neurologicdisorders

7/27/2019 neurologicdisorders

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NURSINGCAREOFCLIENTSWITHNEUROLOGIC

DISORDERS


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OUTLINE

Autoimmune Disorders

Multiple Sclerosis (MS)

Myasthenia Gravis (MG)

Guillen-Barr syndrome (GBS)

Degenerative disorders

Parkinsons Disease

Huntingtons Disease

Amyotrophic Lateral Sclerosis (ALS)


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MULTIPLESCLEROSIS


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MULTIPLESCLEROSIS

Chronic demyelinating

disease of the CNSassociated with abnormal

immune response to

environmental factor


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MULTIPLESCLEROSIS

Periods of exacerbations and remissions

Progression of disease with increasing lossof function

Incidence is highest in young adults (2040); onset between 2050

Affects females more than males

More common in temperate climates

Occurs mainly in Caucasians


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MANIFESTATIONS

FatigueOptic nerve involvement: blurred vision,

haziness

nystagmus, dysarthria,cognitivedysfunctions, vertigo, deafness

Weakness, numbness in leg(s), spasticparesis, bladder and bowel dysfunction

ataxiaSpasticity

Blindness


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STRESS

AGGRAVATESSYMPTOMS.


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COLLABORATIVECARE

Focus is on retaining

optimum functioning and

limiting disability


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DIAGNOSTICTESTS

Neurological exam, careful history

Lumbar puncture with CSF analysis: increased

number of T lymphocytes; elevated level of

immunoglobulin G (IgG)

Cerebral, spinal optic nerve MRI: showsmultifocal lesions

Evoked response testing of visual, auditory,

somatosensory impulses show delayed

conduction CT scan shows density of white matter or plaque

formation


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NO CURE EXISTS

FOR MS


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MEDICATIONS Biologic response modifiers

Interferon beta-1a Interferon beta-1b

Glatiramer acetate

Glucocorticosteroids

Immunosuppressants azathioprine (Imuran)

cyclophosphamide (Cytoxan)

methotrexate

Muscle relaxants to treat muscle spasms

diazepam Medications to deal with bladder problems:

anticholinergics or cholinergics depending onproblem experienced by client


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NURSINGDIAGNOSES

Self care deficit

Impaired physical mobility

Risk for injury

Impaired urinary and bowel elimination

Impaired verbal communication

Risk for aspiration

Disturbed thought processes

Ineffective individual coping

Potential for sexual dysfunction


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NURSINGCARE

Monitor motor movements for interferencewith ADLs

Encourage activity balanced with rest

periodsAssess cognitive function

Explain:

Bladder training

Positioning

Avoid temperature extremes

Medication compliance

Avoid STRESS.


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HEALTHPROMOTION

Client needs to develop strategies to deal with

fatigue, exacerbations

Prevention of respiratory and urinary tract infections


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HOMECARE

Education

Referral to support group and resources

Referral to home health agencies when condition

requires


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MYASTHENIAGRAVIS MG)


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MYASTHENIAGRAVIS(MG)

Chronic autoimmune

neuromuscular disorder

affecting the neuromuscular

joint


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MYASTHENIAGRAVIS(MG)

characterized by fatigue and severe weakness of

skeletal muscles

Occurs with remissions and exacerbations

Occurs more frequently in females, with onsetbetween ages 2030


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MANIFESTATIONS

Seen in the muscles that are affected:

Ptosis (drooping of eyelids), diplopia(double vision)

Weakness in mouth muscles resulting indysarthria and dysplagia

Weak voice, smile appears as snarl

Head juts forward

Muscles are weak but DTRs are normalWeakness and fatigue exacerbated by

stress, fever, overexertion, exposure toheat; improved with rest


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MG is purely a MOTOR

disorder with no effecton sensation or

coordination


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COMPLICATIONS

Pneumonia

Myasthenic Crisis

Sudden exacerbation of motor weakness putting

client at risk for respiratory failure and aspiration Manifestations: tachycardia, tachypnea, respiratory

distress, dysphasia


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COMPLICATIONS

Cholinergic Crisis

Occurs with overdosage of medications(anticholinesterase drugs) used to treat MG

Develops GI symptoms, severe muscleweakness, vertigo and respiratory distress

Both cr ises of ten require vent i lat ion

assistance


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DIAGNOSTICTESTS

Physical examination and history

Tensilon Test: edrophonium chloride (Tensilon)administered and client with myasthenia will showsignificant improvement lasting 5 minutes

EMG: reduced action potentialAntiacetylcholine receptor antibody serum levels:

increased in 80% MG clients; used to follow courseof treatment

Serum assay of circulating acetylcholine receptorantibodies: if increased, is diagnostic of MG


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MEDICATIONS

Anticholinesterase medications

Pyridostigmine bromide (Mestinon)

Immunsuppression medications including

glucocorticoids

Cyclosporineor azathioprine (Imuran)


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SURGERY

Thymectomy is recommended in clients


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PLASMAPHERESIS

Used to remove antibodies

Often done before planned surgery, or when

respiratory involvement has occurred


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NURSINGCARE

Teaching interventions to deal with fatigue

Importance of following medication therapy


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HOMECARE

Avoid fatigue and stress

Plan for future with treatment options

Keep medications available

Carry medical identification Referral to support group, community resources


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GUILLAIN-BARRSYNDROMEGBS)


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GUILLAIN-BARRSYNDROME

(GBS)

Acute autoimmune

inflammatory demyelinating

disorder of peripheralnervous system

characterized by acute onset

of ascending motor paralysis

GUILLAIN BARR SYNDROME


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GUILLAIN-BARRSYNDROME

(GBS)

Cause is unknown but precipitating events includeGI or respiratory infection, surgery, or viralimmunizations

8090% of clients have spontaneous recovery with

little or no disabilities 46% mortality rate, and up to 10% have

permanent disabling weakness

20 % require mechanical ventilation due torespiratory involvement


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MANIFESTATIONS

Most clients have symmetric weakness beginning inlower extremities

Ascends body to include upper extremities, torso, andcranial nerves

Sensory involvement causes severe pain, paresthesia andnumbness

Paralysis of intercostals and diaphragmatic muscle

Autonomic nervous system involvement: blood pressurefluctuations, cardiac dysrhythmias, paralytic ileus, urinaryretention

Weakness usually plateaus or starts to improve in the fourthweek with slow return of muscle strength


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DIAGNOSTICTESTS

diagnosis made thorough history and clinical

examination; there is no specific test

CSF analysis: increased protein

EMG: decrease nerve conduction

Pulmonary function test reflect degree of respiratory

involvement


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MEDICATIONS

supportive and prophylactic care

Antibiotics

Morphine for pain control

Anticoagulation to prevent thromboemboliccomplications


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MEDICALMANAGEMENT

Tracheostomy

Plasmapheresis

Enteral feeding

IVIG


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NURSINGDIAGNOSES

Ineffective breathing pattern

Impaired bed and physical mobility

Imbalanced nutrition

Acute Pain Risk for Impaired Skin Integrity

Impaired Communication

Fear


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HOMECARE

Clients will usually require hospitalization,

rehabilitation, and eventually discharge to home

Client and family will need support; support groups


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DEGENERATIVEDISORDERS


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PARKINSONSDISEASE

characterized by tremor at rest, muscle rigidity andakinesia (poor movement); cause unknown

Affects older adults mostly, mean age 60 with malesmore often than females

Parkinson-like syndrome can occur with somemedications, encephalitis, toxins; these are usuallyreversible


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MANIFESTATIONS

Tremorat rest with pill rolling motion of thumb and

fingers

Worsens with stress and anxietyProgressive impairment affecting ability to

write and eat

Rigidity

Involuntary contraction of skeletal muscles

Cogwheel rigidity: jerky motion


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MANIFESTATIONS

Akinesia

Slowed or delayed movement that affects chewing,speaking, eating

May freeze: loss of voluntary movement

Bradykinesia: slowed movementPosture instability

Involuntary flexion of head and shoulders, stoopedleaning forward position

Equilibrium problems causing falls, and short,accelerated steps

Shuffling gait


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MANIFESTATIONS

Autonomic nervous system Constipation and urinary hesitation or frequency

Orthostatic hypotension, dizziness with position

change

Eczema, seborrhea

Depression and dementia; confusion,

disorientation, memory loss, slowed thinking

Inability to change position while sleeping, sleep

disturbance

Mask-like face

Dysphonia


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MEDICATIONS

Antiparkinsonian- Levodopa (Larodopa) antiviral therapy- amantadine (Symmetrel)

anticholinergics- benztropine mesylate

(Cogentin)

Bromocriptine (Parlodel) pergolide (Permax)inhibit dopamine breakdown

MAOI- selegiline (Eldepryl)

Antihistamine- diphenhydramine hydrochloride

(Benadryl)

Medications may lose their efficacy; response

to drugs fluctuates: on-off effect


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TREATMENTS

Deep brain stimulation

Stereotactic procedures

Pallidotomy: destruction of involved tissue

thalamotomy: destroys specific tissue involved intremor


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NURSINGDIAGNOSES

Impaired Physical Mobility

Impaired Verbal Communication

Impaired Nutrition: Less than body requirements

Self care deficit Constipation

Disturbed Sleep Patterns

Ineffective coping


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NURSINGCARE

Improve mobility

Enhance self care activities

Improving bowel elimination

Improving nutrition Enhancing swallowing

Improving communication supporting coping

abilities


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HOMECARE

Medication education

Adaptation of home environment

Gait training and exercises

Nutritional teaching


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HUNTINGTONSDISEASE(CHOREA)

Progressive, degenerative

inheritedneurologic diseasecharacterized by increasing

dementia and chorea


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HUNTINGTONSDISEASE(CHOREA)

Cause unknown

Autosomal dominant genetic disorder

No cure

Usually asymptomatic until age of 3040

a significant reduction (volume and activity) of

acetylcholine


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DIAGNOSTICTESTS

Genetic testing of blood

CT scan shows cerebral atrophy


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NURSINGCARE

Very challenging: physiological, psychosocial andethical problems

Genetic counseling


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HOMECARE

Referral to agencies to assist client and family,support group and organization


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AMYOTROPHICLATERALSCLEROSIS ALS)LOUGEHRIGSDISE SE


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AMYOTROPHICLATERALSCLEROSIS(ALS)

Progressive, degenerative neurologic disease

characterized by weakness and wasting of muscles

without sensory or cognitive changes

Several types of disease including a familial type onset is usually between age of 4060

higher incidence in males at earlier ages but equallypost menopause

Physiologic problems involve swallowing, managing

secretions, communication, respiratory muscledysfunction

Death usually occurs in 25 years due to respiratoryfailure

MANIFESTATIONS


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MANIFESTATIONS

Initial: spastic, weak muscles with increased DTRs;muscle flaccidity, paresis, paralysis, atrophy; clientsnote muscle weakness and fasciculations; musclesweaken, atrophy; client complains of progressivefatigue; usually involves hands, shoulders, upperarms, and then legs

Atrophy of tongue and facial muscles result indysphagia and dysarthria; emotional lability and lossof control occur

50% of clients die within 25 years of diagnosis,often from respiratory failure or aspirationpneumonia


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DIAGNOSTICTEST

Testing rules out other conditions that maymimic early ALS such as hyperthyroidism,compression of spinal cord, infections,neoplasms

EMG to differentiate neuropathy frommyopathy

Muscle biopsy shows atrophy and loss ofmuscle fiber

Serum creatine kinase if elevated (non-specific)

Pulmonary function tests: to determinedegree of respiratory involvement


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NURSINGDIAGNOSES

Risk for Disuse Syndrome

Ineffective Breathing Pattern: may require

mechanical ventilation and tracheostomy


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NURSINGCARE

Help client and family deal with current healthproblems

Plan for future needs including inability to

communicate


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CREUTZFELDT-JAKOBDISEASE

(CJD, spongiform encephalopathy)


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CREUTZFELDT-JAKOBDISEASE

Rapid progressive

degenerative neurologic

disease causing brain

degeneration without

inflammation


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DESCRIPTION

Transmissible and progressively fatalCaused by prion protein: transmission of

prion is through direct contamination withinfected neural tissue

Variant form of CJD is mad cow disease:

believed transmitted by consumption of beefcontaminated with bovine form of disease

Pathophysiology: spongiform degenerationof gray matter of brain


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No definitive treatment.

Outcome is fatal.


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MANIFESTATIONS

Onset: memory changes, exaggerated startlereflex, sleep disturbances

Rapid deterioration in motor, sensory, language

function

Confusion progresses to dementia

Terminal states: clients are comatose with

decorticate and decerebrate posturing

DIAGNOSTIC TESTS


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DIAGNOSTICTESTS

Clinical pictures, suggestive changes on EEG andCT scan

Similar to Alzheimers in early stages

Final diagnosis made on postmortem exam

N C


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NURSINGCARE

Use of standard precautions with blood and bodyfluids

Support and assistance to client and family


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TRIGEMIN LNEUR LGI

(tic douloureux)

D


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DESCRIPTION

Chronic disease of trigeminal nerve (cranial nerveV) causing severe facial pain

The maxillary and mandibular divisions of nerve are

effected

Occurs more often in middle and older adults,females more than males

Cause is unknown

MANIFESTATIONS


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Severe facial pain occurring for brief seconds

to minutes hundreds of times a day, severaltimes a year

Usually occurs unilaterally in area of mouthand rises toward ear and eye

Wincing or grimacing in response to the painTrigger areas on the face may initiate the pain

Sensory contact or eating, swallowing, talkingmay set off the pain

Often there is spontaneous remission afteryears, and then condition recurs with dullache in between pain episodes


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M C O S


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MEDICATIONS

Anticonvulsants

carbamazepine (Tegretol)

phenytoin (Dilantin)

gabapentin (Neurotin)

SURGERY


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SURGERY

Intractable pain may be treated by severing thenerve root: rhizotomy

Client may have lost facial sensation and have loss

of corneal reflex

NURSING CARE


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NURSINGCARE

Teaching client self-management of pain

Maintaining nutrition

Preventing injury


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DESCRIPTION


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DESCRIPTION

Disorder of seventh cranial nerve and causesunilateral facial paralysis

Occurs between age of 2060 equally in males

and females

Cause unknown, but thought to be related toherpes virus

MANIFESTATIONS


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MANIFESTATIONS

Numbness, stiffness noticed first

Later face appears asymmetric: side of face

droops; unable to close eye, wrinkle forehead or

pucker lips on one side

Lower facial muscles are pulled to one side;appears as if a stroke

PROGNOSIS


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PROGNOSIS

Majority of person recover fully in few weeks tomonths

Some persons have residual paralysis

DIAGNOSIS


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DIAGNOSIS

based on physical examination

COLLABORATIVE CARE


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COLLABORATIVECARE

Corticosteroids are prescribed in some cases butuse has been questioned

Treatment is supportive

NURSING CARE


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NURSINGCARE

Teaching client self-care: prevent injury andmaintain nutrition

Use of artificial tears, wearing eye patch or taping

eye shut at night; wearing sunglasses

Soft diet that can be chewed easily, small frequentmeals

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neurologicdisorders