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Neurological Disorders

Neuro II Objective 10
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Multiple Sclerosis
Progressive, degenerative disease
Myelin sheath is damaged causing an inflammatory response
Damaged myelin removed by astrocytes, forms scar tissue (plaque)
Impulses still transmitted but not as effective
White fiber tracts of brain and spinal cord are usually affected
MS demographics
One of leading causes of neurologic disability in persons 20-40 years
App. 500,000 in U.S. affected
Women slightly higher than men, pregnancy may exacerbate
Seen more often in colder climates
Incidence in 1st degree relatives: 15 X greater
Types of MS
Benign
Relapsing - remitting
Porgressive - relapsing
- primary and secondary
Benign MS
Mild attacks, minimal or no disability
Patient usually does NOT seek medical attention
Relapsing - remitting
Increasingly freq attacks, periods of remission-return to baseline
attacks develop over 1-2 weeks, resolve over 4-8 mos
Most will move into secondary progressive
Progressive - relapsing
No periods of remission, doesn't return to baseline
only about 5% of pts have this kind; progressive, cumulative symptoms and deterioration occur over several yrs
Primary Progressive
Progressive disability with no acute attacks
Usu between 40-60 year of age at onset
Secondary Progressive
Gradual, may or may not have acute relapses
begins with RR course, later becomes steadily progressive
Multiple Sclerosis S/S
Muscle weakness & spasticity
Fatigue
Intention tremors
Dysmetria
Paresthesia
Hypalgesia
Ataxia
Dysarthria
Dysphagia
Diplopia
Nystagmus
Scotomas
Decreased visual & hearing acuity
Tinnitus, vertigo
Bowel and bladder dysfunction
Alterations in sexual function
Cognitive changes
Multiple Sclerosis Tretment
Tx-ABC's of MS = Avonex, Betaseron, Copaxone. Rebif (interferon) - expensive. Meds to treat symptoms. Mitoxantrone - slows or stops the growth of certain cells that affect the body's natural defenses
Parkinsons Disease
Debilitating, neurologic disease affecting motor ability
Acetylcholine transmits excitatory messages
Dopamine is produced in the substantia nigra, inhibits the function of acetylcholine
Degeneration of substantia nigra-decrease production of dopamin
Decreases inhibition of acetylcholine
Lose ability to refine voluntary movement
Initial Stage PD
unilateral limb, minimal weakness, hand and arm trembling
Mild Stage PD
bilateral limb, masklike facies, slow shuffling gait
Moderate Stage PD
postural instability, increased gait disturbances
Severe Stage PD
disability-akinesia, rigidity
Complete ADL dependence
Parkinsons Disease Key Features
Cardinal signs
Tremor
Rigidity
Bradykinesia
Postural instability
Other
Gait abnormalities
"Pill rolling"
Mask-like facies
Speech problems
Autonomic dysfunction
Psychosocial difficulties
Parkinsons Disease Statistics
Symptoms usually appear after age 50
Can occur as early as 30
4th most common neurodegenerative disease
3rd most common in older adults
50,000 new cases each year
Affects men more than women
Affects nearly 1% of population over 60
Pallidotomy
this operation is a probe inserted into brain. A small lesion is made deep in brain to interrupts electrical pathways that cause rigidity and tremors (in Parkinsons)
Amyotrophic Lateral Sclerosis (ALS)
Lou Gehrig's Disease
Progressive degenerative disease involving the motor system
Atrophy of hands, forearms, and legs
Sensory and autonomic nervous systems are not involved, no mental status changes
Excess of glutamate covering the motor neuron leading to destruction of nerve cell
ALS Clinical Manifestations
Fatigue while talking
Tongue atrophy
Dysphagia & dysarthria
Weakness of the hands & arms
Incoordination
Fasciculations of the face
Nasal quality of speech
ALS Statistics
Usual age of onset: 40-70
More prevalent in men
Death usu occurs within 3-5 years after onset of symptoms
No: cause, cure, tx, pattern of progression, or prevention
Rilutek-neuroprotective effect in early stages
Symptomatic tx and rehab
Huntington's Disease
Hereditary disorder transmitted as an autosomal dominant trait at the time of conception
mutation in the HD gene (IT15) located on chromosome 4
Increase in excitatory neurotransmitters
Decrease in inhibitory neurotransmitters
Huntington's Disease Stages
Gradual onset, three stages
1. Onset of neurologic or psychologic symptoms
2. Increasing dependence on others for care
3. Loss of independent function
Each stage lasts roughly 5 years...15 year course of the disease is typical.
Huntington's Disease Manifestations
Decreased attention span
Poor judgment
Memory loss
Personality changes
Dementia (late)
Choreiform movements
Poor balance
Hesitant or explosive speech
Dysphagia
Impaired respiration
Bowel/bladder incontinence
Huntington's Disease Statistics
Offspring of parent w/disease=50%
Men and women equally affected, usu 35-45 years of age
25,000 have disease, 20,000 to 50,000 carriers
Genetic counseling
Management is symptomatic
Guillian-Barré Syndrome
Autoimmune attack and demyelination of the peripheral nerves and some cranial nerves
Acute inflammatory process, varying degrees of motor weakness and paralysis
Dispersion of impulses, slow conduction velocities, or conduction block
Antecedent event precipitates clinical presentation
Schwann cell is spared allowing remyelination
GBS Etiology
• Acute illness
• Gastrointestinal illness
• Campylobacter jejuni bacteria
• Human immune deficiency virus infection
• Mycoplasma pneumoniae
• Surgery
• Upper respiratory infection
• Virus
• Cytomegalovirus
• Epstein-Barr virus
• Varicella-zoster virus
• Vaccination
• Flu
• Group A Streptococcus
• Rabies
• Drugs
• Captopril
• Danazol
• Penicillamine
• Systemic lupus erythematosus
• Hodgkin's disease
Nursing dx for GBS
Ineffective airway clearance related to weakness, problems in swallowing, and respiratory muscle paralysis
GBS Recovery
4-6 months
Remyelination and axonal regeneration
60-75% recover completely
Myasthenia Gravis
a chronic progressive disease characterized by chronic fatigue and muscular weakness (especially in the face and neck)
Myasthenia Gravis Pathophysiology
"Grave muscle weakness"
Chronic, neuromuscular, autoimmune disease
Decrease in # and effectiveness of ACh receptors at neuromuscular junction
Nerve impulses are not transmitted to skeletal muscle
No evidence of CNS or PNS disease or muscle atrophy
Characterized by remissions & exacerbations
Myasthenia Gravis Lab Values
TSH: (0.5-1.5 mU/L) decreased in MG
Serum protein electrophoresis (checking for immuno
disorders)
Acetylcholine Receptor Antibodies (AChR) <0.4 nmol/L
elevated in MG
Tensilon test
Test-used to determine difference between Myathenia Crisis and Cholinergic Crisis
Anticholinesterase-rapid onset, brief duration of action-inhibit breakdown of Ach;
Myasthenic crisis-symptoms improve; cholinergic crisis-doesnot improve, or gets worse.
Myasthenic crisis
usually caused by some type of infection; exacerbation of disease process; not enough anticholinesterase drugs; severe muscle weakness that may lead to resp failure
Cholinergic Crisis
exacerbation of muscle weakness; overmedication with anticholinesterase drugs -rare; muscle tone does NOT improve after giving Tensilon
Myasthenic Gravis treatment
Anticholinesterase (Mestinon)-inhibits breakdown of ACh, inc concentration at NM junction.
Immunosuppressant-reduce production of antibodies.
Corticosteroids-suppress pts immune response, dec amount of antibody production.
IVIG-may be given during exacerbations
Plasmapharesis-temp reduction in antibodies
Thymectomy-completely removed, antigen specific immunosuppression,
Myasthenia Gravis education
Rest and avoid fatigue
Importance of taking medications on schedule
Infection may cause exacerbation