ch59 Chronic Neurologic Problems

• Bilateral, bandlike pressure at base of skull and/or face
• Constant squeezing tightness
• Cycles over several years
• Intermittent for months or years
• Not related to time
• Palpable neck and shoulder muscle stiffness, stiff neck, tenderness

• Unilateral (60%), may switch sides, commonly anterior
• Throbbing, synchronous with pulse
• Periodic, cycles of severaL months to years
• Continuous for hours or days
• May be preceded by prodrome, onset after awakening, better with sleep
• Nausea/vomiting, edema, irritability, sweating, photophobia, phonophobia, prodrome of sensory/motor/psych phenomena, family history (in 65%)

• Unilateral, radiating up or down from one eye
• Severe, bone-crushing
• May have months or years between attacks, attacks occur in clusters, 1-2x/day over a period of 4-8 wks
• 30-90 minutes
• Nocturnal, commonly awakens patient from sleep
• Vasomotor symptoms such as facial flushing or pallor, unilateral lacrimation, ptosis, rhinitis

• Vasoconstrict arteries
• Contraindicated in patients with hypertension

• Verapamil, lithium, ergotamine, divalproex, NSAIDS
• Inhaling 100% oxygen at 7-9 L/min x15-20 min.
• Sumatriptan (Imitrex)
• Methylsergode, if recurrence at a specific time

Nonopioid analgesics (e.g., aspirin, acetaminophen) alone or with sedative, muscle relaxant, tranquilizer, or codeine.

• Involve both sides of the brain
• Characterized by bilateral synchronous epileptic discharges in brain from onset of seizure
• No warning or aura
• In most cases, loss of consciousness for a few seconds to several minutes

• Most common generalized seizure (f.k.a. grand mal)
• Loss of consciousness
• Fall on ground
• Tonic = fall to ground, stiff body for 10-20 seconds
• Clonic = subsequent jerking phase for 30-40 seconds
• Loss of body function control (salivation, incontinence) may occur

Brief staring spell, lasts only a few seconds, often unnoticed. Usually occurs only in children, rarely beyond adolescence. EEG demonstrates 3-Hz spike-and-wave pattern unique to this type of seizure.

Staring spell with other symptoms including brief warnings, peculiar behavior during seizure, or confusion after seizure. EEG demonstrates atypical spike-and-wave patterns, usually >3 Hz.

• Unilateral manifestations, localized in brain, caused by focal irritations
• Begin in specific region of cortex
• May be confined to one side of brain or may spread to involve entire brain, culminating in generalized tonic-clonic seizure

Demyelination of nerve sheath followed by myelin regeneration.

Glial scar tissue, which forms hard, sclerotic plaques and results in slowing/blockage of nerve impulses.

• Corticosteroids - exacerbations
• Immunomodulators - exacerbations
• Immunosuppressants - exacerbations
• Cholinergics - urinary retention
• Anticholinergics - urinary frequency/urgency
• Muscle relaxants - spasticity
• CNS stimulants - fatigue
• Antiviral/antiparkinsonian - fatigue

Disease of basal ganglia characterized by slowness in initiation and execution of movements (bradykinesia), increased muscle tone (rigidity), tremor at rest, and impaired postural reflexes.

• First sign: Tremor
• Second sign: Rigidity
• Third sign: Bradykinesia

• Dopaminergics - enhance supply of dopamine
• Anticholinergics - block effect of overactive cholinergic neurons

• Levodopa + carbidopa = Sinemet
• Levodopa is chemical precursor to dopamine, crosses blood-brain barrier, converts to dopamine in basal ganglia; carbidopa inhibits enzyme dopa-decarboxylase in peripheral tissues, allowing more levodopa to get to the brain.

• An autoimmune disease in which antibodies attack acetylcholine (ACh) receptors, resulting in decreased number of ACh receptor sites on neuromuscular junctions.
• Characterized by fluctuating weakness, with rest restoring strength and progressing weakness through the day.

• Acute exacerbation of muscle weakness triggered by infection, surgery, emotional distress, drug overdose, or inadequate drugs.
• Major complications are muscle weakness with swallowing and breathing.

• Anticholinesterase drugs - enhance function at the neuromuscular junction, prolongs action of acetylcholine by inhibiting enzyme that brakes down acetylcholine; includes neostigmine (Prostigmin) and pyridostigmine (Mestinon).
• Alternate-day corticosteroids.
• Immunosuppressants.

Overdose of anticholinesterase drugs (used to treat myasthenia gravis), resulting in respiratory insufficiency and severe muscle weakness.

• Administer Tensilon (anticholinesterase drug)
• Symptoms improve = myasthenic crisis
• Symptoms worsen = cholinergic crisis

Thymus gland produces anticholinesterase; therefore, removing the thymus gland (thymectomy) results in improvement in majority of patients.

Progressive wasting disorder, loss of motor neurons, leads to death within 2-6 years of diagnosis. Weakness of limbs progressively moving inward until respiratory failure results in death. Patients remain cognitively intact.

• Facilitate communication
• Reduce risk of aspiration
• Decrease pain secondary to muscle weakness
• Decrease risk of injury related to falls
• Provide diversional activities such as reading and companionship
• Help family and patient manage disease process including grieving related to loss of motor function and ultimately death

Autosomal dominant (50% chance of inheritance), deficiency in acetylcholine and GABA, symptoms opposite of Parkinson's. Excessive, abnormal involuntary movements (chorea), writhing, twisting movements. Progressive disease. Death usually within 10-20 years.

• Palliative care
• Antipsychotics (Haldol), antidepressants, and antichorea (clonazepam/Klonopin)
• High-calorie diet (4000-5000 kCal/day)