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. Functions1. Motor – controls body movement2. Sensory – responds to sensory stimuli3. Fast-acting regulatory system that controls all other systems of the body4. Also responsible for consciousness, intelligence, memory

B. Principal Divisions1. Central Nervous System (CNS) – brain & the spinal cord; serves as control mechanism for the entire organism2. Peripheral Nervous System (PNS)

a. 12 Cranial nerves (CN)b. 31 Spinal nervesc. Autonomic nerves

i. Sympatheticii. 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 Neurons1. Sensory (afferent) neurons – from sensory receptors to CNS2. Motor (efferent) neurons – from CNS to effector (muscle/glands)3. Interneurons – connect neuron to neuron found in CNS only

D. Synapses1. An axon transmits a nerve impulse at a specialized junction with another neuron called synapse2. Junction of Presynaptic and Postsynaptic neurons3. Axons may establish synaptic contacts with any portion of the surface of another neuron, except those regions that

are myelinated4. 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. Typesa. Somatic – stimulates skeletal musclesb. Autonomic – stimulates autonomic organs

2. Elementsa. Sensory receptorb. Afferent neuronc. Integration center (CNS)d. Efferent neurone. Effector organ

F. Central Nervous System1. Brain

a. Characteristicsi. 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. Partsi. 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

o Precentral gyrus – motor functiono Broca’s Area – speech production (base of precentral gyrus); damage to broca’s area leads to

expressive (non-fluent) aphasia

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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 Wernicke’s Area – speech comprehension (posterior area of superior temporal gyrus); damage to wernicke’s 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 – body’s 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 body’s 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 contractionso Respiratory center – regulates breathing depth and rateo 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 centerc. Emerges from the base of the brain at the level of the foramen magnum & extends caudally to L2 vertebra, then

cauda equina3. Protection of the CNS

a. Skull bones and vertebral columnb. Meninges – protective covering of the cerebral cortex and spinal cord

i. Dura mater – tough outermostii. Arachnoid mater – middle weblikeiii. 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 mm3) 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 Monroii. Third ventricle (diencephalon)

↓ Cerebral aqueduct of Sylvius (midbrain)iii. Fourth ventricle (posterior to pons & medulla)

↓ Foramen of Lushka and Magendieiv. Central canal of spinal cord (canal inside the spinal cord) and Subarachnoid space (space that surrounds the

brain and spinal cord) ↓ Arachnoid villi

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v. Dural venous sinusesvi. Blood (Venous circulation)

d. Blood-Brain barrier – relatively impermeable capillaries to isolate neural tissues in the CNS from the general circulation

G. Peripheral Nervous System1. Cranial Nerves – “Oh, oh, oh, to touch and feel a girl’s 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 & Plexusesi. Intercostal nerves – anterior rami of spinal nerves T1–T11; travel in the intercostal space sandwiched

between two adjacent ribsii. 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*Superior and inferior gluteal – gluteus

3. Autonomic Nerves – divided into the Parasympathetic, Sympathetic and Enteric Systemsa. 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

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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 Parasympathetic SympatheticOther Name “Housekeeping”

or “Resting and Digesting”

“Fight-or-Flight”

Nerves Included Craniosacral: Cranial nerves 3,

7, 9, 10 and Spinal nerves S2-

S4

Thoracolumbar: Thoracic and

Lumbar Spinal Nerves

Neurotransmitters Acetylcholine Epinephrine, Norepinephrine

Receptor Nicotinic, Muscarinic

α1, α2, β1, β2

Major Effects Constricts Pupil, Constricts

bronchioles, Increases peristalsis,

Dilates vessels, Decreases HR and BP, penile

erection

Dilates Pupil, Dilates

bronchioles, Inhibits

peristalsis, Increases

Blood Glucose, Constricts vessels,

Increases HR and BP,

ejaculation

c. Enteric (ENS) – directly controls the gastrointestinal tract (peristalsis, secretions, churning) Auerbach’s (Myenteric) Plexus – located between the inner and outer layers of muscularis externa Meissner’s (Submucosal) Plexus – located in the submucosa

H. Blood Supply of the Brain1. 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 hippocampusb. 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

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. HeadachePrepared by Dr. Jhason John J. Cabigon 4

B. Conditions that Increase intracranial pressure (ICP)1. Head Trauma2. Cerebrovascular Disorders3. Brain Tumor

C. Seizure Disorders and EpilepsyD. Degenerative Diseases

1. Parkinson’s disease2. Alzheimer’s disease

E. Demyelinating Disease: Multiple SclerosisF. Neuromuscular Disease: Myasthenia GravisG. PNS Diseases

1. Guillain Barre Syndrome2. Trigeminal Neuralgia3. Bell’s Palsy

H. Motor Neuron Disease: Amyotropic Lateral SclerosisI. Spinal Cord Alterations

1. Herniated Nucleus Pulposus2. Spinal cord Injury

J. Pediatric Conditions1. Febrile Seizures2. Meningitis3. Spina bifida4. Hydrocephalus5. Cerebral Palsy6. Reye’s Syndrome

Headache

A. Types:1. Primary

a. Migraine – cerebral vasodilationb. Tension HA – chronic, less severe; muscle spasm of neck and scalp (band-like)c. Cluster HA – most painful; cyclical (wks to months), then remission (months to yrs)d. Cranial arteritis – older people; immune-mediated temporal headache

2. Secondary – organic cause, ex. brain tumor or aneurysmB. 4 Phases of Migraine

1. Prodrome – hours to days before attack; variety of symptoms, but same prodrome each attack2. Aura – less than 1 hr; usually visual disturbances (light flashes or bright spots)3. Headache – Intensifies over 4-72 hours4. Recovery (Postdrome)

C. Medical Management – Vasoconstrictors (contraindicated in HPN and IHD)1. Sumatriptan (Imitrex) 2. Ergotamine (Avamigran)

D. Nursing Care1. Meds on onset of pain2. Quiet, dark environment3. Elevate head 30o4. 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 Trauma1. Most Common Causes:

a. Motor vehicular accidentsb. Violencec. Falls

2. Risk Factors:

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a. Alcohol intakeb. Drugsc. Low Socioecomic level

3. Brain Injury can be Closed (Blunt) Injury or Open Brain Injury4. 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 (Battle’s 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 Traumao Coagulopathieso Ruptured aneurysm

Typeso Acute – symptoms develop over 24 to 48 hourso Subacute – after 48 hours to 2 weekso 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

6. PathophysiologyBrain 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 Traumaa. 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

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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 ScoreEye Opening Spontaneous

To verbal commandTo painNo response

4321

Verbal Response Oriented, conversesDisoriented, conversesUses inappropriate wordsMakes incomprehensible soundsNo response

54321

Motor Response To verbal commandTo localized painFlexes and withdrawsFlexes abnormally (decorticate position)Extends abnormally (decerebrate position)No response

654321

*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 lighto Ipsilateral dilation of pupilo Fixed dilated pupilso Doll’s eyes – oculocephalic reflex

d. Cushing’s 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 +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 8. Diagnostics

a. Radiologic examination confirms the presence and extent of skull fractureb. CT Scanc. MRId. Cerebral angiographye. Positron Emission Tomography (PET) – method of scanning the examines the brain function rather than structure

9. Complications of Traumatic Brain Injurya. Decrease cerebral perfusion b. Cerebral edema and herniation

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c. Impaired oxygenation and ventilationd. 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)

10. Nursing Diagnosisa. Altered Cerebral Tissue Perfusion r/t increased ICPb. Ineffective Breathing pattern r/t compression of respiratory centerc. Aspiration r/t unconsciousnessd. Self-care deficit r/t altered level od consciousnesse. Impaired physical mobility r/t abnormal motor responsef. Impaired nutrition, less than body requirements r/t increased metabolic demands, fluid restriction and inadequate

intakeg. Risk for injury (self-directed and directed at others) r/t seizures, disorientation, restlessness or brain damageh. Risk for imbalanced body temperature r/t damaged temperature-regulating mechanisms in the braini. Risk for impaired skin integrity r/t bed rest, hemiparesis, hemiplegia, immobility, or restlessnessj. 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 checksl. Interrupted family processes r/t unresponsiveness of patient, unpredictability of outcome, prolonged recovery

period, and the patient’s residual physical disability and emotional deficitm. Deficit knowledge about brain injury, recovery and the rehabilitation process

11. Managementa. 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 fractures12. Nursing Care

a. Monitor neurologic checks hourly Level of consciousness (GCS) Pupils DTRs Motor and Sensory CN testing

b. Monitor vital signsc. Lessen constrictive clothing and remove potentially injurious itemd. 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 edemag. Monitor IVF (Isotonic solution; KVO)h. Monitor I/O and F/E (inc in ICP leads à renal vasoconstriction à decrease blood flow to kidneys à 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-q4Prepared by Dr. Jhason John J. Cabigon 8

k. Turning and repositioning q2l. 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 à attracts fluid from

brain tissue to vessels à 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 henleo SE: hyponatremia, hypokalemia

Anti-inflammatory Steroids – Prednisone (Pred), Dexamethasone (Decadron)o MOA: decreases edema by suppressing components of inflammationo SE: peptic ulcer, GI bleeding, Na and H20 retention, delayed wound healing, mood swings,

hyperglycemia, acneC. 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 stroke1. 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 arteriesb. Signs and symptoms

Signs and symptoms mainly depend on what specific part of the brain is affected 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 fieldo Loss of peripheral vision – unaware of objects or the borders of objectso Diplopia – double vision

Motor deficitso 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 gaito Dysarthria – difficulty in forming wordso Dysphagia – difficulty in swallowing

Sensory Deficitso Paresthesia – numbness or tingling of extremity (occurs on opposite side of lesion)

Communication deficitso Dysphasia – impaired speecho Aphasia – loss of speecho Expressive aphasia (Broca’s aphasia) – unable to form words that are understandableo Receptive aphasia (Wernicke’s aphasia) – unable to comprehend the spoken wordo Global (mixed) aphasia – combination

Apraxia – inability to perform a previously learned action/skill Cognitive deficits

o Amnesia – memory is disturbed or losto Decreased attention spano Impaired concentration

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o Poor abstract reasoningo Altered judgment

Emotional deficitso Loss of self-controlo Emotional labilityo Decreased tolerance to stressful situationo Depressiono Withdrawalo Fear, hostility, angero 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 strokesb. Ruptured intracranial aneurysm (dilation of weakened arterial wall) – results to subarachnoid hemorrhagec. Cerebral amyloid angiopathy – damage due to deposits of beta-amyloid protein in small and medium-sized

vessels of the braind. 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 neoplasmsf. Certain medications – anticoagulants, amphetamines

3. Risk Factors of Strokea. 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

b. 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 à ↑viscosity à stasis à thrombosis Stress – ↑sympathetic stimulation à vasoconstriction Physical inactivity – sedentary lifestyle

4. Severity of Strokea. 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

b. Reversible Ischemic Neurologic Disability (RIND) – 24 to 72 hoursc. Complete Stroke – if symptoms persist longer

5. Prognosis of Strokea. Thrombotic CVA – poor prognosis for neurologic and functional recoveryb. Embolic CVA – good prognosisc. Hemorrhagic CVA – 50-70% mortalityd. Lacunar CVA – very good prognosis

6. Emergency Carea. “ABCDE”b. Elevate head 30-45o to prevent ↑ICPc. Loosen constrictive clothes and remove potentially injurious itemsd. Monitor vital signs and level of consciousness

7. Medical Managementa. Thrombolytic therapy – used for dissolving clots in ischemic stroke

Recombinant tissue Plasminogen Activator (rt-PA) must be given within 3 hours à 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

b. Anticoagulants – for secondary thrombus formation; blocks conversion of prothrombin to thrombin; do not breakdown formed clots; ex. Heparin and warfarin

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Heparin – parenteral; use in stroke is controversial because of risk of bleeding o Ex. Heparin sulfateo 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 2.5o SE: Bleeding, N/V, contipationo Antidote: Vitamin K

c. 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

d. Narcotic analgesics – to provide sedation; ex. Morphine sulfate and Meperidine HCl (Demerol)e. Antihypertensivesf. Hyperosmotic Diureticg. Anti-inflammatoryh. Anti-convulsanti. Stool softener

8. Surgical management: for evacuation of blood clots (ex. Craniotomy, burr hole)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 q1d. Monitor V/Se. Provide psychological supportf. Administer meds as orderedg. 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

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Allow sufficient time to answerk. For Apraxia

Guide px through intended movement Keep repeating the movement

D. Brain Tumor1. 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 bodyc. Supratentorial – occuring in anterior 2/3 of brain (primarily cerebrum)d. Infratentorial – posterior 1/3 (primarily cerebellum and brainstem

2. Assessmenta. 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 projectilec. Coordination disturbance (ataxia)d. Hypotonia and hyporeflexiae. Nystagmus (rhythmical activity of the eye)f. Diplopia (double vision)g. Visual field defectsh. Signs of inc. ICP

3. Monitoring ICPa. ICP monitoring – records the pressure exerted w/in the cranial cavity by the brain, cerebral blood and CSFb. 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. Managementa. 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 edemac. Hyperosmotic Diureticd. Stool softenere. Anti-convulsantsf. Analgesicsg. 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 ↑ICPb. Administer meds c. Provide care for neurologic deficitsd. Provide supportive care for effects of radiation and chemoe. Provide psychological support to patient and family due to its diagnosis and poor prognosisf. Prepare patient for surgery

E. Intracranial Surgeries1. 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

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• 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 skulld. 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 headacheb. Provide emotional supportc. Shampoo scalp and check signs of infectiond. Shave haire. Monitor V/S and neuro checksf. Avoid enemas unless indicated – straining ↑ICPg. Give pre-op steroids as orderedh. Insert foley catheter as ordered

3. Post-op Nursing Care:a. Maintain patent airway and adequate ventilation

Supratentorial Incisiono Elevate head off bed 30-45oo Position patient on the back if intubated

Infratentorial Incisiono Keep head flat or elevate 20-30oo Do not flex head to chesto Check respiration closely and report signs of distresso Maintain on NPO for 24 hours – due to possible impairment of swallowing and gag

b. Monitor V/S and neuro checks q1c. Turn q2d. 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 frequentlyf. Administer meds as orderedg. Apply ice to swollen eyesh. Refer px for rehab for residual deficit

Seizures and Epilepsy

A. Definition1. Seizures – episodes of abnormal, motor, sensory, autonomic, or psychic activity (or combination of these) that result

from sudden excessive discharge from cerebral neurons2. 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. Idiopathica. Geneticb. Developmental defects

2. Acquireda. CVDb. Hypoxemia of any cause, including vascular insufficiencyc. Fever (children)

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d. Head injurye. Hypertensionf. 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 withdrawalj. Allergiesk. Encephalopathy (ex. Reye’s syndrome)l. Congenital CNS defect (ex. Hydrocephalus)m. Degenerative diseases (ex. Tay-Sach’s disease)

C. Classification of Seizures1. 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 symptomsc. Complex partial – consciousness is impaired coupled with automatism (lip smacking, chewing, aimless walking,

or other complex motor activities)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. Diagnostics1. Electroencephalography (EEG) – measures abnormal electrical activity of the brain2. Other procedures to detect primary disorders (i.e. MRI for brain tumor)

E. Medications – Anticonvulsants1. Phenobarbital (Luminal) and Phenytoin (Dilantin) – can be used for both grand mal and petit mal seizures2. Carbamazepine (Tegretol) – can be used for refractory seizures not responding to other anticonvulsants3. 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 privacy2. Patient with an aura (warning sign of an impending seizure) may have time to seek a safe, private place3. If with aura, place oral airway4. Do not pry open clenched jaws (putting tongue blade is no longer recommended)5. Ease patient on the floor6. Protect head with a pad7. Push aside any furniture8. Loosen constrictive clothing9. If in bed, remove pillows and raise side rails10. Do not restrain11. If possible, place patient on one side with head forward12. If suction available, use it to clear secretions

G. Nursing Care After the Seizure1. 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 seizure4. Reorrient patient upon awakening5. Use calm persuasion and gentle restraint if patient becomes agitated post-ictal

Neurodegenerative Disorders

A. Parkinson’s Disease1. A slowly progressing neurologic movement disorder that eventually leads to disability2. Associated with decreased levels of dopamine resulting from destruction of pigmented neuronal cells in the

substantia nigra in the basal ganglia region of the brain3. 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

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5. Causative Factors:a. Idiopathic (unknown) – most commonb. 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. Pathophysiologya. Destruction of dopaminergic cells in the substantia nigra in the basal ganglia

↓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. Assessmenta. Tremors – pill-rolling, restingb. Rigidity – cogwheelc. Bradykinesia – slow movementd. Fatiguee. Postural Instability – stooped posture, propulsive, shuffling gait (short steps with feet barely leaving ground, thus

producing a shuffling noise) f. Emotional lability and depressiong. Seborrhea (scaly skin) h. Autonomic symptoms (increased salivation and sweating, constipation, decreased sexual capacity)i. Mask-like facies (emotionless), decreased blinking of eyesj. Micrographia – small handwritingk. Dysphonia – soft, slurred low-pitched and less-audible speech)

8. Medicationsa. 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 tremorsd. Antiviral – amantadine (Symmetrel); early parkinson’s; believed to release dopamine from storage sitese. Dopamine agonists – bromocriptine mesylate (Parlodel) and pergolide (Permax); often employed to postpone the

initiation of carbidopa or levodopa or when carbidopa or levodopa loses effectivenessf. Tricyclic antidepressants – amitriptyline HCl (Elavil); 1/3 to 1/2 of the dosage used in depressed patientsg. MAOIs – selegiline (Eldepryl); inhibits dopamine breakdownh. Antihistamines – diphenhydramine HCl (Benadryl); reduce tremors and anxiety

9. Nursing Carea. Administer drugsb. 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

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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 Allow sufficient time for meals

g. Avoid constipation and maintain adequate bowel elimination Increase fluids High fiber diet Stool softeners

h. Provide psychological supporti. 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 pillow2. Keep head and neck as erect as possible3. Use broad-based gait4. Raise feet while walking

B. Alzheimer’s Disease1. Senile Dementia of the Alzheimer’s type2. Chronic, progressive, and degenerative brain disorder that is accompanied by profound effects on memory, cognition,

and ability for self-care3. Abnormal protein deposits and other structural changes appear4. Theories:

a. Oxidative stress, primarily in the hippocampus and neocortexb. Reduction in brain Ach

5. Anti-Alzheimer Medicationsa. Drugs that do not cure alzheimer’s 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 researchD. Predisposing/Precipitating Factors:

1. Geography – frequent in cool and temperate climates (Europe, New Zealand, Southern Australia, Northern US, Southern Canada)

2. Genetic predisposition3. Viral infection – a virus triggering the autoimmune response4. Emotional and physical stress – may induce relapse (exacerbations and remissions are characteristics of MS)

E. Pathophysiology1. Sensitized T cells cross the blood-brain barrier

↓

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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 tractb. Cerebrumc. Brainstemd. Cerebellume. Spinal Cord

F. Assessment1. Visual disturbance – blurred vision, scotoma (blind spots), diplopia2. Fatigue – most disabling symptom3. Impaired sensation – paresthesia and pain4. Impaired motor function – weakness, paralysis, spasticity5. Mood swings – depression 6. Impaired cerebellar function – nystagmus, tremors, ataxia, difficulty in coordination7. Bladder dysfunction – urinary retention/incontinence8. Bowel dysfunction – constipation9. Sexual dysfunction – impotence in males

G. Secondary Complications1. UTI2. Constipation3. Pressure ulcers4. Contracture deformities5. Dependent pedal edema6. Pneumonia7. Reactive depression8. Decreased bone density

H. Types of MS1. Relapsing – remitting (RR) MS2. Primary progressive (PP) MS3. Secondary progressive (SP) MS4. Progressive-relapsing (PR) MS

I. Diagnostics1. CSF Exam - ↑ protein and immunoglobulins2. Evoked potential studies – define the extent of disease process and monitor changes3. Neuropsychological testing4. MRI – shows area of demyelination

J. Medications1. No cure exists for MS; only delay the progression of the disease or symptom management2. IV methylprednisolone – key agent in treating acute relapse in RR MS3. 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 plaquesK. 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↓

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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 productionD. Assessment

1. MG is a purely motor disorder2. 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 facies5. Laryngeal involvement – dysphonia, hoarseness6. Generalized weakness7. Weakness of intercostal muscles leading to decreased vital capacity and respiratory failure

E. Diagnosis1. Tensilon Test – IV injection of edrophonium or Tensilon® (a fast-acting acetylcholinesterase inhibitor) provides

spontaneous relief of symptoms2. EMG – amplitude of evoked potentials3. Ach receptor antibody test4. MRI – showing enlarged thymus gland

F. Management1. Pyridostigmine bromide (Mestinon) – an anticholinesterase; first line of therapy

SE: fasciculations, abdominal pain, diarrhea and increased oropharyngeal secretions2. Other anticholinesterases – neostigmine (Prostigmin) and ambenomium (Mytelase)3. Corticosteroids – suppresses immune response; ex. prednisone4. Immunosuppressive drugs5. Surgery – thymectomy6. Plasmapheresis (plasma exchange) – used to treat exacerbations; removal of plasma containing acethylcholine

receptor antibodies G. Nursing Care

1. Administer drugs as ordered and observe SE2. Monitor effectiveness of drug; assess muscle strength before and after medication3. Avoid the following drugs:

a. Certain antibiotics, like neomycin, streptomycin , kanamycin and other aminoglycosides – agranulocytosisb. Cardiovascular meds, like procainamide – arrhythmiac. Sedatives, like morphine – respiratory depressiond. Quinine – hypotensione. Procaine (Novocaine)f. Beta-blockersg. Antiseizure and psychotropic drugs

4. Provide optimal nutritiona. Check gag reflexb. Provide soft dietc. Do not leave alone if with difficulty in swallowing

5. Monitor respiratory status frequently6. Keep emergency airway and suction equipment nearby7. 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 Cause S/Sx’s ManagementMultiple sclerosis Demyelinating dse of CNS; plaques

appear on demyelinated axons scotoma (blind spots), diplopia & BOV; then variety of neuro sx

*Methylprednisolone: key*Anti-spastics: diazepam, baclofen, dantrolene (Dantrium)

Myasthenia gravis Destruction of post-synaptic acetylcholine receptor leading to muscle weakness

diplopia and ptosis; then muscle weakness that increases w/ activity (purely motor)

*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

Guillain-Barre Syndrome

Demyelinating dse of PNS leading to ascending weakness

Ascending weakness (lower extremities à respiratory

Emergency intubationIVIG

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muscles)

Motor Neuron Disease: Amyotropic Lateral Sclerosis

A. Amyotropic Lateral Sclerosis (Lou Gehrig’s Disease) – progressive loss of motor neurons leading to atrophy of musclesB. Death usually occurs as a result of respiratory infection secondary to respiratory insufficiencyC. Incidence: 1.5 cases per 100,000; men>women; onset occurring in the 5th or 6th decade of lifeD. Theories about the cause of ALS:

1. Autoimmune2. Free radical damage3. Oxidative stress

E. Assessment1. Clinical manifestations depend on the location of the afftected motor neurons2. 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 ALSG. Management

1. No specific therapy for ALS2. Main focus: maintain or improve function, well-being and quality of life3. Riluzole (Rilutek) – glutamate antagonist; slows the deterioration of motor neurons

PNS Diseases

A. Guillain-Barré Syndrome1. 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 paresthesia2. Incidence: men > women3. 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 changesc. Antecedent event usually 2 weeks before symptoms begind. Cranial nerve involvement – blindness, inability to swallow and clear secretion, dysphagiae. Ventilatory insufficiency if paralysis ascends to the respiratory musclesf. Autonomic dysfunction – HPN, bradycardia/tachycardia, orthostastic hypotensiong. Do not affect cognitive function

5. Diagnosticsa. CSF – elevated proteinsb. Evoked potential studies – demonstrate a progressive loss of nerve conduction velocity

6. Managementa. Because of the possibility of rapid progression and neuromuscular respiratory failure, GBS is a medical

emergencyb. Respiratory therapy or mechanical ventilation may be necessaryc. Elective intubation before onset of respiratory insufficiencyd. IVIG – therapy of choicee. 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/ MS4. Etiology: unknown; but vascular compression and pressure are suggested5. Assessment

a. The pain ends abruptly as it starts and is described as unilateral shooting and stabbing sensationb. Associated with involuntary contractions of the facial muscles – sudden closing of the eye, twitching of mouth

6. Managementa. Antiseizure agents – carbamazepine (Tegretol), gabapentin (Neurontin) and phenytoin (Dilantin) relieves painb. Nerve Block – injection of phenol/alcohol; temporary effect (last 6-18 months)

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c. Surgery Microvascular decompression of the trigeminal nerve Radiofrequency Thermal Coagulation Percutaneous Baloon Microcompression

7. Nursing Carea. Assess character of pain including triggering factors and pain management techniquesb. Administer meds and monitor responsec. Maintain room in moderate temperatured. Provide small frequent feedings of lukewarm, semisolid or soft foodse. Hygiene; Provide patient with soft cloth and lukewarm water (perform only during periods of ↓pain)f. Prepare patient for surgery if necessaryg. 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 careii. Chew on the unaffected sideiii. Avoid hot fluids/foodsiv. Mouthcare after mealsv. Good oral hygiene and visit dentist q6movi. Protect face during extreme temp

C. Bell’s Palsy1. Bell’s 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 weeks2. Predisposing factors:

a. Unknownb. Vascular ischemiac. Viral infection (herpes simplex, herpes zoster)d. Autoimmunee. Brain Tumor

3. Assessmenta. Loss of taste (anterior 2/3)b. Complete paralysis on one side of the facec. Pain behind ear

4. Nursing Carea. Assess facial nerve regularlyb. Administer meds as ordered (corticosteroids and mild analgesic)c. Provide soft diet with supplementary feedingsd. Instruct px to chew on unaffected sidee. Avoid hot fluids/foodsf. Perform mouth care after each mealg. 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. Causesa. Traumatic

Motor vehicle crashes – most common Violence-related Falls Sports-related

b. Non-traumatic Hematoma Ruptured vessel Congenital defect (ex. Spina bifida)

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2. Predominant Risk factorsa. Age – common among 16-30 y/ob. Gender – male>femalec. Alcohold. Drug Use

3. Most commonly involved vertebraa. C5-C7b. T12c. L1

4. Clinical manifestations: depending on type and level of injury5. 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-S5b. 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 3d. 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 greatere. E (Normal) – motor and sensory functions are normal

6. Classification of SCI according to the area of spinal cord damagea. 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 intactc. Lateral cord syndrome (Brown-Sequard syndrome) – ipsilateral paralysis or paresis with ipsilateral loss of touch,

pressure and vibration and contralateral loss of pain and temperature7. Diagnostics

a. X-ray of spineb. CT Scan and MRIc. Myelogram – if MRI is contraindicated

8. Nursing Carea. 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 Managementa. 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 Position patient as ordered

1. Low Spinal Surgery – generally flat2. High Spinal Surgery – slight elevation of head

Maintain proper body alignment Reposition q1-2 by log-rolling Place pillows between legs while on theside

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Assess for post-op complications:1. Respiratory distress2. Constipation3. Abdominal distention and pain4. Hypoactive bowel sounds

Pediatric Alterations

A. Febrile Seizures1. 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 years5. Between 95 and 98 percent of children who have experienced febrile seizures do not go on to develop epilepsy

B. Hydrocephalus – “water in the brain”; abnormal accumulation of CSF in the ventricles, or spaces, of the brain1. Classification

a. Non-communicating – flow of CSF from ventricles to subarachnoid space is obstructedb. Communicating – flow of CSF is not obstructed, but CSF is inadequately reabsorbed in the subarachnoid space

2. Assessmenta. 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

sign3. 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 sizec. CT Scand. MRIe. 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

b. 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 hemorrhage5. Nursing Care

a. Provide routine pre-op care with special attention to monitoring neurologic statusb. 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

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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

C. Meningitis – inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges1. Etiology

a. Viral or aseptic – Enterovirusb. Bacterial – H. influenzae (in children), N. meningitides (in adolescents), S. pneumoniae (in elderly)c. Protozoal – Naegleria and Acanthamoebad. Fungal – Cryptococcus neoformans

2. Assessmenta. 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 adultsc. Opisthotonus – rigid arching of backd. (+) Kernig’s sign and Brudzinski sign (pathognomonic sign)

Kernig’s sign – px supine, hip and knee 90o; passively extend knee; (+) Kernig's sign – knee extension à pain

Brudzinski’s sign – px supine; flex neck; (+) Brudzinski’s – neck flexion à involuntary flexion of knee and hipe. Projectile vomiting – due to increased ICPf. Photophobia and phonophobiag. Chills, anorexiah. Irritabilityi. Generalized body malaisej. Weight lossk. Abnormal posturing (decorticate/decerebrate)l. Possible seizurem. Rapidly spreading petechial rash (if meningococcal bacteria)

3. Diagnostic test – Lumbar/Spinal tapa. 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)

4. Nursing Carea. 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 seizured. Prevent complications of immobilitye. Maintain F/E balancef. Monitor V/S, I/O, neuro checkg. Observe for signs of hydrocephalush. Provide client teaching and discharge plan

Nutrition – increase calories and carbohydrates; protein for tissue repair Small frequent feedings Prevent complications Prevent seizures

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Mental retardation Delay in psychomotor development Visual and Hearing impairment Urinary retention

D. 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 areas1. Predisposing factors:

a. If sibling has a neural tube defectb. Virusc. Environmentd. Radiation

2. Types of Spina Bifidaa. 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 myelomeningocoele3. Assessment

a. Examine the defect for size, level, covering and CSF leakageb. 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. Diagnosticsa. Prenatal

UTZ – may show spinal defect Amniocentesis – elevated Alpha Fetoprotein (AFP) leve

b. Postnatal X-ray of spine, CT Scan – shows vertebral defect Myelogram – shows extent of neural defect Encephalogram – shows hydrocephalus

5. Nursing Carea. 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 child’s positiond. Provide sensory stimulation – objects for visual stimulation; stimulate also other senses e. Provide emotional support to parents and familyf. Provide patient teaching

Wound care Passive ROM exercises Signs of infection Medication and SE

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Feeding, diapering, positioning Availability of appropriate support groups, genetic counseling

E. 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 three1. Incidence: 1.5-5 in 1,000 live births2. 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. Classificationa. Spastic – most common type; increase muscle tone leading to stiff and difficult movement

Common types of spastic CP – hemiparesis, quadriparesis, paraplegiab. 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 normalc. Athetoid/Dyskinetic – mixed muscle tone: trouble holding themselves in an upright, steady position for sitting or

walking, and often show involuntary and uncontrolled motions 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 yearsd. Hypotonic – limp and can move only a little or can't move at alle. Mixed

4. Associated problemsa. Mental retardationb. Hearing lossc. Defective speechd. Seizurese. Attention deficit disorderf. Sensory impairment

5. Assessmenta. Delayed gross motor development – most common clinical manifestationb. 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 Carea. 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.

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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 child’s 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 accomplishments2. Set realistic and attainable goals3. Encourage and appealing physical appearance4. 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 individual’s 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 child’s inability to accomplish certain tasks.2. Urge them to relax and demonstrate patience.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.F. Reye’s 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 use2. Signs and symptoms

a. Stage I 1. Persistent, heavy vomiting that is not relieved by eating2. Generalized lethargy3. General mental symptoms, e.g. confusion4. Nightmares5. High fever6. Headaches

b. Stage II 1. Stupor caused by minor brain inflammation2. Hyperventilation3. Fatty liver (found by biopsy)4. Hyperactive reflexes

c. Stage III 1. Continuation of Stage I and II symptoms2. Possible coma3. Possible cerebral edema4. Rarely, respiratory arrest

d. Stage IV 1. Deepening coma2. Large pupils with minimal response to light3. Minimal but still present hepatic dysfunction

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e. Stage V 1. Very rapid onset following stage IV2. Deep coma3. Seizures4. Multiple organ failure5. Flaccidity6. Extremely high blood ammonia (above 300 mg/dL of blood)7. Death

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