusinasi yang berkomentar secara terus menerus terhadap prilaku pasien .

– Mendiskusikan perihal pasien di antara mereka sendiri (diantara berbagai suara yang

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berbicara atau

– Jenis suara halusinasi lain yang berasal dari salah satu bagian tubuh.

d. Waham-waham menetap jenis lainnya, yang menurut budaya setempat dianggap tidak
wajar dan sesuatu yang mustahi,misalnya perihal keyakinan agama atau politik tertentu atau
kekuatan dan kemampuan diatas manusia biasa (misalnya mampu mengendalikan cuaca
atau berkomunikasi dengan mahluk asing atau dunia lain)

2. Atau paling sedikitnya dua gejala dibawah ini yang harus selalu ada secara jelas:

e. Halusinasi yang menetap dari panca indera apa saja , apabila disertai baik oleh waham
yang mengambang maupun yang setengah berbentuk tanpa kandungan afektif yang jelas,
ataupun disertai oleh ide-ide berlebihan (over-valued ideas) yang menetap, atau apabila
terjadi setiap hari selama berminggu-minggu atau berbulan-bulan terus menerus.

f. Arus pikiran yang terputus (break) atau yang mengalami sisipan (interpolation) yang
berakibat inkoherensia atau pembicaraan yang tidak relevan atau neologisme.

g. Perilaku katatonik seperti keadaan gaduh gelisah (excitement), posisi tubuh tertentu
(posturing) atay fleksibilitas cerea, negativisme, mutisme, dan stupor.

h. Gejala negatif seperti sikap apatis, bicara yang jarang dan respons emosional yang
menumpul tidak wajar, biasanya yang mengakibatkan penarikan diri dari pergaulan sosial
dan menurunya kinerja sosial, tetapi harus jelas bahwa semua hal tersebut tidak disebabkan
oleh depresi atau medikasi neureptika.

3. adapun gejala-gejala khas tersebut diatas telah berlangsung selama kurun waktu satu
bulan atau lebih (tidak berlaku untuk setiap fase nonpsikotik prodromal);

4. Harus ada suatu perubahan yang konsisten dan bermakna dalam mutu keseluruhan
(overall quality) dari beberapa aspek perilaku pribadi (personal behavior), bermanifestasi
sebagai hilangnya minat, hidup tak bertujuan, tidak berbuat sesuatu, sikap larut dalam diri
sendiri (self absorbed attitute), dan penarikan diri secara sosial.

F.20 Skizofrenia Paranoid

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Pedoman diagnostik

1. Memenuhi kriteria umum diagnosis skizofrenia

2. Sebagai tambahan:

- Halusinasi dan/ waham arus menonjol;

(a) Suara-suara halusinasi yang mengancam pasien atau memberi perintah, atau halusinasi
auditorik tanpa bentuk verbal berupa bunyi pluit (whistling), mendengung (humming), atau
bunyi tawa (laughing).

(b) Halusinasi pembauan atau pengecapan rasa, atau bersifat seksual , atau lain-lain
perasaan tubuh, halusinasi visual mungkin ada tetapi jarang menonjol.

(c) Waham dapat berupa hampir setiap jenis, tetapi waham dikendalikan (delusion of
control), dipengaruhi (delusion of influence) atau passivity (delussion of passivity), dan
keyakinan dikejar-kejar yang beraneka ragam, adalah yang paling khas;

· Gangguan afektif, dorongan kehendak dan pembicaraan, serta gejala katatonik secara
relatif tidak nyata / tidak menonjol.

Diagnosa Banding :

– Epilepsi dan psikosis yang diinduksi oleh obat-obatan

– Keadaan paranoid involusional (F22.8)

– Paranoid (F22.0)

F20.1 Skizofrenia Hebefrenik

Pedoman Diagnostik

– Memenuhi Kriteria umum diagnosis skizofrenia

– Diagnosis hebefrenik untuk pertama kali hanya ditegakkan pada usia remaja atau dewasa
muda (onset biasanya 15-25 tahun).

– Kepribadian premorbid menunjukan pemalu dan senang menyendiri (solitary), namun tidak
harus demikian untuk memastikan bahwa gambaran yang khas berikut ini

– Untuk meyakinkan umumnya diperlukan pengamatan kontinu selama 2 atau 3 bulan

lamanya, untuk memastikan bahwa gambaran yang khas berikut ini memang benar
bertahan :perilaku yang tidak bertanggung jawab dan tidak dapat diramalkan, serta

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manerisme, ada kecenderungan untuk menyendiri (solitaris) dan perilaku menunjukan
hampa tujuan dan hampa perasaan. Afek pasien yang dangkal (shallow) tidak wajar
(inaproriate), sering disertai oleh cekikikan (gigling) atau perasaan puas diri (self-satisfied),
senyum-senyum sendiri (self absorbed smiling) atau sikap tinggi hati (lofty manner), tertawa
menyerigai, (grimaces), manneriwme, mengibuli secara bersenda gurau (pranks), keluhan
hipokondriakalI dan ungkapan dan ungkapan kata yang diulang-ulang (reiterated phrases),
dan proses pikir yang mengalamu disorganisasi dan pembicaraan yang tak menentu
(rambling) dan inkoherens

– Gangguan afektif dan dorongan kehendak, serta gangguan proses pikir biasanya
menonjol, halusinasi dan waham biasanya ada tapi tidak menonjol ) fleeting and fragmentaty
delusion and hallucinations, dorongan kehendak (drive) dan yang bertujuan (determnation)
hilang serta sasaran ditinggalkan, sehingga prilaku tanpa tujuan (aimless) dan tanpa
maksud (empty of purpose) Tujuan aimless tdan tampa maksud (empty of puspose). Adanya
suatu preokupasi yang dangkal, dan bersifat dibuat-buar terhadap agama, filsafat, dan tema
abstrak lainnya, makin mempersukar orang memahami jalan pikirannya.

F20.3 Skizofrenia Tak terinci (undifferentiated )

Pedoman diagnostik :

(1) Memenuhi kriteria umu untuk diagnosa skizofrenia

(2) Tidak memenuhi kriteria untuk skizofrenia paranoid, hebefrenik, katatonik.’

(3) Tidak memenuhi kriteria untuk skizofrenia residual atau depresi pasca skiszofrenia

F20.5 Skizofrenia Residual

Pedoman diagnostik:

Untuk suatu diagnostik yang menyakinkan , persyaratan berikut harus di penuhi semua:

(a) Gejala “Negatif” dari skizofrenia yang menonjol misalnya perlambatan psikomotorik,
aktifitas menurun, afek yang menumpul, sikap pasif dan ketidak adaan inisiatif, kemiskinan
dalam kuantitas atau isi pembicaraan, komunikasi non verbal yang buruk, seperti ekspresi
muka, kontak mata, modulasi suara, dan posisi tubuh, perawatan diri, dan kinerja sosial
yang buruk.

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(b) Sedikitnya ada riwayat satu episode psikotik yang jelas dimasa lampau yang memenuhi
kriteria untuk diagnosa skizofrenia

(c) Sedikitnya sudah melampaui kurun waktu satu tahun dimana intensitas dan frekuensi
gejala yang nyata seperti waham dan halusinasi telah sangat berkurang (minimal) dan telah
timbul sindrom negatif dari skizofrenia

(d) Tidak terdapat dementia, atau penyakit/gangguan otak organik lainnya, depresi kronis
atau institusionla yang dapat menjelaskan disabilitas negatif tersebut.

F20.6 Skizofrenia Simpleks

Pedoman diagnostik

– Skizofrenia simpleks sulit dibuat secara meyakinkan karena tergantung pada pemantapan
perkembangan yang berjalan berlahan dan progresif dari: (1) gejala negatif yang khas dari
skizofrenia residual tanpa didahului riwayat halusinasi waham, atau manifestasi lain dari
episode psikotik. Dan (2) disertai dengan perubahan-perubahan perilaku pribadi yang
bermakna, bermanifestasi sebagai kehilangan minat yang mencolok, tidak berbuat sesuatu
tanpa tujuan hidup, dan penarikan diri secara sosial.

– Gangguan ini kurang jelas gejala psokotiknya dibanding dengan sub type skisofrenia
lainnya.

F21 Schizotypal

Pedoman diagnostic

 Rubric diagnostic ini tidak dianjurkan ntuk digunakan secara umum Karena tidak
membatasi secara tegas dengan schizophrenia simpleks atau dengan gangguan
kepribadian schizoid atau paranoid

 Bila istilah ini digunakan untuk diagnosis 3 atau 4 gejala khas berikut ini harus sudah
ada, secara terus menerus atau secara periodic, sedikitnya untuk 2 tahun lamanya :

a) Afek yang tidak wajar atau yang menyempit / “constricted” (individy tampak
dingin dan acuh tak acuh)

b) Perilaku atau penampilan yang aneh, eksentrik atau ganjil

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 c) Hubungan sosial yang buruk dengan orang lain dan tendensi menarik diri dari
pergaulan sosial

d) Kepercayaan yang aneh atau berpikiran bersifat magik, yang mempengaruhi

perilaku dan tidak serasi dengan norma-norma budaya setempat

e) Kecurigaan atau ideide paranoid

f) Pikiran obsesif berulang-ulang yang tak terkendali,sering dengan isi yang

bersifat “dsymorphophobic” (keyakinantentang bentuk tubuh yang tidak
normal/ buruk dan tidak terlihat secara objektif oleh orang lain), seksusal atau
agresif

g) Persepsi-persepsi pancaindera yang tidak lazim termasuk mengenai tubuh

(somatosensory) atau ilusi-ilusi lain, depersonalisasi atau dereliasisasi.

h) Pikiran yang bersifat samar-samar (vague), berputar-putar (circumstantial),

penuh kiasan (metaphorocical), sangat terinci dan ruwet (overelaborate), atau
stereotipik, yang bermanifestasi dalam pembiicaraan yang aneh atau cara
lain, tanpa inkoherensiyang jelas dan nyata.

i) Sewaktu-waktu ada episode menyerupai keadaan psikotik yang bersifat

sementara dengan iluso, halusiansi auditorik, atau yang lainnya yang bertubi-
tubi, dan gagasan yang mirip waham, biasanya terjadi tanpa provokasi dari
luar.

 Individu harus tidak pernah memenuhi kriteria schizophrenia dalam stadium

manapun.

 Suatu riwayat pada salah seorang anggota keluarga yang terdekat memberikan
bobot tambahan untuk diagnosis ini, tetapi merupakan prasyarat.

F22 Gangguan Waham Mentetap

 Kelompok ini mengikuti serangkaian gangguan dengan waham-waham yang

berlangsung lama, sebagai satu-satunya gejala klinis yang khas atau yang paling
mencolok dan tidak dapat digolongkan sebagai gangguan mental organic,
schizofrenik, atau gangguan afektif.

 Pentingnya faktor genetic, ciri-ciri kepribadian dan situasi kehidupan dalam

pembentukan gangguan kelompok ini tidak pasti dan mungkin bervariasi

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.

F22.0 Gangguan Waham

Pedoman diagnostic

 Waham-waham merupakan satu-satunya ciri khas klinis atau gejala yang paling
mencolok. Waham-waham tersebut (baik tunggal maupun sebagia suatu system
waham) harus sudah ada sedikitnya 3 bulan lamanya dan harus bersifat pribadi
(personal) dan bukan budaya setempat.

 Gejala-gejala depresif atau bahkan episode depresif yang lengkap/ “full-blown” (F32)
mungkin terjadi secara intermitten dengan syarat bahwa waham-waham tersebut
menetap pada saat-saat tidak terdapat gangguan afektif itu.

 Tidak boleh ada bukti-bukti tentang adanya penyakit otak.

 Tidak boleh ada halusinasi auditorik atau hanya kadang-kadang saja ada bersifat
sementara.

 Tidak ada riawayat gejala-gejala schizophrenia (waham dikendalikana, siar pikiran,

penumpukan afek, dsb.)

F22.8 Gangguan Waham Menetap Lainnya

 Kategori sisa untuk gangguan-gangguan waham mentap yang tidak memenuhi

kriteria untuk gangguan waham (F22.0).

 Gangguan waham yang berlangsung kurang dari 3 bulan lamanya, tidak memenuhi
kriteria schizophrenia, harus dimasukkan dalam kode F23.- (gangguan psikotik akut
dan sementara), walaupun untuk sementara.

F22.9 Gangguan Waham Menetap YTT

F23 Gangguan Psikotik Akut dan Sementara

Pedoman diagnosis

 Menggunakan urutan diagnosis yang mencerminkan urutan prioritas yang diberikan

untuk ciri-ciri utama terpilih dari gangguan ini. Urutan prioritas yang dipakai ialah :

 Onset yang akut (dalam masa 2 minggu atau kurang = jangka waktu gejala-
gejala psikotik menjadi nyata dan mengganggu sedikitnya beberapa aspek
kehidupan dan perkerjaan sehari-hari, tidak termasuk dalam periode

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 prodromal yang gejalanya sering tidak jelas) sebagai ciri khas yang
menentukan seluruh kelompok

 Adanya sindrom yang khas (berupa “polimorfik” = beraneka-ragam dan

berubah cepat, atau “schizophrenia-like” = gejala schizophrenia yang khas)

 Adanya stress akut yang berkaitan (tidak selalu ada, sehingga dispesifikasi
dengan karakter ke 5; x0=tanpa penyerta stress akut; x1=dengan penyerta
stress akut). Kesulitan atau problem yang berkepanjangan tidka boleh
dimasukkan sebagai sumber stress dalam konteks ini.

 Tanpa diketahui berapa lama gangguan akan berlangsung

 Tidak ada gangguan dalam kelompok ini yang memenuhi kriteria episode manik
(F30.-) atau episode depresif (F32.-), walaupun perubahan emonsional dan
gejala0gejala afektif individual dapat menonjol dari waktu ke waktu.

 Tidak ada penyebab organic seperti trauma kapitism delirium dan dementia. Tidak
merupakan intoksikasi akibat penggunaan alcohol / obat-obatan.

F24 Gangguan waham induksi

Pedoman diagnosis:

 Diagnosis gangguan waham karena induksi harus dibuat hanya jika:

a) Dua orang atau lebuh mengalami waham atau system waham yang sama,
dan saling mendukung dalam keyakinan waham itu.

b) Mereka mempunyai hubungan dekat yang tak lazim dalam bentuk seperti
diuraikan diatas.

c) Ada bukti dalam kaitan waktu dan konteks lainya bahwa waham tersebut
diinduksi pada anggota yang pasif dari suatu pasangan atau kelompok
melalui kontak dengan anggota yang aktif (hanya satu orang anggota aktif
yang menderita gangguan psikotik yang sesungguhnya, waham diinduksi
pada anggota pasif, dan biasanya waham tersebut menghilang mereka
dipisahkan.

 Jika ada alsan untuk percaya bahwa 2 orang yang tinggal bersama mempunyai
gangguan psikotik yang terpisah maka tidak satupun diantaranya boleh dimasukkan
dalam kode didiagnosis ini, walaupun beberapa diantara waham-waham diyakini
bersama.

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F25 Gangguan Schizoaffective

Pedoman diagnisus:

 Diagnosis gangguan skizoafektif hanya dibuat apabila gejala-gejala definitive adanya

schizophrenia dan gangguan afektif sama-sama menonjol pada saat bersamaan
(simultaneously), atau dlaam beberapa hari yang satu sesudah yang lain, dalam satu
episode penyakit yang sama, dan bilamana, sebagai konsekuensi dari ini, episode
penyakit tidak memenuhi kriteria baik schizophrenia maupun episode manik dan
depresif.

 Tidak dapat digunakan untuk pasien yang menampilkan gejala schizophrenia dan
gangguan afektif tetapi dalam episode penyakit yang bebeda.

 Bila seseorang pasien schizophrenia menunjukkan gejala depresif setelah

mengalami suatu episode psikotik, diberi kode diagnosis F20.4 (depresi pasca
schizophrenia). Beberapa pasien dapat mengalami episode skizoafektif berulang,
baik berjenik main (F25) maupun depresif (F25.1) atau campuran (F25.2). Pasien
lain mengalami satu atau dua episode skizoafektif terselip di antara episode maik
atau depresif (F30-F33).

Pharmacology and Clinical Treatment of Antipsychotic

Typical antipsychotics (1st generation) Atypical antipsychotics (2nd generation)

Chlorpromazine (Thorazine) Aripiprazole (Abilify)

Fluphenazine (Prolixin) Clozapine (Clozaril)

Haloperidol (Haldol) Iloperidone (Fanapt)

Loxapine (Loxitane) Olanzapine (Zyprexa)

Molindone (Moban) Paliperidone (Invega)

Perphenazine (Trilafon) Quetiapine (Seroquel)

Thioridazine (Mellaril) Risperidone (Risperdal)

Thiothixene (Navane) Ziprasidone (Geodon)

Trifluoperazine (Stelazine)

 Typical

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 Typical antipsychotic are drugs that antagonize dopamine D2 receptors. The first-
generation antipsychotic drugs tend to cause extrapyramidal adverse effects and
elevated prolactin levels. The conventional antipsychotic agents are available in generic
forms and are less expensive than the newer agents. They are available in a variety of
vehicles, including liquid and intramuscular (IM) preparations.

Extrapyramidal symptoms (EPSs), such as akathisia, dystonia, psuedoparkinsonism,

and dyskinesia.

 Akathisia

One of the most common EPSs is akathisia. This disturbing symptom of inner motor
restlessness can have both a subjective and objective component. Subjectively, clients
may verbalize that they are unable to remain calm, have disturbed sleep patterns, or have
impaired concentration. Symptoms are often described as "anxiety," which is concerning
because it may prompt a clinician to administer an additional APM. Objectively, clients
may demonstrate restlessness through actions such as pacing, marching, shuffling, foot-
taping, rocking motion, or shifting body weight from leg to leg. Restlessness can be
throughout the entire body or confined to a section of the extremities. Akathisia can
surface within a few days of administration of the APM or up to several weeks later.

Symptoms of akathisia typically respond to discontinuation of the APM coupled with

anxiolytic medications such as lorazepam (Ativan), diazepam (Valium), or alprazolam
(Xanax). Beta-Blockers such as propranolol (Inderal) have also proven effective.

 Dystonic Reactions

Dystonic reactions are involuntary muscle contractions of the head, neck, trunk, and
extremities. The neck and head muscles are the most commonly affected areas, including
the tongue, throat, face, eyes, and jaw. Symptoms affecting the tongue and throat
muscles can affect the vocal cords, causing a hoarse voice, stiff or thick tongue,
dysphagia, laryngeal or pharyngeal spasms, and potential obstruction, which becomes a
medical emergency. Neck and trunk symptoms include torticollis, contorting or twisting of
the cervical spine muscles, and opisthotonos, a severe form of back arching. In addition,
clients may experience oculogyric crisis which is rolling of the eyes in a locked upward
position. This condition can easily be mistaken as delusional behavior. Dystonic reactions
can occur after a single dose of the APM or days after initiating treatment.

Dystonic reactions, which can develop acutely, require immediate interventions to

minimize symptoms. Anticholinergic and antiparkinsonian agents are the first line of
defense during acute dystonic reactions. These medications relieve dystonic symptoms

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 within minutes; however, the anticipation for the onset of relief can be frightening to an
anxious client who is experiencing involuntary muscle contractions. However, they should
be prescribed with caution because the potential risks of lethality with overdose,
dependence, psychosis, dry mouth, blurred vision, constipation, tachycardia, urinary
hesitancy, dizziness, confusion, and the potential to aggravate tardive dyskinesia.

 Pseudoparkinsonism

Pseudoparkinsonism, or neuroleptic-induced parkinsonism, includes slow pill-rolling

finger tremors, masklike facial expression, weakened voice, absence of arm swing when
walking, stiff stooped posture, and an impaired shuffling gait. Cogwheeling rigidity,
assessed frequently in the arms, is a ratchet-like motion of the extremities during
extension. Mentally, the client can display bradyphrenia, or a slowed ability to think
through familiar situations. One unique manifestation after prolonged use of the APM is
the rabbit syndrome which is tremors of the lips and a constant chewing motion.
Pseudoparkinsonism can develop after the first dose of medication is administered or
weeks later; however, it is usually seen early in treatment or when the APM dosage is
increased.

 Tardive dyskinesia

Tardive dyskinesia is characterized by rapid, repetitive, involuntary movements of the

face, trunk, respiratory muscles, and extremities. Facial movements, which often occur in
the oral area, can include a protruding or rolling tongue, lip smacking, grimacing,
frowning, sucking or kissing motions, and facial distortions. Stereotypic movements of the
limbs can be irregular, rapid, purposeless motions or slow serpentine movements. A
client's trunk may rock, twist, jerk, or thrust forward. Unlike the other EPSs, dyskinesia is
a late-appearing side effect that can emerge months to years after the APM has been
administered, and it is identified as tardive dyskinesia. In some cases, about 6%, the
symptoms are irreversible. However, if the antipsychotic agent is removed quickly, the
tardive dyskinesia may be reversed. The symptoms of tardive dyskinesia can be
disfiguring and embarrassing for clients; therefore, potential for social isolation is a
concern. Age, race, and sex appear to place some persons at a higher risk of tardive
dyskinesia.

Management of tardive dyskinesia begins with prevention of the symptoms.

Screening for tardive dyskinesia is strongly recommended at least every 3 to 6
months. Other sources of symptom management for tardive dyskinesia are being
explored such as treatment with vitamin B6 and vitamin E.

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 Atypical

Atypical antipsychotics have lower D2 receptor affinity or higher serotonin 5-HT2A

receptor affinity which lead to lower rates of EPS. The second-generation drugs are more
likely to cause weight gain and abnormalities in glucose and lipid control; in addition, they
are often more expensive than the first-generation drugs. Of the second-generation
agents, risperidone is available as a long-acting injection that uses biodegradable
polymers; olanzapine, paliperidone, and aripiprazole are also now available in long-acting
injectable forms.

They have side effects that many find even more distressing. These include:

 Diabetes mellitus
 Weight gain
 Hyperlipidemia
 Sexual dysfunction
 Cardiac dysfunction

Dopamine Pathway of Schizophrenia and Presynaps & Postsynapse of

action Central Neurotransmitter
Main dopamine pathway:

1. Mesolimbic pathway
2. Mesocortical pathway
3. Nigrostriatal pathway
4. Tuberoinfundibular pathway

Mesolimbic pathway
The mesolimbic pathway transmits dopamine from the ventral tegmental area (VTA) to
the nucleus accumbens. The VTA is located in the midbrain, and the nucleus accumbens is
in the ventral striatum.

Functions:
 reward-related cognition
 incentive salience ("wanting")
 pleasure ("liking") response from certain stimuli
 positive reinforcement
 aversion-related cognition

Associated dosorders:

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  ADHD (Attention Deficit Hyperactivity Disorder)
 Addiction
 Positive symptom schizophrenia

Mesocortical pathway
The mesocortical pathway transmits dopamine from the VTA to the frontal cortex. The "meso"
prefix in "mesocortical" refers to the VTA, which is located in the midbrain, and "cortical" refers
to the cortex.

Functions:
 Cognitive control of behavior

Associated dosorders:
 ADHD (Attention Deficit Hyperactivity Disorder)
 Addiction
 Negative symptom schizophrenia

Nigrostriatal pathway
The nigrostriatal pathway transmits dopamine from the substantia nigra pars compacta (SNc)
to the caudate nucleus and putamen. The substantia nigra is located in the midbrain, while
both the caudate nucleus and putamen is located in the dorsal striatum.

Functions:
 motor function
 reward-related cognition
 associative learning

Associated dosorders:
 Addiction
 Chorea
 Parkinson's disease

Tuberoinfundibular pathway

The tuberoinfundibular pathway transmits dopamine from the hypothalamus (arcuate

nucleus aka "infundibular nucleus") to the pituitary gland. This pathway influences the
secretion of certain hormones, including prolactin.

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Associated dosorders:
 Hyperprolactinaemia

+ Positive symptoms:
 Delusions
 Auditory hallucinations
 Thought disorder: a pattern of disordered language use that is presumed to reflect
disordered thinking.
o pressure of speech (speaking incessantly and quickly),
o derailment or flight of ideas (switching topic mid-sentence or inappropriately),
o thought blocking,
o rhyming,
o 'word salad’

+ Negative symptoms:
 Avolition: general lack of desire, drive, or motivation to pursue meaningful goals.
 Flat affect: a lack of emotional reactivity on the part of an individual (“blunted of affect”).
 Alogia: a general lack of additional, unprompted content seen in normal speech.
 Anhedonia: an inability to experience pleasure from normally pleasurable life events such
as eating, exercise, and social or sexual interaction.

Neurotransmitter

Neurotransmitters are stored in a synapse in synaptic vesicles, clustered beneath

the membrane in the axon terminal located at the presynaptic side of the synapse.
Neurotransmitters are released into and diffused across the synaptic cleft, where they bind to
specific receptors in the membrane on the postsynaptic side of the synapse.

Most neurotransmitters are about the size of a single amino acid, however, some
neurotransmitters may be the size of larger proteins or peptides. A released neurotransmitter
is typically available in the synaptic cleft for a short time before it is metabolized by enzymes,
pulled back into the presynaptic neuron through reuptake, or bound to a postsynaptic receptor.
Nevertheless, short-term exposure of the receptor to a neurotransmitter is typically sufficient
for causing a postsynaptic response by way of synaptic transmission.

In response to a threshold action potential or graded electrical potential, a neurotransmitter is

released at the presynaptic terminal. Low level "baseline" release also occurs without electrical
stimulation. The released neurotransmitter may then move across the synapse to be detected
by and bind with receptors in the postsynaptic neuron. Binding of neurotransmitters may

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influence the postsynaptic neuron in either an inhibitory or excitatory way. This neuron may
be connected to many more neurons, and if the total of excitatory influences are greater than
those of inhibitory influences, the neuron will also "fire". Ultimately it will create a new action
potential at its axon hillock to release neurotransmitters and pass on the information to yet
another neighboring neuron.

Substance Abuse and Psychological Aspect, Law Aspect and the

Antidote
Psychological aspect:

Substance Intoxication Withdrawal Antidote

Alcohol & Impair attention & Insomnia, agitation, Benzodiazepine
sedative / memory, amnesia, labile delirium, auditory Opiate antagonist
hypnotic affect, delirium, hallucination, (naltrexone)
hallucination irritability Alcohol :
disulfiram,
thiamine
Cocaine & Euphoric, irritable, labile Dysphoric, fatigue, Beta –
amphetamine mood, anxiety, hypersomnia, noradrenergic
psychosis, delirium suicidal thought, Benzodiazepine
guilt, hopeless (lorazepam)
Opioid Euphoria, sedation, Dysphoric, anxiety, Methadone
reduce sexual desire, irritability, insomnia, Naloxone
restlessness

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 impair memory &
attention
Cannabis Euphoria, amotivation, Insomnia, irritability, Benzodiazepine
perceptual disturbances, restlessness (lorazepam)
psychosis, delirium Antipsychotic
Phencyclidine Auditory hallucination, No symptom Beta–
delusion, blunted affect, noradrenergic
inattention (propanolol)
Benzodiazepine
Hallucinogen Hallucination, illusion, No symptom Beta–
synesthesia, noradrenergic
depersonalization, (propanolol)
derealization, paranoia Benzodiazepine
Antipsychotic
Inhalant Euphoria, disorientation, No symptom Oxygen
confusion

Law aspect  prohibited, except on medication with doctor prescription

Emergency Psychiatry
Yang termasuk kondisi kegawat daruratan psikiatri:

 Kondisi gaduh gelisah

 Dampak kekerasan
 Suicidal
 Extra pyramidal symptoms
 Delirium
 Kondisi gaduh gelisah
Kekerasan pada diri sendiri = mutilasi diri atau tingkah laku bunuh diri / suicidal
behavior
Ada 3 symptoms: Agitasi, agresuf, kekerasan
Management: Lindungi diri sendiri  waspada  pastikan cukup orang untuk
pengikatan pengikatan  evaluasi diagnostik  eksplorasi kemungkinan
intervensi  dirawat  melibatkan aparat hukum bila perlu  peringatkan calon
korban.
Medikasi: antipsikotik / benxodiazepine (pilih salah satu)

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  Flufenazin, trifluoperazin, atau haloperidol 5 mg per-oral / IM
 Olanzapine 2,5 – 10 mg IM, max 4 injeksi/hari
 Lorazepam 2 – 4 mg, diazepam 5 – 10 mg IV secara perlahan (2 mnt)
 Bunuh diri (suicidal)
Management:
Rawat inap
Terapi psikofarma  lorazepam 3x1 mg / hari, selama 2 minggu + antidepresan
Terapi non farmakologik  psikoterapi
 Sindrom neuroleptik maligna
Symptoms: febrile fever, rigidity, instabilitas otonomik (takikardia, hyperhydrosis),
gangguan kesadaran
Management: Diagnosa sindrom neuroletik maligna (rigiditas tidak berespon
terhadap antikolinergik)  stop pemberian antipsikotik  monitor TTV  cek lab
(CBC, diff count, kimia darah, fungsi hati ginjal) (biasanya terjadi lekositosis dan
peningkatan creatine phospokinase (CPK))  turunkan suhu badan dengan ice
bath, ice packs, cooling blanket, ice water enema, evaporative cooling (antipiretik
biasanya tidak berespon)  hidrasi  setelah sindrom neuroleptik maligna
sembuh, beri antipsikotik beda kelas dengan sebelumnya.
 Delirium
Symptoms: prodromal (lelah, cemas, iritabilitas, gangguan tidur), penurunan
kesadaran, kewaspadaan (hiperaktivitas atau hipoaktivitas)
Management: jika karena toksisitas antikolinergik  pisostigmin salisilat 1-2 mg
IV/IM, dapat diulang 15-30 mnt bila perlu

Classification and Evaluation Multiaxial Psychiatry

Diagnosis multiaxial ada 5 aksis (PPDGJ hal 11-16):

Aksis I  gangguan klinis (boleh >1)

 kondisi lain yang jadi fokus klinis

Aksis II  gangguan kepribadian

 retardasi mental

Aksis III  kondisi medik umum

Aksis IV  masalah psikososial dan lingkungan

Aksis V  penilaian fungsi secara global, pake global assesment of functioning (GAF)

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Tujuan:

 Mencakup informasi secara komprehensif, sehingga membantu dalam

o therapy planning
o mengetahui outcome / prognosis
 Format mudah & sistematik, sehingga membantu dalam
o Memberi tahu informasi klinis
o Mengetahui kompleksitas situasi klinis
o Menggambarkan heterogenitas individual dengan diagnosis yang sama
 Memacu penggunaan :model bio-psiko-sosial” dalam klinis, pendidikan, dan penelitian

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