NEUROLOGIC DISORDERS
NIO C. NOVENO, RN, MAN, MSN
ALZHEIMER’S DISEASEALZHEIMER’S DISEASE
ALZHEIMER’S DISEASE
A progressive, degenerative neurological disorder characterized by:
Behavioral dysfunctionSevere cognitive impairmentSevere cognitive impairment
Personality changes
Most common non-reversible form of dementia� Forgetfulness → mental incapacitation
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ALZHEIMER’S DISEASE
Degenerative disorder of the cerebral cortex
(frontal lobe)
Poor prognosisPoor prognosis
No cure or definitive treatment
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ALZHEIMER’S DISEASE
Pathophysiolgy…
Brain damage caused
Chromosome 21
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Neurofibril tangles
Neuritic plaques Granulovacuolar degeneration
Brain damage caused genetic substance
(amyloid)
1
2
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3
ALZHEIMER’S DISEASE
Risk factors
� Neurochemical
� Environmental� Aluminum and manganese
� Slow-growing CNS viruses
� Trauma
� Genetic abnormality (C 21)
� Old age
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ALZHEIMER’S DISEASE: Symptoms
Stage 1: 1-3 years•Short-term memory loss
•Decreased attention span
•Subtle personality changes
•Mild cognitive deficits
•Difficulty with depth
perception
Stage 2: 2-10 years•Obvious memory loss
•Confusion
•Wandering behavior
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perception •Wandering behavior
•“Sundowning”
•Irritability and agitation
•Decreased spatial
orientation
•Impaired motor skills
•Impaired judgment
Stage 3: 8-10 years•Absent cognitive abilities
•Disoriented to time & place
•Severely altered communication
skills
•Impaired or absent motor skills
•Bowel & bladder incontinence
NURSING CARE
Prevent injury
Safe environment
Assess changes in mental status
Maintain improve hygiene, nutrition, healthMaintain improve hygiene, nutrition, health
Labels
Keep routines
Frequent rest periods
Encourage exercises to maintain mobility
Provide emotional support to the family
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Pharmacology
Anti-cholinesterase1. Tacrine HCl (Cognex)
� Check liver function weekly x 18 weeks
2. Donepezil (Aricept)� OD in the early stages
3. Rivastigmine 3. Rivastigmine
Cholinergics[Ach precursors: choline, lecithin, deanol]
Anti-depressantsAmitriptyline, desipramine, fluoxetine, nortryptilline, trazodone
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Pharmacology
Vitamin E & selegiline
� Delay the progress of AD
Ginkgo bilobaGinkgo biloba
� Improves cognitive function for 6-12 mos.
Propentofylline
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Pharmacology
Anti-psychotics
� Haloperidol (Haldol): agitation and confusion
� Taken HS
� A/E: WOF extrapyramidal symptoms (EPS)� A/E: WOF extrapyramidal symptoms (EPS)
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Pharmacology
CORTICAL CHANGES
ABSENT COGNITIVE ABILITIES
LABELSLABELSIMPROVE COGNITION
MAINTAIN A NORMAL LIFESTYLE
OLD AGE
TACRINE
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PARKINSON’S DISEASEPARKINSON’S DISEASE(PARALYSIS AGITANS)(PARALYSIS AGITANS)
Motor Motor modulationmodulation
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Motor cortex: Planning & initiationMotor cortex: Planning & initiation
Cerebellum: Motor coordinationCerebellum: Motor coordination
Parkinson's Disease (Paralysis Agitans)
A. Etiology and pathophysiology
1. Progressive disorder:
bradykinesia, tremor, rigidity (BRT)
� ♂ than ♀ (3:2)� ♂ than ♀ (3:2)
2. Suspected causes include:
a. neuromuscular imbalance
(dopamine and acetylcholine)
b. unknown virus
c. cerebral vascular disease
d. chemical or physical trauma
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PATHOPHYSIOLOGY
Dopamine producing neurons degenerate▼
Depletion of dopamine & excess acetylcholine
▼▼
Basal ganglia further deteriorates� Initiate movement� Control posture
� Maintain muscle tone� Autonomic movements
SYMPTOMS DO NOT APPEAR UNTIL 70-80% OF SUBSTANTIA NIGRA NEURONS ARE LOST
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Parkinson's Disease (Paralysis Agitans)
B. Clinical findings
1. Subjective
a. Mild, diffuse, muscular pain
b. Feelings of stiffness and rigidity, particularly of b. Feelings of stiffness and rigidity, particularly of
large joints
c. Defects in judgment and emotional lability
may be present
d. Depression
e. Cognitive and memory deficits
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Parkinson's Disease (Paralysis Agitans)2. Objective
a. Increased difficulty in performing usual activities
b. Generalized tremor; "pill-rolling“
c. Various disorders of locomotion c. Various disorders of locomotion
d. Mask-like facial expression with unblinking eyes
e. Low-pitched, slow, poorly modulated, poorly articulated speech
f. Drooling
g. Various autonomic symptoms
h. In the elderly, dementia, confusion, and psychosis
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PARC DARKPARC DARKPPILL ROLLING
AABOUT TO FALL
RRIGIDITY
CCAN’T SWALLOW/SPEAK (DROOLS)
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DDOPAMINE/L-DOPA
AARTANE
RRESTRICT COFFEE
KKEEP TREMORS DOWN (ANTI-H1)
Parkinson's Disease (Paralysis Agitans)
C.Therapeutic interventionsMedical regimen is palliative rather than curative
1. Levodopa [coverts to dopamine] + Carbidopa (Sinemet) [prevents brekdown of levodopa](Sinemet) [prevents brekdown of levodopa]� Decrease CHON in diet
� Withheld until symptoms become disabling
� SE: dyskinesias, hallucinations, and nightmares, orthostatic hypotension, NV
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Parkinson's Disease (Paralysis Agitans)
2.Dopamine agonists: postpone initiation of levodopa and carbidopa therapytherapy� Pergolide (Permax)
� Bromocritine mesylate (Parlodel)
� Ropinirole
� Pramipexole
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Parkinson's Disease (Paralysis Agitans)
3. Anticholinergic agents
4. Amantadine HCl (Symmetrel) – unknown
mechanism in PDmechanism in PD
5. MAO inhibitors – increases dopamine levels
� Selegiline (Elepryl)
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Parkinson's Disease (Paralysis Agitans)
6. Budipine
� Reduces akinesia, rigidity and tremors
7. Anti-histamine7. Anti-histamine
� Allays tremors
8. Physiotherapy to reduce rigidity of
muscles and prevent contractures
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Parkinson's Disease (Paralysis Agitans)
Surgical intervention
a. Thalamotomy – stereotactic surgical technique which localizes and destroys VL thalamic nucleus
b. Pallidotomy – experimental procedure for intractable procedure
c. Fetal neural tissue transplant to basal ganglia (experimental)
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Parkinson's Disease (Paralysis Agitans)
Complications Fluctuations in mobility
1. Wearing-off effects
2. On-off symptoms – unpredictable symptoms of rapid fluctuation between dyskinesia (“on” rapid fluctuation between dyskinesia (“on” symptoms) and rigidity or bradykinesia (“off” symptoms)
3. Psychiatric effects
� Confusion� Visual hallucinations
� Paranoia 4. Sleep disturbances
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Parkinson's Disease (Paralysis Agitans)
Prognosis:
• NO cure
• Slowly progressive• Slowly progressive
• Declines over several years
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Nursing Care of Clients with Parkinson's DiseaseAssessment
1. History of onset and progression of symptoms
2. Observations of tremors, gait, facial expression, and bradykinesia and bradykinesia
3. Nutritional status
4. Elimination status
5. Blood pressure in horizontal and vertical positions to identify postural hypotension
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Nursing Care of Clients with Parkinson's DiseasePlanning/Implementation
1. Provide a safe environment
2. Teach the client or family to cut food into small bite-sized pieces or alter the consistency to prevent choking sized pieces or alter the consistency to prevent choking
3. Provide small, frequent meals
4. Encourage an adequate intake of roughage and fluids
5. Teach the client activities to limit postural deformities
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Nursing Care of Clients with Parkinson's DiseaseC. Planning/Implementation cont…
6. Teach the client activities to maintain gait as normal as possible
7. Teach and encourage daily physical therapy to limit rigidity 7. Teach and encourage daily physical therapy to limit rigidity and prevent contractures
8. Attempt to administer care
9. Encourage the client to continue taking medications even though results may be minimal
10. Advise client to report side effects to physician
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Nursing Care of Clients with Parkinson's Disease
11. Encourage diet rich in nutrient-dense foods
12. Teach clients taking levodopa to limit intake 12. Teach clients taking levodopa to limit intake of foods high in vitamin B6
13. Assist client in setting achievable goals
14. Suction when necessary
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(Lou Gehrig Disease)(Lou Gehrig Disease)
Amyotrophic Lateral SclerosisAmyotrophic Lateral Sclerosis
Amyotrophic Lateral Sclerosis(Lou Gehrig’s Disease)
Etiology and pathophysiology
1. Cause unknown2.Progressive degenerative process involving the spinal, corticobulbar, and lower motor the spinal, corticobulbar, and lower motor
neurons, with subsequent atrophic and spastic
changes in the cranial as well as the spinal
nerves
3.Occurs more frequently in men than in women in the fourth and fifth decades of life
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Amyotrophic Lateral Sclerosis(Lou Gehrig’s Disease)
Clinical findings
1. Subjective
a. Muscular weakness
b. Malaise and fatigue
2.Objective
a. Irregular spasmodic twitching in small muscle groups
(fasciculations)
b. Atrophy
c. Spasticity
d. Difficulty in breathing, chewing, swallowing, speaking
e. Outbursts of laughter or crying
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Amyotrophic Lateral Sclerosis(Lou Gehrig’s Disease)
C. Therapeutic interventions
1. Physiotherapy may be helpful in relieving
spasticityspasticity
2. Support respiratory functions
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Nursing Care of Clients with Amyotrophic Lateral SclerosisA. Assessment
1. History of onset and progression of
symptoms
2. Neurologic status
3. Respiratory status including rate, depth, and
effort
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Nursing Care of Clients with Amyotrophic Lateral SclerosisC. Planning/Implementation
1. Encourage activity
2. Encourage range-of-motion exercises
3. Prevent aspiration 3. Prevent aspiration
4. Provide alternate means of communication
5. Allow client to discuss feelings
6. Monitor respiratory function
7. Support natural defense mechanisms
8. Teach the avoidance of situations that may
contribute to infection
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Myasthenia Gravis
A. Etiology and pathophysiology1. A chronic, progressive, neuromuscular disorder
2. Reduced number of acetylcholine receptors (AChR) and altered membrane of the muscle end-(AChR) and altered membrane of the muscle end-plate
3. Autoimmune process
4. Highest incidence in young adult females
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Myasthenia Gravis
A. Etiology and pathophysiology cont…
5. Myasthenic crisis
6. Two peaks of onset:6. Two peaks of onset:
� 20-30 years: ♂than♀� >50 years: ♀than ♂
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Myasthenic crisis
Abrupt onset of severe, generalized muscle weakness
with inability to swallow, speak or maintain
respirations
Administration of Tensilon provide relief
Cholinergic crisisCholinergic crisis
Symptoms similar to myasthenic crisis and also, the side
effect of anticholinesterase drugs
Administration of Tensilon worsen the symptoms
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Myasthenia Gravis
A. Etiology and pathophysiology cont…
7. Risk factors
a. Stress
b. Hormonal changesb. Hormonal changes
c. Drugs
• Alcohol
• Aminoglycosides
• Morphine
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Pathophysiology
Thymic lymphocytes▼
Acetylcholine-receptor antibodies ▼
Attack post synaptic muscle membraneAttack post synaptic muscle membrane▼
Fewer receptors to combine with acetylcholine▼
Altered action potential▼
Weakness
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Myasthenia GravisB. Clinical findings
1. Subjective
a. Extreme muscle weakness
• progressively worsens as the muscle is used, but disappears with rest
b. Dysphagia (difficulty chewing and swallowing) b. Dysphagia (difficulty chewing and swallowing)
c. Diplopia
d. Dysarthria (difficulty speaking)
e. Dyspnea
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Myasthenia Gravis
2. Objective
a. Ptosis
b. Weak voice (dysphonia)
c. Myasthenic smile (snarling, nasal smile)c. Myasthenic smile (snarling, nasal smile)
d. Strabismus
e. Diagnostic measures
� TENSILON TEST: Edrophonium is used to
distinguish myasthenic crisis from cholinergic
crisis (toxic effects of excessive neostigmine)
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Myasthenia Gravis
C. Therapeutic interventions1. Anticholinesterases
a. Neostigmine (Prostigmin)
b. Pyridostigmine bromide (Mestinon)
c. Ambenonium chloride (Mytelase)
2. X-ray therapy or thymectomy may cause partial remission
3. Corticosteroids or ACTH
4. Tracheostomy with mechanical ventilation
5. Plasmapharesis
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Nursing Care of Clients with Myasthenia Gravis
A. Assessment1. History of onset and progression of motor
and sensory loss and sensory loss
2. Factors that intensify symptoms
3. Neurologic status
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Nursing Care of Clients with Myasthenia GravisC. Planning/Implementation
1. Administer medications on strict time schedule
2. Observe for signs of:� Dyspnea
� Dysphagia ► myasthenic crisis� Dysphagia ► myasthenic crisis� Dysarthria
3. T-SET on bed side
4. Provide plenty of rest
5. Avoid people with URTI
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Nursing Care of Clients with Myasthenia Gravis
6. Carry a medic alert band
7. NO morphine
8. Allay anxiety
9. Proper nutrition
10. Prevent corneal damage
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GUILLAINGUILLAIN--BARRÉ SYNDROME BARRÉ SYNDROME (POLYRADICULONEURITIS)(POLYRADICULONEURITIS)
Guillain-Barré Syndrome
(Polyradiculoneuritis)A. Etiology and pathophysiology
1. Cause unknown; � immunologic status
� follows respiratory or gastrointestinal infection
2. Changes in the motor cells of the spinal cord and medulla with areas of demyelination
3. After initial and plateau periods, recovery may take up to a year� some experience residual deficits or die of complications
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Guillain-Barré Syndrome
(Polyradiculoneuritis)B. Clinical findings
1. Subjective
a. Generalized weakness
b. Paresthesia
c. Diplopia
2. Objective
a. Ascending paralysis; 24-72 hours
b. Respiratory paralysis
c. Hypertension, tachycardia, and low-grade fever
d. Incontinence
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Guillain-Barré Syndrome
(Polyradiculoneuritis)C. Therapeutic interventions
1. Steroids
2. Plasmapheresis2. Plasmapheresis
3. Support of vital functions
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Guillain-Barré Syndrome
(Polyradiculoneuritis)Nursing Care of Clients with Guillain-Barré
Syndrome
Assessment1. Respiratory characteristics1. Respiratory characteristics
2. Neurologic status
3. History of any recent illness (particularly viral infections)
4. Onset and progression of symptoms
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Guillain-Barré Syndrome
(Polyradiculoneuritis)Nursing Care of Clients with Guillain-Barré Syndrome
Planning/Implementation
1. Monitor vital signs, vital capacity, breath sounds,
and arterial blood gasesand arterial blood gases
2. Keep airway and tracheostomy set at the bedside
3. Suction, provide fluid replacement therapy, and
monitor functioning of the respirator as required
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Guillain-Barré Syndrome
(Polyradiculoneuritis)Nursing Care of Clients with Guillain-Barré Syndrome
Planning/Implementation
5. Prevent complications of immobility
a. Skin carea. Skin care
b. Range-of-motion exercises
c. Position changes
d. Coughing and deep breathing
e. Antiembolic stockings
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MULTIPLE SCLEROSIS MULTIPLE SCLEROSIS (DISSEMINATED SCLEROSIS)(DISSEMINATED SCLEROSIS)
Multiple Sclerosis (Disseminated Sclerosis)A. Etiology and pathophysiology
1. Chronic, debilitating, progressive disease� periods of remission and exacerbation
� randomly scattered patches of demyelination
� brainstem, cerebrum, cerebellum, and spinal cord� brainstem, cerebrum, cerebellum, and spinal cord
2. Cause unknown; viral and immunologic
3. Onset in early adult life (20 to 40 years)
4. Fatigue, stress, and heat tend to increase symptoms
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Multiple Sclerosis (Disseminated Sclerosis)B. Clinical findings
1. Subjective
a. Paresthesia
b. Altered position sense b. Altered position sense
c. Dysphagia
d. Ataxia
e. Weakness
f. Diplopia
g. Blurred vision
h. Inappropriate emotional affect
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Multiple Sclerosis (Disseminated Sclerosis)
2. Objectivea. Nystagmus
b. Blindness
c. Intention tremors
d. Slurred or scanning speech
e. Spastic paralysis and gaite. Spastic paralysis and gait
f. Impaired bowel function
g. Impaired bladder function
h. Impotence
i. Cognitive loss (a late sign)
j. Increased deep tendon reflexes
k. Pallor of optic discs evident on examination with ophthalmoscope
l. Increased gamma globulin levels in the CSF
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Multiple Sclerosis (Disseminated Sclerosis)C. Therapeutic interventions
1. Generally palliative
2. Corticosteroids or ACTH
3. Baclofen is used to control spasticity 3. Baclofen is used to control spasticity
4. Interferon beta-1b, recombinant (Betaseron)
5. Physiotherapy, rehabilitation, and psychotherapy
6. Nerve blocks may be used for severe spasticity
7. Immunosuppressive drugs are being investigated
as treatment
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Nursing Care of Clients with Multiple SclerosisA. Assessment
1. History of onset and progression of motor
and sensory lossand sensory loss
2. Factors that intensify symptoms
3. Neurologic status
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Nursing Care of Clients with Multiple SclerosisB. Planning/Implementation
1. Rest periods
2. Avoid hot baths
3. Use assistive devices3. Use assistive devices
4. Assist the client and family to plan and
implement a bowel and bladder regimen
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Nursing Care of Clients with Multiple SclerosisB. Planning/Implementation
5. Allay anxiety
� NO false hopes during periods of remission
� Allow to ventilate feelings � Allow to ventilate feelings
� Seek counseling and rehabilitation
� Explain the disease to client and family
� Help the client reestablish a realistic self-image
� Teach the client to compensate for problems
with gait
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Nursing Care of Clients with Multiple Sclerosis
6. Provide care to prevent decubiti and
contractures
a. Provide special skin care
b. Provide special attention to jointsb. Provide special attention to joints
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SSCCLLEERR
pasm; slurred speech
ognitive loss
oss of bowel & bladder function
motional affect is inappropriate; eye problems
estRROOSSIISS
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wallowing problems
est
ptic discs are pale
teroids
mpotence; increased DTR
Characteristics Multiple Sclerosis Myastenia Gravis Guillaine- BarreSyndrome
Weakness Weakness Weakness
Causes Demyelination of
the myelin sheath
inflammatory
disease of the CNS
A disease of the
“white matter”
Decrease in
functioning
acetylcholine
receptor site due to
antibodies
Inflammatory
disorder of the
peripheral nerves
with demyelination
SignificantHistory
May be
environmental
remissions may be
exacerbated by
stress, illness etc
No precipitating
factors
Precipitated by viral
or bacterial illness
approx. 2 weeks
before
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Characteristics Multiple Sclerosis Myastenia Gravis Guillaine- Barre
Syndrome
Characteristics of weakness
No pattern,
assymetrical
Increase weakness
with prolong activity
Ascending, bilateral,
symmetrical
Diplopia Ataxia
Diplopia, ptosis,
Severe weakness
and numbness in Signs Numbness, tingling,
muscle weakness
and spasm, pain
Diplopia, ptosis,
dysphagia
and numbness in
arms and legs
characterize GBS
Epidemiology Female 20-40 Y/O
caucasian Female of
reproductive age
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Characteristics Multiple Sclerosis Myastenia GravisGuillaine- Barre
Syndrome
Diagnostic Tools
EMG Tensilon Test EMG
Complications Respiratory distress
Contractures
Aspiration
Respiratory distress
Myasthenic
Cholinergic
Crisis
Respiratory distress
Contractures
Aspiration
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BRAIN TUMORSBRAIN TUMORS
Brain Tumors
A. Etiology and pathophysiology
1. Either benign or malignant
2. Classified according to tissue of origin
a. Meningiomaa. Meningioma
b. Acoustic neuroma and optic nerve spongioblastoma
c. Gliomas: originate in neural tissue; usually malignant
(1)Astrocytoma
(2)Glioblastoma
(3)Oligodendroglioma
d.Hemangioblastomas and angiomas
e. Metastatic tumors
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Brain TumorsB. Clinical findings
1. Subjective
a. Headache that increases with stooping
b. Lethargy
2. Objective
a. Vomiting
b. Papilledema (noted on ophthalmoscopy)
c. Abnormal brain waves on the EEG
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Brain TumorsSymptoms may vary depending on location of
tumor
a. Frontal lobe
b. Temporal lobe
c. Parietal lobec. Parietal lobe
d. Occipital region
e. Cerebellar region
f. Signs of increased intracranial pressure
g. Motor and sensory deficits
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Brain Tumors
C. Therapeutic interventions
1. Radiation therapy and/or chemotherapy
2. Surgery for partial or complete removal of the 2. Surgery for partial or complete removal of the
lesion
a. Craniotomy with removal of lesion and invaded tissue
b. Stereotaxic laser surgery; employs computer-directed
laser to eradicate tissue
3. Steroids, anticonvulsives, and osmotic diuretics to
control symptoms may be ordered
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Nursing Care of Clientswith Brain TumorsA. Assessment
1. History from client and family to identify behavioral changes, coping skills, and behavioral changes, coping skills, and neurologic deficits
2. Neurologic status
3. Signs of increased intracranial pressure
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Nursing Care of Clientswith Brain TumorsC. Planning/Implementation
1. Provide emotional support
2.Maintain the client’s comfort 2.Maintain the client’s comfort
3.Support client's nutrition
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Nursing Care of Clientswith Brain TumorsC. Planning/Implementation
4. Provide care for the client requiring brain
surgery
a. Obtain consent for surgery and removal of a. Obtain consent for surgery and removal of
hair After surgery keep the client's head
elevated 30 degrees (12 inches) to aid
drainage
b. Support respiratory function
c. Assess the client's level of consciousness and
neurologic status for changes
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Nursing Care of Clientswith Brain Tumors
e. Observe for signs of increased intracranial pressure
(ICP)
(1) Decreased level of consciousness
(2)Restlessness
(3)Weakness or paralysis (3)Weakness or paralysis
(4)Visual and other sensory disturbances
(5) Increased systolic pressure; widening pulse
pressure
(6)Decreased pulse rate
(7)Changes in respiratory pattern
(8)Unilateral nonreactive and/or dilated pupil
progressing to bilateral
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Nursing Care of Clientswith Brain Tumors
(9)Headache
(10)Rapid rise in body temperature
(11)Vomiting
(12)Seizures
(13)Papilledema(13)Papilledema
(14)Use strict aseptic technique with ICP monitoring
(15)Observe dressings for cerebrospinal spinal (CSF) leakage or hemorrhage
(16)Maintain accurate intake and output records
(17)Utilize hypothermia as ordered if the client is febrile; fever increases metabolic needs of the brain
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EPILEPSYEPILEPSY(SEIZURE DISORDERS)(SEIZURE DISORDERS)
Epilepsy (Seizure Disorders)
A. Etiology and pathophysiology1. Abnormal discharge of electric impulses by the
nerve cells in the brain
2. Onset of idiopathic epilepsy generally before age 30
3. Other conditions associated with seizures include brain tumor, CVA, hypoglycemia, and head trauma
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Epilepsy (Seizure Disorders)
4.Types of seizuresa. Partial seizures (seizures beginning locally)
(1)Simple
(2)Complex
b. Generalized seizures (bilaterally symmetric and without local onset) (1)Absence (petit mal)
(2)Myoclonic
(3)Tonic-clonic (grand mal)
c. Status epilepticus
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Seizure Disorders
Generalized seizures1. Grand mal seizure
2. Absence (petit mal)
• preceded by an aura
• tonic- clonic phases
• ends with post- ictal phase
• sudden vacant facial expression
• all motor activity ceases
3. Myoclonic Seizures • possible loss of muscle tone
• brief flexor muscle spasm: may have
arm extension, trunk flexion
• May be generalized or local
• occurs only when fever is rising
• Common to less than 5 years old
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Seizure Disorders
Partial Seizures1. Simple Partial Seizure •Motor, sensory or autonomic
symptoms without loss of
consciousness
•Begins in focal area but 2. Complex partial seizure
•Begins in focal area but
progresses to grand mal
seizures
Status Epilepticus • Recurrent generalized
seizures without gaining
consciousness
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Epilepsy (Seizure Disorders)
B. Clinical findings (tonic-clonic seizures) 1. Subjective
a. Aura or warning sensation
b. Loss of consciousness during seizure
c. Lethargy often follows return to consciousness (postictal phase)
d. Dyspnea d. Dyspnea
2. Objective
a. Pupils become fixed and dilated
b. Often the client cries out as seizure begins or as air is exhaled forcefully
c. Tonic and clonic movement of the muscles
d. Incontinence
e. Abnormal EEG
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Epilepsy (Seizure Disorders)
C. Therapeutic interventions1. Anticonvulsant therapy continued throughout life
a. Phenytoin sodium (Dilantin), carbamazepine (Tegretol), valproic acid (Depakene), mephenytoin (Mesantoin) and primidone (Mysoline) often used to control tonic-clonic seizures
b. Trimethadione (Tridione), phensuximide (Milontin), and b. Trimethadione (Tridione), phensuximide (Milontin), and ethosuximide (Zarontin) to control absence seizures
c. Diazepam (Valium) given IV to treat status epilepticus
2. Sedatives (e.g., phenobarbital) used to reduce emotional stress
3. Neurosurgery is sometimes indicated if seizures are caused by tumors, abscesses, or vascular problems
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NURSES NOTES
Therapeutic level of Dilantin: 10-20 mcg/ml
WOF: � Gingival hyperplasia� GI disturbances� Hepatotoxicity� Ataxia� Ataxia� Hypocalcemia� Decreased absorption of vitamin D
REMEMBER:
� GOOD ORAL HYGIENE
� REPORT TO MD IF Sx WORSENS
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COUNSELLING
CALM
ANTI-CONVULSANTS
APNEA/CYANOSIS
EVALUATE CHANGES IN LOC
S
Phenobarbital (Sodium luminal), Primidone (Mysoline), Carbamazepine (Tegretol), Phenytoin (Dilantin)
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SAFETY
AVOID ALCOHOL
ACTIVITIES?
R EDUCE STIMULI;
REMAIN WITH CLIENT
REORIENT
Nursing Care of Clients with EpilepsyA. Assessment
1. History of type, frequency, and duration of
seizures
2. History to identify precipitating factors
3. Sensations associated with the seizure that may
constitute an aura
4. Detailed list of client's medications
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Nursing Care of Clients with EpilepsyB.Planning/Implementation
1. Provide protection for the client during and after the seizure
2. Help the client who can identify an aura2. Help the client who can identify an aura
3. Encourage the client to carry and wear a medical alert tag
4. Help the client plan a schedule
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Nursing Care of Clients with Epilepsy
5. Instruct the client to refrain from excessive use of
alcohol
6. Teach the client and family to:6. Teach the client and family to:
� observe the aura
� initial point of seizure
� type of seizure
� level of consciousness
� loss of bladder and bowel control
� progression of seizure
� postictal condition
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Nursing Care of Clients with Epilepsy
7. Encourage the client to express feelings.
8. Lifetime medication use
9. Teach client about anticonvulsant therapy
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INCREASED INCREASED INTRACRANIAL INTRACRANIAL INTRACRANIAL INTRACRANIAL PRESSUREPRESSURE
INCREASED INTRACRANIAL PRESSURE
Monroe- Kellie Doctrine: An increase in the volume of any one of the components of the brain will lead to a change in the volume of the other components in order to maintain the ICP maintain the ICP
Condition associated with increased ICP:1. Mass Lesions
2. Head Injuries
3. Infections
4. Vascular Insult
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INCREASED INTRACRANIAL PRESSURE
• LOC changes
• Increasing systolic BP
• Headache
• Vomiting
Clinical Manifestations
• Increasing systolic BP
• Bradycardia
• Cheyne-Stokes breathing
• Fever
• Vomiting
• Anisocoria
• Papilledema
• Hemiplegia/hemiparesis
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INCREASED INTRACRANIAL PRESSURE
Laboratory Diagnostics� CT Scan
� MRI
Medical Management • Osmotic diuretics
• Loop diuretics � MRI
� Cerebral Angiography
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• Loop diuretics
• Corticosteroids
• Barbiturates
• Surgery
INCREASED INTRACRANIAL PRESSURE
Nursing Interventions
HOB elevated; Semi- Fowler’s
Evaluate and prevent increase of ICP Evaluate and prevent increase of ICP
Airway
Drainage; Drugs (e.g. mannitol)
Safety
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CEREBROVASCULAR CEREBROVASCULAR ACCIDENT ACCIDENT ACCIDENT ACCIDENT
CEREBROVASCULAR ACCIDENT
� Either hemorrhagic or
ischemic in origin
� Men> women
Risk Factors
• Diabetes mellitus
• Cardiac disease
• Hypertension� Men> women
� TIAs are warning
signals!!!
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• Hypertension
• Obesity
• Smoking
• Use of OCPs
• Stress
• Inactivity
Clinical Manifestations
1. Signs of increased
ICP
2. Cognitive deficits
� Short and long- term
memory recall
4. Communication loss
5. Apraxia
6. Agnosia
7. Visual-perceptual
dysfunction
� Homonymous � Altered judgment
3. Motor deficits
� Hemiplegia/
hemiparesis
� Dysarthria
� Dysphagia
� Homonymous
hemianopsia
� Diplopia
8. Sensory changes
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Left Hemisphere Stroke
Right Hemisphere Stroke
Paralysis on the right
side
Paralysis on the left
side
Right visual field
defects
Left visual field
defects
Aphasia Spatial- perceptual
deficits
Altered intellectual
ability
Increased
distractibility
Slow, cautious
behavior
Impulsive behavior
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Laboratory Diagnostics1. CT Scan/ MRI
2. Cerebral angiography
Medical Management
1. Hyperosmotic
agents
2. Corticosteroids
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2. Corticosteroids
3. Anticonvulsants
4. Thrombolytics
5. Anticoagulants
6. Antihypertensives
Nursing Interventions:Acute Phase
� Maintain patent airway and adequate
ventilation
� Monitor VS, neuro checks and signs of � Monitor VS, neuro checks and signs of
increased ICP, shock and seizures
� Provide complete bedrest as ordered
� Maintain IV fluid and electrolyte balance and
ensure adequate hydration
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Nursing Interventions:
Acute Phase
� Maintain proper body positioning
� Head of bed maybe elevated at least 30-45 degrees
� Turn and reposition patient every 2 hours on
unaffected side and 20 minutes on the affected side unaffected side and 20 minutes on the affected side
� Passive ROM every 4 hours
� Promote skin integrity
� Maintain adequate elimination
� Maintain a quite and restful environment
� Administer medications and monitor for side- effects
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Nursing Interventions
Rehabilitation Phase
Hemiplegia
� Turn every 2 hours
� Use footboards to prevent footdrop
� Support paralyzed arm with pillows or a sling prevent � Support paralyzed arm with pillows or a sling prevent
subluxation of shoulder
� Provide active and passive ROM every 4 hours
� Apply lotion over bony prominences
� Avoid too much drying and too much moisture in skin
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Nursing Interventions
Rehabilitation Phase
Dysphagia
� Check gag reflex before feeding
� Offer soft foods
� Place food in unaffected side of mouth � Place food in unaffected side of mouth
� Have patient sit upright when eating and 30 minutes afterward
Homonymous hemianopsia
� Early in care, approach client on unaffected side
� Place personal belongings, food on unaffected side
� Teach client the technique of scanning
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Nursing Interventions
Rehabilitation Phase
Receptive aphasia
� Give simple slow directions
� Use short, simple questions
� Use nonverbal communication techniques � Use nonverbal communication techniques
Expressive aphasia
� Allow sufficient time for patient to answer question
� Anticipate needs of patient
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CEREBRAL CEREBRAL ANEURYSMANEURYSM
Cerebral Aneurysm
Etiology and pathophysiology
1. Sac formed by dilation of the walls of an artery within the cranial cavity
2. May be the result of a congenital weakness in the vessel, trauma, or arteriosclerosisarteriosclerosis
3. Symptoms occur when the aneurysm compresses nearby nerves or when it ruptures
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Cerebral Aneurysm
Clinical findingsSubjective
a. Unilateral headache
b. Pain in the eye
c. Diplopiac. Diplopia
d. Tinnitus
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Cerebral Aneurysm
Objective
a. Rigidity of the back of the neck and spine
b. Ptosis of the eyelid
c. Hemiparesisc. Hemiparesis
d. Decreased level of consciousness
e. Deviations from normal results in CT scan and lumbar puncture
f. Signs of increased ICP if rupture occurs
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Cerebral Aneurysm
C. Therapeutic interventions
1. Attempt to keep the client hypotensive
2. Clips: If there is a stalk connecting the
aneurysm; cut off blood supply to the
aneurysm permanently
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Nursing Care of Clients with Cerebral AneurysmsA. Assessment
1. Neurologic status
2. Presence of signs of increased ICP
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Nursing Care of Clients with Cerebral AneurysmsB. Planning/Implementation
1. Continue neurologic assessment
2. Assist with lumbar puncture
3. Teach client the need to continue antihypertensive medications
4. Teach client to avoid straining, lifting, exerting, and acutely flexing the neck
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HEAD INJURYHEAD INJURY
Head InjuryTypes:
1. Concussion – results in temporary neurologic
dysfunction
2. Contusion – more severe blow that bruises the
brain
3. Hemorrhage
a. Epidural hematoma
b. Subdural hematoma
c. Subarachnoid hemorrhage
d. Intracerebral hemorrhage
4. Fractures
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Head Injury
Clinical Manifestations:� Depends on the type of injury
� Signs of increased ICP
� Compound fractures:
Rhinorrhea − Rhinorrhea
− Otorrhea
− Raccoon’s sign
− Battle’s sign
− Conjunctival hemorrhage
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Laboratory Diagnostics:• Skull X- ray
• CT Scan
Nursing Interventions:• Similar to care patients with increased ICP
• Care of patients with basal skull fracture
- Have patient lie in bed unless contraindicated
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- Have patient lie in bed unless contraindicated
- Place a loose collection pad under the nose or over
the ear
- Caution patient not to blow the nose or sneeze
- Placing NGT is contraindicated
- Nasotracheal suctioning is contraindicated
� Observe for complication (e.g. meningitis)
CRANIOTOMYCRANIOTOMY
Craniotomy
Nursing Care1. Airway
� Position to side to prevent aspiration
� Vigorous coughing is contraindicated
2. Positioning 2. Positioning a. Supratentorial Surgery
� Avoid positioning on operated side if large tumor was removed
� Place on his side with HOB elevated at 45 degrees
b. Infratentorial Surgery � Keep patient flat; on either side with head aligned to
spinal column
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3. Observe for signs of complications
(increased ICP, meningitis, seizures)
4. Monitor the incision site for signs of
infection
5. Provide pain medications for the headache
6. Nutrition 6. Nutrition
� Supratentorial: no contraindications
� Infratentorial: NPO for 24 hours post-op
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Craniotomy
6. Avoid:� Suctioning nose if without written order
� Placing patient in T-berg position
� Flexing neck of patient � Flexing neck of patient
� Positioning on operated side if large tumor
was removed
� Take temperature orally
� Sedating heavily
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MENINGITISMENINGITIS
Meningitis
A.Most common CNS infection of infants and children
B. Inflammation of the meninges by bacteria that travel via the cerebrospinal fluid
C. Classification: culture of cerebrospinal fluid used to help identify organism
1. Bacterial: caused by pus-forming bacteria
2. Tuberculous
3. Viral or aseptic
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Meningitis
D. Clinical findings• Opisthotonos
• Headache
• Irritability and high-pitched cry
• Signs of increased intracranial pressure • Signs of increased intracranial pressure
• Fever, nausea, and vomiting
• Meningococcal meningitis: petechiae and purpuric skin rash
E. Therapeutic intervention - massive doses of intravenous antibiotics
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Nursing Care of Patients with MeningitisA. Assessment
1. Fever
2. Headache, irritability
3. Vomiting
4. Seizures
5. Nuchal rigidity5. Nuchal rigidity
B. Analysis/Nursing Diagnoses1. Altered family processes related to having a child with a
serious illness
2. Risk for infection related to presence of infective organisms
3. Risk for injury related to presence of infection
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Nursing Care of Patients with MeningitisC.Planning/Implementation
1. Provide for rest
2. Decrease stimuli from the environment
3. Position on the side with head gently supported in extensionextension
4. Institute respiratory isolation
5.Maintain fluid balance because of meningeal edemaa. Record intake and output carefully
b. Correct any deficits
c. Monitor IV fluid
d. Daily weights
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Nursing Care of Patients with MeningitisC. Planning/Implementation
6. Provide emotional support for parents, since
child usually becomes ill suddenly
7. Administer antibiotic therapy as prescribed 7. Administer antibiotic therapy as prescribed
8. Observe for complications such as septic
shock and circulatory collapse
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Meningitis Encephalitis Brain Abscess
Causative
Organisms
Bacteria, fungi,
yeasts, viruses
Bacteria, fungi,
yeast, viruses,
parasites
Bacteria
Clinical
Manifestations
• Nuchal rigidity
• (+) Brudzinski
• (+) Kernigs
• s/sx of increased
ICP
• Fever
• Mental
deterioration
• Amnesia
• Personality
changes
•Hemiparesis
S/sx of increased ICP
• Fever •Hemiparesis
Diagnostics • Stained smears and
sensitivity
• Lumbar puncture
• Viral studies • CT Scan, skull x-
ray
Medical
Management
Antibiotics with
sensitivity tests
Supportive
treatment vidarabine
Antibiotics Incision
and drainage
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Meningitis
Predisposing Factors:
� Basilar skull fracture
� Brain/spinal surgery
� Sinus, upper respiratory or ear infections
Laboratory Diagnostics:
� Stained Smears and sensitivity
� Lumbar puncture
or ear infections
Clinical Manifestations:
� Nuchal rigidity � Kernig’s sign� Brudzinski sign� Fever
� Seizures
Medical Management:
� Antibiotics
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INTRACRANIAL INFECTIONS
Nursing Management:
1. Assess level of consciousness, VS and neurologic
checks regularly
2. Minimize environmental stimulation 2. Minimize environmental stimulation
3. Have a family member at the bedside when possible
4. Administer sedatives and mild analgesics as indicated
5. Monitor and initiate seizures precautions
6. Monitor for residual side effects such as vision,
hearing, activity and cognitive processes
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NEUROLOGIC DISORDERS
NIO C. NOVENO, RN, MAN, MSN
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