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179 Cards in this Set
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Beta-blockers - eg. propranolol (Inderal), which is nonselective, and atenolol which is selective
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Migraine Prophylaxis
MOA: Blocks beta-1 and beta-2 receptors; if drug only blocks beta-1 receptors it is considered beta-selective; selectivity is lost at higher doses Other uses: Hypertension, ischemic heart disease/myocardial infarction, heart failure Contraindications: Asthma/COPD, bradycardia (AV block), hypotension, peripheral vascular disease and Raynaud’s disease, uncontrolled heart failure, cardiogenic shock, sick sinus syndrome, Wolff-Parkinson-White syndrome S/E: Fatigue, hypotension, bradycardia, depressive symptoms, heart failure, dizziness, cold extremities Monitoring parameters: Blood pressure, pulse Comments: Considered first line therapy, when d/c, taper over 2-3 weeks |
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Valproic acid (Depakene) or divalproex sodium (Depakote), (Depacon is intravenous)
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Migraine Prophylaxis/anticonvulsant
MOA: Blocks sodium current, blocks T-calcium current, blocks penicillin-induced bursting, increases GABA in vitro Other uses: Migraine prophylaxis and acute therapy, bipolar disorder Contraindications: Hepatitis S/E: Weight gain, GI distress, tremor, pancreatitis, hepatotoxicity, polycystic ovary disease, alopecia, thrombocytopenia, other blood dyscrasias (more in children), hyperammonemia, parkinsonism, sensorineural hearing loss, edema Monitoring parameters: Serum concentrations, liver function tests, platelets; CBC/diff for blood dyscrasias esp in children Comments: Taper in patients with seizures (FDA-approved for both szs and migraines) |
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Tricyclic antidepressants -eg. amitriptyine (Elavil), nortriptyline (Pamelor, Aventyl)
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Migraine Prophylaxis
MOA: Blocks reuptake of NE, serotonin Other uses: Depression, neuropathy, urge incontinence Contraindications: Recent myocardial infarction, arrhythmia, heart block; closed-angle glaucoma, avoid MAO-inhibitors S/E: Hypotension, QT prolongation, drowsiness, dry mouth, constipation, blurry vision Monitoring parameters: Orthostatic hypotension, esp in elderly, heart rate, EKG Comments: Taper over 2-3 weeks |
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Calcium channel blockers (eg. verapamil, diltiazem)
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Migraine Prophylaxis
MOA: Calcium channel blocker Other uses: Hypertension, ischemic heart disease, rate control agent in atrial fibrillation and paroxysmal supraventicular tachycardia (verapamil and diltiazem only), achalasia Contraindications: Prolonged P-R interval (verapamil and diltiazem only), heart failure (systolic dysfunction), critical aortic stenosis S/E: Edema, headache (worse with dihydropyridine calcium channel blockers like amlodipine or Norvasc), fatigue, gingival hyperplasia Monitoring parameters: Blood pressure, heart rate (for verapamil and diltiazem) Comments: Taper over 2-3 weeks |
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ACE-inhibitors (eg. lisinopril)
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Migraine Prophylaxis
MOA: Angiotensin converting enzyme inhibitor Other uses: Hypertension, heart failure, microalbuminuria and nephrotic syndrome Contraindications: Hyperkalemia, volume depletion, bilateral renal artery stenosis, angioedema, critical aortic stenosis, pregnancy, caution in renal failure S/E: Dry cough, hyperkalemia, renal impairment Rare: angioedema Monitoring parameters: Blood pressure, potassium, serum creatinine |
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Botulinum toxin type A (BoTox), type B (Myobloc)
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Migraine Prophylaxis
MOA: Inhibits acetylcholine release Other uses: Blepharospasm, cervical dystonia, hyperhidrosis, strabismus, bladder muscle dysfunction Contraindications: Neuromuscular disease (ALS, myasthenia, Lambert-Eaton syndrome), aminoglycosides, other drugs with neuromuscular block S/E: Dysphagia, dry mouth, ptosis, headache, flu-like syndrome, injection site pain Rare: anaphylaxis, dyspnea Monitoring parameters: Comments: ? efficacy in headache; intramuscular injections |
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Gabapentin (Neurontin)
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Migraine Prophylaxis/Epilepsy
MOA: Increases GABA synthesis and release, limits high frequency action potential firing, reduces L-calcium current, increases serotonin, protects against glutamate neurotoxicity, may upregulate Ih (H-channel) Other uses: Used more for pain, including neuropathy, migraine, essential tremor Contraindications: S/E: Drowsiness, weight gain, dizziness, muscle twitching, diplopia Monitoring parameters: Comments: Taper in patients with seizures |
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Lithium (Lithobid)
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Migraine Prophylaxis
MOA: Alters neuronal sodium transport Other uses: Migraine, bipolar disorder, acute mania, schizoaffective disorder Contraindications: Inability to monitor serum concentrations S/E: Tremor, polyuria (diabetes insipidus), diarrhea, vomiting, seizures, hypothyroidism Monitoring parameters: Serum creatinine, lithium concentrations, TSH Comments: Serum concentration 0.6-1.2mEq/L |
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Magnesium
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Migraine Prophylaxis
MOA: Gates channel at NMDA-receptor Other uses: Migraine- prophylaxis and acute therapy Contraindications: Renal insufficiency, cardiac conduction abnormalities S/E: Dyspepsia, diarrhea Monitoring parameters: |
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Riboflavin
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Migraine Prophylaxis
MOA: Vitamin B, use 400mg daily Other uses: Contraindications: S/E: Monitoring parameters: Comments: |
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Baclofen
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Migraine Prophylaxis
MOA: Centrally-acting muscle relaxant Other uses: Spasticity Contraindications: Epilepsy S/E: Sedation, confusion, dry mouth, fatigue, hypotension, dizziness Monitoring parameters: Comments: Taper |
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Tizanadine (Zanaflex)
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Migraine Prophylaxis
MOA: Central alpha-2 agonist; decreases NE, blocks NMDA receptor Other uses: Spasticity Contraindications: S/E: Sedation, dry mouth, fatigue, hypotension, dizziness, constipation Monitoring parameters: Serum creatinine, LFTs, hypotension Comments: Taper |
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Cyclobenzaprine (Flexeril, Amrix, Fexmid)
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Migraine Prophylaxis
MOA: Centrally-acting muscle relaxant Other uses: Muscle spasm Contraindications: MAO inhibitor, recent myocardial infarction, heart block, heart failure, closed-angle glaucoma, arrhythmia, alcohol use S/E: Sedation, dry mouth, fatigue, dizziness Monitoring parameters: Comments: Taper |
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Cyproheptadine
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Migraine Prophylaxis
MOA: Serotonin antagonist, antihistamine, anticholinergic Other uses: Allergic rhinitis, urticaria, anorexia nervosa, serotonin syndrome Contraindications: Closed-angle glaucoma, urinary retention, MAO-inhibitors S/E: Dry mouth, drowsiness, nausea, dizziness, headache, weight gain Monitoring parameters: |
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Montelukast (Singulair)
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Migraine Prophylaxis
MOA: Leukotriene inhibitor Other uses: Asthma, allergic rhinitis Contraindications: S/E: Headache, flu-like syndrome, abdominal pain Rare: angioedema, anaphylaxis Monitoring parameters: Comments: |
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Atypical antipsychotic agents
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Migraine Prophylaxis
MOA: Dopamine antagonist Other uses: Schizophrenia, bipolar disorder Contraindications: Gastrointestinal or genitourinary obstruction, hyperthermia, closed-angle glaucoma S/E: Dry mouth, constipation, somnolence, weight gain, stroke, neuroleptic malignant syndrome, extrapyramidal disorders, hyperprolactinemia Monitoring parameters: Blood glucose, HbA1c, weight, lipid panel Comments: Black box warning for increased stroke and mortality in elderly with dementia |
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Triptans (eg sumatriptan- Imitrex)
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Acute therapy for Migraine
MOA: Serotonin agonist at 5HT1A and 1D receptors (produces vasoconstriction) Other uses: Contraindications: Ischemic disease, uncontrolled hypertension, coronary vasospasm, basilar migraine, hemiplegic migraine, ergot use within 24 hours S/E: MI, hypertension, CVA, nausea, paresthesias, jaw neck or chest pain, pressure, tightness, dizziness, drowsiness Monitoring parameters: Blood pressure, do not overuse (analgesic- induced headache) Comments: SC, nasal; if cardiac risk factors check EKG, lipid and if benefit outweighs risk, give 1st dose in office |
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Ergotamine (eg dihydroergotamine _DHE)
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Acute therapy for Migraine
MOA: Produces vasoconstriction Other uses: Contraindications: Same as triptans; triptan use within 24 hours S/E: MI, hypertension, CVA, nausea, paresthesias, dizziness Monitoring parameters: Same as triptans Comments: Not used as much except for nasal spray and IV |
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Acetaminophen, dichloralphenazone, isometheptene (Midrin, etc)
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Acute therapy for Migraine
MOA: Dichloralphenazone –sedative Isometheptane – cerebral vasoconstriction Other uses: Contraindications: Hypertension, coronary artery disease, MAO-I use, peripheral vascular disease S/E: Dizziness Monitoring parameters: Limit to 5/day, 15/week Comments: Older medication; Schedule IV controlled substance |
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Corticosteroids (eg prednisone)
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Acute therapy for Migraine
MOA: Corticosteroid; ? mechanism – used IV in severe migraine Other uses: Contraindications: Hypertension S/E: Psychosis, mood changes, nausea, hyperglycemia, heart failure, hypertension (short term use) Monitoring parameters: Comments: IV; other side effects with long-term use |
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Metoclopramide (Reglan)
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Acute therapy for Migraine
MOA: Dopamine blocker, acetylcholine agonist, 5-HT antagonist Other uses: Diabeteic gastroparesis, GERD Contraindications: S/E: EPS, depression, sedation, hyperprolactinemia Monitoring parameters: Comments: |
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Antipsychotic/antiemetic (eg prochlorperazine – Compazine)
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MOA: Dopamine blocker
Other uses: Contraindications: S/E: EPS. drowsiness, anticholinergic side effects Monitoring parameters: Comments: IV |
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Phenobarbital
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Anticonvulsants
MOA: Enhances GABA-evoked chloride currents, reduces L-and N-calcium currents, blocks AMPA glutamate receptor subtype Other uses: Sedation, essential tremor Contraindications: Porphyria, absence seizures S/E: Sedation, cognitive impairment, hyperactivity in children and elderly, ataxia, diplopia, allergic rash including Stevens-Johnson syndrome, osteopenia, frozen shoulder syndrome, folic acid deficiency Monitoring parameters: Serum concentrations, CBC/diff Comments: Taper over 6 weeks-1 year; available IV, IM |
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Primidone (Mysoline)
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Anticonvulsants
MOA: Active parent drug, also breaks down to phenobarbital and active metabolite PEMA Other uses: Sedation, essential tremor Contraindications: Porphyria, absence seizures S/E: Same as phenobarbital, may be more sedating; impotence Monitoring parameters: Serum concentrations, CBC/diff Comments: Taper over 6 weeks-1 year |
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Phenytoin (Dilantin); one IV form is fosphenytoin (Cerebyx)
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Anticonvulsants
MOA: Blocks sodium current, blocks L-type calcium current and uptake, blocks NMDA responses, depresses basal level of cGMP, increases GABA Other uses: Porphyria, absence seizures; avoid IV if pt has arrhythmia, radiotherapy (increases allergic reaction risk) Contraindications: S/E: Diplopia, ataxia, dysarthria, tremor, headache, sedation, allergic rash including Stevens-Johnson syndrome, allergic hepatitis, lymphadenopathy, gingival hyperplasia, osteopenia, peripheral neuropathy Monitoring parameters: Serum concentrations (draw at least 2 hours after IV fosphenytoin), CBC/diff, LFTs Comments: Taper |
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Carbamazepine (Tegretol, Tegretol XR, Carbatrol)
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Anticonvulsants
MOA: Blocks sodium current, blocks L-calcium current, increase 5-HT release, blocks NMDA current, blocks adenosine A1 receptors Other uses: Neuralgia, trigeminal neuralgia, bipolar disorder Contraindications: MAO-I use, blood dyscrasias, hyponatremia, absence and myoclonic seizures S/E: Diplopia, headache, nausea, diarrhea, ataxia, hyponatremia, neutropenia, rarely other blood dyscrasias, allergic rash including Stevens-Johnson syndrome, cardiac conduction problems, impotence Monitoring parameters: Serum concentrations, CBC/diff, LFTs, sodium Comments: Taper |
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Ethosuximide (Zarontin)
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Anticonvulsants
MOA: Blocks T-calcium current Other uses: Contraindications: S/E: Nausea, hiccups, insomnia, agitation, psychosis, allergic rash, blood dyscrasias Monitoring parameters: Serum concentrations, liver function tests, platelets; CBC/diff Comments: |
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Felbamate (Felbatol)
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Anticonvulsants
MOA: Blocks NMDA-induced current, enhances GABA-evoked chloride currents, limits sodium action potential firing Other uses: Contraindications: S/E: Hepatotoxicity and aplastic anemia (black box warnings), anorexia, insomnia, headache Monitoring parameters: Serum concentrations, liver function tests, platelets; CBC/diff Comments: Taper |
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Lamotrigine (Lamictal)
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Anticonvulsants
MOA: Blocks sodium current, blocks calcium currents, increases brain GABA, decreases glutamate release, provides neuroprotective effects secondary to inhibition of glutamate release, may upregulate Ih (H-channel) Other uses: Bipolar disorder, neuropathy Contraindications: S/E: Allergic rash including Stevens-Johnson syndrome (see pkg insert before dosing), ataxia, diplopia, nightmares, flushing, headache, rare cases of hepatotoxicity Monitoring parameters: Serum concentrations Comments: Taper |
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Tiagabine (Gabitril)
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Anticonvulsants
MOA: Inhibits GABA reuptake by blocking its selective transporter Other uses: Generalized anxiety Contraindications: S/E: Sedation, diplopia, dizziness, muscle weakness, tremor, nonconvulsive status epilepticus, psychosis Monitoring parameters: Comments: Taper |
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Topiramate (Topamax)
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Anticonvulsants
MOA: Blocks sodium current, blocks AMPA glutamate receptor subtype, increase brain GABA, enhances GABA-evoked chloride currents, inhibits carbonic anhydrase, possibly inhibits L-calcium channels Other uses: Epilepsy, bipolar disorder Contraindications: Nephrolithiasis, anorexia S/E: Slowed thinking, dysarthria, mood changes, weight loss, dysarthria, paresthesias, nephrolithiasis, rare: hypohydrosis esp in children, rare cases of closed-angle glaucoma Monitoring parameters: Serum bicarbonate in children Comments: Taper |
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Zonisamide (Zonegran)
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Anticonvulsants
MOA: Blocks sodium and T-calcium channels, increases brain dopamine Other uses: Contraindications: Hypersensitivity to sulfonamides S/E: Sedation, anorexia, mood changes, dizziness, diplopia, nephrolithiasis, oligohidrosis, rare blood dyscrasias Monitoring parameters: CBC/diff Comments: taper |
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Oxcarbazepine (Trileptal)
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Anticonvulsants
MOA: Blocks sodium channels, may be effects at calcium, potassium channels Other uses: Neuralgia, bipolar disorder Contraindications: Absence seizures S/E: Dizziness, diplopia, headache, allergic rash, hyponatremia, rare blood dyscrasias Monitoring parameters: CBC/diff Comments: Congener of carbamazepine but less neurological side effects and less rash, more hyponatremia; taper |
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Levetiracetam (Keppra)
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Anticonvulsants
MOA: Inhibits presynaptic neurotransmitter release by binding to presynaptic vesicle protein SV2A; may have effect at potassium channels; may reduce mossy fiber sprouting, gliosis and alter GABAA receptor; effects at calcium channels Other uses: Contraindications: S/E: Sedation, depression, irritability, asthenia, poor coordination, psychosis Monitoring parameters: Comments: Taper; available IV |
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Benzodiazepines eg. clonazepam (Klonopin), lorazepam (Ativan), diazepam (Diastat is the rectal form)
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Anticonvulsants
MOA: Agonist for GABA receptor Other uses: Sedation, anxiety, chemotherapy-induced nausea, status epilepticus Contraindications: IV products that contain benzyl alcohol - avoid in neonates; also IV products with propylene glycol – avoid in children and those with renal impairment S/E: Dependency, respiratory depression, dizziness, ataxia Monitoring parameters: Respirations when given IV Comments: Taper |
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Interferon-beta 1b (Betaseron)
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MOA: Peptides with antiviral and immunoregulatory; decrease interferon-gamma; affect T-helper cells
Other uses: First-line treatment for relapsing-remitting MS Contraindications: Pregnancy, depression, myelosuppression S/E: Flu-like symptoms, anemia, hepatotoxicity, injection site reactions, depression Monitoring parameters: Monitor liver function tests, CBC/diff, TSH Comments: High dose interferon, given as a daily subcutaneous injection |
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Interferon-beta 1a (Avonex)
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MOA: Peptides with antiviral and immunoregulatory; decrease interferon-gamma; affect T-helper cells
Other uses: First-line treatment for relapsing-remitting MS Contraindications: Pregnancy, depression, myelosuppression S/E: Flu-like symptoms, anemia, hepatotoxicity, injection site reactions, depression Monitoring parameters: Monitor liver function tests, CBC/diff, TSH Comments: Low dose interferon, lower incidence of neutralizing antibodies, intramuscular injection weekly |
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Interferon-beta 1a (Rebif)
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MOA: Peptides with antiviral and immunoregulatory; decrease interferon-gamma; affect T-helper cells
Other uses: First-line treatment for relapsing-remitting MS Contraindications: Pregnancy, depression, myelosuppression, alcohol use S/E: Flu-like symptoms, anemia, hepatotoxicity, injection site reactions, depression Monitoring parameters: Monitor liver function tests, CBC/diff, TSH Comments: High dose interferon, subcutaneous injection 3x/week |
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Glatiramer (Copoxone)
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MOA: Possible effect on CD4 T cells, produces brain-derived neurotrophic factor
Other uses: First-line treatment for relapsing-remitting MS Contraindications: Immunosuppression S/E: Injection site reactions; 10-15% have a single post-injection reaction consisting of chest pain, palpitations and difficulty breathing Monitoring parameters: Comments: Subcutaneous injection |
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Natalizumab (Tysabri)
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MOA: Monoclonal antibody
Other uses: Relapsing-remitting MS Contraindications: Immunosuppression S/E: Infusion reactions, headache, fatigue, depression, joint pain, abdominal pain, urinary tract infections, multifocal leukoencephalopathy Monitoring parameters: MRI at baseline Comments: Restricted distribution program; intravenous injection every month; antibody reaction can reduce effect |
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Mitoxantrone (Novantrone)
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MOA: Reduces migration of T cells into the CNS (effect on DNA)
Other uses: Relapsing-remitting MS; progressive MS Contraindications: Avoid use with natalizumab (increased risk of multifocal leukoencephalopathy); pregnancy; heart failure (ejection fraction < 50%), neutropenia, pulmonary disease S/E: Blue-green color in urine, sclera may turn bluish, blood dyscrasias, acute myelogenous leukemia, nausea, menstrual irregularities, alopecia, urinary and respiratory tract infections Monitoring parameters: Cardiac function testing, LFTs, CBC/diff Comments: Intravenous injection every 3 months |
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Acetylcholinesterase inhibitors – eg. donepezil (Aricept)
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Alzheimer’s disease
MOA: Acetylcholinesterase inhibition Other uses: Vascular dementia (for donepezil) Contraindications: Cardiac conduction problems, COPD, neuromuscular block S/E: Nausea, confusion, insomnia, bradycardia Monitoring parameters: LFTs with tacrine (Cognex) – rarely used Comments: 2 are FDA-approved for mild-moderate Alzheimer’s disease; donepezil is approved for all stages |
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Memantine (Namenda)
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Alzheimer’s disease
MOA: NMDA-receptor antagonist Other uses: Epilepsy Contraindications: Renal tubular acidosis, urinary alkalinization S/E: Dizziness, confusion, headache, constipation, somnolence Monitoring parameters: Comments: For moderate- severe disease |
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Levodopa/carbidopa (Sinemet, Parcopa); levodopa/carbidopa/entacapone (Stalevo)
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Parkinson’s disease
MOA: Dopamine replacement Other uses: Restless legs syndrome Contraindications: MAO-inhibitors, melanoma S/E: Nausea, orthostatic hypotension, dyskinesia, mood changes, hallucinations Monitoring parameters: Orthostatic hypotension Comments: Taper , carbidopa is “suicide inhibitor” of dopa-decarboxylase; use about 100mg daily |
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Dopamine agonists (eg. ropinirole - Requip); apomorphine (Apokyn) is available for SC injection for intermittent hypomobility
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Parkinson’s disease
MOA: Stimulates post-synaptic dopamine receptor Other uses: Restless legs syndrome; for bromocriptine: acromegaly, hyperprolactinemia, neuroleptic malignant syndrome Contraindications: Breastfeeding S/E: Nausea, orthostatic hypotension, dyskinesia, hallucinations, “sleep attacks;” retroperitoneal fibrosis from bromocriptine Monitoring parameters: Orthostatic hypotension Comments: Taper |
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Anticholinergic agents (eg. trihexyphenidyl)
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Parkinson’s disease
MOA: Anticholinergic, antihistaminic Other uses: Urge incontinence, irritable bowel syndrome, extrapyramidal reactions Contraindications: Closed angle glaucoma, urinary retention, benign prostatic hypertrophy, ileus, tardive dyskinesia, tachycardia S/E: Dry mouth, urinary retention, constipation, tachycardia, blurry vision, psychosis, sedation Monitoring parameters: Comments: Taper |
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COMT-inhibitor (eg entacapone - Comtan)
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Parkinson’s disease
MOA: Inhibition catechol O-methyltransferase Other uses: Nonselective MAO-inhibitors, impaired liver function Contraindications: S/E: Side effects of levodopa Monitoring parameters: Orthostatic hypotension Comments: Taper; hepatotoxicity with tolcapone (Tasmar) |
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MAO-inhibitor B (eg. selegiline –Eldepryl)
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Parkinson’s disease
MOA: Monamine oxidase inhibitor B Other uses: Selegiline transdermal (Emsam) patch available for depression Contraindications: High tyramine foods, serotonergic medication, pheochromocytoma, melanoma S/E: Orthostatic hypotension, confusion, dizziness, nausea, headache, dyskinesia, hypertensive crisis (rare) Monitoring parameters: Orthostatic hypotension Comments: Serious drug interactions; taper |
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Amantadine (Symmetrel)
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Parkinson’s disease
MOA: NMDA-receptor antagonist, anticholinergic, dopamine agonist Other uses: Influenza A prophylaxis and treatment, extrapyramidal syndromes Contraindications: S/E: Nausea, dizziness, insomnia, depression, livedo reticularis, edema, orthostatic hypotension Monitoring parameters: Orthostatic hypotension Comments: Taper |
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Opioids agonist
(eg. morphine – rapid-release formulations; – MS Contin, which is long-acting, etc) |
Analgesics
MOA: Opiate receptor agonist Other uses: Acute therapy for migraine Contraindications: CNS depression, impaired pulmonary function, alcoholism S/E: Abuse potential, sedation, dizziness, constipation, urinary retention, nausea, headache, confusion Monitoring parameters: Respirations Comments: Schedule II-IV controlled substance; IM, IV, SC, epidural, rectal; meperidine metabolite accumulates in renal failure causing seizures; taper |
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Partial opioid agonists (eg. butorphanol-Stadol)
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Analgesics
MOA: Partial opioid agonist Other uses: Acute therapy for migraine Contraindications: CNS depression, impaired pulmonary function, alcoholism S/E: Abuse potential, sedation, dizziness, constipation, urinary retention, nausea, headache, confusion Monitoring parameters: Respirations Comments: Schedule III-IV controlled substance; IM, IV, nasal formulations; taper |
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Tramadol (Ultram)
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Analgesics
MOA: Opiate agonist, inhibits norepinephrine and serotonin reuptake Other uses: Epilepsy, serotonin syndrome Contraindications: CNS depression, impaired pulmonary function, alcoholism S/E: Abuse potential, sedation, dizziness, constipation, urinary retention, nausea, headache, confusion, allergic rash Monitoring parameters: Respirations Comments: Taper |
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Nonsteroidal antiinflammatory agents or NSAIDs (eg. ibuprofen Motrin, etc)
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Analgesics
MOA: Prostaglandin inhibition Other uses: Fever, acute therapy for migraine Contraindications: Avoid 3rd trimester, aspirin allergy, hypertension, heart failure, bleeding risk S/E: Nausea, GI ulceration, cardiovascular and GI risk (black box warning), renal impairment, hepatotoxicity, bronchospasm, edema, tinnitus Monitoring parameters: Creatinine, CBC Comments: Limit use, especially in elderly |
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Capsaicin (Zostrix) – topical made from peppers
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Analgesics
MOA: Blocks substance P Other uses: Contraindications: S/E: Burning, erythema Monitoring parameters: Comments: Especially used for neuropathic pain; do not get in eyes |
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Acetaminophen (Tylenol)
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Analgesics
MOA: Unknown Other uses: Fever, acute therapy for migraine Contraindications: Alcoholism, liver disease, anorexia S/E: Hypertension, dizziness Monitoring parameters: LFTs if high dose Comments: Limit to 4 g daily in adults- causes hepatotoxicity on overdose |
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Modafinil (Provigil)
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MOA: Alpha stimulant? used for narcolepsy, obstructive sleep apnea, shift work sleep disorder, multiple sclerosis
Other uses: Contraindications: Left ventricular hypertrophy, mitral valve disease, unstable angina, recent MI, substance abuse history S/E: Arrhythmias, syncope, headache, nausea, anorexia, anxiety Monitoring parameters: Blood pressure Comments: Schedule IV controlled substance |
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Amphetamines (eg. Dexedrine); also many long-acting formulations
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MOA: Alpha stimulant for narcolepsy
Other uses: ADHD Contraindications: High abuse potential (not in children with ADHD), MAO-I use, cardiomyopathy, hypertension, glaucoma, bipolar disorder, hyperthyroidism S/E: Tachycardia, hypertension, insomnia, euphoria, headache, tremor, anorexia, psychosis, mania, MI, CVA, growth retardation in children Monitoring parameters: Blood pressure, pulse; height and weight in children Comments: Schedule II controlled substance; taper |
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Methylphenidate (Ritalin etc); also many long-acting formulations
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MOA: Alpha stimulant for narcolepsy
Other uses: ADHD Contraindications: High abuse potential (not in children with ADHD), MAO-I use, cardiomyopathy, hypertension, glaucoma, bipolar disorder, hyperthyroidism Monitoring parameters: Blood pressure, pulse; height and weight in children Comments: Schedule II controlled substance; taper |
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Acetylcholinesterase inhibitors (eg. pyridostigmine -Mestinon)
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MOA: Acetylcholinesterase inhibitor used for myasthenia gravis
Other uses: Contraindications: GI obstruction, GU obstruction, COPD, bradycardia, arrhythmia S/E: Arrhythmias, hypotension, diarrhea, headache, dizziness, hypersalivation, diaphoresis, miosis, urinary frequency, rhinitis Monitoring parameters: Comments: |
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Riluzole (Rilutek)
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MOA: For ALS, inhibits glutamate release, blocks NMDA and kainate-type postsynaptic receptors, inhibits voltage-dependent Na channels
Other uses: Contraindications: Impaired hepatic function, neutropenia, hypertension S/E: Asthenia, nausea, rhinitis, headache Monitoring parameters: LFTs Comments: |
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Serotonin Syndrome
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Recommended criteria (3 must be present): mental status changes, confusion, hypomania, agitation, poor coordination, myoclonus, hyperreflexia, diaphoresis, shivering, tremor, diarrhea, fever
Causative agents: typically SSRIs and MAOIs, w/ lithium, levodopa, TCAs, tramadol, DM cough med, meperidine |
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Antiepileptic-induced seizures
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Phenobarbital, phenytoin, carbamazepine aggravate absence seizures
Carbamazepine/oxcarbazepine sometimes aggravates primary generalized tonic-clonic seizures Antiepileptic drugs have the potential to aggravate seizures in individual patients even when used appropriately Higher doses more likely to cause problems |
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Common Seizure Precipitants
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Missed medication
Sleep loss Illness Fever Heat Hypoglycemia Stress Meds that lower seizure threshold Hyperventilation Flashing lights Drug interaction reducing AED concentration AED-induced seizures |
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Drugs for Partial seizures
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First line: Lamotrigine, Carbamazepine, Oxcarbazepine, Levetiracetam, Topiramate, Gabapentin
Second line: Phenytoin, Tiagabine, Zonisamide Valproic acid Other alternatives: Phenobarbital, Primidone, Felbamate, Pregabalin |
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Drugs for Primary generalized tonic-clonic seizures
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First line: Lamotrigine, Valproic acid
Second line: Topiramate, Zonisamide, Phenytoin, Levetiracetam, Gabapentin Other alternatives: Felbamate, Phenobarbital, Primidone, Carbamazepine, Oxcarbazepine |
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Drugs for Absence seizures
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First line: ethosuximide, valproic acid (FDA approved for typical absence only), lamotrigine
Second line: levetiracetam (especially for myoclonus), topiramate, zonisamide Other alternatives: felbamate |
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Drugs for atypical absence, atonic, myoclonic seizures
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First line: topiramate, zonisamide
Lamotrigine (sometimes aggravates myoclonus) Levetiracetam (especially for myoclonus) Second line: ethosuximide (atypical only) Other alternatives: felbamate |
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Distinguish between weakness arising from CNS sources versus PNS
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Sensory level is strong evidence for a CNS source
Distribution of weakness (restricted to lower extremities) Reflex asymmetry upper versus lower extremities (spinal shock) In GBS, reflexes are lost very early in all limbs Presence of a Babinski sign The involvement of bowel and bladder is strongly suggestive of a CNS source (spinal cord) |
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Differential Diagnosis of Acute Paralysis of Peripheral Nervous System Origin
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Gullian Barre Syndrome
Hypokalemic Periodic Paralysis Botulium intoxication Tick paralysis Organophosphate intoxication Myasthenia Gravis |
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Early Warning Signs of acute paralysis
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Mild lower extremity weakness
May take the form of fatiguability of strength Inability to urinate or urinary incontinence Sudden onset of symmetric numbness and parasthesias Pain: either localized or more severe radiating in a myotomal distribution |
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Objective Signs of Spinal Cord Involvement in acute paralysis
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Weakness!! Proximal lower extremity weakness and distal upper extremity weakness
Post void residual volume greater than 100 cc Sensory level to pin prick or other tactile stimuli Impaired rectal sphincter function Reflexes that are asymmetric between upper and lower extremities |
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Acute Paralysis of CNS Origin
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Will almost always be due to spinal cord pathology
First exclude the presence of a surgically treatable lesion Localize lesion on the basis of neurologic exam Imaging is emergent and MRI is by far the best modality If an MRI cannot be carried out a CT scan may be useful but is much less sensitive to most forms of pathology |
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Structural Lesions Associated with Acute Paralysis
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Metastatic tumor
Epidural abscess Epidural hematoma Herniated disc Primary spinal cord tumor Hematomyelia Arteriovenous malformation |
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Cervical Disk Herniation
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May result in significant spinal cord compression with acute or subacute paralysis
In cases of suspected cervical cord injury including disc herniation the neck should be immobilized No attempt at physical therapy should be made until the anatomy has been defined by MRI The usual presentation is that of subacute weakness with very brisk lower extremity reflexes |
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Secondary Extramedullary Tumors
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Most common form of spinal cord tumor
Carcinoma, lymphoma, myeloma Most common presentation is with gradual onset of symptoms consisting of numbness, weakness, sensory loss, spasticity, bladder and bowel dysfunction May be accompanied by Fruend’s Syndrome - Complete block of CSF flow with very high protein in CSF Do not do an LP until after an imaging study has been carried out showing adequate CSF flow |
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Epidural Hematoma
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Most commonly seen after trauma or laminectomy
Beware - Patients with auto-anticoagulation due to hepatic failure - Coumadin - Lovenox - Rapid onset of paralysis Sensory loss Sphincter dysfunction |
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Epidural Abscess
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Diagnosis is usually not made until paraplegia or quadriplegia has set in
May occur in non-immunocompromised individuals Seen commonly in the setting of diskitis Prognosis is usually poor Treat early and aggressive Presents with pain at the level of the abscess Fever, radicular pain, headache, nuchal rigidity, and weakness Beware the patient with FUO: - Especially post surgical - Especially with diskitis - Especially in IV drug users Staph Aureus, streptococcus, gram negatives, anaerobes |
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Acute Transverse Myelitis
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The acute or subacute onset of paraplegia or quadriplegia accompanied by a spinal segmental level of sensory disturbance and an impairment of sphincter function which occurs in the absence of a structural lesion.
A functional, inflammatory transection of spinal cord function May be partial or complete as above To make this diagnosis one must exclude a structural lesion |
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Anterior Spinal Artery Infarct
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Diagnosis is made on clinical grounds
Imaging may be helpful (Owls eye sign) Complete transverse myelitis with sensory level and loss of sphincter function, but with preservation of vibration and position sense Most commonly seen at T-10 Often due to occlusion of the artery of Adamkieviwcz Associated with aortic dissection |
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Management of Acute Paralysis
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Exclude hemorrhagic lesions and spinal cord infarct
If a mass lesion is found treat with decadron at high dose - 10 mg IV followed by 4 mg q 6hr If no mass lesion is seen (i.e. transverse myelitis) and there is no evidence of a vascular pattern Treat with solumedrol at 1000 mg daily for five days, then taper |
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Acute Medical Issues in Acute Paralysis
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Beware of DVTs!!!
- Use both sub q heparin as well as pneumatic compression boots - Patients are at extremely high risk for DVT Insert foley catheter - Patients are insensate below the level of their lesion They can hide very serious pathology |
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Workup of Acute Paralysis of PNS Origin
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Measure forced vital capacity
- If 1.5 L or lower monitor in ICU - If 1.2 L or lower elective intubation Perform lumbar puncture - In GBS protein will be very high but cell count will be WNL Plan for EMGs and PNCVs |
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Acute Paralysis Prognosis
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Depends on underlying process
Severity of presentation Epidural abscesses and hematomas are among the worst In general there is little recovery The hope is to institute definitive therapy as early as possible to prevent progression 50%-80% of SCI injuries are <30 years old 79.6% are male The most common MISSED fracture on xray is C7/T1 ~25%of SCI patients also have TBI (traumatic brain injury) MVA- 45-55% 1st In geriatric population, falls 2nd In <30, violence and falls tie for 2nd Bimodal distribution <30 yrs old >65 yrs old |
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ASIA B
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Incomplete: Sensory but not motor function below level of injury; has sacral sparing. Better prognosis if has intact pinprick.
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ASIA Classification
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to classify patients with SCI - a standardized classification of SCI severity and level. It helps determine expected functional gains and overall prognosis.
It is best done 72 hours after initial injury with high correlation of corresponding prognosis. If done in ED or in first 24 hours, as well as weeks to months afterwards, it has been found to have less reliable correlation. |
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ASIA A
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Complete: No motor or sensory function below level of injury; no sacral sparing. (Can have zone of partial preservation)
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ASIA C
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Incomplete: Motor function is preserved below the neurological level, and>50% of muscles <3/5.
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ASIA D
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Incomplete: Motor function is preserved below the neurological level, and >50% of muscles have 3/5 of greater.
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ASIA E
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Normal: Motor and sensory function are normal.
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Brown Sequard Syndrome
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involves a relatively greater ipsilateral loss of proprioception and motor function, with contralateral loss of pain and temperature sensation.
Very rare; usually found in combination with other SCI syndromes. Has been found in knife injuries and tumors. Best prognosis of ambulation at 1 year of all SCIs. |
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Central Cord Syndrome
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usually involves a cervical lesion, with greater motor weakness in the upper extremities than in the lower extremities. Weakness more distally than proximally.
**This motor exam needs to be present in first few days after injury.** Sensory loss is variable, and the patient is more likely to lose pain/temperature sensation than proprioception/ vibration. Dysesthesias, especially in upper extremities common. Good prognosis overall for functional independence at one year. |
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Anterior Cord Syndrome
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involves variable loss of motor function and pain and/or temperature sensation, with preservation of proprioception.
Rare Often used to confuse students/residents on exam. |
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Conus Medullaris Syndrome
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is a sacral cord injury.
with or without involvement of the lumbar nerve roots. This syndrome is characterized by areflexia in the bladder, bowel, and to a lesser degree, lower limbs. Motor and sensory loss in the lower limbs is variable. Important to differentiate from traditional spinal cord injuries. Permanent flaccid bladder, bowel, and lower extremities, while traditional SCI will begin to develop increased tone and spasticity after spinal shock (LMN vs. UMN). |
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Cauda Equina Syndrome
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Is a nerve root injury rather than a true SCI, the affected limbs are areflexic.
Is an injury to the lumbosacral nerve roots. Is characterized by an areflexic bowel and/or bladder, with variable motor and sensory loss in the lower limbs. This injury is usually caused by a central lumbar disk herniation. Clinically, lower motor nerve injury. Will not develop spasticity. |
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Spine Clearance
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Done while patient on spine board.
Plain films with 3 views: anteroposterior, lateral, and odontoid. Must include C7-T1 junction If these images are normal, flexion/ extension views done to search for instability. Collars cannot be removed, nor therapy provided until cervical spine cleared. External immobilization with cervical collar vs. external fixation. - If need to control cervical flexion/extension, use cervical collar. - If need to also control cervical rotation or lateral bending, need HALO. Surgical stabilization is done with cervical collar used post-surgery. |
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Spinal shock
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Spinal shock- a state of temporary depression of cord function with loss of all motor/sensory functions.
Is below level of injury. Hypotension Flaccid paralysis as well as flaccid bowel/bladder Last hours-a few weeks (+) bulbocavernous reflex-end of spinal shock Can obtain true ASIA exam during spinal shock. |
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Pressure Ulcers
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Most common place to start pressure ulcers is when patient in ED!
In insensate, immobilized patient, can develop in ONE to TWO hours. Pressure ulcers form from inside out. Get patient off spine board as soon as possible (spine clearance). Remove belts, keys, wallets, anything in pockets. Increased pressure areas are: sacrum/coccyx, occiput, scapulae, heels, and between knees Extensive wound care including: Wound VACs, pulsatile lavage or Ultrasonic mist, 1-3x/day dressing changes. Surgical interventions include: extensive debridement, grafts, and muscle flaps. |
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DVT prophylaxis in spinal cord injury
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Patients are at very high risk for VTE
Higher risk than cancer patients Virchow’s triad (venous stasis, endothelial damage, hypercoaguable state). Overall, incidence of DVT in untreated patients is 81%, but symptomatic DVT 12-23%. DVT prophylaxis is suggested for 3 months post injury, when patients return to regular population’s risk of VTE. Use SQ Heparin TID or Lovenox daily CHEST guidelines 2008- IVC filters NOT prophylaxis for DVTs. - If unable to use chemical prophylaxis, place IVC filters in SCI patients. - SCDs used 23 hours/day are ~20% effective. - ASA, Plavix, TEDs are NOT effective DVT prophylaxis. Have seen bilateral DVTs on appropriate prophylaxis! |
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Post-Thrombotic Syndrome
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Post-thrombotic syndrome (PTS)- prelude to venous stasis and venous insufficiency.
This puts SCI patients at high risk of venous insufficiency ulcers as early as 25-30 yrs old. PTS develops in up to 20% of patients with DVTs (some studies now saying up to 50%). Develops within 2-5 years (now as early as 1-2 yrs). Probably more likely in SCI patients, because they are less likely to recanalize vessels. To decrease risk of PTS, use TEDS x2 years. |
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Heterotopic Ossification
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HO is the formation of lamellar bone in abnormal areas (non-skeletal tissue), usually soft tissue, near large joints or long bones.
Incidence of 16-53% in SCI HO most common in: Hips, Knees, Shoulders, Elbows, sometimes in the paravertebral area. Some reports shown occurance at the ankles. Also been called myositis ossificans (MO)-term usually used by radiologists to define abnormal bone formation on imaging. Usually forms within 3-4 months of initial injury (2 weeks to 12 months). Patients with multiple traumatic injuries have a higher incidence of HO. On exam, it can present as: painless decreased ROM at joint Inflammatory process including: erythema, heat, pain, and low grade fever. SCI patients with HO below level of lesion might not present with pain. Need to rule out cellulitis and DVT. |
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Diagnosis of Heterotopic Ossification
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Xray, triple phase bone scan (7-10 days earlier)
Important to diagnose since can only prevent more HO, not reduce it (?) using NSAIDs for prevention, but the literature is not conclusive. “Treatment” is with bisphonates- Etidronate 20mg/kg x 2 weeks, then 10mg/kg x 8 weeks. Literature not conclusive, but only medical intervention Surgical intervention: - Have to wait until bone matured (12-18 months) - Try to avoid surgical removal of HO because extremely “bloody”. - Only a few surgeons seem to improve function (joint irradiated after surgery) Remember, if patient high risk for HO formation, high risk of reformation. |
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Cardiac Issues in spinal cord injury
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Bradycardia- in 1st 6 weeks
- More common in cervical injuries. - Secondary to overriding parasympathetic tone (absent sympathetic input to heart). - Can be triggered by suctioning (vaso-vagal reflex)- can pretreat with atropine. Usually resolves in ~6 weeks, but some patients require pacemaker in severe cases. (Some clinical reports of Theophylline) Resting Low Blood pressure- Due to interruption of the descending sympathetic tracts. Lasts lifelong, but symptomatic 6-12 weeks in 95% of cases. Caused by: - Decreased compensatory vasoconstriction - Decreased venous return due to decrease muscle activity - Causes reduction in stroke volume and blood pressure. - NOT CAUSED BY VENOUS POOLING - Orthostasis- usually symptomatic 6-12 weeks Venous pooling can play a role |
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Treatment for Cardiac Issues in spinal cord injury
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ACE wraps and Abd binders-1st line
NaCl tablets-to increase volume Florinef-to increase volume Midodrine-to increase peripheral resistance *If SCI patient put back to bed for ~ 1week, will have lost accommodation* |
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Cardiac issues in spinal cord injury cause and diagnosis
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Increased risk of cardiovascular disease:
- Abnormal/elevated lipid profiles (increased LDL and decreased HDL) not uncommon with chronic SCI, even seen in Para-Olympian athletes. - Length of time since injury more reflective of CAD and MI risk than diet and activity. Diagnosis: - Need to do EKG, Stress test (ex: adenosine) much earlier than other patients. - Also need to test for metabolic syndrome/diabetes more closely (SCI patients more likely to develop than walking population) Direct cause unknown, but adrenal dysfunction is a likely source. |
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UTI and spinal cord injury
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If patient has Foley for >3 days, will most likely develop UTI in acute hospitalization.
SCI patients can become colonized within 2-4 weeks Is important to ascertain when patient has UTI vs. just colonization So always check U/A with microscopy and Urine Cx with sensitivities. If patient has response to bacteria (i.e. nitrites, WBC) can be termed UTI. No nitrites-rarely an UTI. UTI can present with fever, impending sepsis (low BP), or bladder spasms with sudden incontinence. |
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Neurogenic Bowel
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Initially, bowel and bladder flaccid (no rectal tone!)
At EXTREMELY high risk of adynamic ileus Constipation is not cause of lack of BMs- have to be on DAILY PO and PR meds. Bowel program: - will require agents to increase movement of stool through GI system. - If patient has diarrhea, usually stool coming around impaction. Decreased peristalsis initially. Might need manual disimpaction. |
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Treatment of Neurogenic Bowel/Bladder
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In acute hospital:
- Need scheduled bowel meds- usually Senokot (not just Colace) 2 tabs daily. - scheduled suppository (Magic Bullet) daily or QOD - If not done, could require surgical disimpaction. In rehab: - As above, scheduled bowel meds - Suppository and/or digital stimulation Can get on schedule bowel regimen, so no incontinence- in 3-6 weeks |
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Neurogenic Bowel/Bladder
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A flaccid bladder will continue to expand as filled by urine (can get up to 2000cc).
Cathing is required to empty. Once in rehab, we remove Foley catheter to see if patient regains any bladder sensation and voiding. Cathing needed in flaccid and spastic bladder; however, will probably require Detrol/Ditropan to increase bladder volume. Cathing usually q4-6 hours, depending on cath volumes (if <500cc, cath at 6 hours; >500cc cath at 4 hours). If patient continues with high volumes, can get reflux up ureters and cause hydronephrosis. To spontaneously void can use: Crede’ maneuver (pushing down on abdomen) valsalva (abdominal strain) suprapubic tapping thigh scratching (elicits cremaster reflex) Anal manipulation can also start voiding reflex. If continue with Foley/indwelling catheter or suprapubic cather, patient is at increased risk for patients for UTIs, kidney stones, and long term bladder cancer. |
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spasticity
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Definition: is a velocity-dependent increase in stretch reflexes that is part of the upper motor neuron syndrome. It may be accompanied by clonus and spasms.
Usually begins to develop during inpatient rehab stay Can be helpful to: allow functional use of upper and lower extremities decreases risk of DVT helps with venous pooling which decreases orthostatic hypotension decreases risk of osteoporosis However: increases risk of contractures Increases risk of pressure ulcers It can also be painful and impair function (along with make hygiene more difficult) Rule of thumb- do not treat with medications unless impairs function or is painful! |
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Treatment of Spasticity
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1st line treatment- range of motion!!!!
No medication will work if ROM not done. Meds- Baclofen- (start 5-10 mg TID) Valium (start 5-10 mg BID or TID) Zanaflex (tabs or capsules- start 4-8 mg QHS) Dantrium (start 25 mg daily). Most common adjuvant- Clonidine All have side effects! Other treatments are Botox and Phenol injections for localized spasticity and Intrathecal Baclofen pump. |
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Autonomic Dysreflexia
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ONLY REHAB EMERGENCY!!!!
AD is a syndrome of imbalanced reflex sympathetic discharge occurring in SCI with lesions above T5/T6 (i.e. above the splanchnic sympathetic outflow) that can develop once spinal shock is resolved. Clinically diagnosed with elevated BP above patient’s baseline with headache. Patients with complete SCI are at higher risk of developing than incomplete SCI. |
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Pathophysiology Autonomic Dysreflexia
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below the injury, intact peripheral sensory nerves transmit impulses that ascend in the spinothalamic and posterior columns to stimulate sympathetic neurons (centered in thoracic cord).
The inhibitory outflow above the SCI from cerebral vasomotor centers is increased, but it is unable to pass below the block of the SCI. This large sympathetic outflow causes release of NE and Dopamine. This causes sudden elevation in blood pressure. Vasomotor brainstem reflexes attempt to lower blood pressure by increasing parasympathetic stimulation to the heart. This is done via the vagus nerve which causes compensatory bradycardia. There is vasoconstriction below level of lesion with increased sympathetic tone and vasodilitation above level of injury secondary to overriding parasympathetic tone. |
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Presentation of Autonomic Dysreflexia
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Above level of lesion, flushing and profuse sweating.
Below the lesion, piloerection, skin pallor, and decreased sweating. Patients will also complain of anxiety, blurred vision, and nasal congestion. Most common cause is urinary!!!! So if has Foley, FLUSH IT! Other causes include: bowel (full rectal vault), MI, pancreatitis, ingrown toenail, LABOR (even if patient not c/o any labor pains), invasive testing (heart cath through femoral vessels), menstruation, sexual intercourse, UTI, DVT, pressure ulcer, sunburn. ALWAYS need to speak with surgeon about operations or procedures due to the high risk of developing AD without proper care. |
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Treatment of Autonomic Dysreflexia
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First line treatment- SIT PATIENT UP!!
Next, flush foley, cath patient, clear rectal vault; check and clear offending stimulus. Also need to loosen tight clothing Meds- BITE and swallow Nifedipine Can also place nitropaste (can wipe off easily) or use Clonidone, **Important to remember, must act quickly with high index of suspicion to treat** |
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Neuropathic and SCI Pain
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Above level of lesion-
musculoskeletal pain have overuse injuries from using upper extremities as weight bearing limbs. Treat extremely aggressively At level of injury- can be neuropathic or from cause of their injury- ex: GSW- bullet still in patient, vertebral fx- if neuropathic, many patients c/o band of pain- burning, stinging, compressing, making it “hard to breathe”. Treat with neuropathic pain agents- try to avoid Elavil b/c will exacerbate urinary retention. Below level of injury pain- is either neuropathic or possible visceral pain referred from underlying pathology- ex: gallbladder, cardiac chest pain. |
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Osteoporosis in spinal cord injury
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Below level of lesion
Usually 2-5 years after injury, but depends on age, level of activity, complete vs. incomplete. Need bone density scan and calcium replacement (if not hypercalcemic). Can have osteoporotic fracture as early as 18 months. |
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Long-term bladder issues in spinal cord injury
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Nephrolithiasis- kidney stones frequent in patients with in-dwelling foleys or suprapubic catheters.
Bladder Cancer- high risk in patients with in-dwelling foleys or suprapubic catheters. Ostomy- for easier cathing - pull part of bowel to make compartment to cath from. Site is on the right side of abdomen. Helps increase independence. |
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Syrinx Formation
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Syrinx- formation of CSF fluid pocket- can press on spinal cord and causes sensory or motor deficits, as well as increased spasticity.
ASIA exam yearly essential to determine if clinically significant. |
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Spinal Cord Injury: C1- C3
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Movement possible includes: neck flexion, extension, and rotation.
Paralysis of: trunk, upper extremities, lower extremities. Ventilator dependent Goal of rehab is family training and fitting for power W/C- patient should be able to direct others to complete their care. Ventilator dependent Inability to clear secretions W/C propulsion- power with sip/puff, head, or chin control If no injury to phrenic nerve, can be assessed for phrenic nerve pacer |
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Spinal Cord Injury: C4
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Movements possible include: neck flexion, extension, rotation, as well as scapular elevation, and inspiration.
Paralysis of: trunk, upper extremities, lower extremities. Also has inability to cough and have low respiratory reserve secondary to intercostal paralysis. Goal of rehab is family training and fitting for power W/C- patient should be able to direct others to complete their care. May be able to breath without ventilator, but at high risk for mucus plugging. W/C propulsion- power with head, chin, or sip/puff control |
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Spinal Cord Injury: C5
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Movement possible includes: shoulder flexion, extension, abduction as well as elbow flexion and supination. Also has scapular abduction and adduction.
Paralysis of: elbow extension, pronation, as well as all wrist and hand movement. Has paralysis of trunk and lower extremities. Will probably have low respiratory endurance and vital capacity secondary to paralysis of intercostals. Requires assistance with secretion management, cough Is independent with power W/C with arm drive control Can propel manual W/C on flat non-carpeted surfaces for shorter distances-independent for pressure relief with adaptive equipment/techniques |
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Spinal Cord Injury: C6
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Movement possible include: scapular protraction, some horizontal adduction, forearm supination, and radial wrist extension.
Weakness/paralysis of: wrist flexion, elbow extension, hand movements, and trunk and lower body paralysis. Will still probably need assistance to clear secretions and quad cough secondary to intercostal paralysis. May require help with secretions, quad cough-With lesions at C3 through C6, vital capacity is 20% of normal, and cough is weak and ineffective Can use power W/C with standard arm drive Can also use manual W/C indoors, but requires assist-dependent outdoors. Power assist chair is good option. Independent with equipment to do pressure relief. First level that in shape younger male might be able to live independently. Is extremely rare. |
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Spinal Cord Injury: C7- C8
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Movement possible includes: elbow extension, wrist extension and flexion, finger flexion and extension, thumb flexion and extension/abduction
Paralysis includes: trunk and lower extremities as well as limited grasp/release and dexterity secondary to hand intrinsics. Might still require help with secretion control and quad cough C7 is the first true level that a patient can live independently. Usually require aide, however don’t need 24 hour care. May require help with secretions and quad cough Independent with: pressure relief, level transfers, eating, grooming, manual W/C propulsion, and bathing and dressing upper body. Most patients use modified van, but this is first level they might be able to load/unload W/C, depending on upper body strength. Patients require hand controls for driving |
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Spinal Cord Injury: T1- T9
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Patients have upper extremities completely intact, but limited truncal stability. Also have lower extremity paralysis.
They do have some intercostal innervation, but is secondary. Still increased risk of pneumonia- the higher the level, the higher the risk. Overall reduced vital capacity and endurance-With high thoracic cord injuries (ie, T2 through T4), vital capacity is 30-50% of normal, and cough is weak. Independent with: feeding, grooming, bathing, dressing, bladder and bowel management, bed mobility, transfers, W/C propulsion, and driving with hand controls |
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Spinal Cord Injury: T10 – L1
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Patients have completely innervated intercostals, external obliques, rectus abdominus, with good trunk stability.
Paralysis of lower extremities Intact respiratory function and endurance Independent with: feeding, grooming, dressing, bathing, toileting, bowel/bladder management, bed mobility, transfers, pressure relief, W/C propulsion, driving with hand controls. Patients usually can load/unload own folding W/C Also independent with standing; some patients can walk with assistance; literature notes it as functional, but overall require 3/5 HFs and 3/5 of 1 KE (HF- iliopsoas- L2,L3; KE- quadraceps femoris-L2-L4) |
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Spinal Cord Injury: L2 – S5
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Patients have good truncal stability and partial to full control of lower extremities.
Have partial paralysis of hips, knees, ankles, and feet. These lesions include conus medullaris syndrome and cauda equina syndrome. |
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Metabotropic receptor
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G-protein coupling receptors -> coupling G-proteins -> effector enzymes (2nd messenger) such as phospholipid C or adenyl cyclase; OR can affect an ion channel
Includes muscarinic, 1 type of GABA receptor, glutamate, biogenic amines and peptide receptors |
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Ionotropic receptor
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Ligand-gated ion channels (ionophore receptors) – regulated by binding of neurotransmitters – nicotinic, GABA, glycine, many glutamate receptors.
Several neurotransmitters can be released from one axon terminal (presynaptic receptor) and a single neuron can house numerous types of receptors. There is also ‘cross-talk’ |
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Nicotinic receptor
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excitatory receptor, present at the neuromuscular junction, autonomic ganglia, adrenal medulla. Receptor is a ligand-gated ion channel. Works through increased cation permeability (Na, K). Nicotinic receptors have 8 α and 3 β subunits. Mediate pre- and post-synaptic excitation in the CNS. Mediates prejunctional control of transmitter release. (α7)5 receptors in the CNS are sensitive to botulinum toxin.
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Muscarinic receptor
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Present at parasympathetic end organs, in cortex and amygdala. Muscarinic receptors are metabotropic receptors. There are 5 subtypes (M1-M5). M1 and M2 > M3 in the CNS. Stimulating M1 (excitatory) is related to improved cognition, seizure activity, decreased dopamine and increased secretions. M2 is related to neuronal inhibition, increased tremors, hypothermia and analgesia. M4 is related to dopamine release and analgesic effects. M5 facilitates dopamine release and can increase drug-seeking behaviors.
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Beta 1 receptor
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Found in heart, stimulation mediates positive ionotropic (increase contractility of the heart) and chronotropic (increases heart rate through the SA node) effects; found in CNS.
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Beta 2 receptor
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Lung (bronchodilation), smooth muscles (relaxation), arterioles (vasodilation); can also enhance release of other neurotransmitters when functioning as a presynaptic heteroreceptor; found in CNS
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Alpha 1 receptor
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Postsynaptic, excitatory (alpha 1A vasoconstriction, alpha 1B heart, alpha 1D – aortic)
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Alpha 2 receptor
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Presynaptic, inhibitory in autonomic nervous system and decreases sympathetic outflow in CNS, can be extrajunctional (does it work far away from the axon terminal that is releasing the major neurotransmitter); can also be postsynaptic.
Alpha 2A mediates antinociception (pain relief), sedation, hypothermia, hypotension Alpha 2B – mediates vasoconstriction Alpha 2C – mediates dopaminergic neurotransmission, behavior |
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MAOA
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Especially in the locus ceruleus
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MAOB
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Nucleus raphe dorsalis, posterior hypothalamus, glia
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Simple partial seizures
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result when the ictal discharge occurs in a limited and often circumscribed area of cortex, the epileptogenic focus. Almost any symptom or phenomenon can be the subjective (aura) or observable manifestation of a simple partial seizure. Especially common auras include an epigastric rising sensation, fear, a feeling of unreality or detachment, deja vu and jamais vu experiences, and olfactory hallucinations. Patients are aware of their surroundings and may interact with others during these episodes.
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Complex partial seizures
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on the other hand, are defined by impaired consciousness and imply bilateral spread of the seizure discharge, at least to basal forebrain and limbic areas. In addition to loss of consciousness, patients with complex partial seizures usually exhibit automatisms such as lip smacking, repeated swallowing, clumsy per severation of an ongoing motor task, or some other complex motor activity that is undirected and inappropriate. Postictally, patients are confused and disoriented for several minutes, and determining the transition from ictal to postictal state may be difficult without simultaneous EEG monitoring. Of complex partial seizures, 70-80% arise from the temporal lobe; foci in the frontal and occipital lobes account for most of the remainder.
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Generalized tonic-clonic seizures
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characterized by abrupt loss of consciousness with bilateral tonic extension of the trunk and limbs (tonic phase), often accompanied by loud vocalization as air is forcedly expelled across contracted vocal cords (epileptic cry), followed by synchronous muscle jerking (clonic phase). In some patients, a few clonic jerks precede the tonic-clonic sequence; in others, only a tonic or clonic phase is apparent. Postictally, patients are briefly unarousable, then lethargic and confused, often preferring to sleep.
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Absence (petit mal) seizures
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momentary lapses in awareness that are accompanied by motionless staring and arrest of ongoing activity. Absence seizures begin and end abruptly; they occur without warning or postictal period. Longer attacks may be accompanied by myoclonic jerks of the eyelid or facial muscles, variable loss of muscle tone and automatisms. When the beginning and the end of the seizure are less distinct, or if tonic and autonomic components are included, the term atypical absence seizure is used. Atypical absences are seen most often in retarded children with epilepsy or in epileptic encephalopathies, such as Lennox-Gastaut syndrome.
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Myoclonic seizures
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characterized by rapid, brief muscle jerks that can occur bilaterally, synchronously or asynchronously, or unilaterally. These range from isolated small movements of the face, arm, or leg muscles, to massive bilateral spasms simultaneously affecting the head, limbs, and trunk.
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Atonic (astatic) seizures
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also called drop attacks. These are characterized by sudden loss of muscle tone, which may be fragmentary (head drops) or generalized, resulting in a fall.
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Childhood Absence Epilepsy
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disorder begins most often between the ages of 4 and 12 years of age and is characterized predominantly by recurrent absence seizures, which, if untreated, can occur literally hundreds of times per day. EEG activity during the absence attacks is characterized by stereotyped, bilaterally synchronous 3Hz spike and wave discharges. Generalized tonic-clonic seizures also occur in 30 to 50% of cases. Most children are intellectually and neurologically intact. Ethosuximide and valproate are effective in treating these.
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Benign Focal Epilepsy of Childhood
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(benign Rolandic Epilepsy). Onset is between 4 and 13 years; children are usually otherwise normal. Some children have attacks only at night. Sleep promotes secondary generalization, so the parents only report generalized seizures, any focal manifestations usually go unnoticed. In contrast, seizures that occur during the day are usually focal with twitching of one side of the face, speech arrest, drooling from a corner of the mouth, and paresthesia of the tongue, lips, inner cheeks, and face. Seizures may progress to include clonic jerking or tonic posturing of the arm and leg on one side. Consciousness is usually preserved.
The interictal abnormality is distinctive and stereotyped di- or triphasic sharp waves over the central-midtemporal (Rolandic) regions. The prognosis is uniformly good. Seizures disappear by mid to late adolescence in all cases. Carbamazepine is the drug of choice, although phenytoin and phenobarbital are also effective. |
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Lennox-Gastaut Syndrome
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term is applied to a heterogeneous group of childhood epileptic encephalopathies that are characterized by mental retardation, uncontrolled seizures, and a distinctive EEG pattern. The syndrome is not a pathologic entity, because clinical and EEG manifestations result from brain malformations, perinatal asphyxia, severe head injury, CNS infection, or, rarely, a progressive degenerative or metabolic syndrome. A cause can be identified in 50 to 60% of cases. Seizures usually begin before the age of 4 years, and about 25% of children have a history of infantile spasms. No treatment is effective. Refractory cases may be considered for corpus callosotomy.
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Juvenile Myoclonic Epilepsy
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Usually occurs in otherwise normal individuals between the ages of 8 and 20 years. The fully developed syndrome comprises morning myoclonic jerks, generalized tonic-clonic seizures that occur just after waking, normal intelligence, a family history of similar seizures, and an EEG that shows generalized spikes, 4-6Hz spike wave discharges and multiple spike discharges.
Valproate is the treatment of choice. |
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Temporal Lobe Epilepsy
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most common epilepsy syndrome in adults. In most cases, the epileptogenic region involves the mesial temporal structures, especially the hippocampus, amygdala, and parahippocampal gyrus. Seizures usually begin in late childhood and adolescence and a history of febrile convulsions in infancy is common. Virtually all patients have complex partial seizures. Fifty percent of patients are not controlled with anticonvulsant medications; for these anterior temporal lobectomy is the treatment of choice.
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Frontal Lobe Epilepsy
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seizures are usually brief, tending to cluster, occur at night in a high number of patients, have bizarre motor manifestations, and may have minimal EEG changes on surface EEG. There is a high incidence of status epilepticus with these seizures.
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Post-traumatic Epilepsy
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Seizures occur within 1 year in about 7% of civilian and about 34% of military head injuries. The differences relate mainly to the much high proportion of penetrating wounds in military cases. The risk of developing post-traumatic epilepsy is directly related to the severity of the injury and also correlates with the total volume of brain lost as measured by CT. Depressed skull fractures may or may not be a risk. Head injuries are classified as severe if they result in brain contusion, intracerebral or intracranial hematoma, unconsciousness, or amnesia for more than 24 hours, or in persistent neurologic abnormalities, such as aphasia, hemiparesis, or dementia. Mild head trauma; brief loss of consciousness, no skull fracture, no focal neurologic signs, no contusion or hematoma, do not increase the risk of seizures above the general population rates.
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Febrile Seizures
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These are generalized convulsions that occur during a febrile illness that does not involve the brain. Most occur in children between the ages of 6 months and 4 years; they are occasionally seen in children as old as 6 or 7 years.
Typically the seizure occurs early in febrile illness, while the temperature is rapidly rising. Although generalized convulsions are the rule, focal features or Todd paralysis are seen in about 10% of patients. |
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Neonatal seizures
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are the most common sign of neurologic dysfunction in the newborn. They occur in 0.5% of all newborns, more often in preterm babies, and frequently signify injury to the developing brain.
The current classification recognizes four general patterns: subtle, clonic, tonic, and myoclonic. The prognosis is directly related to the etiology of the seizures. |
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Myopathy
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A generic term indicating disease of the muscle. Includes muscular dystrophies, inflammatory myopathies (myositis), myalgias, rhabdomyolysis, etc.
Normal cranial nerves Proximal weakness Decreased reflexes No sensory changes CK is elevated in almost all myopathic diseases. EMG is used to diagnose the presence of a myopathy and to differentiate the type of myopathy. |
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Duchenne’s Muscular Dystrophy
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The most common childhood muscular dystrophy
Incidence: 1 in 3500 live male births Prevalence: 3 per 100,000 X-linked recessive inheritance Presentation: delayed crawling, delayed walking, Gower’s sign, proximal weakness noted by age 3, calf pseudohypertrophy, contractures, scoliosis Most patients die in the late teens to early twenties Heart, brain, and smooth muscle are also affected CK greatly elevated (10-50,000). Diagnosis through testing for dystrophin gene (positive in 70%) Weekly prednisone helps improve strength some |
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Polymyositis
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Incidence: 5 per 1,000,000
Prevalence: 5 per 100,000 Age of onset 45-65 Women to men is 2:1 Presentation: rapid onset proximal weakness (difficulty standing from seated position, falls, trouble lifting arms above head), can have lung and cardiac involvement Diagnosed with CK, EMG, and biopsy Treated with immunosuppression |
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Dermatomyositis
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Incidence: 5 per 1,000,000
Prevalence: 5 per 100,000 Bimodal distribution, 5-14 and 45-65 Women to men is 2:1 Presentation: rapid onset proximal weakness similar to polymyositis, rash (heliotrope, Gottron’s sign), can have lung and cardiac involvement Approximately 25% associated with malignancy Diagnosed with CK, EMG, and biopsy (skin and muscle) Treated with immunosuppression |
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Inclusion Body Myositis
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Most common inflammatory myopathy in those older than 50
Incidence: 7 per 1,000,000 Prevalence: 13 per 100,000 More common in men Presentation: slow onset proximal and distal weakness (finger/wrist flexors, quads > hip flexors), dysphagia Diagnosed with CK, EMG, and biopsy Poor response to immunosuppression |
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Statin Associated Myopathy
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Incidence: < 0.5% of those taking statins
Increased risk with “stronger” statins and when used in combination with fibrates Statin associated muscle disease ranges from mild myalgias with normal CK to overt rhabdomyositis Presentation: proximal weakness and myalgias CK is typically very high Treatment is discontinuation of statin |
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Disease of the Neuromuscular Junction
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Any condition in which transmission is interrupted within the neuromuscular junction. By far the most common condition is myasthenia gravis, but other examples include Lambert-Eaton myasthenic syndrome, botulism, and tetanus.
Cranial neuropathies are common – ptosis, diplopia, dysarthria, and dysphagia Proximal weakness Decreased reflexes No sensory changes Fatigability is an important aspect, both by history and exam. Workup: There are specific antibodies for each NMJ disease, but acetylcholine receptor antibodies are seen in myasthenia gravis. Nerve conduction studies for repetitive stimulation. CT of the chest will sometimes show a thymoma. |
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Myasthenia Gravis
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Incidence: 10 per 1,000,000
Prevalence: 5 per 100,000 Bimodal distribution: teens-30 (females) and 50-70 (males) Presentation: can be generalized, bulbar, or ocular, symptoms worse at end of day Diagnosed with NCS (rep stim) and AchRec abs Treated with pyridostigmine and immunosuppression |
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Neuropathy - Exam
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Cranial nerves are normal
Distal weakness Decreased reflexes Sensory loss The combination of distal weakness and sensory loss can lead to deformities of the hands and feet. Workup: Bloodwork often includes testing for diabetes (HgbA1C, fasting glucose, glucose tolerance), B12 deficiency, and hypothyroidism. Other tests include heavy metal screen and protein electrophoresis. Nerve conduction studies are key. |
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Inherited Neuropathies
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The most common inherited neuropathy is Charcot-Marie-Tooth Disease. While overall this is uncommon, there is a large amount of CMT in western North Carolina.
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Acquired Neuropathies
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There is a wide range of diseases that can be fit into this category, including:
Entrapment neuropathies – carpal tunnel, cubital tunnel, etc Diabetic polyneuropathy Autoimmune neuropathies – Guillain-Barre syndrome, CIDP Motor neuron disease – Amyotrophic lateral sclerosis (ALS), spinal muscular atrophy |
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Carpal Tunnel Syndrome
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The most common nerve entrapment syndrome
Incidence: 100-1000 per 1,000,000 Prevalence: 1000-5000 per 100,000 (rates are even higher in certain groups) Presentation: numbness and pain over the palm (digits 1-3), weakness with advanced cases Diagnosed clinically or with NCS Conservative treatment: rest, wrist braces, NSAIDS Aggressive treatment: steroid injections, ligament release surgery |
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Diabetic Polyneuropathy
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The leading cause of neuropathy in the US and Europe
Prevalence: 60-70% of diabetics have some degree of neuropathy Presentation: stocking-glove sensory loss, burning, and weakness in advanced cases Diagnosed clinically or with NCS Treat the neuropathy with glycemic control, treat the symptoms with TCAs, gabapentin, other AEDs, topical capscaisin |
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Amyotrophic Lateral Sclerosis
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Incidence: 20 per 1,000,000
Prevalence: 10 per 100,000 Peak age of onset is 65-70 5-10% of ALS is familial Presentation: upper and lower motor neuron signs (spasticity, atrophy, fasiculations), asymmetric onset, bulbar involvement Mean symptom onset to death time is 4 yrs Diagnosis supported by EMG Rilutek (riluzole) is the only FDA approved treatment. Supportive care is important. |
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Guillain-Barre Syndrome
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Incidence=Prevalence: 1 per 100,000
Most common between age 30-50 Presentation: preceding event (viral GI or respiratory illness, vaccine, surgery), ascending weakness and numbness (difficulty walking, falls, trouble with ADLs), absent reflexes, respiratory compromise Diagnosed with NCS, LP Treated with either IVIG or PEx |
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Transient Ischemic Attack
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ischemic (low-blood-flow) stroke without permanent damage
“angina” of the brain <24 h by definition, but usually 2-20 min important warning of impending stroke prompt evaluation urgent to prevent future stroke–find out the cause! |
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Cortical strokes
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Imply large-vessel, often embolic events
At risk for recurrence if embolic At risk for swelling, increased ICP and herniation Signs - language abnormalities (aphasias) - gaze preferences - neglect syndromes - cortical sensory findings - Personality changes |
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Subcortical Strokes
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hemibody motor or sensory symptoms without cortical involvement
the so-called “lacunar” syndromes |
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Brainstem Strokes
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May present with consciousness ranging from completely comatose to fully awake
Hallmark is crossed findings Think of brainstem longitudinally and cross-sectionally |
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Hemorrhage vs. Ischemic Infarct
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Both present with sudden, acute deficit
Supporting evidence for hemorrhage - severe H/A at onset (especially worst H/A of patient’s life with SAH) - younger age with h/o of HTN - Greater than expected obtundation with hemispheric stroke than usually seen in patients with ischemic infarcts CANNOT make definitive dx clinically *** Non-contrast head CT *** |
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ACA syndrome
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Very uncommon
hemiparesis ( leg >> arm and face) gaze preference sensory loss ( leg > arm/face) behavioral disorders incontinence |
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PCA Syndrome
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Hemianopia or cortical blindness if bilateral
Visual behavioral disorders - Palinopsia - Prosopagnosia - Alexia - color anomia Temporal lobe involvement may cause aphasia and memory loss Thalamic involvement can cause sensory loss |
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Small-Vessel Syndromes
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Small, deep infarcts in the distribution of the lenticulostriates, thalamoperforators or paramedian branches of the basilar
25% of strokes Pathology is fibrinoid necrosis, lipohyalinosis and microatheroma Risk factors are HTN, DM, tobacco abuse, hyperlipidemia No cortical findings on exam |
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Classic Lacunar Syndromes
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Pure motor hemiparesis
Pure sensory stroke Clumsy-hand, dysarthria syndrome Sensorimotor stroke Ataxic hemiparesis |
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Emergency Stroke Care
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Detection of the onset of stroke signs and symptoms
Dispatch through activation of the EMS system and prompt EMS response Delivery of the victim to the receiving hospital while providing appropriate pre-hospital assessment and care and pre-arrival notification Door (emergency department triage) Data (emergency department evaluation, including CT scan) Decision about potential therapies Drug therapy |
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Risks of Reperfusion Therapy
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Hemorrhage into infarcted tissue
- Risk goes up as size of stroke increases and as time interval increases Lack of efficacy: if tissue already infarcted then reperfusing does no good Distal embolization of thrombotic material Risk of dissection |
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Emergency Stroke Care Medical Management
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Begin aspirin therapy within 48 hours
Initiate DVT prophylaxis Avoid hypotonic solutions Maintain adequate nutrition/hydration Prioritize early mobilization and discontinue invasive lines and Foley catheter ASAP Initiate PT/OT/ST ASAP if clinically indicated |
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Infantile spasms
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may be idiopathic or symptomatic. When all clinical data are considered, including results of imaging studies, only about 15% of the patients are now classified as idiopathic.
Symptomatic cases have various etiologies: cerebral dysgenesis, tuberous sclerosis, phenylketonuria, intrauterine infections, or hypoxic-ischemic injury. Seizures are characterized by sudden flexor or extensor spasms that involve the head, trunk, and limbs simultaneously. The attacks usually begin before 6 months of age. The EEG is grossly abnormal, showing chaotic, high voltage slow activity with multi focal spikes, a pattern termed hypsarrhythmia. The treatment of choice is adrenocorticotropic hormone (ACTH); spasms are notoriously refractory to usual anticonvulsant medications, with the exception of Vigabatrin (not available in the US). ACTH controls the spasms and normalizes the EEG. Only 5-10% of children with infantile spasms have normal or near normal development, and more than 66% have severe disabilities. |
