Medical-Surgical Nursing 2

Prepared by Dr. Jhason John J. Cabigon

Neurology: Nursing Management of Patients with Neurologic Dysfunction Review of Anatomy and Physiology A. Functions 1. Motor controls body movement 2. Sensory responds to sensory stimuli 3. Fast-acting regulatory system that controls all other systems of the body 4. Also responsible for consciousness, intelligence, memory B. Principal Divisions 1. Central Nervous System (CNS) brain & the spinal cord; serves as control mechanism for the entire organism 2. Peripheral Nervous System (PNS) a. 12 Cranial nerves (CN) b. 31 Spinal nerves c. Autonomic nerves i. Sympathetic ii. Parasympathetic 3. Neurons transmits electrical impulses; parts: a. Cell body/Soma w/ Nissl bodies (RER) b. Axons transmitting end; may be covered by myelin sheath (hastens impulse transmission) c. Dendrites receiving end C. Types of Neurons 1. Sensory (afferent) neurons from sensory receptors to CNS 2. Motor (efferent) neurons from CNS to effector (muscle/glands) 3. Interneurons connect neuron to neuron found in CNS only D. Synapses 1. An axon transmits a nerve impulse at a specialized junction with another neuron called synapse 2. Junction of Presynaptic and Postsynaptic neurons 3. Axons may establish synaptic contacts with any portion of the surface of another neuron, except those regions that are myelinated 4. Chemical synapse the most numerous type of synapse Facilitates most interactions between neurons and all communications between neurons and effectors At these junctions, the presynaptic membrane releases a signaling molecule called a neurotransmitter, such as acetylcholine (ACh) E. Reflex rapid, predictable, involuntary response 1. Types a. Somatic stimulates skeletal muscles b. Autonomic stimulates autonomic organs 2. Elements a. Sensory receptor b. Afferent neuron c. Integration center (CNS) d. Efferent neuron e. Effector organ F. Central Nervous System 1. Brain a. Characteristics i. Average human brain weighs about 3 pounds (1300-1400 g) ii. The brain reaches its full size at ~6 y/o iii. If brain cells do not get oxygen for 3 to 5 min, they begin to die b. Parts i. Cerebrum the largest part of the human brain, is divided into left and right hemispheres connected to each other by the corpus callosum; The hemispheres are covered by a thin layer of gray matter known as the cerebral cortex; The hemispheres exhibit gyri (elevated ridges) and sulci (shallow grooves); Divided into lobes: Frontal lobe primary motor area, speech, thought process
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o Precentral gyrus motor function o Brocas Area speech production (base of precentral gyrus); damage to brocas area leads to expressive (non-fluent) aphasia o Pre-frontal gyrus controls morals, values, judgement and decision making Parietal lobe somatic sensory area o Post-central gyrus general sensation (i.e. touch, pressure, pain) Temporal lobe auditory area, language processing o Wernickes Area speech comprehension (posterior area of superior temporal gyrus); damage to wernickes area leads to receptive aphasia (fluent) aphasia o Olfactory area deep inside the temporal lobe Occipital lobe visual area Limbic lobe includes: o Hypothalamus controls temperature, emotions, food and water intake, sexual behavior; also influences the endocrine system o Amygdala and Hippocampus convert information into long-term memories Insula not well understood * Basal Ganglia islands of gray matter; regulates voluntary motor activities * Homunculus bodys representation in the brain; motor and sensory homunculus ii. Diencephalon between Cerebrum and Brain Stem Thalamus: relay station for sensory impulses Hypothalamus: regulatory center of Autonomic Nervous System (temperature regulation, food and water intake, sexual behavior); part of limbic system (emotional brain); also influences the pituitary gland (the master endocrine gland) Epithalamus: pineal gland (produces melatonin which controls the bodys sleep-wake cycle) & choroid plexus (produces cerebrospinal fluid) iii. Brain stem midbrain, pons, medulla Connects brain to the spinal cord Pathway for nerve tracts Contains nuclei of cranial nerves Contains the Reticular Activating System (RAS) along the entire length of brainstem w/c plays a role in consciousness Pons also contains neurons involved with spontaneous respiration Medulla contains: o Cardiac center adjusts force and rate of myocardial contractions o Respiratory center regulates breathing depth and rate o Vasomotor center regulates BP iv. Cerebellum large cauliflower-like part of the brain; coordinates timing of muscle activities and balance/equilibrium 2. Spinal Cord a. Two-way conduction pathway to and from the brain b. Major reflex center c. Emerges from the base of the brain at the level of the foramen magnum & extends caudally to L2 vertebra, then cauda equina 3. Protection of the CNS a. Skull bones and vertebral column b. Meninges protective covering of the cerebral cortex and spinal cord i. Dura mater tough outermost ii. Arachnoid mater middle weblike iii. Pia mater innermost delicate c. Cerebrospinal fluid water cushion that occupies the space between the arachnoid layer; continually formed (by the choroids plexus) and continually drained *Characteristics: clear, colorless, alkaline, SG 1.007, total amount of 100-160 ml (replaced 3x/day; total ~500ml/day), contains traces of glucose and proteins, with minimal WBCs (0-5 cells per mm 3) and no RBCs; Normal pressure: 80-100 mmH20 in newborns; <200 mmH20 in normal children and adult *Flow of CSF: i. Lateral ventricles (cerebrum) Foramen of Monro ii. Third ventricle (diencephalon) Cerebral aqueduct of Sylvius (midbrain) iii. Fourth ventricle (posterior to pons & medulla)
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Foramen of Lushka and Magendie Central canal of spinal cord (canal inside the spinal cord) and Subarachnoid space (space that surrounds the brain and spinal cord) Arachnoid villi v. Dural venous sinuses vi. Blood (Venous circulation) d. Blood-Brain barrier relatively impermeable capillaries to isolate neural tissues in the CNS from the general circulation Peripheral Nervous System 1. Cranial Nerves Oh, oh, oh, to touch and feel a girls vagina, ah heaven I Olfactory Sensory (Smell) II Optic Sensory (Vision) III Oculomotor Motor (most eyes movements, upper eyelid elevation); Autonomic (pupillary constriction) IV Trochlear Motor (downward and inward eye movement) V Trigeminal Sensory (sensation of face, cornea and scalp); Motor (chewing) VI Abducens Motor (lateral eye movement) VII Facial Sensory (taste, anterior 2/3 of tongue); Motor (muscles of expressions of the face, eyes and mouth); Autonomic (salivary glands) VIII Auditory (Vestibulocochlear) Sensory (hearing and balance) IX Glossopharyngeal Sensory (taste, posterior 1/3 of tongue); Motor (swallowing); Autonomic (salivating) X Vagus Sensory (sensations of the throat, larynx and abdominal viscera); Motor (gag and swallowing; also vocal cord movement); Autonomic (regulates heart and digestive activity) XI Accessory Spinal Motor (sternocleidomastoid and trapezius head rotation and shoulder shrug) XII Hypoglossal Motor (tongue movements) 2. Spinal Nerves a. 31 pairs from spinal cord: i. Cervical nerves (8) ii. Thoracic nerves (12) iii. Lumbar nerves (5) iv. Sacral nerves (5) v. Coccygeal nerve (1) b. Dermatomal levels a specific segment of skin supplied by a single spinal nerve; all spinal nerves except for C1 innervate a segment of skin, and so each of these nerves is associated with a dermatome c. Spinal nerve groups & Plexuses i. Intercostal nerves anterior rami of spinal nerves T1T11; travel in the intercostal space sandwiched between two adjacent ribs ii. Nerve Plexuses networks of interweaving anterior rami of spinal nerves; anterior rami of most spinal nerves form nerve plexuses on both the right and left sides of the body; nerve plexuses then split into multiple named nerves that innervate various body structures Cervical plexus C1 to C5 (serves head, neck shoulders) Important nerve: *Phrenic serves diaphragm and muscles of neck and shoulder Brachial plexus C5 to T1 (serves chest, shoulders, arms and hands) Important nerves: *Axillary deltoid *Radial arm and forearm extensors *Musculocutaneous arm flexors *Median forehand flexors and some muscles of hand *Ulnar wrist and many hand muscles Lumbar plexus L1 to L4 (serves back abdomen, groin, thighs, knees and calves) Important nerves: *Femoral lower abdomen, buttocks, anterior thigh and skin of anteromedial leg and thigh *Obturator adductor muscles and skin of medial thigh and hip joint Sacral plexus L4 to S4 (serves the pelvis, buttocks, genitals, thighs, calves and feet) Important nerves: *Sciatic lower trunk and posterior surface of thigh and leg; splits into: Common fibular, also known as peroneal nerve (lateral leg/foot) and Tibial (posterior leg/foot) *Pudendal somatic nerve of external genitalia; sphincters of bladder and rectum

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*Superior and inferior gluteal gluteus Autonomic Nerves divided into the Parasympathetic, Sympathetic and Enteric Systems a. Parasympathetic (PNS) housekeeping or resting-and-digesting system; in general, causes constriction and contraction of organs, EXCEPT for the CVS organs (heart and blood vessels) Constriction of pupils Constriction of bronchioles and increase in secretions Increase in peristalsis and secretions Contraction of bladder Increase in salivation Decrease in heart rate Dilation of blood vessels (decrease BP) Penile erection (due to vasodilation) b. Sympathetic (SNS) fight-or-flight Increase in heart rate Increase in blood pressure Ejaculation Differences Other Name Nerves Included Parasympathetic Housekeeping or Resting and Digesting Craniosacral: Cranial nerves 3, 7, 9, 10 and Spinal nerves S2S4 Acetylcholine Nicotinic, Muscarinic Constricts Pupil, Constricts bronchioles, Increases peristalsis, Dilates vessels, Decreases HR and BP, penile erection Sympathetic Fight-or-Flight Thoracolumbar: Thoracic and Lumbar Spinal Nerves Epinephrine, Norepinephrine 1, 2, 1, 2 Dilates Pupil, Dilates bronchioles, Inhibits peristalsis, Increases Blood Glucose, Constricts vessels, Increases HR and BP, ejaculation

Neurotransmitters Receptor Major Effects

c. Enteric (ENS) directly controls the gastrointestinal tract (peristalsis, secretions, churning) Auerbachs (Myenteric) Plexus located between the inner and outer layers of muscularis externa Meissners (Submucosal) Plexus located in the submucosa H. Blood Supply of the Brain 1. Internal Carotid (right and left) gives rise to: a. Anterior cerebral artery supplies the frontal lobes and medial aspects of the parietal and occipital lobes b. Middle cerebral artery, also called the artery of stroke supplies the frontoparietal somatosensory cortex. Infarcts in its territory result in contralateral hemiparesis 2. Basilar artery comes from the fusion of left and right vertebral arteries; the basilar artery then gives rise to: a. Posterior cerebral artery supplies the occipital and inferior temporal lobes including the hippocampus b. Cerebellar arteries supplies the cerebellum and brain stem Superior cerebellar artery (SCA) Anterior cerebellar artery (AICA) Posterior cerebellar artery (PICA) actually a branch of vertebral artery
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3. The Circle of Willis a circle of arteries that supply blood to the brain; creates redundancies in the cerebral
circulation. If one part of the circle becomes blocked or narrowed (stenosed) or one of the arteries supplying the circle is blocked or narrowed, blood flow from the other blood vessels can often preserve the cerebral perfusion well enough to avoid the symptoms of ischemia; components a. Internal carotid arteries (left and right) b. Anterior cerebral arteries (left and right) c. Posterior cerebral arteries (left and right) d. Anterior communicating artery (connects left and right anterior cerebral arteries) e. Posterior communicating artery (connects posterior cerebral arteries and internal carotids) Alterations A. Headache B. Conditions that Increase intracranial pressure (ICP) 1. Head Trauma 2. Cerebrovascular Disorders 3. Brain Tumor C. Seizure Disorders and Epilepsy D. Degenerative Diseases 1. Parkinsons disease 2. Alzheimers disease E. Demyelinating Disease: Multiple Sclerosis F. Neuromuscular Disease: Myasthenia Gravis G. PNS Diseases 1. Guillain Barre Syndrome 2. Trigeminal Neuralgia 3. Bells Palsy H. Motor Neuron Disease: Amyotropic Lateral Sclerosis I. Spinal Cord Alterations 1. Herniated Nucleus Pulposus 2. Spinal cord Injury J. Pediatric Conditions 1. Febrile Seizures 2. Meningitis 3. Spina bifida 4. Hydrocephalus 5. Cerebral Palsy 6. Reyes Syndrome Headache A. Types: 1. a. b. c. d. Primary Migraine cerebral vasodilation Tension HA chronic, less severe; muscle spasm of neck and scalp (band-like) Cluster HA most painful; cyclical (wks to months), then remission (months to yrs) Cranial arteritis older people; immune-mediated temporal headache Secondary organic cause, ex. brain tumor or aneurysm

2. B. 4 Phases of Migraine 1. Prodrome hours to days before attack; variety of symptoms, but same prodrome each attack 2. Aura less than 1 hr; usually visual disturbances (light flashes or bright spots) 3. Headache Intensifies over 4-72 hours 4. Recovery (Postdrome) C. Medical Management Vasoconstrictors (contraindicated in HPN and IHD) 1. Sumatriptan (Imitrex) 2. Ergotamine (Avamigran) D. Nursing Care 1. Meds on onset of pain 2. Quiet, dark environment
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3. Elevate head 30o 4. Heat, massage, analgesics, muscle relaxants (for tension HA) Conditions that Increase ICP

A. Intracranial pressure pressure inside the rigid cranial vault; normal ICP: 10-20 mmHg as measured from the lateral
ventricles; maintained by the equilibrium of 3 components: 1. Brain tissue (1400g) 2. Blood (75 ml) 3. CSF (75 ml) B. Head Trauma 1. Most Common Causes: a. Motor vehicular accidents b. Violence c. Falls 2. Risk Factors: a. Alcohol intake b. Drugs c. Low Socioecomic level 3. Brain Injury can be Closed (Blunt) Injury or Open Brain Injury 4. Types of Brain injury: a. Cerebral Concussion mild traumatic brain injury with temporary loss of neurologic function with no apparent structural damage b. Cerebral Contusion more severe injury, the brain is bruised with possible surface hemorrhage; patient loses consciousness for more than a few seconds or minutes c. Diffuse axonal Injury widespread damage to axons in the cerebrum, corpus callosum and brain stem; patient experiences no lucid intervals, immediate coma, abnormal posturing and global cerebral edema d. Skull Fracture open or closed; can be classified into simple, comminuted, depressed and basilar fractures; manifestations of Basilar skull fracture: Hemorrhage from the nose, pharynx, ears or conjunctiva Ecchymosis over the mastoid (Battles sign) CSF leakage in the ears (CSF otorrhea) and nose (CSF rhinorrhea) Halo sign on bed linens is highly suggestive of CSF leak (blood stain surrounded by yellowish stain) e. Intracranial Hemorrhages hematomas (collection of blood) that develop within the cranial vault; types: 5. Types of Intracranial Hemorrhage a. Epidural/Extradural Hemorrhage blood accumulation between skull and dura Most serious type Can result from skull fracture that causes laceration of middle menigeal artery (hemorrhage from this artery causes rapid pressure in the brain) Considered as an extreme emergency Marked neurologic deficit or even respiratory arrest within minutes b. Subdural Hemorrhage blood accumulation between dura and brain Causes o Trauma o Coagulopathies o Ruptured aneurysm Types o Acute symptoms develop over 24 to 48 hours o Subacute after 48 hours to 2 weeks o Chronic after 3 weeks to months c. Intracerebral Hemorrhage bleeding into the substance of the brain; causes: Direct penetration (bullet, stab wounds) Systemic HPN w/c causes vessel rupture Rupture of Aneurysm Vascular anomalies Intracranial tumors Bleeding disorders Complication of anticoagulant therapy
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Pathophysiology Brain suffers traumatic injury Brain swelling or bleeding Rigid cranium allows no room for expansion of contents so Intracranial Pressure (ICP) increases Pressure on blood vessels w/in the brain causes blood flow to the brain to slow Cerebral hypoxia and ischemia occur ICP continues to rise. Brain may herniate. Cerebral blood flow ceases 7. Assessment of Head Trauma a. Level of consciousness the single most valuable indicator of neurologic function Alert. The patient is awake and verbally and motorally responsive; oriented x3 Lethargic. The patient is sleepy or drowsy and will awaken and respond appropriately to command; somnolent, obtunded Stupor. The patient becomes unconscious spontaneously and is very hard to awaken. Semi-coma. The patient is not awake but will respond purposefully to deep pain; no spontaneous movement Coma/Deep Coma. The patient is completely unresponsive; vegetative state; sphincters absent; reflexes minimal/absent; posture - decorticate or decerebrate b. Glasgow Coma Scale Faculty Measured Response Score Eye Opening Spontaneous 4 To verbal command 3 To pain 2 No response 1 Verbal Response Oriented, converses 5 Disoriented, converses 4 Uses inappropriate words 3 Makes incomprehensible sounds 2 No response 1 Motor Response To verbal command 6 To localized pain 5 Flexes and withdraws 4 Flexes abnormally (decorticate position) 3 Extends abnormally (decerebrate 2 position) 1 No response *GCS Score of 10 or less emergency attention *GCS Score of 7 or less is interpreted as comatose c. Pupillary Reaction Normal: PERRLA (pupils equally round, reactive to light and accomodation) Abnormal: o Pupils react sluggishly to light o Ipsilateral dilation of pupil o Fixed dilated pupils o Dolls eyes oculocephalic reflex d. Cushings Triad sign of increased ICP HPN (progressively increasing systolic BP) which results to widening pulse pressure (an increase in difference between systolic and diastolic pressure over time) Bradycardia Irregular respiration (ie. Cheyne-Stokes respiration alternating shallow and deep breathing) e. Test Reflexes grading of reflexes 0 No reflex +1 Minimal activity (hypoactive) +2 Normal response
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+3 More active than normal +4 Maximal activity (hyperactive or with clonus*); Clonus repeated rhythmic contractions f. Test Motor Function grading of muscle strength 5 Active motion against full resistance 4 Active motion against some resistance 3 Active motion against gravity 2 Active motion with gravity eliminated 1 barely detectable motion 0 no motion or muscular contraction detected g. Observe for other signs: sensory deficits, changes in behavior, judgment and decision-making; aphasia; hearing difficulty; ataxia; convulsions h. Note headache, vomiting and nuchal rigidity Diagnostics a. Radiologic examination confirms the presence and extent of skull fracture b. CT Scan c. MRI d. Cerebral angiography e. Positron Emission Tomography (PET) method of scanning the examines the brain function rather than structure Complications of Traumatic Brain Injury a. Decrease cerebral perfusion b. Cerebral edema and herniation c. Impaired oxygenation and ventilation d. Impaired fluid, electrolyte and nutritional balance (hyponatremia 2o to shifts in ECF and SIADH; hypokalemia; hyperglycemia) e. Risk for post-traumatic seizures Immediate (w/in 24 hours) Early (w/in 1-7 days) Late (after 7 days) Nursing Diagnosis a. Altered Cerebral Tissue Perfusion r/t increased ICP b. Ineffective Breathing pattern r/t compression of respiratory center c. Aspiration r/t unconsciousness d. Self-care deficit r/t altered level od consciousness e. Impaired physical mobility r/t abnormal motor response f. Impaired nutrition, less than body requirements r/t increased metabolic demands, fluid restriction and inadequate intake g. Risk for injury (self-directed and directed at others) r/t seizures, disorientation, restlessness or brain damage h. Risk for imbalanced body temperature r/t damaged temperature-regulating mechanisms in the brain i. Risk for impaired skin integrity r/t bed rest, hemiparesis, hemiplegia, immobility, or restlessness j. Disturbed thought process (deficits in intellectual function, communication, memory, information processing) r/t brain injury k. Disturbed sleep pattern r/t brain injury and frequent neurologic checks l. Interrupted family processes r/t unresponsiveness of patient, unpredictability of outcome, prolonged recovery period, and the patients residual physical disability and emotional deficit m. Deficit knowledge about brain injury, recovery and the rehabilitation process Management a. Transport on board and cervical collar (any patient with head injury is presumed to have cervical spine injury until proven otherwise) b. Prevent secondary injury and maintain adequate cerebral oxygenation Endotracheal intubation Fluid resuscitation Oxygenation c. Surgery is required for evacuation of blood clots, debridement and elevation of depressed fractures Nursing Care a. Monitor neurologic checks hourly Level of consciousness (GCS) Pupils DTRs
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Motor and Sensory CN testing b. Monitor vital signs c. Lessen constrictive clothing and remove potentially injurious item d. Maintain open airway and provide adequate ventilation Maintain unconscious patient in position that facilitates draining of oral secretions, w/ head elevated about 30o to decrease intracranial venous pressure Establish effective suctioning procedures Guard against aspiration and respiratory insufficiency Closely monitor ABGs Monitor for pulmonary complications such as Acute respiratory distress syndrome (ARDS) and pneumonia e. Prevent increase in ICP Maintain calm quiet environment Provide psychological support to prevent stress Avoid bending, sneezing, coughing, straining at bowel movement Avoid valsalva manuever (forced exhalation against a closed airway) f. Decrease fluid intake to decrease cerebral edema g. Monitor IVF (Isotonic solution; KVO) h. Monitor I/O and F/E (inc in ICP leads renal vasoconstriction decrease blood flow to kidneys results to decrease UO) i. Maintain Seizure precaution Keep padded tongue blade by bedside Keep bed in low position Adjust side rails up at all times j. Monitor temperature q2-q4 k. Turning and repositioning q2 l. Provide psychological support and measure even if patient is comatose (Hearing- last sense lost) m. Administer meds as ordered: Hyperosmotic Diuretic Mannitol (Osmitrol) o MOA: Decreases brain edema; Increases osmotic pressure w/in the vasculature attracts fluid from brain tissue to vessels renal excretion o SE: headache, N/V, chills, rebound edema when d/c, hyponatremia, hypokalemia Loop Diuretic Furosemide (Lasix) o MOA: promote excretion of Na and H20 along loop of henle o SE: hyponatremia, hypokalemia Anti-inflammatory Steroids Prednisone (Pred), Dexamethasone (Decadron) o MOA: decreases edema by suppressing components of inflammation o SE: peptic ulcer, GI bleeding, Na and H20 retention, delayed wound healing, mood swings, hyperglycemia, acne Cerebrovascular Diseases or Stroke refers to a functional abnormality of the CNS that occurs when the normal blood supply of the brain is disrupted; types: ischemic and hemorrhagic stroke 1. Ischemic Stroke (Brain Attack) also known as cerebrovascular accident (CVA) or brain attack; occurs when the normal blood supply of the brain is disrupted due to occlusion, like thrombosis and embolism; a. Types of Ischemic stroke: Large artery thrombotic strokes (20%) thrombus formation and occlusion at the site of atherosclerosis result in ischemia and infarction (deprivation of blood supply) Small penetrating artery thrombotic strokes (25%) most common cause; affects one or more vessels; also known as lacunar strokes because it forms cavities after death of infracted brain tissue Cardiogenic embolic stroke (20%) associated with cardiac dysrrhythmia, usually AF; emboli originate from the heart with valvular heart disease or thrombi in left ventricle Cryptogenic stroke (30%) unknown cause Others (5%) stroke from illicit drug use, coagulopathies, migraine and spontaneous dissection of carotid or vertebral arteries b. Signs and symptoms Signs and symptoms mainly depend on what specific part of the brain is affected
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Prepared by Dr. Jhason John J. Cabigon

 Main presenting sign: Numbness or weakness of the face, arm, or leg, especially on one side of the body Confusion or change in mental status Trouble speaking or understanding speech Visual disturbances Difficulty walking, dizziness, or loss of balance or coordination Sudden severe headache c. Neurologic deficits Visual Field Deficits o Hemianopsia loss of half of visual field o Loss of peripheral vision unaware of objects or the borders of objects o Diplopia double vision Motor deficits o Hemiparesis weakness of half of the body (due to lesion in opposite hemisphere) o Hemiplegia paralysis of half of the body (due to lesion in opposite hemisphere) o Ataxia staggering, usteady gait o Dysarthria difficulty in forming words o Dysphagia difficulty in swallowing Sensory Deficits o Paresthesia numbness or tingling of extremity (occurs on opposite side of lesion) Communication deficits o Dysphasia impaired speech o Aphasia loss of speech o Expressive aphasia (Brocas aphasia) unable to form words that are understandable o Receptive aphasia (Wernickes aphasia) unable to comprehend the spoken word o Global (mixed) aphasia combination Apraxia inability to perform a previously learned action/skill Cognitive deficits o Amnesia memory is disturbed or lost o Decreased attention span o Impaired concentration o Poor abstract reasoning o Altered judgment Emotional deficits o Loss of self-control o Emotional lability o Decreased tolerance to stressful situation o Depression o Withdrawal o Fear, hostility, anger o Feelings of isolation 2. Hemorrhagic Stroke (2o to intracerebral hge or cerebral aneurysm) caused by bleeding into the bran tissue, the ventricles, or the subarachnoid space; 15-20% of cerebrovascular disorders; Causes: a. Spontaneous rupture of small vessels due to uncontrolled HPN 80% of hemorrhagic strokes b. Ruptured intracranial aneurysm (dilation of weakened arterial wall) results to subarachnoid hemorrhage c. Cerebral amyloid angiopathy damage due to deposits of beta-amyloid protein in small and medium-sized vessels of the brain d. Arteriovenous malformations (AVMs) - abnormal connection between veins and arteries, usually congenital; the resulting tangle of vessels do not contain capillaries, thus high-pressure arteries and low-pressure veins are directly connected; extremely fragile and prone to bleeding e. Intracranial neoplasms f. Certain medications anticoagulants, amphetamines 3. Risk Factors of Stroke a. Non-modifiable Factors Advance age >55 y/o; the incidence of stroke more than doubles in each successive decade Gender men>women Race african-americans almost twice than caucasians
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4. a. b. c. 5. a.

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Modifiable Risk Factors HPN major risk factor MI and CHF - cardiac output Valvular disease (like endocarditis) and Atrial Fibrillation Atherosclerosis wall thickens as the result of a build-up of fatty materials such as cholesterol Asymptomatic carotid stenosis Obesity and Hyperlipidemia Alcohol and Smoking leads to vasoconstriction DM - blood sugar viscosity stasis thrombosis Stress sympathetic stimulation vasoconstriction Physical inactivity sedentary lifestyle Severity of Stroke Transient Ischemic Attack (TIA) a neurologic deficit less than 24 hours, with most episodes resolving in less than 1 hour; results from temporary ischemia (impairment of blood flow) to a specific region of the brain; serves as a warning sign for impending stroke Reversible Ischemic Neurologic Disability (RIND) 24 to 72 hours Complete Stroke if symptoms persist longer Prognosis of Stroke Thrombotic CVA poor prognosis for neurologic and functional recovery Embolic CVA good prognosis Hemorrhagic CVA 50-70% mortality Lacunar CVA very good prognosis Emergency Care ABCDE Elevate head 30-45o to prevent ICP Loosen constrictive clothes and remove potentially injurious items Monitor vital signs and level of consciousness Medical Management Thrombolytic therapy used for dissolving clots in ischemic stroke Recombinant tissue Plasminogen Activator (rt-PA) must be given within 3 hours decrease in size of stroke and an overall improvement in functional outcome after 3 months Rt-PA is given at 0.9 mg/kg, max 90 mg; 10% given IV bolus, 90% given IV over 1 hr via infusion pump Most common SE: bleeding Anticoagulants for secondary thrombus formation; blocks conversion of prothrombin to thrombin; do not breakdown formed clots; ex. Heparin and warfarin Heparin parenteral; use in stroke is controversial because of risk of bleeding o Ex. Heparin sulfate o Lab reference: aPTT (activated partial thromboplastin time) o SE: Bleeding, ecchymosis, petechiae, hematuria, hemorrhage o Antidote: Protamine sulfate Warfarin oral o Ex. Warfarin Sodium (Coumadin) o Lab reference: PT (prothrombin time) INR (international normalized ratio) target is 2.5 o SE: Bleeding, N/V, contipation o Antidote: Vitamin K Anti-platelets if warfarin is contraindicated Ex: aspirin (aspilets), clopidogrel (Plavix), ticlopidine (Ticlid), dipyridamol (Persantine) + aspirin; dipyridamol inhibits thrombus formation if given chronically and is also a vasodilator at high doses Decrease the incidence of cerebral infarction in patients who have experienced TIA and stroke SE of aspirin: prolonged bleeding time, gastric irritation, N/V, tinnitus Narcotic analgesics to provide sedation; ex. Morphine sulfate and Meperidine HCl (Demerol) Antihypertensives Hyperosmotic Diuretic Anti-inflammatory Anti-convulsant Stool softener Surgical management: for evacuation of blood clots (ex. Craniotomy, burr hole)
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9. Nursing Care a. Acute care (1st 24-48 hours) Maintain open airway and provide adequate ventilation O2 at 6-8 L/min by nasal cannula Cough and deep breathing q2 Suction secretions b. Turn q2; if sensation is impaired, decrease amount of time on affected side; if possible place patient in prone position for 15-30 mins several times a day c. Monitor neurologic checks q1 d. Monitor V/S e. Provide psychological support f. Administer meds as ordered g. For Hemiplegia prevent deformities Use proper positioning Turn q1-q2 Put paralyzed arm on pillows Elevate affected extremity above level of heart to prevent edema Passive ROM exercises to build strength on affected muscle Prevent flexion of fingers squeeze rubber ball To prevent hip flexion contracture, keep bed flat except when px participates in ADLs Use footboard for flaccid paralysis h. For Dysphagia prevent aspiration Check gag reflex before feeding Offer soft food Place px in upright position Place food on unaffected side Instruct px to chew and swallow on unaffected side Provide mouth care Maintain calm approach i. For Hemianopsia prevent injury Approach patient on unaffected side Place personal belongings, food, articles on unaffected side Gradually teach scanning turning px head to see things on the affected side j. For Aphasia prevent miscommunication Give simple, slow direction Give 1 command at a time Gradually shift topics Use non-verbal techniques Anticipate px needs to prevent frustrations and feelings of helplessness Allow sufficient time to answer k. For Apraxia Guide px through intended movement Keep repeating the movement D. Brain Tumor 1. Types of Tumors a. Primary Brain Tumors Tumors arising from the protective covering of the brain (ex. Dural meningioma) Tumors arising from cranial nerves (ex. Acoustic neuroma tumor developing in or around 8th cranial nerve) Tumors originating within brain tissue (ex. Glioma infiltrate any portion of brain; most common) Tumors from other brain structure (ex. Tumors of pituitary gland, pineal gland and cerebral vessels Developmental tumors ex. Angioma (mass of abnormal blood vessels, teratoma (tumor with tissue or organ components, like hair, teeth, bone, eyes, hands, feet) and craniopharyngioma (tumor derived from pituitary gland embryonic tissue, that occurs most commonly in children and pxs in their 50s and 60s; iIt arises from odontogenic (tooth-forming) epithelium, therefore, contains deposits of calcium, which are evident on an x-ray) b. Secondary Tumors (Metastatic Lesions) tumor originating else where in the body
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E.

c. Supratentorial occuring in anterior 2/3 of brain (primarily cerebrum) d. Infratentorial posterior 1/3 (primarily cerebellum and brainstem 2. Assessment a. Headache (recurrent, progressive, more severe in the morning, affected by positioning); infants (persistent, irritative crying and head-rolling) b. Vomiting w/ or w/o nausea; progressive, becomes projectile c. Coordination disturbance (ataxia) d. Hypotonia and hyporeflexia e. Nystagmus (rhythmical activity of the eye) f. Diplopia (double vision) g. Visual field defects h. Signs of inc. ICP 3. Monitoring ICP a. ICP monitoring records the pressure exerted w/in the cranial cavity by the brain, cerebral blood and CSF b. Types of Monitoring device Intraventricular cath inserted in the lateral ventricle to give direct measurement of ICP; also allows drainage of CSF if needed (normal 10-20 mmHg) Subarachnoid screw or bolt inserted to the skull and dura mater into the SA space Epidural sensor the least invasive; placed between skull and dura mater; indirect measurement of ICP (normal ICP 0-10 mmHg) c. When using monitoring devices: (1) use strict aseptic technique when handling any part of the device, (2) check insertion site for signs of infection, (3) monitor temperature, (4) assess for CSF leak, loose connections, air bubbles and occlusions in tubing 4. Management a. Radiation and Chemo for inaccesible tumor and metastatic tumor; may also follow surgery; Radiation therapy cornerstone of tx for many tumors; Brachytherapy surgical implantation of radiation sources to deliver high doses at a short distance) b. Corticosteroids to reduce edema c. Hyperosmotic Diuretic d. Stool softener e. Anti-convulsants f. Analgesics g. Intracranial surgery; goal is to remove or destroy the entire tumor w/o increasing neurologic deficits (paralysis, blindness) or to relieve symptoms by partial removal (decompression) 5. Nursing Care a. Monitor V/S and neuro; check signs of ICP b. Administer meds c. Provide care for neurologic deficits d. Provide supportive care for effects of radiation and chemo e. Provide psychological support to patient and family due to its diagnosis and poor prognosis f. Prepare patient for surgery Intracranial Surgeries 1. Types: a. Craniotomy opening of skull to gain access to intracerebral structures; used to remove tumors, relieve elevated ICP, evacuate blood clot or control hemorrhage Supratentorial above the tentorium Infratentorial below the tentorium Transsphenoidal through mouth and nasal sinuses (usually to gain access to the pituitary gland) b. Burr holes circular openings made in the skull by hand drill or automatic craniotome; used to assess cerebral swelling and injury and the size and position of ventricles; also a means of evacuation of intracranial hematoma or abscess; also for allowing access to the ventricles for decompression, ventriculography, or shunting procedures c. Craniectomy excision of portion of skull d. Cranioplasty repair of cranial defects 2. Pre-op Nursing Care: a. Explain to px about the procedure to prevent anxiety; explain head will be shaved, large bandaging on the head, possible temporary swelling and discoloration around the eye, and possible headache b. Provide emotional support c. Shampoo scalp and check signs of infection d. Shave hair e. Monitor V/S and neuro checks f. Avoid enemas unless indicated straining ICP
13

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g. Give pre-op steroids as ordered h. Insert foley catheter as ordered 3. Post-op Nursing Care: a. Maintain patent airway and adequate ventilation Supratentorial Incision o Elevate head off bed 30-45o o Position patient on the back if intubated Infratentorial Incision o Keep head flat or elevate 20-30o o Do not flex head to chest o Check respiration closely and report signs of distress o Maintain on NPO for 24 hours due to possible impairment of swallowing and gag b. Monitor V/S and neuro checks q1 c. Turn q2 d. Monitor F/E balance Assess dressing frequently Administer meds as ordered Apply ice to swollen eyes Refer px for rehab for residual deficit Monitor F/E balance Monitor I/O Restrict fluids Avoid overly rapid infusion Watch out for signs of Diabetes insipidus (dec. UO, hunger, thirst, irritabilty, muscle weakness, dec. LOC) e. Assess dressing frequently f. Administer meds as ordered g. Apply ice to swollen eyes h. Refer px for rehab for residual deficit Seizures and Epilepsy A. Definition 1. Seizures episodes of abnormal, motor, sensory, autonomic, or psychic activity (or combination of these) that result from sudden excessive discharge from cerebral neurons 2. Epilepsy unprovoked, recurrent seizures due to a chronic underlying process; can be primary (idiopathic) or secondary (due to another underlying condition, such as brain tumor) B. Causes of Seizures 1. Idiopathic a. Genetic b. Developmental defects 2. Acquired a. CVD b. Hypoxemia of any cause, including vascular insufficiency c. Fever (children) d. Head injury e. Hypertension f. CNS infections (e. Meningitis, encephalitis) g. Metabolic and toxic conditions (ex. Renal failure, hyponatremia, hypocalcemia, hypoglycemia, pesticides) h. Space occupying lesions (ex. Brain Tumor, subdural hematoma) i. Drug and alcohol withdrawal j. Allergies k. Encephalopathy (ex. Reyes syndrome) l. Congenital CNS defect (ex. Hydrocephalus) m. Degenerative diseases (ex. Tay-Sachs disease) C. Classification of Seizures 1. Partial (or focal) seizures begin in one part of the brain b. Simple partial consciousness remains intact and may have motor, sensory, autonomic or psychic symptoms c. Complex partial consciousness is impaired coupled with automatism (lip smacking, chewing, aimless walking, or other complex motor activities)
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2. Generalized seizures involve electrical discharges in the whole brain a. Tonic-clonic (grand mal) cause sudden loss of consciousness, loss of postural control, tonic muscular contraction producing teeth-clenching and rigidity in extension (tonic phase) followed by rhythmic muscular jerking (clonic phase) b. Absence (petit mal) sudden, brief impairment of consciousness without loss of postural control (10-20 secs) c. Others: atypical absence, infantile spasms, and tonic, clonic, and myotonic seizures D. Diagnostics 1. Electroencephalography (EEG) measures abnormal electrical activity of the brain 2. Other procedures to detect primary disorders (i.e. MRI for brain tumor) E. Medications Anticonvulsants 1. Phenobarbital (Luminal) and Phenytoin (Dilantin) can be used for both grand mal and petit mal seizures 2. Carbamazepine (Tegretol) can be used for refractory seizures not responding to other anticonvulsants 3. Diazepam (Valium) is primarily used for status epilepticus (continuous uninterrupted seizure activity or rapid succession of epileptic seizures) 4. Ethosuximide (Zarontin) - control absence/petit mal seizure 5. Others gabapentin (Neurotonin), topiramate (Topamax), valproate (Depakote) SE of anticonvulsants: gastrointestinal irritation, sedation, gum hyperplasia (phenytoin); phenytoin and valproic acid are teratogenic (pregnancy category D) F. Nursing Care During a Seizure 1. Provide privacy 2. Patient with an aura (warning sign of an impending seizure) may have time to seek a safe, private place 3. If with aura, place oral airway 4. Do not pry open clenched jaws (putting tongue blade is no longer recommended) 5. Ease patient on the floor 6. Protect head with a pad 7. Push aside any furniture 8. Loosen constrictive clothing 9. If in bed, remove pillows and raise side rails 10. Do not restrain 11. If possible, place patient on one side with head forward 12. If suction available, use it to clear secretions G. Nursing Care After the Seizure 1. Keep patient on one side to prevent aspiration (keep airway patent) 2. Expect a period of confusion post-ictal (grand mal) 3. A short apneic period may occur during or immediately after a generalized seizure 4. Reorrient patient upon awakening 5. Use calm persuasion and gentle restraint if patient becomes agitated post-ictal Neurodegenerative Disorders A. Parkinsons Disease 1. A slowly progressing neurologic movement disorder that eventually leads to disability 2. Associated with decreased levels of dopamine resulting from destruction of pigmented neuronal cells in the substantia nigra in the basal ganglia region of the brain 3. Four cardinal manifestations: tremors, rigidity and bradykinesia, postural changes 4. Incidence: symptoms usually appear in the 5th decade of life; however, cases have been diagnosed as early as 30 y/o 5. Causative Factors: a. Idiopathic (unknown) most common b. Secondary Genetics Atherosclerosis Excessive accumulation of oxygen free radicals Viral infections, like encephalitis Head trauma Chronic use of antipsychotics, like chlorpromazine (Thorazine) and haloperidol (Haldol); other drugs: methyldopa, reserpine Some environmental exposures (manganese and carbon monoxide) 6. Pathophysiology a.Destruction of dopaminergic cells in the substantia nigra in the basal ganglia
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 b.Depletion of dopamine stores c. Degeneration of dopaminergic nigrostriatal pathway d.Imbalance of excitatory (acetylcholine) and inhibitory (dopamine) neurotransmitters in the corpus striatum e.Impairment of extrapyramidal tracts controlling complex body movements f. Tremors, Rigidity, Bradinesia, Postural changes 7. Assessment a. Tremors pill-rolling, resting b.Rigidity cogwheel c. Bradykinesia slow movement d.Fatigue e.Postural Instability stooped posture, propulsive, shuffling gait (short steps with feet barely leaving ground, thus producing a shuffling noise) f. Emotional lability and depression g.Seborrhea (scaly skin) h.Autonomic symptoms (increased salivation and sweating, constipation, decreased sexual capacity) i. Mask-like facies (emotionless), decreased blinking of eyes j. Micrographia small handwriting k. Dysphonia soft, slurred low-pitched and less-audible speech) 8. Medications a.Levodopa (L-dopa) most effective agent; mainstay MOA: provides levodopa to brain cells for conversion to dopamine in the basal ganglia SE: orthostatic hypotension, nausea and vomiting, headache, anxiety, loss of appetite, mental changes (confusion, hallucinations, depression, sleep alteration), cardiac arryhythmia; on-and-off syndrome, occasional involuntary movements (dyskinesia), neuroleptic malignant syndrome (severe rigidity, stupor, hyperthermia) Nursing Implications: contraindicated in patients with glaucoma, cardiovascular, renal or hepatic disease; advise client to change position slowly to prevent orthostatic hypotension; nausea can be helped by taking drug with food; but avoid high protein diet because there will be absorption impairment of L-dopa; avoid taking Vitamin B6 since it will inhibit the conversion of L-dopa to dopamine; monitor BP; use cautiously in clients with peptic ulcers and psychoses b.Levodopa-carbidopa (Sinemet) maximizes the beneficial effect of levodopa by preventing its breakdown and reducing its adverse reactions c. Anticholinergics trihexyphenidyl HCl (Apo-trihex) and benztropine (Cogentin); controls rigidity and tremors d.Antiviral amantadine (Symmetrel); early parkinsons; believed to release dopamine from storage sites e.Dopamine agonists bromocriptine mesylate (Parlodel) and pergolide (Permax); often employed to postpone the initiation of carbidopa or levodopa or when carbidopa or levodopa loses effectiveness f. Tricyclic antidepressants amitriptyline HCl (Elavil); 1/3 to 1/2 of the dosage used in depressed patients g.MAOIs selegiline (Eldepryl); inhibits dopamine breakdown h.Antihistamines diphenhydramine HCl (Benadryl); reduce tremors and anxiety 9. Nursing Care a.Administer drugs b.Provide safe environment Side rails on bed; handle bars on toilet, bathtub and hallways; prevent scattered rugs Hard-back or spring-loaded chairs to make getting up easier c. Provide measures to increase mobility Physical therapy (active and passive ROM and stretching exercises) Assistive devices d.Encourage independence in self-care activities Alter clothing for ease in dressing Use assistive devices Do not rush patient e.Improve communication abilities instruct patient to practice reading aloud, listen to own voice and enunciate each syllable clearly; refer to speech therapy if indicated f. Maintain adequate nutrition Cut food into bite-size pieces Provide small frequent feedings q30mins
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 Allow sufficient time for meals g.Avoid constipation and maintain adequate bowel elimination Increase fluids High fiber diet Stool softeners h.Provide psychological support i. Provide Teaching/Discharge Planning Nature of disease Use of meds and SE Importance of daily exercise Promotion of active participation in self-care activities Activities to limit postural deformities 1. Firm mattress w/ small pillow 2. Keep head and neck as erect as possible 3. Use broad-based gait 4. Raise feet while walking B. Alzheimers Disease 1. Senile Dementia of the Alzheimers type 2. Chronic, progressive, and degenerative brain disorder that is accompanied by profound effects on memory, cognition, and ability for self-care 3. Abnormal protein deposits and other structural changes appear 4. Theories: a.Oxidative stress, primarily in the hippocampus and neocortex b.Reduction in brain Ach 5. Anti-Alzheimer Medications a. Drugs that do not cure alzheimers disease but only improve the cognitive function and disability for mild to moderate disease by increasing the amount of Ach by inhibiting acetylcholinesterase (an enzyme that breaks down acetylcholine) b.Examples: tacrine (Cognex), donepezil (Aricept), galantamine (Reminyl), rivastigmine (Exelon) c. SE: headache, nausea, vomiting, anorexia, diarrhea, tiredness, myalgia, insomnia, dizziness, confusion, allergies, signs of cholinergic overstimulation (unusual sweating, brochospasms, bradycardia, hypotension, urinary difficulties); tacrine is known to produce hepatotoxicity Demyelinating Disease: Multiple Sclerosis

A. Multiple Sclerosis immune-mediated, progressive demyelinating disease of the CNS; results to impaired transmission of
nerve impulses B. Incidence: women>men; may occur at any age but typically manifests in young adults between 20-40 y/o (Great crippler of young adult) C. Cause: ongoing research D. Predisposing/Precipitating Factors: 1. Geography frequent in cool and temperate climates (Europe, New Zealand, Southern Australia, Northern US, Southern Canada) 2. Genetic predisposition 3. Viral infection a virus triggering the autoimmune response 4. Emotional and physical stress may induce relapse (exacerbations and remissions are characteristics of MS) E. Pathophysiology 1. Sensitized T cells cross the blood-brain barrier 2. The immune system attack leads to inflammation that destroys the myelin (fatty, protein layer that insulates axons and speed up impulse transmission); plaques appear on demyelinated axons 3. Disruption to the flow of nerve impulses 4. Variety of manifestations Areas commonly affected: a. Optic nerve, chiasm and tract b. Cerebrum c. Brainstem d. Cerebellum
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e. Spinal Cord F. Assessment 1. Visual disturbance blurred vision, scotoma (blind spots), diplopia 2. Fatigue most disabling symptom 3. Impaired sensation paresthesia and pain 4. Impaired motor function weakness, paralysis, spasticity 5. Mood swings depression 6. Impaired cerebellar function nystagmus, tremors, ataxia, difficulty in coordination 7. Bladder dysfunction urinary retention/incontinence 8. Bowel dysfunction constipation 9. Sexual dysfunction impotence in males G. Secondary Complications 1. UTI 2. Constipation 3. Pressure ulcers 4. Contracture deformities 5. Dependent pedal edema 6. Pneumonia 7. Reactive depression 8. Decreased bone density H. Types of MS 1. Relapsing remitting (RR) MS 2. Primary progressive (PP) MS 3. Secondary progressive (SP) MS 4. Progressive-relapsing (PR) MS I. Diagnostics 1. CSF Exam - protein and immunoglobulins 2. Evoked potential studies define the extent of disease process and monitor changes 3. Neuropsychological testing 4. MRI shows area of demyelination J. Medications 1. No cure exists for MS; only delay the progression of the disease or symptom management 2. IV methylprednisolone key agent in treating acute relapse in RR MS 3. For spasticity: diazepam (Valium), baclofen (lioresal), dantrolene sodium (Dantrium) 4. For urinary retention bethanicol (Urecholine) 5. Interferon beta-1a (Rebif), interferon beta-1b (Betaseron), glatinamer acetate (Copaxone) reduce frequency and duration of relapse and decrease size and number of plaques K. Nursing Care (p. 2281-2284) Neuromuscular Disease: Myasthenia gravis

A. Myasthenia gravis an autoimmune disorder affecting the neuromuscular junction causing varying degrees of weakness of
the voluntary muscles

B. Incidence: Women (20-40 y/o) >Men (60-70 y/o)

C. Pathophysiology 1. Auto-antibodies destroy acetylcholine receptor sites in post-synaptic neurons 2. Fewer receptors are available for acetylcholine stimulation 3. Deceased transmission of impulses across the NMJ 4. Voluntary muscle weakness 80% of people with MG have thymic hyperplasia or thymic tumor the thymus gland is believed to be the site of antibody production D. Assessment 1. MG is a purely motor disorder 2. Diplopia and ptosis (drooping of eyelid) 3. Extreme muscle weakness that increases with activity (relieved by rest) 4. Weakness of muscles of face and throat Dysphagia and Mask-like facies 5. Laryngeal involvement dysphonia, hoarseness
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6. Generalized weakness 7. Weakness of intercostal muscles leading to decreased vital capacity and respiratory failure E. Diagnosis 1. Tensilon Test IV injection of edrophonium or Tensilon (a fast-acting acetylcholinesterase inhibitor) provides spontaneous relief of symptoms 2. EMG amplitude of evoked potentials 3. Ach receptor antibody test 4. MRI showing enlarged thymus gland F. Management 1. Pyridostigmine bromide (Mestinon) an anticholinesterase; first line of therapy SE: fasciculations, abdominal pain, diarrhea and increased oropharyngeal secretions 2. Other anticholinesterases neostigmine (Prostigmin) and ambenomium (Mytelase) 3. Corticosteroids suppresses immune response; ex. prednisone 4. Immunosuppressive drugs 5. Surgery thymectomy 6. Plasmapheresis (plasma exchange) used to treat exacerbations; removal of plasma containing acethylcholine receptor antibodies G. Nursing Care 1. Administer drugs as ordered and observe SE 2. Monitor effectiveness of drug; assess muscle strength before and after medication 3. Avoid the following drugs: a. Certain antibiotics, like neomycin, streptomycin , kanamycin and other aminoglycosides agranulocytosis b. Cardiovascular meds, like procainamide arrhythmia c. Sedatives, like morphine respiratory depression d. Quinine hypotension e. Procaine (Novocaine) f. Beta-blockers g. Antiseizure and psychotropic drugs 4. Provide optimal nutrition a. Check gag reflex b. Provide soft diet c. Do not leave alone if with difficulty in swallowing 5. Monitor respiratory status frequently 6. Keep emergency airway and suction equipment nearby 7. Observe for myasthenic crisis a. Caused by undermedication, physical and emotional stress, infection b. Abrupt onset of severe generalized weakness with inability to swallow, speak and maintain respiration 8. Observe for cholinergic crisis a. Caused by overmedication b. Unusual sweating, brochospasms, bradycardia, hypotension, urinary difficulties c. Atropine sulfate antidote Summary of Autoimmune Diseases
Autoimmune Dse Multiple sclerosis Myasthenia gravis Cause Demyelinating dse of CNS; plaques appear on demyelinated axons Destruction of post-synaptic acetylcholine receptor leading to muscle weakness S/Sxs scotoma (blind spots), diplopia & BOV; then variety of neuro sx diplopia and ptosis; then muscle weakness that increases w/ activity (purely motor) Management *Methylprednisolone: key *Anti-spastics: diazepam, baclofen, dantrolene (Dantrium) *Edrophonium (Tensilon): Dx *Pyridostigmine (Mestinon): Tx ( Ach); overdose may lead to cholinergic crisis; underdosage may lead to myasthenic crisis *Corticosteroids: immunosupression *Atropine: antidote for cholinergic crisis Emergency intubation IVIG

Guillain-Barre Syndrome

Demyelinating dse of PNS leading to ascending weakness

Ascending weakness (lower extremities respiratory muscles)

Motor Neuron Disease: Amyotropic Lateral Sclerosis A. Amyotropic Lateral Sclerosis (Lou Gehrigs Disease) progressive loss of motor neurons leading to atrophy of muscles B. Death usually occurs as a result of respiratory infection secondary to respiratory insufficiency C. Incidence: 1.5 cases per 100,000; men>women; onset occurring in the 5th or 6th decade of life
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D. Theories about the cause of ALS: 1. Autoimmune 2. Free radical damage 3. Oxidative stress E. Assessment 1. Clinical manifestations depend on the location of the afftected motor neurons 2. Chief symptoms: fatigue, progressive muscle weakness, cramps, fasciculations (twitching), and incoordination F. Diagnosis ALS is diagnosed on the basis of signs and symptoms because no clinical or lab tests are specific for ALS G. Management 1. No specific therapy for ALS 2. Main focus: maintain or improve function, well-being and quality of life 3. Riluzole (Rilutek) glutamate antagonist; slows the deterioration of motor neurons PNS Diseases

A. Guillain-Barr Syndrome
1. Autoimmune attack on the peripheral nerve leading to acute, rapid segmental demyelination of peripheral nerves and some cranial nerves producing ascending weakness with dyskinesia, hyporeflexia, and paresthesia 2. Incidence: men > women 3. Precipitating factors: a. Antecedent viral infection (cytomegalovirus, EBV and HIV); other bacterial infection (Campylobacter jejuni, Mycoplasma pneumoniae, Haemophilus influenzae) b. Immunization (influenza vaccine) 4. Assessment a. Begins with symmetric muscle weakness and diminished reflexes of the lower extremity; progresses upward; may progress to tetraplegia b. Mild sensory changes c. Antecedent event usually 2 weeks before symptoms begin d. Cranial nerve involvement blindness, inability to swallow and clear secretion, dysphagia e. Ventilatory insufficiency if paralysis ascends to the respiratory muscles f. Autonomic dysfunction HPN, bradycardia/tachycardia, orthostastic hypotension g. Do not affect cognitive function 5. Diagnostics a. CSF elevated proteins b. Evoked potential studies demonstrate a progressive loss of nerve conduction velocity 6. Management a. Because of the possibility of rapid progression and neuromuscular respiratory failure, GBS is a medical emergency b. Respiratory therapy or mechanical ventilation may be necessary c. Elective intubation before onset of respiratory insufficiency d. IVIG therapy of choice e. Plasmapheresis 7. Nursing Care (p. 2289-2292) B. Trigeminal Neuralgia 1. Trigeminal neuralgia (Tic Douloureux) paroxysms of pain in the area innervated by any of the 3 branches (most common V2 and V3) 2. The pain ends abruptly as it starts and is described 3. Incidence: 5th-6th decade of life; elderly women; people w/ MS 4. Etiology: unknown; but vascular compression and pressure are suggested 5. Assessment a. The pain ends abruptly as it starts and is described as unilateral shooting and stabbing sensation b. Associated with involuntary contractions of the facial muscles sudden closing of the eye, twitching of mouth 6. Management a. Antiseizure agents carbamazepine (Tegretol), gabapentin (Neurontin) and phenytoin (Dilantin) relieves pain b. Nerve Block injection of phenol/alcohol; temporary effect (last 6-18 months) c. Surgery Microvascular decompression of the trigeminal nerve Radiofrequency Thermal Coagulation Percutaneous Baloon Microcompression
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7. Nursing Care a. Assess character of pain including triggering factors and pain management techniques b. Administer meds and monitor response c. Maintain room in moderate temperature d. Provide small frequent feedings of lukewarm, semisolid or soft foods e. Hygiene; Provide patient with soft cloth and lukewarm water (perform only during periods of pain) f. Prepare patient for surgery if necessary g. Provide patient teaching; d/c planning Avoid outdoor activities during cold, windy and rainy weathers Importance of good nutrition/hygiene Use of meds and SE Specific instructions following surgery: i. Protective eye care ii. Chew on the unaffected side iii. Avoid hot fluids/foods iv. Mouthcare after meals v. Good oral hygiene and visit dentist q6mo vi. Protect face during extreme temp C. Bells Palsy 1. Bells Palsy (facial paralysis) unilateral inflammation of the facial nerve, which results to weakness or paralysis of the facial muscles on the affected side; majority of patients recover completely in 3-5 weeks 2. Predisposing factors: a. Unknown b. Vascular ischemia c. Viral infection (herpes simplex, herpes zoster) d. Autoimmune e. Brain Tumor 3. Assessment a. Loss of taste (anterior 2/3) b. Complete paralysis on one side of the face c. Pain behind ear 4. Nursing Care a. Assess facial nerve regularly b. Administer meds as ordered (corticosteroids and mild analgesic) c. Provide soft diet with supplementary feedings d. Instruct px to chew on unaffected side e. Avoid hot fluids/foods f. Perform mouth care after each meal g. Provide special eye care to protect cornea Dark glasses Artificial tears Ointment and eye patch at night to keep eyelids close h. Provide support and reassurance Spinal Cord Alterations A. Herniated Nucleus Pulposus (refer to orthopedic nursing) B. Spinal cord Injury 1. Causes a. Traumatic Motor vehicle crashes most common Violence-related Falls Sports-related b. Non-traumatic Hematoma Ruptured vessel Congenital defect (ex. Spina bifida) 2. Predominant Risk factors a. Age common among 16-30 y/o
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Gender male>female c. Alcohol d. Drug Use 3. Most commonly involved vertebra a. C5-C7 b. T12 c. L1 4. Clinical manifestations: depending on type and level of injury 5. Classification of SCI according to degree of sensory and motor impairment; American Spinal Injury Association (ASIA) Impairment Scale: a. A (Complete) no motor or sensory function in the sacral segments S4-S5 b. B (Incomplete) sensory, but not motor function, is preserved below the neurologic level c. C (Incomplete) motor function is preserved below the neurologic level, but more than half of key muscles below the neurologic level have a muscle grade less than 3 d. D (Incomplete) motor function is preserved below the neurologic level, at least more than half of key muscles below the neurologic level have a muscle grade of 3 or greater e. E (Normal) motor and sensory functions are normal 6. Classification of SCI according to the area of spinal cord damage a. Central cord syndrome motor deficits (in the upper extremities compared to the lower extremities); sensory loss varies but is more pronounced in the upper extremities; bowel/bladder function may be affected or preserved b. Anterior cord syndrome loss of pain, temperature and motor function below the lesion; light touch, position and vibration sensation remain intact c. Lateral cord syndrome (Brown-Sequard syndrome) ipsilateral paralysis or paresis with ipsilateral loss of touch, pressure and vibration and contralateral loss of pain and temperature 7. Diagnostics a. X-ray of spine b. CT Scan and MRI c. Myelogram if MRI is contraindicated 8. Nursing Care a. Emergency Care ABCDE (Airway, Breathing, Circulation, Disability, Exposure) Immobilize using a spinal (back) board, with head and neck secured on neutral position (to prevent an incomplete injury from becoming complete) b. Acute Care Administer drugs as ordered high dose methylprednisolone, a corticosteroid, has been found to improve motor and sensory outcomes at 6 weeks, 6 months and 1 year if given within 8 hours after injury Administer oxygen to maintain high partial pressure of oxygen (PaO2) Care of reduction and traction devices (ex. Use of skeletal tongs or halo device for cervical fracture) Monitor vital signs Maintain F/E Watch out for spinal shock (sudden depression of reflex activity below the lesion which may also affect bladder and bowel function) Watch out for neurogenic shock (loss of autonomic function below lesion; vital organs are affected) Prevent complications of immobilization 9. Surgical Management a. Laminectomy excision of posterior arches and spinous process of vertebra); indications: Progressive neurologic deficit Suspected epidural hematoma Bony fragments Penetrating injuries that require surgical debridement Direct visualization and exploration of the cord b. Pre-op care Teach patient log-rolling turning patient as a unit while maintaining alignment of the spinal column c. Post-op care
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b.

1. 2.

1. 2. 3. 4.

Position patient as ordered Low Spinal Surgery generally flat High Spinal Surgery slight elevation of head Maintain proper body alignment Reposition q1-2 by log-rolling Place pillows between legs while on theside Assess for post-op complications: Respiratory distress Constipation Abdominal distention and pain Hypoactive bowel sounds

Pediatric Alterations

A. Febrile Seizures 1. Convulsions brought on by a fever in infants or small children 2. During a febrile seizure, a child often loses consciousness and shakes, moving limbs on both sides of the body;
less commonly, the child becomes rigid or has twitches in only a portion of the body, such as an arm or a leg, or on the right or the left side only 3. Most febrile seizures last a minute or two, although some can be as brief as a few seconds while others last for more than 15 minutes 4. Occur in children between the ages of 6 months and 5 years 5. Between 95 and 98 percent of children who have experienced febrile seizures do not go on to develop epilepsy Hydrocephalus water in the brain; abnormal accumulation of CSF in the ventricles, or spaces, of the brain 1. Classification a. Non-communicating flow of CSF from ventricles to subarachnoid space is obstructed b. Communicating flow of CSF is not obstructed, but CSF is inadequately reabsorbed in the subarachnoid space 2. Assessment a. Infants Bulging, non-pulsating fontanels and separated sutures Enlarged head Eyes that appear to gaze downward (sunset eyes) Irritability Seizures Lethargy/Sleepiness Poor feeding Vomiting High pitched cry Abnormal muscle tone b. Older Children Changes in head size is less common Signs of ICP (vomiting, ataxia, headache) Alterations in neurologic status Papilledema (or papilloedema) optic disc swelling that is caused by increased intracranial pressure; late sign 3. Diagnosis a. Serial transillumination transmission of light through the skull of the infant; if there is an excess of CSF, light is scattered to different parts of the skull, producing patterns characteristic to hydrocephalus b. Ultrasonography shows pathologic increase in ventricle size c. CT Scan d. MRI e. ICP monitoring techniques 4. Surgical Management (Shunt procedure) a. Placement of a ventricular catheter (a tube made of silastic), into the cerebral ventricles to bypass the flow obstruction/malfunctioning arachnoidal granulations and drain the excess fluid into other body cavities, from where it can be resorbed
23

B.

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C.

Most shunts drain the fluid into the peritoneal cavity (ventriculo-peritoneal shunt), but alternative sites include the right atrium (ventriculo-atrial shunt), pleural cavity (ventriculo-pleural shunt), and gallbladder c. Complications of shunts: infection, obstruction, overdrainage, intraventricular hemorrhage 5. Nursing Care a. Provide routine pre-op care with special attention to monitoring neurologic status b. Provide post-op care Maintain patency of shunt Position child on the operative side Pump the shunt as ordered Observe for signs of infection Position head slightly elevated c. Instruct parents regarding: Wound care Signs of Infection Signs of increased ICP Need for repeated shunt if it becomes blocked or infected Expected level of development Availability of support group Meningitis inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges 1. Etiology a. Viral or aseptic Enterovirus b. Bacterial H. influenzae (in children), N. meningitides (in adolescents), S. pneumoniae (in elderly) c. Protozoal Naegleria and Acanthamoeba d. Fungal Cryptococcus neoformans 2. Assessment a. Triad of meningitis: Nuchal rigidity (inability to flex the neck forward passively due to increased neck muscle tone and stiffness) Sudden high fever Altered mental status b. Headache most common symptom in adults c. Opisthotonus rigid arching of back d. (+) Kernigs sign and Brudzinski sign (pathognomonic sign) Kernigs sign px supine, hip and knee 90o; passively extend knee; (+) Kernig's sign knee extension pain Brudzinskis sign px supine; flex neck; (+) Brudzinskis neck flexion involuntary flexion of knee and hip e. Projectile vomiting due to increased ICP f. Photophobia and phonophobia g. Chills, anorexia h. Irritability i. Generalized body malaise j. Weight loss k. Abnormal posturing (decorticate/decerebrate) l. Possible seizure m. Rapidly spreading petechial rash (if meningococcal bacteria) 3. Diagnostic test Lumbar/Spinal tap a. Lumbar/Spinal tap use of hollow spinal needle into the subarachnoid space (L3-L4 or L4-L5) b. CSF Analysis confirms meningitis: Increase proteins and WBC Decrease glucose Increase CSF opening pressure (normal: 50-160 mmHg) (+) Culture microorganism c. Side Effects CSF leak (prone 2-3 hours) Headache (flat on bed for 12-24 hours; hydrate)
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b.

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D.

4. Nursing Care a. Administer meds Broad-spectrum penicillin (for bacterial meningitis) o SE: Organ toxicity, Superinfection, Allergic reaction Corticosteroids to prevent complications of overactive inflammation Antipyretic Mild analgesic b. Strict respiratory isolation (safe after 24 hours of antibiotic therapy) c. Comfortable and dark room due to photophobia and seizure d. Prevent complications of immobility e. Maintain F/E balance f. Monitor V/S, I/O, neuro check g. Observe for signs of hydrocephalus h. Provide client teaching and discharge plan Nutrition increase calories and carbohydrates; protein for tissue repair Small frequent feedings Prevent complications Prevent seizures i. Rehab for neurologic deficit Mental retardation Delay in psychomotor development Visual and Hearing impairment Urinary retention Spina bifida a neural tube defect characterized by failure of posterior vertebral arches to fuse during embryonic development; if the opening is large enough, this allows a portion of the spinal cord to protrude through the opening in the bones; the most common location of the malformations is the lumbar and sacral areas 1. Predisposing factors: a. If sibling has a neural tube defect b. Virus c. Environment d. Radiation 2. Types of Spina Bifida a. Spina bifida occulta hidden spina bifida; spinal cord and meninges are still in normal anatomic position; defect may not be visible (maybe identified by a dimple, lipoma, birthmark or tufts of hair in the spine); child is asymptomatic or may have slight neuromuscular deficit; no treatment if asymptomatic (treatment is aimed at specific symptoms) b. Spina bifida cystica a cyst protrudes through the defect in the vertebral arch; most common problem is rupture of sac; 2 types: Spina bifida meningocoele outpouching of meninges, not no nerve in the sac (thus no neuro deficit); good prognosis after surgery; the least common form Spina bifida myelomeningocoele the most common and most serious; the meningeal sac contains spinal elements, like spinal nerves; child will have neuro deficits below the site of lesion; 80% of children will have multiple handicaps. Encephalocoele cranial meningocoele or myelomeningocoele 3. Assessment a. Examine the defect for size, level, covering and CSF leakage b. Motor and sensory involvement include: Movement problems of lower extremities Withdrawal of lower extremities or crying Paralysis of lower extremities Joint deformities Hydrocephalus Neurogenic bowel 4. Diagnostics a. Prenatal UTZ may show spinal defect Amniocentesis elevated Alpha Fetoprotein (AFP) leve b. Postnatal
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X-ray of spine, CT Scan shows vertebral defect Myelogram shows extent of neural defect Encephalogram shows hydrocephalus 5. Nursing Care a. Prevent trauma to the sac Cover with sterile dressing, soak with NSS Position infant prone/side-lying Keep are free from contamination by urine/feces (protective barrier drape maybe necessary) Inspect the sac for intactness or signs of infection Administer antibiotics b. Prevent complications Observe for signs of hydrocephalus, meningitis and joint abnormalities Clean, intermittent catheterization to manage neurogenic bladder Administer meds to prevent urinary complications Perform passive ROM exercise to lower extremities c. Provide adequate nutrition adopt diet and feeding techniques according to childs position d. Provide sensory stimulation objects for visual stimulation; stimulate also other senses e. Provide emotional support to parents and family f. Provide patient teaching Wound care Passive ROM exercises Signs of infection Medication and SE Feeding, diapering, positioning Availability of appropriate support groups, genetic counseling Cerebral Palsy neuromuscular disorder resulting from damage to the motor control centers of the developing brain and can occur during pregnancy, during childbirth or after birth up to about age three 1. Incidence: 1.5-5 in 1,000 live births 2. Possible Causes: a. Prenatal Altered neurologic development Poor oxygen supply before birth Exposure to radiation Drugs before birth Infections, such as rubella, toxoplasmosis, or cytomegalovirus b. Perinatal Birth injuries Perinatal asphyxia Drugs during birth c. Postnatal Physical brain injury ex. child falls out of crib Incidents involving hypoxia to the brain (such as drowning) Toxins and Infections (encephalitis or meningitis) Severe dehydration Tumors Kernicterus high levels of bilirubin in the blood that leads to brain damage 3. Classification a. Spastic most common type; increase muscle tone leading to stiff and difficult movement Common types of spastic CP hemiparesis, quadriparesis, paraplegia b. Ataxic caused by damage to the cerebellum; lack of balance, poor coordination, dizziness, impaired depth perception and hypotonia Manifested by a wide-based gait and rapid repetitive movements are performed poorly May also suffer from intention tremors, a shaking that begins with a voluntary movement; muscles and reflexes are normal c. Athetoid/Dyskinetic mixed muscle tone: trouble holding themselves in an upright, steady position for sitting or walking, and often show involuntary and uncontrolled motions
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 Major manifestations are athetosis (wormlike movement), dyskinetic movement of mouth, drooling and dysarthria Movements may become choreoid (irregular, jerky) and dystonic (disordered muscle tone), especially when stressed and during the adolescent years d. Hypotonic limp and can move only a little or can't move at all e. Mixed 4. Associated problems a. Mental retardation b. Hearing loss c. Defective speech d. Seizures e. Attention deficit disorder f. Sensory impairment 5. Assessment a. Delayed gross motor development most common clinical manifestation b. Alterations of muscle tone (e.g. increased or decrease resistance to passive movements, child feels stiff when handling or dressing, difficulty in diapering or opisthotonos) c. Abnormal postures (e.g. scissoring legs or persistent infantile posturing) d. Reflex abnormalities (e.g. persistent primitive reflexes, such as tonic neck of hyperreflexia) 6. Nursing Care a. Prevent physical injury by providing the child with a safe environment, appropriate toys, and protective gear (helmet, kneepads) if needed. b. Prevent physical deformity by ensuring correct use of prescribed braces and other devices and by performing ROM exercises. c. Promote mobility by encouraging the child to perform age-and condition-appropriate motor activities. d. Promote adequate fluid and nutritional intake. e. Foster relaxation and general health by providing rest periods. f. Administer prescribed medications which may include sedatives, muscle relaxants and anticonvulsants. g. Encourage self-care by urging the child to participate in activities of daily living (ADLs) (e.g. using utensils and implements that are appropriate for the childs age and condition). h. Facilitated communication 1. Talk to the child deliberately ad slowly, using pictures to reinforce speech when needed. 2. Encourage early speech therapy to prevent poor or maladaptive communication habits. 3. Provide means of articulate speech such as sign language or a picture board. 4. Technology such as computer use may help children with severe articulation problems. i. As necessary, seek referrals for corrective lenses and hearing devices to decrease sensory deprivation related to vision and hearing losses. j. Help promote a positive self-image in the child: 1. Praise his accomplishments 2. Set realistic and attainable goals 3. Encourage and appealing physical appearance 4. Encourage his involvement with age and condition- appropriate peer group activities. k. Promote optimal family functioning 1. Encourage family members to express anxieties, frustrations and concerns and to explore support networks. 2. Provide emotional support and help with problem solving as necessary. 3. Refer the family to support organizations such as the United Cerebral Palsy Association. l. Prepare the child and family for procedures, treatments, appliances and surgeries if needed. m. Assist in multidisciplinary therapeutic measures designed to establish locomotion, communication and self-help, gain optimal appearance and integration of motor functions; correct associated defects as effectively as possible and provide educational opportunities based on the individuals needs and capabilities. Therapeutic measures include: 1. Braces to help prevent or reduce deformities, increase energy of gait, and control alignment. 2. Motorized devices to permit self-propulsion. 3. Orthopedic surgery to correct deformities and decrease spasticity (medications are not helpful for spasticity). 4. Medications to control possible seizure activity or attention deficit disorder. 5. Speech therapy and physical therapy. n. Inform parents but their child will need considerable help and patience in accomplishing each new task. 1. Encourage them not to focus solely on the childs inability to accomplish certain tasks. 2. Urge them to relax and demonstrate patience.
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3. Explain the importance of providing positive feedback. o. Encourage the family to seek appropriate functional, adaptive and vocational training for the child. p. Encourage family members to achieve balance in their lives between caring for their disabled child and other family and personal matters. Reyes Syndrome a potentially fatal disease that causes numerous detrimental effects to many organs, especially the brain and liver, as well as causing hypoglycemia; the disease causes fatty liver with minimal inflammation and severe encephalopathy (with swelling of the brain) 1. The exact cause is unknown, and while it has been associated with aspirin consumption by children with viral illness, it also occurs in the absence of aspirin use 2. Signs and symptoms a. Stage I 1. Persistent, heavy vomiting that is not relieved by eating 2. Generalized lethargy 3. General mental symptoms, e.g. confusion 4. Nightmares 5. High fever 6. Headaches b. Stage II 1. Stupor caused by minor brain inflammation 2. Hyperventilation 3. Fatty liver (found by biopsy) 4. Hyperactive reflexes c. Stage III 1. Continuation of Stage I and II symptoms 2. Possible coma 3. Possible cerebral edema 4. Rarely, respiratory arrest d. Stage IV 1. Deepening coma 2. Large pupils with minimal response to light 3. Minimal but still present hepatic dysfunction e. Stage V 1. Very rapid onset following stage IV 2. Deep coma 3. Seizures 4. Multiple organ failure 5. Flaccidity 6. Extremely high blood ammonia (above 300 mg/dL of blood) 7. Death

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