Disturbance of Conciousness

Pukovisa Prawiroharjo
 Pukovisa Prawiroharjo
Jakarta, 5 April 1983
Islam

FKUI : dokter 2006

FKUI : dokter spesialis saraf 2011

@pukovisa

Email: dr.pukovisa@yahoo.co.id
0811139043

Dewan Pendiri FULDFK

Ketua DEP FULDFK pertama 2005-6.

CV
 Anggota Tim P2KB 2006-2008
Sekretaris Tim P2KB IDI Jakarta Pusat 2008-2011
Wasekjen MKEK Pusat 2012-2015
Wakil Ketua IDI cabang Jakarta Pusat 2011-2014
Anggota MKEK Wilayah DKI Jakarta 2012-2015
Anggota Tim Penyusun Revisi Kode Etik Kedokteran
(KODEKI) Indonesia 2012  Buku KODEKI Baru 2012

Staf Pengajar Departemen Neurologi

Staf Divisi Bioetika Departemen Pendidikan Kedokteran

Sekretaris Jenderal Perhimpunan Angiologi Indonesia

(PANGI) 2012-2015

Medical Service Coordinator PacHealth@ThePlaza

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 Jones, 1923
• Men ought to know that from the brain, and from
the brain only, arise our :
– Pleasures, joys, laughters and jests, as well as our
sorrows, pains, griefs and tears.
– Through it we think, see, hear, and distinguish the ugly
from the beautiful, the bad from the good, the
pleasant from the unpleasant , sleeplessness, in-
opportune mistakes, aimless anxieties, absent-
mindedness, and acts that are contrary to habit.
– These things that we suffer all come from the brain.
Madness comes from its moistness
 Wakefullness vs Awareness
• Wakefullness : State of conciousness, not sleep or
coma
– We can degree : full awake, half awake, deep
anestized  Glasgow Coma Scale : E4M6V5 / E1M1V1
(Teasdale and Jennett, 1974)
– Awake it means aware
• Awareness : Content of conciousness
– Changeable : relative stable in short periode
– Depend on our spectrum psycological capacities
– Many factors that can change : sensations, desire,
emotions, memories, thoughts, and intention
 Self Conciousness
• Colloquial sense of self Conciousness : SADAR
DIRI
• Self Conciousness as self detection : fell your
body
• Self Conciousness as self monitoring :
cognitive abilities
• Self Conciousness as self recognition :
recognize our own body as our own
 Confusion
• Impaired attention and concentration, manifest
disorientation in time, place, and person early
sign
• Deterioration in memory, perception,
comprehension, problem solving, language, praxis,
visuospatial function and various aspects of
emotional behavior
• Single higher cortical function deficit is defined by
dominant behavioral change (agnosia, apraxia,
aphasia) rather than characterizing the state as
confusion
 Confusion
• Fluctuate in severity
• Acute confusion: delirium
– Hyper- agitated, positive symptoms
– Hypo- muted, negative symptoms
• Chronic confusion: dementia (final)
• Beclouded dementia
Patophysiology -Coma & Confusion
• Interruption of energy substrate delivery
(hypoxia, ischemia, hypoglycemia )

• Alteration of the neurophysiologic response of

neuronal membranes (drug or alcohol
intoxication, toxic endogenous metabolites,
anesthesia, or epilepsy)
 Transient loss of Conciousness
• Hypotensive syncope
– Vasovagal syncope : sudden drop in blood presure
– Micturition and cough syncope
– Postural hypotension
– Carotid sinus disease
– Syncope due to primary cardiac dysfunction
• Seizure
• Vertebrobasilar ischemia
• Hypoglicemia
• Hyperventilation
 Coma
• DD/
– Akinetic mutism : damage bilateral frontal lobe
– Locked in syndrome : ventral pons ( corticospinal
and corticobulbar paralyse) but Reticular system
remain intact
– Vegetative state
– Catatonia
– Non convulsive status epilepticus
 Disturbance of Conciousness
• Person loss of awareness of their external
environment
• Neuroanotomical and neurophysiological :
uncertain
• Anatomy related :
– Cerebral hemisphere
– Reticular system in brainstem
 Conciousness Anatomy
Two (2) Component Anatomy :
Reticular formation and cerebral hemisphere
Retikularis formatio : a diffuse collection of neurons that extends
throughout the brainstem (center : pons).
Reticular Activating System : a diffuse collection of neuron in the
reticular formation, plays an essential role in keeping the concious
brain.
ARAS : Ascending Reticular Activating System from Formasio
reticularis through bilateral cerebral hemisphere. Blocking 
disturbance of conciousness
FORMATIO RETIKULARIS
Wakefulness
Awareness
Sistem Norefinefrin
NEUROTRANSMITER
Cholinergic System
 Sistem Modulasi Difus
Sistem Tempat Neuron Struktur Inervasi Fungsi Modulasi dari
Neuromodulator Berasal Sistem

Norepinephrine Lokus koerolus di Kosteks Serebri, talamus, Atensi, Arousal, Siklus

pons hipotalamus, bulbus tidur-bangun,
oktaforius, Midbrain, pembelajaran, memori,
medula spinalis anxiety, nyeri dan mood
Serotonin Raphe nuklei Proyeksi ke nukleus Nyeri dan lokomosi
sepanjang garis bawah sampai medula
tengah brain stam spinalis
Nukleis atas ke otak Siklus tidur bangun,
mood dan emosi,
perilaku agresi dan
depresi
Dopamine Substansi nigra di Korteks dan bagian Motor control “Reward”
midbrain dan VTA sistem limbik pusat perilaku
kecanduan
Acetylcholine Dasar otak : pons Serebrum hipokampus Siklus tidur bangun,
dan Midbrain dan talamus arousal, pembelajaran,
memori, Informasi
sensoris ke arah talamus
Consciousness
Concious
Coma
BRAIN DEATH
VEGETATIVE STATE
Minimally Conciousness
Lock-in Syndrome
 Evaluation of Conciosness
• Qualitative :
– Inatention
– Confusion
– Stupor
– Coma
• Quantitative :
– Glasgow Coma Scale
• Eye max : 4
• Motor responds max : 6
• Verbal max : 5
 Grading
Alert
Composmentis
Drowsiness Be aroused by touch or noise, can maintain
Somnolence alertness for some time

Stupor Be awakened by vigorous stimuli, have an

effort to avoid uncomfortable stimulation

Coma Cannot be aroused by stimulation, no

purposeful attemp is made to avoid painful
stimuli
 Glasgow Coma Scale

Eye Opening Verbal Motor Response

(E) (V) (M)
1 None None None
2 To pain Sounds Decerebrate
3 To speech Words Decorticate
4 Spontaneous Confused Withdraw to pain
5 Oriented Localizing to pain
6 Obey commands
 GLASGOW COMA SCORE
• Scoring from the best response
• Verbal response will not correct in the
condition of aphasia, intubation, and facial
injury
• Sensory loss may interfere painful stimulation
• Eye opening may be interfered by orbital
swelling and 3rd CN palsy
• Arm movements may be impaired from local
trauma or cervical cord lesion
How to exam patient response if
not concious

Supra orbital Nails bed

Sternum Temporo mandibular joint

 Causes of Disturbance Conciousness
• Extracerebral :
– Metabolic or endocrine
– Circulatary collapse
– Toxin
– Drugs
– Psychiatric
• Intracerebral :
– Hemorhage
– Tumor
– Meningitis encephalitis
– Dementia
 Examination of the comatose patient
• Signs of head injury : rhinorhea, otorhea, brill
hematom, battle sign
• Pupil response :
– Pin point : toxin opiat
– Bilateral fixed mid position : mesencephalon
– Anisokor : herniation
– Slowly reactive : metabolic
• Respiratory pattern :
– Cheyne stokes respiration : alternate hyper and
hypoventilation ( thalamus)
– Hyperventilation : metabolic
– Ataxic respiration : irregular pattern ( medulla
oblongata lession)
 cheyne stok pattern

Hiperventilasi neurogenik sentral

Apnestik pattern

cluster & pernafasan ataxic pattern

Apnoe
 Cheyne Stokes Pattern

• Pattern : periodc hiperpnoe with periodic

apnoe about 10-20 seconds.
• Location
– Dysfunction bilateral hemisphere (level diencephalon)
– Process : metabolic disturbance : uremic, hepatic coma, or
bilateral infarction or mass that cause herniation at diencephalon
level
 Neurogenic Central Hyperventilation

Location : Disfunction brainstem or upper pons

Hyperventilation in freq. 40-50x/mnt
PO2 araise more than 70-80 mmHg
Jika level PO2 di bawah normal  hipoksemia
Could be : Cardiac disease, lung problem, and metabolic
problem
 Apneustic Pattern

Location : lower pons,

Long inspiration phase than stop at maximal
inspiration.
 Cluster Pattern

Only at lower pons, with characterize  apnoe

process
 Ataxic Pattern

Location at medullar
No specific pattern with chest respiration
 Examination of the comatose patient
• Ocular movement :
– Dolls eye movement
– Caloric test : cold to eye conjugate to irigated ear
• Funduscopic exam :
– Papil edema
– Subhyaloid hemorhage
• Limb position :
– Hemiparesis
– Decerebrate posture
– Decorticate posture
Pupil changes in coma
patient
 Eyes Movement
• Rest position:
– Gaze Deviation contra lesion  lession at contralateral hemisphere

– Gaze deviation ~ hemisfer  lession at contralateral pons

– Down Deviation  lession at brain tectum mecencephalon

• Okulocefalik reflexes(doll’s eye)

– Disfunction of bilateral hemisphere

• Okulovestibular reflexes
– Negatif  Lession at brain stem
 Supporting examination
• ECG
• Check for metabolic finding :
– Blood gas analysis
– Electrolyte
– Glucose
– Toxin
– Drugs
 Supporting Examination
• Brain Function : EEG or PET Scan
• Brain vascular : TCD or MRA or Angiography
• Brain Imaging : CT Scan or MRI
– Mass :
• Hemmorhage
• Tumor
• Abcess
– Large infarction or multiple infarct at brainstem
– Hydrocephalus
 Death

Clasic = Asistol + Apnea

After resuscitation
Brain death = Brainstem death

Loss of conciousness with loss brainstem

function including respiration

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IDI No. 336/PB/A.4/88

Death :

No spontan respiration and cardiac stop firmly or

There is brainstem death

How we conclude brainstem death ??

 Three component

Inclusion to do the Brain stem death

test
Brain stem death test positive
Confirmation test positive

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 Inclusion Criteria
As clinic or neuroimaging : damage in CNS  Brainstem
death
Exclusion medical condition that could mask the clinical
exam (Severe disturbance Electrolyte and acid base, or
endocrin disturbance)
Not intoxication cases or poisoned
Body Temp. (core) ≥ 32 C

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 Brainstem test

• Coma or no response
• No brainstem reflexes
• Complit Apneu confirmed with apneu test

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 Coma
or No response

No motoric response !!
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Brainstem Reflexes

Pupil
Kornea
Okulosefalik
Respon motorik
pd distribusi
saraf kranialis
Okulo-Vestibular
Gag reflexes
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 Loss of Brainstem reflexes
• Pupil
– No light response. Mid position and pupil dilatation
diameter (4 – 6 mm)

• Eyes movement
– Doll’s eye movement : negative
– Vestibulo-okular reflexes : Caloric test with cold water
irigation (7 oC under body temp) 50 ml each ear (interval 5
minute)
Exam motoric and sensoric response

No motoric response with pain stimulation : jaw reflex, and face

movement

No sensoric response : cornea reflexes

No gag reflexe and cough mechanism  loss of pharyng and

trachea reflexes.

Gag reflexes : posterior pharing stimulation with tounge spatel

Cough reflexe : Suction Trakeal/ bronchial

Apnea Test

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 Apnea test
Inclusion criteria :

Widjick (1995) apnea test could be done if:

Temperatur sentral >36,5˚C.
Sistolic pressure >90 mmHg
Euvolemia
pCO2 normal (optional pCO2 arterial >40mmHg)
pO2 normal (optional pO2 >200mmHg)
 Cont’
1. Preoksigenasi w/ oksigen 100% ( 10-20 minutes).

2. Put pulse oxymetri dan Disconect ventilator.

3. Oxygenation 6L/minutes to trakhea (or canul O2 at karina).

4. Observe respiration movement (abdominal and chest)

Disconection from ventilator ( 8-10 minutes), count pO2 dan
pCO2 arterial.  connect again to ventilator.

5. If no respiration movement and pCO2 arterial >60 mmHg,

apnea test : positif.

6. If dont : test negative and re exam : 25 minutes – 24 hours

 TES KONFIRMASI
MATI BATANG OTAK

Meliputi cerebral angiography, TCD, EEG, dan

cerebral scintigraphy.
Di Indonesia tidak memerlukan tes-tes
konfirmasi.
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 Algorithm of Brain Death
Determination
Comatose patient
Yes Exclude
Reexamine
- Metabolic disorders
- Drugs screening
- Drug Intoxication
No - Laboratory results
- Residual Effect from drug Therapy
Yes
Clinical Brain Death? Reexamine
- Normothermia ? – Areactive coma ? Consider baseline
- Normotension ? – Absent brain stem reflexes ? No EEG
- Apnea ?
Yes
Change in
Observation period
exam
- Neonates – 2 mo : 48 h - >1 yr : 12 – 24 hrs
- 2 mos – 1 yr : 24 h - Adults : 6 – 12 hrs
Unchange
dExam Consider confirmatory testing
- Patients < 1 yr
- Brain pathology not consistent with clinical
course or neurologic exam
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Brain Death From Christoper N et el. Textbook of Neurointensive Care.2004; 647
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 Pitfalls in diagnose Brain Stem Death
Hasil pemeriksaan
1. Pupil terfiksasi
2.Refleks okulo vestibuler
3. Tidak ada nafas
4.Tidak ada aktivitas motorik
5. EEG isolelektrik
Kemungkinan kausa
obat anti kolinergik
obat pelumpuh otot
penyakit sebelumnya
vestibuler supressan
ototoksik agents
penyakit sebelumnya
henti nafas pasca hiperventilasi
obat pelumpuh otot
obat pelumpuh otot
locked in state
obat sedativa
obat sedativa
anoksia
hipotermi
ensefalitis
trauma
 Drugs that could influence conciousness

Drugs T½ (hr) Therapeutic range

Lorazepam 10-20 0.1-0.3 mcg/ml
Midazolam 2-5 50-150 ng/ml
Diazepam 40 0.2-0.8 mcg/ml
Carbamazepine 10-60 2-10 mcg/ml
Phenobabitone 100 20-40 mcg/ml
Pentobarbitone 10 1-5 mcg/ml
Thiopentone 10 6-35 mcg/ml
Morphine 2-3 70-450 ng/ml
Amitriptyline 10-24 75-200 ng/ml
Alcohol 10 ml/h 800-1500 mg/l
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