5 Flashcards
What is the CT–scan appearance of subdural hematomas?
Subdural hematomas are crescent–shaped and epidural hematomas are lens–shaped.
What are the indications for cervical spine x–rays after head trauma?
Cervical spine x–rays should be obtained in head trauma if there are focal findings consistent with a cervical radiculopathy or if spinal tenderness is present.
What is the treatment for severe intracranial hemorrhage?
Lowering intracranial pressure with hyperventilation to pCO2 of 30–35, mannitol, elevation of head of bed. Surgical evacuation. Maintain the SBP 110–160. Slight degree of HTN maintains cerebral perfusion.
A 50–year–old woman with sudden loss of consciousness, severe headache, nuchal rigidity, photophobia, and a temperature of 38.5 C (101.3 F). What is the diagnosis?
Subarachnoid hemorrhage
What is subarachnoid hemorrhage?
Bleeding into caused by aneurysm. Around the circle of Willis. Association with polycystic kidney disease, Ehlers–Danlos syndrome. Occurs spontaneously. Head trauma is a rare cause.
What is the presentation of subarachnoid hemorrhage?
Sudden, severe headache, loss consciousness 50%. Focal neurologic symptoms 30% from compression of occulomotor nerve. Nuchal rigidity, photophobia, headache, papilledema. Seizures.
What are the long–term outcome of subarachnoid hemorrhage?
One–year mortality 50%, with half of the people dying immediately. Longer–term manifestations include focal deficits, seizures, rebleeding, hydrocephalus.
How is subarachnoid hemorrhage diagnosed?
CT of head without contrast has 95% sensitivity. If CT is normal and SAH is suspected, lumbar puncture is done. Lumbar puncture is most sensitive. The absence of red cells in CSF excludes SAH.
What is the treatment for subarachnoid hemorrhage?
Maintain SBP 110–160. Seizure prophylaxis with phenytoin. Nimodipine is a calcium–channel antagonist that lowers risk of blood vessel spasm.
What test should be done after subarachnoid hemorrhage has been diagnosed?
Angiography to determine the site of the bleeding. Surgical clipping of the AVM should occur before rebleeding develops.
What is the management of hydrocephalus after subarachnoid hemorrhage?
If hydrocephalus occurs, then shunting should be done.
What is the treatment for spinal headache after lumbar puncture?
A spinal headache is treated with a blood patch.
What are the signs of respiratory injury in burn injuries?
Soot in the mouth or nose, stridor, wheezing, altered mental status, burned nasal hairs, and burns involving closed spaces are signs of impending pulmonary and laryngeal edema.
What are the signs of carbon monoxide overdose?
Altered mental status, dyspnea, headache, and chest pain are clues to severe carbon monoxide poisoning.
What are the signs of pulmonary thermal injury?
Laryngeal edema can result in stridor, hoarseness, and dyspnea. Soot in the nose and mouth can imply impending airway compromise.
How is the severity of burn injury assessed?
Carboxyhemoglobin elevated in severe burns. Severe burns are defined as combined second– and third–degree burns >20% in adults or >10% in the old or very young or third–degree burns >5% of body surface area.
What is the management of severe respiratory injury?
If there are signs of severe respiratory injury, intubate the patient. If the carboxyhemoglobin level is significantly elevated (>5–10%), give 100% oxygen.
How is the fluid resuscitation requirement determined for burns?
Fluid resuscitation over first 24 hours is 4 ml per % BSA/kg. Ringer’s to provide half fluid in first 8 h, with 1/4 in second 8 h, and 1/4 in final 8 h (Parkland formula). Maintain a urine output >0.5–1 mL/kg/h.
What is the treatment for burns?
Stress ulcer prophylaxis with H2 blockers. Silver sulfadiazine. Do not break blisters. Escharotomy for circumferential burns. Skin grafting.
What are heat cramps?
Mild fluid and electrolyte depletion. Painful muscular contractions lasting a few minutes. Body temperature normal. Treatment is oral rehydration and salt replacement.
What is heat exhaustion?
Weakness; body temperature slightly elevated; headache, anxiety. The patient is still able to sweat. Treatment with oral fluid and electrolyte replacement; may need intravenous hydration.
What is heat stroke?
Loss of ability to lose heat, inability to sweat. T >40 C, confusion, disorientation, nausea, blurred vision, seizures; hemoconcentration, rhabdomyolysis, elevation BUN, creatinine, WBC. Anuria, DIC, lactic acidosis.
What is the treatment of heat stroke?
Treatment with intravenous fluid replacement and rapid cooling. The body should be sprayed with water. Chlorpromazine and diazepam to control shivering.
What is malignant hyperthermia?
Nonexertional idiosyncratic heat reaction of rhabdomyolysis caused by anesthetic agents such as halothane or succinylcholine. Treatment is dantrolene.
What is neuroleptic malignant syndrome?
Idiosyncratic reaction to phenothiazines or butyrophenones, such as haloperidol. Muscular rigidity and rhabdomyolysis.
What is the treatment of neuroleptic malignant syndrome?
Treatment is bromocriptine or dantrolene.
What is hypothermia?
Core body temperature below 35 C (normal 37 C). Severe hypothermia is a core temperature below 30 C. Hypothermia often occurs with alcohol intoxication.
What is the presentation of hypothermia?
Lethargy, confusion, and weakness. Death from arrhythmia. Ventricular fibrillation or ventricular tachycardia. J–wave elevation may mimic ST segment elevation.
What is the effect of ionizing radiation on the body?
Ionizing radiation destroys DNA molecules. Lethal and can cause cancer. Nonionizing radiation includes infrared, ultraviolet, microwave radiation, which are less destructive and causes burns.
What are the symptoms of radiation exposure?
Nausea and vomiting early; intestinal ulceration, bleeding, infection later. Injury to skin, salivary glands, respiratory epithelium, thyroid, bone marrow.
What is the treatment of radiation exposure?
Antiemetics, platelets and RBC transfusions. Colony–stimulating factors (G–CSF, GM–CSF) to restore marrow. Bone marrow transplantation.
What is the presentation of near drowning?
Agitation, coma, cyanosis, coughing, and pulmonary edema, tachypnea, tachycardia, and blood–tinged sputum. Rales and rhonchi. Hypothermia. Hypoxia, hypercarbia, metabolic acidosis, hyperkalemia, hemolysis.
What is the presentation of anaphylaxis?
Urticaria, dyspnea, stridor, tachycardia, hypotension, and hemodynamic collapse.
What is the treatment of anaphylaxis?
Antihistamine (diphenhydramine), epinephrine injections, intravenous fluids, H2 blockers, and systemic corticosteroids.
What is the bacteriology of cat and dog bites?
Infections are most often polymicrobial. Cat bites are associated with Pasteurella multocida; dog bites are associated with Pasteurella, Eikenella, and Capnocytophaga canimorsus.
What is the treatment of cat and dog bites?
Wound care. Prophylactic antibiotic is amoxicillin/clavulanate (clindamycin and either ciprofloxacin or trimethoprim/ sulfamethoxazole or azithromycin if penicillin allergic).
What is the bacteriology of human bites?
Human bites carry an infection rate of 15%. Anaerobic and aerobic bacteria. Hepatitis B and HIV can also be transmitted through bites.
What is the treatment for human bite wounds?
Irrigate wound; cultures are not useful. If the bite is
Which animals carry rabies?
Raccoons, rats, wild dogs, woodchucks, skunks, foxes. 100% fatal. Less than 10 persons per year are infected in the US.
What is the presentation of rabies?
Incubation period up to one year. Prodrome of 2–10 days of fever and paresthesias at the bite site. Aphasia, paralysis, hypersalivation, and myoclonus.
How is rabies diagnosed?
Viral cultures from saliva, CSF, or serum
What is the treatment for rabies infection?
Ribavirin. Prophylaxis with human rabies immunoglobin provides immediate passive immunity. Human diploid cell vaccine should be given at 0, 3, 7, 14, and 28 days (5 shots total).
How many deaths per year are caused by snake bites?
What is the treatment of snake bites?
Decrease the spread of venom with compression bandages. Antivenin may cause anaphylactic reactions. Hypotension is managed with fluids. Ventilatory support for laryngeal edema.
What are the causes of spinal cord compression?
Commonly caused by lymphoma, multiple myeloma, carcinomas of prostate, lung, breast, kidney, or colon; herniated disk, epidural abscess, hematoma, or trauma.
What is the presentation of spinal cord compression?
Sensory loss, lower extremity weakness; sphincter dysfunction or sexual dysfunction. History of cancer, fever, and bowel or bladder incontinence or retention.
How is spinal cord compression diagnosed?
Plain x–rays are abnormal. The diagnostic test of choice is an MRI of the spine.
What is the treatment for spinal cord compression?
High–dose dexamethasone immediately, then MRI. For lymphoma or multiple myeloma, radiation therapy should be started. Surgical decompression for a herniated disk, epidural abscess, or hematoma.
What is syringomyelia?
Cavitation of spinal cord. Communicating with CSF or noncommunicating. Associated with congenital Arnold Chiari; caused by trauma, tumors.
What are the signs of syringomyelia?
Impaired pain, temperature; intact sensation to light touch. Loss of pain and temperature occurs in a cape–like distribution. Sparing of tactile sensation, position, and vibratory sense. Areflexia.
What is subacute combined degeneration?
B12 deficiency. Distal paresthesias and weakness of extremities followed by spastic paresis and ataxia. Deficit of vibration and proprioception with pyramidal signs (plantar extension, hyperreflexia). Low B12.
What is the presentation of anterior spinal artery infarct?
Flaccid paralysis, spastic paresis. Loss pain, temperature; sparing vibration and position. Motor, sensory, autonomic is lost below the level of the infarction with retained vibration and position. Treatment is supportive.
What is the Brown–Sequard syndrome?
Hemisection of the cord with ipsilateral spastic paresis. Ipsilateral loss of joint position sense, tactile discrimination, and vibratory sensations. Contralateral loss of pain and temperature.
A 60–year–old woman with sudden onset of right upper extremity weakness, aphasia, pronator drift and right facial nerve palsy. What is the most likely cause?
Ischemic stroke
What is a stroke?
Sudden onset of a focal neurologic deficit.
What are the mechanisms of strokes?
Large artery thrombosis, small artery thrombosis (lacunar), embolic (cardiogenic or artery–to–artery), vascular dissection, systemic hypotension, intracranial bleeding.
What is the presentation of ischemic stroke?
Acute onset of a focal neurologic deficit.
What is the blood supply to the brain?
Two major systems: carotid (anterior) circulation, and vertebrobasilar (posterior) circulation. The anterior circulation include the anterior cerebral artery and middle cerebral artery.
What are the signs of occlusion of the anterior cerebral artery?
Contralateral weakness in arm and sensory loss in leg more than in the upper extremity. Urinary incontinence, confusion, behavioral disturbances. Lower extremity weakness exceeds upper extremity.
What are the signs of occlusions of the middle cerebral artery?
Contralateral hemiplegia, hemisensory loss, homonymous hemianopia, eyes deviated toward lesion. Dominant results in aphasia. Nondominant results preserved speech, comprehension with confusion, apraxia.
What parts of the brain are supplied by the posterior circulation?
Cerebellum, brain stem, occipital lobe of the cortex, and pons. The major blood vessels of the posterior circulation are the posterior cerebral artery, basilar artery, and vertebral arteries.
What are the signs of posterior cerebral artery occlusion?
Contralateral homonymous hemianopia, hallucinations, agnosias. Occlusion of the penetrating branches of the PCA can result in CN III palsy with contralateral hemiplegia (Weber syndrome) or CN III palsy.
What is Wallenberg syndrome?
Occlusion of posterior inferior cerebellar artery, which presents as ipsilateral facial sensory loss, contralateral body sensory loss, vertigo, ataxia, dysarthria, dysphagia, and Horner syndrome (ptosis).
What are the signs of occlusion of the major cerebellar arteries?
Vertigo, vomiting, nystagmus, and ipsilateral limb ataxia.
How is stroke diagnosed?
Noncontrast CT to distinguish between hemorrhagic and ischemic stroke. CT often negative for ischemia within the first 48 hours. Diffusion–weighted MRI is the most accurate test for cerebral ischemia.
What tests will find the embolic source after an acute ischemic stroke?
Echocardiogram, carotid duplex, and 24–hour Holter monitor. Evaluation for inherited hypercoagulability.
What is the treatment for ischemic stroke?
Tissue plasminogen activator if within 4.5 hours of symptom onset.
What are the contraindications to tissue plasminogen activator for ischemic stroke?
Stroke or head trauma within 3 mo, hemorrhage (GI, GU), surgery within 14 d, intracranial hemorrhage, arterial puncture within 7 d, BP > 185/110, anticoagulants; platelets 15 sec).
What is the prognosis for patients who receive tissue plasminogen activator?
39% of all patients treated with tPA have a good functional outcome. Only 26% of untreated have a good outcome. Intracranial hemorrhage occurs in 5.8%. The fatality rate after intracranial hemorrhage is 45%.
What is the secondary prevention of ischemic stroke?
Started 24 hours after TPA. When patients have allergy to aspirin or continue to have recurrent cerebrovascular events on aspirin, dipyridamole may be added or the patient may be switched to clopidogrel.
When should heparin be given to patients with ischemic stroke?
Heparin in acute ischemic stroke is limited to patients with atrial fibrillation, basilar artery thrombosis, or stroke in evolution.
What is the treatment of subarachnoid hemorrhage?
Nimodipine to reduce the risk of ischemic stroke. Early surgical clipping of the aneurysm or embolization of the vessel. Aspirin is contraindicated.
What is the management of intracranial aneurysms that are found incidentally?
Unruptured aneurysms found incidentally should be repaired if they exceed 10 mm.
What are the indications for carotid endarterectomy?
Carotid endarterectomy for occlusion > 70% and the lesion is symptomatic. Endarterectomy may benefit those who are asymptomatic if there is >60% stenosis in men who are
What is a seizure?
Paroxysmal event caused by abnormally discharging central nervous system neurons. Epilepsy is a condition of recurrent seizures due to a chronic underlying process.
What are the causes of seizures?
Stroke, bleed, AV malformation; meningitis, abscess, encephalitis, trauma, vasculitis, hypoNa, hypoCa, hypoMg, hypoglycemia, hypoxia, drug overdose/withdrawal, idiopathic, neoplasm, psychiatric.
What is the presentation of a seizure?
Paroxysmal, involuntary, abnormal movement or change of consciousness. Sudden onset, with or without an aura. Disorientation, sleepiness, muscle aches. Incontinence, tongue biting, headache.
How is syncope different from a seizure?
Patients with syncope will not complain of significant postictal symptoms. Syncope patients will recover consciousness within several minutes of the event, and will not have incontinence or tongue biting.
How are seizures classified?
Partial or generalized and complex or simple.
What are partial seizures?
Partial seizures affect discrete portions of the brain, such as causing involuntary jerking of a finger or hand.
What is a simple partial seizure?
Consciousness is maintained for the duration of a simple seizure, and the seizure affects a discrete portion of brain. When there is a change in consciousness, the seizure is termed a complex partial seizure.
What are generalized seizures?
Arise from both cerebral hemisphere. Generalized tonic–clonic seizures are tonic contraction of muscles throughout the body followed by intermittent relaxation (clonic phase).
What are absence seizures?
Sudden, brief loss of consciousness without loss of postural tone. The ECG shows a generalized, symmetric 3–Hz spike–and–wave discharge pattern.
What are atonic seizures?
Atonic seizures are characterized by sudden loss of postural tone, lasting 1 to 2 seconds.
What are myoclonic seizures?
Myoclonic seizures are characterized by a sudden, brief muscle contraction.
What is status epilepticus?
Recurrent or continuous seizures lasting at least 5–30 min.
How are seizures diagnosed?
Electroencephalogram, serum electrolytes, glucose, toxicology, and arterial blood gas to exclude hypoxia. A CT scan or MRI of the head is indicated to exclude a structural lesion as the cause of seizure.
What is the treatment for status epilepticus?
Secure airway, breathing, circulation. Evaluate and treat causes. Lorazepam, which potentiates GABA receptor. If seizure continues, phenytoin or fosphenytoin to add phenobarbital.
What are the side effects of phenytoin?
Diplopia, dizziness, ataxia. Gum hyperplasia, lymphadenopathy, hirsutism, and rash.
What are the side effects of phenobarbital?
Sedation, ataxia, and rash.
What drug should be given if patients continue to seize after administration of lorazepam, phenytoin and Phenobarbital?
Midazolam or propofol anesthesia.
When should anticonvulsant therapy be started in patients with a first–time seizure?
Anticonvulsants should be started only if the patients has an abnormal neurologic exam, presented with status epilepticus, has a strong family history of seizure, or has an abnormal EEG.
What is the treatment for primary generalized tonic–clonic seizures?
Valproic acid. Valproic acid increases the availability of GABA. Lamotrigine, carbamazepine, or phenytoin are alternatives.
What are the side effects of valproic acid?
Side effects include ataxia, tremor, hepatotoxicity, thrombocytopenia, gastrointestinal irritation, and hyponatremia.
What is the mechanism of action of lamotrigine?
Lamotrigine decreases glutamate release. Side effects: Stevens–Johnson syndrome.
What is the treatment of absence seizures?
Ethosuximide. Valproic acid is an acceptable option.
What is the treatment for myoclonic and atonic seizures?
Valproic acid.
What is the treatment for partial seizures?
Carbamazepine and phenytoin are first–line therapy. Valproic acid, lamotrigine, and levetiracetam are alternatives.
What is vertigo?
False sensation of movement.
What are the causes of vertigo?
Mèniére, labyrinthitis, positional vertigo, traumatic, perilymphatic fistula, cervical vertigo. Brain stem disease, AV malformations, tumor, multiple sclerosis, drug overdose, vertebrobasilar migraine.
What are the characteristics of central vertigo?
No tinnitus or hearing loss is present. There are is often diplopia, cortical blindness, dysarthria, extremity weakness or numbness. Nystagmus is pure, vertical, does not suppress with fixation, and multidirectional.
What are the characteristics of peripheral vertigo?
Tinnitus and hearing loss. Absence of diplopia, cortical blindness, dysarthria, extremity weakness or numbness. Nystagmus is mixed, horizontal, suppresses with fixation, and unidirectional.
What are the signs of Mèniére disease?
Tinnitus, hearing loss, episodic vertigo of 1 to 8 h. Symptoms wax and wane as the endolymphatic pressure rises and falls. Most common causes of Mèniére disease are syphilis and head trauma.
What are the signs of labyrinthitis?
Sudden onset of severe vertigo that lasts for several days with hearing loss and tinnitus. Occurs with an upper respiratory tract infection.
What are the signs of benign paroxysmal positional vertigo?
Peripheral vertigo that characteristically is exacerbated by head movement or change in head position. Episodes occur in clusters that persist for several days. The vertigo usually lasts 10 to 60 seconds.
What are the causes of perilymphatic fistula?
Form of peripheral vertigo related temporally to head trauma (slap to the ear) or extreme barotrauma during air flight, scuba diving, or vigorous Valsalva maneuver.
What are the causes of central vertigo?
Caused by cerebellar or brain–stem tumor, bleed, or ischemia. Drug toxicity or overdoses. In young patient with unexplained central vertigo, consider multiple sclerosis.
What is the treatment of peripheral vertigo?
Meclizine or diazepam.
What is the treatment of Mèniére disease?
Low–salt diet and diuretics. Surgical decompression.
What is the treatment of benign paroxysmal positional vertigo?
Positional maneuvers that attempt to move the otolith out of the circular canals (e.g., Dix Hallpike and Barany maneuvers).
What is the treatment of vertigo caused by labyrinthitis?
Meclizine and diazepam.
28–year–old woman with throbbing, right–side headache; nausea; worsened by walking, loud noise, bright light. What is the diagnosis?
Migraine
What are the primary headache syndromes?
Migraine, cluster, and tension headache. Migraine affects 15% of the population.
What are the secondary causes of headache?
Intracranial hemorrhage, brain tumor, meningitis, temporal arteritis, and glaucoma.
What type of headache is characterized by fever and nuchal rigidity?
Meningitis.
What are the clinical symptoms of brain tumors?
Deep, dull, aching pain that disturbs sleep. Vomiting before the onset of headache, or a history of headache induced by coughing, lifting or bending is typical of posterior fossa brain tumors.
What are the characteristics of temporal arteritis?
Unilateral pounding headache with visual changes; dull and boring with lancinating pains. Polymyalgia rheumatica, jaw claudication, fever, weight loss, scalp tenderness; elderly.
What are the laboratory abnormalities associated with temporal arteritis?
Increased sedimentation rate; diagnosed with biopsy of the temporal artery. Initiate therapy with steroid immediately.
What cause of headache syndrome is associated with eye pain?
Glaucoma
What are the characteristics of migraine headaches?
Benign and recurrent syndrome of headache, nausea, vomiting, and focal neurologic deficits. Pulsatile, throbbing, unilateral, aggravated by movement. Photophobia, phonophobia.
What are the triggers of migraine?
Alcohol, chocolate, cheeses, monosodium glutamate, hunger, or irregular sleep patterns.
What is migraine without aura?
Migraine without a preceding focal neurologic deficit. Migraine with aura is a migraine headache that is accompanied by a preceding motor, sensory, or visual symptoms. Focal neurologic symptoms.
What is the pathognomonic aura for migraine?
Scintillating scotoma. Only 20% of migraine has aura. Stars, sparks, and flashes of light. Migraine equivalent is defined as focal neurologic symptoms without headache.
What are complicated migraines?
Migraines with severe neurologic deficits that persist after the resolution of pain.
What are basilar migraines?
Migraine headaches associated with vertigo, diplopia, ataxia, or dysarthria.
What are the characteristics of tension–type headaches?
Tension–type headaches are tight, band–like headaches are bilateral.
What are the characteristics of cluster headaches?
Excruciating, unilateral, periorbital headache without warning 30 min–3 hrs; 1–3 times a day for 4–week period. Red eye, lacrimation, nasal stuffiness, nausea, sensitivity to alcohol. Horner syndrome (ptosis).
How is migraine headache diagnosed?
Severe, sudden onset of a first–time headache with signs of an underlying cause should have a CT scan of the head.
What is the treatment of migraine headache?
Abortive sumatriptan, which is a serotonin receptor agonist. Dihydroergotamine is an alternative. The triptans are contraindicated in cardiovascular disease. Almotriptan, naratriptan, zolmitriptan, and eletriptan.
What is the prophylactic treatment for migraine?
Prophylactic treatment for migraine should be initiated when acute migraine headaches occur more than three to four times per month. Propranolol, timolol, valproic acid, and topiramate. Verapamil and tricyclics.
What is the treatment of cluster headaches?
The most effective treatment is 100% oxygen. Cluster headaches are treated with prednisone, lithium, ergotamine, and verapamil. Sumatriptan.
What is pseudotumor cerebri?
Idiopathic increase in intracranial pressure. 8–10 times more common in women. Association with obesity, chronic lung disease, Addison disease, oral contraceptives, tetracycline, and vitamin A toxicity.
What is the presentation of pseudotumor cerebri?
Headache, diplopia, and 6th cranial nerve (abducens) palsy. Papilledema, blind spot on visual field testing. The CT and MRI are normal, CSF is normal except for an increase in pressure.
What is the treatment for pseudotumor cerebri?
Weight loss, discontinue oral contraceptives, acetazolamide, furosemide, prednisone. Repeated lumbar punctures; placement of ventriculoperitoneal shunt.
What is trigeminal neuralgia?
Idiopathic, sudden, severe, sharp pain side of the mouth and progressing to ear, eye, or nostril. Triggered by touch or movement; pain lasts a few seconds. Compression of the trigeminal nerve root by a vessel, MS, tumor.
What is the treatment of trigeminal neuralgia?
Carbamazepine. Phenytoin, baclofen, or gabapentin. Surgery or alcohol injection into the affected nerve.
16–year–old boy with leg weakness. 3 weeks ago had diarrhea. Bilateral lower–extremity weakness and a loss of reflexes. What is the diagnosis?
Guillain–Barre syndrome
What is Guillain–Barre syndrome?
Acute, often severe polyradiculopathy caused by autoimmune destruction of myelin by an immune response.
What is the presentation of Guillain–Barre syndrome?
Sudden weakness begins lower extremities and moves upward. Loss of reflexes. Legs are more affected than arms and face. Pain, tingling. Loss of large sensory fibers, loss of reflexes and proprioception.
What autonomic instabilities are associated with Guillain–Barre syndrome?
Profuse sweating, postural hypotension, labile blood pressure, cardiac dysrhythmia occurs in severe GBS.
What is the etiology of Guillain–Barre syndrome?
75% have history of infection 1–3 weeks prior; respiratory or GI © jejuni). GBS may be preceded by HSV, CMV, EBV. Influenza vaccine associated with one case per million. HIV, SLE, lymphoma.
How is Guillain–Barre syndrome diagnosed?
A lumbar puncture has an elevated protein without an associated rise in the cell count. Electromyography will show demyelination of the peripheral nerves.
