Transcript NEUROLOGICDISORDERSstudentcopyF2009

NEUROLOGIC DISORDERS
Myasthenia Gravis
Parkinsons Disease
Multiple Sclerosis
Amyotrophic Lateral Schlerosis
Spinal Cord Injury
Intervertebral Disc Herniation
Cranial Nerve Problems
2009
Myasthenia Gravis
DEFINITION
• problem in neurotransmission
• severe fatigue of voluntary muscles
• defect of acetylcholine receptor sites
 at the myoneuronal junction
• theories indicate autoimmune problem
• Remissions/exacerbations
• Progressive proximal muscle weakness
improving with rest
CLINICAL MANIFESTATIONS
• Patients indicate abnormal fatigue of the
voluntary muscles of the eye, the respiratory
tract and the limb muscles
• Also have difficulty with speech and swallowing
• End up choking with meals
• Ptosis, diplopia, dysphagia
• MOST ADVANCED: all muscles weakened: no
respiratory function, no bladder and bowel
function
DIAGNOSTIC TESTS
• Tensilon test:
– give patient a short acting anticholinesterase
(Tensilon or edrophonium chloride) that
enhances neurotransmission and results in
abrupt, but short term improvement of symptoms
• Atropine : antidote for Tensilon
• EMG: electromyography:
LABORATORY ASSESSMENT
• THYROID FUNCTION STUDIES DONE: thyrotoxicosis
seen with MG
• Serum protein electrophoresis: for immunologic
disorders
• Acetylcholine receptor antibodies (AChR): important
diagnositic criterion 80-90% of clients with MG have
elevated AChR
• Often have thymoma or hyperplasia of thymus gland
DRUG THERAPY
Anticholinesterase medications:
– Pyridostigmine bromide (Mestinon),
neostigmine bromide (Prostigmin) Increases
acetylcholine at the neuromuscular junction
– Dosage regulated based on improved strength
and less fatigue
– MUST BE GIVEN ON TIME to keep stable blood
levels
• RESULT: pt weakness worse
DRUGS TO AVOID: increase weakness
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Magnesium
Morphine
Curare
Quinine
Quinidine
Procainamide
Hypnotics
sedatives
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Antibiotics:
Neomycin
Kanamycin
Polymyxin B
tetracyclines
DRUG THERAPY
• Corticosteroids used to control and improve
symtoms:
• prednisone(Deltasone, Winpred)
– As steroids increased anticholinesterase dosage
decreased
• Cytotoxic medications used:
– why they work unknown
TREATMENT
• PLASMAPHERESIS: plasma exchange
– Used to treat exacerbations
– HOW IS THIS DONE: Blood cells and antibody
containing plasma separated out then the cells
and a plasma substitute reinfused
– Improves symptoms in 75% of patients
TREATMENT CONTINUED
• IV immune globulin (IVIG)
• Works as well as plasmapheresis during
exacerbations
Summary of therapies
• Not a cure
• Does not stop the production of acetylcholine
receptor antibiodies
SURGICAL TREATMENT
• Thymectomy continues to be associated with
improvement in 50-92%% of patients
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produces antigen specific immunosuppression
Results in clinical improvement
Decreases need for medication
Takes a year for benefit to be seen because of the long life
of circulating T cells
MYASTHENIC CRISIS
• SEEN WITH UNDERMEDICATION WITH
CHOLINESTERASE INHIBITORS
• Severe generalized weakness and respiratory failure
• Seen after stress (URI, infection, medication change,
surgery, obstetrical delivery, high environmental
temperature)
• Patient needs ventilatory support
• Patient will need help with all ADL
• Suctioning, chest PT
CHOLINERGIC CRISIS
• RESULT OF OVERMEDICATION WITH
ANTICHOLINESTERASE DRUGS
• Can mimic symptoms of myasthenic crisis
• Differentiated via Tensilon test
• Pt with Myasthenic Crisis will show immediate
improvement following Tensilon administration
• Pt with Anticholinergic Crisis will show no
improvement and may get worse
TREATMENT OF CHOLINERGIC CRISIS
• STOP ALL ANTICHOLINESTRASE MEDICATIONS
• Give Atropine sulfate given IV
• SE: secretions thickened
NURSING DIAGNOSIS
THYMECTOMY:
• REMOVAL OF THYMUS GLAND DONE EARLY IN
DISEASE
• May take several years for remission to occur
if it occurs at all
• Review p 1017 Iggy
NURSING CARE
• Most pts seen on outpatient basis
• Teaching:
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use of medications
S&S of myasthenic crisis and choinergic crisis
How to conserve energy
Ways to avoid aspiration
Have suction at home
Gastrostomy feeding instruction
Avoid factors that increase crisis
Eye care
PARKINSONS DISEASE
DEFINED
Presence of motor dysfunction with 4 cardinal
symptoms
• resting tremor
• akinesia (slowness of body movement)
• rigidity
• Postural instability
NO PREVENTION, NO CURE
AGE RANGE: 40-70, PEAK 60
Michael J. Fox dx at age 30
PATHOPHYSIOLOGY
Reduced amount of dopamine
• Result: inhibition effect lost
• Excitatory effect predominant
Reduced norepinephrine in sympathetic NS of
the heart:
• Orthostatic hypotension
ASSESSMENT:
• Initially: one limb involved with mild weakness and
arm and hand trembling
• Progresses to both limbs involved, slow shuffling gait
• Continues to worsen: gait disturbances(slow
shuffling, short hesitant steps, propulsive gait
• Severe involvement: akinesia, rigidity, CANNOT GET
OOD
FURTHER ASSESSMENT:
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Rigidity of facial muscles:
masklike facies
Drooling
Dysphagia
Dysarthria: Rapid slurred speech
Echolalia: repetition
ASSESSMENT CONTINUED
• PSYCHOSOCIAL
• Emotionally labile
• Delayed reaction time
DRUGS
• ANTIPARKINSON AGENT: monoamine oxidase
type b inhibitor: selegiline (Eldepryl, Carbex,
Novo-Selegiline): used to protect the neurons,
successful in reducing the use of Levodopa
until later
• Catechol O-methyltransferase (COMT)
inhibitors:
– Tolcapone (Tasmar)
– Entacapone (Comtan)
Block breakdown of levodopa in body so more can go
to brain and convert to dopamine
DRUGS
• DOPAMINE AGONISTS: providing
dopamine that is missing
– Levodopa (Dopar, L-dopa) and
– carbidopa (Sinemet):
ANTIPARKINSON AGENT/ANTIVIRAL:
• amantadine (Symmetrel): potentiates
action of dopamine in CNS, treats
tremor; also treats symptoms of
“wearing off”
TREATMENT
• Meds may need drug holiday - effectiveness
after used for long time; admit to hospital to
try other drugs
• p693 FOR SURGICAL tx
• Stereotactic Pallidotomy/Thalamotomy
Deep brain stimulation
fetal Tissue transplant
NURSING DIAGNOSIS
• Self-care deficit related to slowness of
movement and muscle rigidity
• Risk for injury related to postural instability
and muscular rigidity
• Impaired verbal communication related to
slowness of movement
• Altered nutrition related to poor muscle
control
NURSING DIAGNOSIS CONTINUED
• Knowledge deficit related to complexity of and
fluctuations in treatment regimen
• Ineffective coping relate to progressive nature
of illness
IMPLEMENTATION
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Establish routine for personal care
Safety in bathing, transferring, walking
AROM, PROM
Encourage pt to take a deep breath before
initiating a conversation, using gestures
• Rigidity of facial expression hides pts true
feelings
IMPLEMENTATION
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Meals thickened liquids, semisolids
Eat sitting up
Suction
Daily wgts
Increase fluids/day for constipation
Drug flowsheet to document response to
medications
• Keep patient active as long as possible
MULTIPLE SCLEROSIS
AUTOIMMUNE DISORDER
DEFINED
• Demyelinating disease affecting nerve fibers of the
brain and spinal cord
• CAUSE unknown. Thought to be an autoimmune
problem with a viral trigger
• Lesions scattered through the white matter of the
brain around the ventricles; some in grey matter
• Inflammatory response triggers phagocytosis with
myelin as the target
OLDER DRUG THERAPY
• The most widely accepted drug treatment is
corticosteroids :
• Methylprednisolone(Solumedrol)
• Given IV followed by oral prednisone
– Steroids decrease the inflammatory
response, decrease the edema,
improvement of symptoms
• Cyclophosphamide (Cytoxan) used for chronic
progressive disease to produce temporary
remission from 1-3 years
DEFINITION CONTINUED
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Edema around lesions
Eventually a hard plaque forms
Characterized by exacerbations and remissions
Progressive from benign with few symptoms to
chronic with complete paralysis.
• 70% of pts lead active productive lives with long
periods of remission
DIAGNOSIS
• lumbar puncture: CSF shows increase protein,
lymphocytes, IgG, presence of oligoclonal
bands and increased myelin basic protein
• EMG: prolonged impulse conduction
• MRI: demonstrates white matter lesions
(plaques) of brain, brainstem and spinal cord
NEW DRUG THERAPY
BIOLOGICAL RESPONSE MODIFIERS:
recommended to use one of these three:
• Interferon beta -1a (Avonex) - weekly IM
• Interferon beta-1b recombinant (Betaseron) every other day SQ
• PURPOSE AND SIDE EFFECTS OF BOTH
– Slows physical disability, decreases physical
worsening of disease
– Major SE: suicidal tendency, depression
• Glatiramer acetate (formerly Copolymer I)
(Copaxone) - every other day SQ
SYMPTOMS
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Blurred vision
Double vision
Dysphagia
Facial weakness
Numbness
Pain
Weakness
Symptoms Continued
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paralysis
abnormal gait
tremor
vertigo
fecal and urinary incontinence
decreased short term memory
word finding trouble
Symptoms Continued
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decreased concentration
mood alteration
decreased libido for women
ejaculatory dysfunction for men
overwhelming weakness
DRUGS
• Baclofen (Lioresal), Diazepam (Valium), Dantrolene
sodium(Dantrium) - for spasticity
• Carbamazepine (Tegretol), tricyclic antidepressants
(amitriptyline),: paresthesia
• propranolol (Inderal), clonazepam (Klonopin) – used
for cerebral ataxia
• Amantadine hydrochloride (Symmetrel): fatigue
• oxybutynin chloride (Ditropan), propantheline
bromide (ProBanthine) - decreased urinary urgency,
incontinence
• Bulk additives (Metamucil) - constipation
• Colace - improved bowel control
• Dulcolax – stimulant
• Tizanidine (Sanaflex) antispasmodic for pain
NURSING INTERVENTIONS
• Self-care deficit: balance assistance with
independence; promote own routine
• Urinary retention/incontinence: intermittent
catherization, Texas catheter for men
• Bowel incontinence: regular routine, high fiber diet,
and fluids
• Impaired skin integrity related to immobility: skin
assessment
NURSING INTERVENTION
• Fatigue related to disease process: pace self
AMYOTROPHIC LATERAL SCLEROSIS
Lou Gerhig’s Disease
Amyotrophic Lateral Sclerosis or Lou Gehrig’s
disease
• Progresive degenerative disease involving the
motor system (motor neurons)
• Sensory and autonomic systems not involved
• No mental status changes
Cause
• Excess of glutamate: chemical responsible for
relaying messages between the motor
neurons
• As the motor neurons die the muscle cells
they supply undergo atrophic changes leading
to paralysis
PROGRESSION OF DISEASE
• Muscle weakness and atrophy develop leading
to flaccid quadriplegia
• Eventually respiratory muscles become
affected leading to respiratory compromise,
pneumonia and death
• No known cure, treatment symptomatic
WHAT DO YOU SEE?
• FATIGUE
• Fatigue while talking
• Muscle
weakness/atrophy
• Tongue atrophy
• Dysphagia (difficulty
swallowing)
• Weakness hands and
arms
• Fasciculations
(twitching) of face
• Nasal quality of
speech
• Dysarthria (difficulty
speaking)
CARE
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Focus on symptoms
Monitor respiratory status
Prepare to initiate respiratory support
Assess complications of immobility
SPINAL CORD INJURY
DEFINED
• Fractures, contusions, or compression of the
vertebral column with damage to the spinal cord
• The injury affects motor and sensory function at the
level of injury and below
SPINAL CORD INJURIES are classified as complete or
incomplete
• Complete: total cord transection
• Incomplete: partial transection
FOUR TYPES OF INJURIES OCCUR
• HYPERFLEXION: compresses vertebral bodies and
disrupts ligaments and discs
• HYPEREXTENSION: disrupts ligaments and causes
vertebral fractures
• AXIAL LOADING: application of excessive vertical
force and may cause compression fractures
• EXCESSIVE ROTATION: tears ligaments and fractures
articular surfaces and causes compression fractures
SPINAL SHOCK
• With cord damage spinal shock occurs and areflexia
(temporary loss of reflex functioning)
• Loss of motor sensory, and autonomic activity below
the level of injury
• Then leads to decrease in blood pressure and
bradycardia
• The parts of body below the level of the cord injury
are paralyzed without sensation or diaphoresis
• Lasts days or months after injury
DEFINITIONS OF PARALYSIS
• PARAPLEGIA: paralysis of the lower portion of
the body; occurs when the injury level is in the
thoracic spine or lower
• Tetraplegia: formerly quadriplegia is paralysis
of the arms, trunk, legs and pelvic portion;
occurs when the level of injury is in the
cervical spine
EMERGENCY TREATMENT
• DO NOT MOVE THE CLIENT until adequate
personnel and equipment are available
• Keep the neck aligned
• Immobilize the head and neck
• Maintain a patent airway (with cervical injury
edema may cause respiratory difficulty
ADMINISTER DRUGS
• High dose corticosteroids:
– reduces disability in 8hrs of injury
• Osmotic diuretics: mannitol (Osmitrol)
– Decreases edema around spinal cord
• Muscle relaxants: baclofen (Lioresal)
– Reduces spasticity
• Dextran
– prevents BP; improves capillary blood flow
• dopamine hydrochloride (Intropin) and isoproterenol
(Isuprel): inotropic and sympathomimetic agents for severe
hypotension
IMMOBILIZATION
• Goal: reduce dislocations and stabilize cervical
vertebral column
HOW?
• Skeletal traction (skeletal tongs such as Gardner–
Wells tongs or Crutchfield tongs)
• Halo traction
CARE: weights hang freely, never remove weights, clean
tongs, assess for infection
SURGERY
• Surgical immobilization via anterior and posterior
decompression and fusion with bone grafts
• DECOMPRESSION WITH LAMINECTOMY: remove bony
fragments that cause compression, remove foreign
body causing compression
• FUSION: anterior, posterior or anterior/posterior
using Harrington rods
IMMOBILIZATION AFTER SURGERY
• SOMI JACKET
• CTLSO
AUTONOMIC DYSREFLEXIA
DEFINED:
• Exaggerated sympathetic response that occurs in
clients with T6 injuries or higher
• Response seen after spinal shock occurs when stimuli
cannot ascend the cord
• Stimulus (urge to void) triggers massive
vasoconstriction below the injury, vasodilation above
the injury, and bradycardia
CAUSES OF AUTONOMIC DYSREFLEXIA
MOST COMMON: overdistended bladder
• Bowel impaction, rectal exam
• UTI, bladder spasms, renal calculi
• Pressure sores, ingrown toenail
• Burns, blows to body
• Tight clothing, tight cast
S & S AUTONOMIC DYSREFLEXIA
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Sudden pounding severe HA
Severe hypertension, bradycardia
Flushing, sweating above the level of injury
Piloerection (goose bumps)
Nasal congestion
Apprehension
Blotching above the level of injury
TX OF AUTONOMIC DYSREFLEXIA
SERIOUS MEDICAL EMERGENCY! ACT QUICKLY!
DO NOT WAIT!
• Identify/remove the stimulus
• Reduce the BP
• Administer drugs
• Teach pt how to deal with it
TX OF AUTONOMIC DYSREFLEXIA
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REQUEST HELP
HOB up!
Check BP q 5 minutes
Do straight cath of bladder; eval bowel
Remove tight clothing, check orthotics
Check skin, toenails
Report to MD if BP still won’t decrease
DRUGS FOR AUTONOMIC DYSREFLEXIA
ACUTE PHASE:
• Nitropaste (vasodilator)
• Arfonad IV (ganglionic blocker to lower BP fast)
• Apresoline IV (relaxes arterolar smooth muscle)
• Low spinal anesthetic at L4 if no results with drugs
PREVENTION: antihypertensives
BLADDER PROBLEMS
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INCONTINENCE
UTI
URINARY CALCULI
BLADDER SPASMS
SPASTIC BLADDER
• Clients have Injury above the sacrum
• End up with upper motor neuron spastic bladder
• May be able to stimulate voiding by
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Stroking inner thigh
Pullin on pubic hair
Pouring warm water over perineum
Tapping bladder to stimulate detrusor muscle
Taking bethanechol chloride (Urecholine); cholinergic
agent which helps contraction of detrusor mucle: take 1
hour before trying to void
FLACCID BLADDER
• Clients with lumbosacral injury
• Have lower motor neuron flaccid bladder
• Able to empty bladder by:
– Tightening abdominal muscles
– Intermittent cath two or three times daily
TREATMENT OF THE URINARY
PROBLEMS
• Intermittent catherization :Clean cath
• Prevents incontinence, dysreflexia, UTI, calculi
CAUTION: never drain more than 700cc/ leads
to hypovolemic shock
• increase fluid, water, high acidity fluids, no
alcohol, low soda (hi salt), low milk, avoid
alkaline fluids
DRUGS FOR ELIMINATION PROBLEMS
• oxybutynin (Ditropan) : decreases urinary incontinence
• propantheline(Pro Banthine): reduces bladder spasms
• ascorbic acid (Vitamin C): increases urine acidity;
prevents UTI; works with Mandelamine
• methenamine (Mandelamine): urinary tract antisepticto
prevent UTI; do not combine with carbonic annhydrase
inhibitors, sulfa drugs or diuretics
• Imipramine (Tofranil) antidepressant used to tx urinary
incontinence (side effect: urinary retention))
BOWEL ELIMINATION PROBLEMS
Constipation
Loss of bowel control
TREATMENT: Bowel Program
• Combination of stool softeners, bulk formers,
laxatives
• High fiber diet, high fluids
Bowel Program
• Consitent time
• High fluid intake
• High fiber diet
DRUGS FOR BOWEL ELIMINATION
PROBLEMS
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docusate sodium(Colace): stool softener
senna (Senekot): laxative
bisacodyl (Dulcolax): laxative
dibucaine (Nupercainal): ointment anesthetic
used prior to beginning bowel program to
prevent autonomic dysreflexia
• psyllium (Metamucil): bulk forming agent
OTHER PROBLEMS
Mostly related to immobility
• RESPIRATORY: pneumonia, PE
• MOBILITY: contractures, spasticity, decubitus, burns,
bruises, fractures, osteoporosis
• CIRCULATORY: DVT/edema, postural hypotension, GI
bleed
• SEXUAL: males have decreased fertility, females can
bear children
INTERVERTEBRAL DISC
HERNIATION
DEFINED
• Disorder involving impingement of a vertebral disk’s
nucleus pulposus on spinal nerve roots causing pain
and possible neuromuscular deficit
TREATMENT conservative:
• with muscle relaxants: cyclobenzaprine
hydrochloride (Flexeril)
• Nonsteroidal anti-inflammatory drugs (NSAIDS):
naproxen (Naprosyn)
• Epidural or local steroid injection
• Rest, heat, muscle strengthening exercises, pelvic
tilts, straight leg raises
MINIMALLY INVASIVE SURGERY
(see page 980 of Iggy)
ADVANTAGE: ambulatory procedure or
shortened hospital stay with less spinal cord
complications
• Percutaneous lumbar diskectomy
• Microdiskectomy
• Laser-assisted laparoscopic lumbar diskectomy
SURGERY see p980 of Iggy
• Diskectomy: spinal nerve is lifted to remove
the offending portion of the disk
• Laminectomy: removal of 1 or more vertebral
lamina and the herniated nucleus pulposus
• Spinal fusion (arthrodesis): to stabilize area
using chips of bone from iliac crest grafted to
vertebrae
SURGICAL MANAGEMENT
LAMINECTOMY: surgical incision of the lamina to relieve
symptoms related to herniated intervertebral disc
POST OP CARE:
• Neurological and neurovascular assessment, assessment of
bowel and bladder function
• Assess for c/o severe HA or leakage of CSF
• Log roll, proper alignment
• Bedrest 24-48 hours; rise as a unit when getting OOB first
time
• Paresthesias may not be relieved immediately
AMPUTATION
COMMON AMPUTATION SITES
TYPES OF SURGERY
FEMUR
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femur patella
PATELLA
TYPES OF PROSTHESES
• TOTAL CONTACT RIGID DRESSING: applied in OR to
protect stump swelling
• PERMANENT LEG PROSTHESIS: rigid dressing that
connects to an adjustable pylon and foot ankle
assembly to permit walking; need 3-4 of these,
stump shrinks with healing
• SOFT DRESSING: when frequent inspection needed;
may have drainage device
COMPLICATIONS
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Bleeding
Infection
Skin breakdown
PHANTOM LIMB PAIN
FLEXION CONTRACTURES
NURSING CARE
1. Proper positioning to
minimize contractures
2. Watch use of pillow
under stump
3. Lie prone
4. Phantom limb pain
5. Monitor for excessive
bleeding
6. Prevent stump edema
7. Assess for infection
8. Assess for hematoma
formation
9. Teach stump care
10. Teach use of prosthesis
11. Provide referral to
National Amputee
Foundation and
Amputee Shoe and
Glove Exchange
CRANIAL NERVE DISORDERS
Trigeminal Neuralgia
Bells Palsy
Guillan-Barre Syndrome
Trigeminal Neuralgia
• DEFINED: chronic disease of the trigeminal nerve causing
severe facial pain unknown cause
• Pain occurs briefly, intense skin surface pain 100 times/day or
a few times a year
• Starts peripherally and advances centrally
• Some trigger zones initiate pain
• TREATED WITH: seizure drugs: carbamazepine (Tegretol);
phenytoin (Dilantin)
• SURGICAL TREATMENT: removal of blood vessel from
posterior trigeminal root or severing nerve root
• NURSING DX: risk for imbalanced nutrition; pain
Bell’s Palsy
• DEFINED: unilateral paralysis of facial muscles; unknown
cause; inflammation of the nerve and viral cause suggested;
recover within few weeks/months, some have permanent
paralysis
• SEE: one sided paralysis of facial muscles and upper eyelid,
loss of taste on affected side, increased tearing of eye on
affected side
• TREATMENT: corticosteroids (decreases edema of nerve
tissue) – Prednisone; and antiviral medications
• NURSING DX: altered body image; altered nutrition
GUILLAIN BARRE SYNDROME
• Autoimmune attack of the peripheral nerve myelin
• RESULT: acute rapid demyelination of peripheral nerves and
some cranial nerves
• PRODUCES:
– ***Ascending weakness with dyskinesia (inability to execute voluntary
movements)
– Weaknss starts in legs and progresses upward for 1 month
– ***Hyporeflexia
– Paresthesias (numbness and pain)
– MAXIMUM WEAKNESS:
• neuromuscular respiratory failure and
• bulbar muscle weakness (demylelination of glossopharyngeal and vagus
nerves leads to inability to swallow or clear secretions)
S & S CONTINUED
• VAGUS NERVE DEMYELINATION:
– Leads to autonomic dysfunction
– Manifested by instability of cardiovascular system
– S & S: tachycardia, bradycardia, hypertension,
orthostatic hypotension
• NO COGNITIVE DYSFUNCTION
SYMPTOMS CONTINUED
• PRECIPITATING EVENT: respiratory or GI
infection, vaccination, surgery, pregnancy
• DURATION OF SYMPTOMS: may take up to
two years to recover; some symptoms are
permanent due to damage to nerves
TREATMENT
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MEDICAL EMERGENCY: ICU
Rapid progression
Neuromuscular respiratory failure
May need mechanical ventilation
suctioning
Prevention of complications of immobility
FOR CARDIOVASCULAR RISKS
• EKG
• beta blocking agents for tachycardia and
hypertension
• IV fluid for hypotension
NURSING DIAGNOSIS