What are the main kinds of epileptic seizures?

Describe the clinical features of partial simple seizures.
Most partial simple seizures encountered in a medical setting consist of the focal jerking or twitching of an arm or leg on one side of the body. This is usually due to a structural lesion in the brain (such as a stroke, abscess, or tumor) that leads to local irritation and an epileptic discharge. If this discharge spreads, the focal seizure also spreads, sometimes involving the other side of the brain and causing twitching or jerking of both arms and legs (generalized tonic-clonic or grand mal seizure). Occasionally, metabolic lesions, especially hyperglycemia and hyperosmolar states, can cause focal lesions and focal partial seizures.

Describe the clinical features of partial complex seizures.
Partial complex seizures may be preceded by an aura of abnormal smells or tastes, visual sensations, or mental phenomena, such as deja-vu. The seizure itself may consist of an episode of staring, lip smacking, and automatic, semipurposeful movements, such as picking at clothes. Often there is no jerking of muscles, no loss of tone, and no falling down. Patients, however, are in a state of significantly altered mental status and often completely unresponsive. After a minute or two, the seizure passes, leaving a postictal state of confusion and lethargy.

Which group is most likely to develop generalized absence seizures?
Generalized absence seizures, sometimes referred to as petit mal, are seen almost exclusively in children. These seizures usually do not have a significant aura or postictal state but may consist of just a few seconds of staring and altered mental status. This may be so brief as to escape detection by untrained observers. At other times, children are thought to be daydreaming rather than experiencing a seizure.

How do generalized tonic-clonic seizures present?
Generalized tonic-clonic seizures, the so-called grand mal seizures, consist of the sudden onset, often without any preceding aura, of jerking tonic and clonic activity of both arms and both legs, with a generalized increase in muscle tone and loss of consciousness. There may be tongue biting or incontinence. Seizures usually last a minute or two and then resolve, often with a period of postictal lethargy and confusion.

How do the identifiable causes of seizures vary by age?

COMMON CAUSES OF SEIZURES BY AGE

What are the most common causes of seizures seen in the emergency department or on the medical ward?
Anticonvulsant withdrawal. Most patients seen here are known epileptics who have been taking medicine and, for one reason or another, are noncompliant with their drugs. Alcohol withdrawal, drug overdose, and metabolic derangements such as hyponatremia are other common causes. Structural brain disease, including stroke and meningitis, is a less common cause of seizures.

How do alcohol withdrawal seizures present?
Such seizures generally occur 12-48 hours after cessation or abrupt reduction in the intake of alcohol. These seizures are always generalized tonic-clonic seizures, without focality. They are often single, isolated seizures, but sometimes patients may have two or more over a span < 6 hours. Status epilepticus is rare after alcohol withdrawal but does occasionally occur. Alcohol withdrawal seizures seldom persist and are self-limited.

What are the most important principles of seizure management?
Most seizures can be controlled completely, or nearly so, by following three basic principles:

1. Pick the most appropriate anticonvulsant for the type of seizure that the patient is experiencing.
2. Steadily increase the dose of that drug, guided by serum anticonvulsant levels, until seizures are controlled. If drug toxicity develops before the seizures stop, the drug is not the appropriate one; try a different one. Obviously, increase the new anticonvulsant to therapeutic levels before tapering of the old drug.
3. Monotherapy is preferable. Good therapeutic levels of one drug are preferable to subtherapeutic levels of multiple drugs.

How is status epilepticus treated?

• Rapid history and physical examination, including airway, breathing, circulation.
• Start IV and draw blood for complete blood count (CBC), electrolytes, anticonvulsant levels. Administer thiamine and glucose.
• Infuse fosphenytoin by slow IV push at 50 mg/min to a dose of ∼20 mg/kg (1500 mg). To break a continuous seizure, give diazepam up to 20 mg or lorazepam up to 8 mg.
• Infuse IV phenobarbital, 100 mg/min up to 600 mg.
• Institute general anesthesia.

When should you intubate a patients with status epilepticus?
Experts disagree about when to intubate that patient. Some do it in step 2; others wait until step 4. You should always be prepared to immediately intubate any patient in status epilepticus.

References
WEB SITES
www.neuroguide.com
www.aan.com (American Academy of Neurology)
www.medmatrix.org
www.internets.com/mednets/sneurolo.htm
www.medwebplus.com/subject/Neurology.html

BIBLIOGRAPHY

• Treiman DM: Convulsive status epilepticus. Curr Treat Options Neurol 1:359-369, 1999.
• Aminoff M: Neurology and General Medicine, 3rd ed. Philadelphia, Churchill-Livingstone, 2001.
• Bradley WG, Daroff RB, Fenichel GM, Jankovic J: Neurology in Clinical Practice, 4th ed. Philadelphia, Butterworth-Heinemann, 2004.
• Caplan LR: Stroke: A Clinical Approach, 3rd ed. New York, Butterworth-Heinemann, 2000.
• Samuels MA, Feske S (eds): Office Practice of Neurology, 2nd ed. Boston, Churchill-Livingstone, 2003.
• Johnson RT, Griffin JW: Current Therapy in Neurologic Disease, 6th ed. St. Louis, Mosby, 2002.
• Victor M, Ropper AH: Prinicples of Neurology, 7th ed. New York, McGraw-Hill, 2001.
• Wyllie E: The Treatment of Epilepsy: Principles and Practice, 3rd ed. Philadelphia, Lea & Febiger, 2002.

What is the most common cause of aphasia in adults?
The most common cause of aphasia in adults is cerebrovascular disease.

Define fluent aphasias.
Fluent aphasias are due to lesions in the cortex in the posterior part of the dominant hemisphere, around the posterior temporal lobe. Such aphasias-also known as Wernicke’s, sensory, receptive, or posterior aphasia-result in speech that is fluent and even loquacious, but senseless. These patients can talk but make no sense. They have many neologisms and paraphasic errors, inventing words and sounds as they go along and stringing words together in nongrammatical, meaningless fashions. Patients usually have impaired naming, repetition, and severely impaired comprehension as well.

How do nonfluent aphasias differ from fluent aphasias?
Nonfluent aphasias are generally produced by lesions in the cortex, in the anterior part of the dominant hemisphere around the sylvian fissure, and are often referred to by other expressions such as Broca’s, motor, expressive, or anterior aphasia. Such patients have difficulty producing language and either cannot speak or do so only in monosyllables and short telegraphic phrases. Naming and repetition are also impaired, but comprehension is relatively preserved.

Compare the two main types of aphasia.

COMPARISON OF THE TWO MAIN TYPES OF APHASIA

References
WEB SITES
www.neuroguide.com
www.aan.com (American Academy of Neurology)
www.medmatrix.org
www.internets.com/mednets/sneurolo.htm
www.medwebplus.com/subject/Neurology.html

BIBLIOGRAPHY

• Aminoff M: Neurology and General Medicine, 3rd ed. Philadelphia, Churchill-Livingstone, 2001.
• Noseworthy JH (ed): Neurologic Therapeutics. London, Martin Dunitz, 2003.
• Bradley WG, Daroff RB, Fenichel GM, Jankovic J: Neurology in Clinical Practice, 4th ed. Philadelphia, Butterworth-Heinemann, 2004.
• Caplan LR: Stroke: A Clinical Approach, 3rd ed. New York, Butterworth-Heinemann, 2000.
• Samuels MA, Feske S (eds): Office Practice of Neurology, 2nd ed. Boston, Churchill-Livingstone, 2003.
• Johnson RT, Griffin JW: Current Therapy in Neurologic Disease, 6th ed. St. Louis, Mosby, 2002.
• Rolak LA (ed): Neurology Secrets, 4th ed. Philadelphia, Hanley & Belfus, 2005.
• Victor M, Ropper AH: Prinicples of Neurology, 7th ed. New York, McGraw-Hill, 2001.

Distinguish among the four main kinds of stroke.

What are the clinical features of a thrombotic stroke?
Thrombotic strokes are the most common type and account for approximately 40% of all strokes. They may have a gradual, stuttering, or stepwise onset rather than an abrupt deficit. The cause is generally atherosclerosis affecting large intracranial vessels. The large-vessel involvement explains why these strokes tend to cause considerable neurologic deficit. About one-third to one-half of thrombotic strokes are preceded by transient ischemic attacks (TIAs), which are focal but totally reversible deficits that last a few minutes.

Describe the major clinical features of an embolic stroke.
Embolic strokes generally arise from the heart with an underlying cardiac disease, such as atrial arrhythmias, valvular disease, or mural thrombus. They tend to be abrupt in onset, with more rapid resolution, and tend to cause smaller neurologic deficits than a thrombotic stroke. Because the embolus travels in the arterial stream until it reaches a blood vessel of sufficiently small caliber to occlude it, it often travels distally all the way to the cortex. Cortical deficits, such as aphasia, are thus characteristic of embolic strokes.

Explain the mechanisms of a lacunar stroke.
Lacunar strokes are very small, discrete infarcts, < 1 cm3 in size, occurring deep within the brain or brain stem (lacune means little lake or pond). These strokes are due to occlusion of tiny penetrating arterioles that supply the deep brain substance, usually in the region of the basal ganglia, thalamus, and internal capsule, as well as the brain stem. These small strokes may cause discrete clinical symptoms, such as a pure motor stroke (hemiparesis without sensory loss) or pure sensory stroke.

How do hemorrhagic strokes differ from the other three types?
An intracerebral hemorrhage is classified as a stroke because of its abrupt onset with focal neurologic deficits, but it is due to rupture of a blood vessel, with subsequent bleeding and intracerebral mass, rather than to ischemia directly. Intracerebral bleeds have an abrupt onset and are usually accompanied by a significant headache and other signs of increased intracranial pressure, such as nausea, vomiting, and a diminished mental status. These are often devastating events with a poor prognosis. Bleeds tend to occur in the same deep locations as lacunae (i.e., the basal ganglia and brain stem).

What are the leading causes of death shortly after a stroke?
The three leading causes of death in the first 30 days after a stroke are not related primarily to the stroke itself or to neurologic deficits:

1. Pneumonia
2. Pulmonary embolus
3. Ischemic heart disease

Discuss the medical management of the patient with acute stroke.
Medical management of the stroke patient should focus on the complications that develop after the stroke. Since the leading cause of death is pneumonia, care should be taken that the patient does not aspirate-keep the patient NPO until it is clear that swallowing is not impaired by neurologic damage. Fever should always be presumed to be pneumonia until proved otherwise. Measures to prevent pulmonary embolus should be instituted, including early mobilization. Ischemic heart disease commonly causes death, since atherosclerosis affecting the cerebral vasculature probably also involves the coronary arteries. Cardiac assessment should be individualized.

When should thrombolysis be used to treat acute ischemic strokes?
Recombined tissue plasminogen activator (TPA) is approved for the acute treatment of ischemic stroke, but only in certain settings. It must be given as soon as possible after the stroke and certainly within the first 3 hours. A CT scan of the head must not show any evidence of infarction (i.e., tissue damage must not be severe or hemorrhage). The patient must have significant deficits (the drug should not be used if the patient will recover well without it), and there should be no other contraindications, such as active bleeding or severe hypertension. Few patients, in fact, meet all these requirements and are candidates for TPA.

How is thrombolytic therapy given?
Patients are treated with 0.9 mg/kg TPA given over 1 hour after an initial 10% bolus. Studies suggest that such patients show approximately 30% more recovery of function than untreated patients. The risk of intracranial hemorrhage is approximately 6%; patients should be carefully monitored.

When is anticoagulation indicated in cerebrovascular disease?
The role of anticoagulation in cerebrovascular disease is highly controversial. The consensus among neurologists is that anticoagulation is mainly of benefit to prevent embolic stroke from the heart. Following an initial brain embolus from a cardiac source, the risk of subsequent emboli is high, especially within the first few days and weeks, and evidence suggests that immediate anticoagulation reduces the risk. Although there is a chance that anticoagulation will worsen a stroke by converting the ischemia into hemorrhage, data suggest that this worsening is more than outweighed by the benefits in preventing further emboli.

Discuss the role of aspirin in the management of cerebrovascular diseases.
Aspirin, given at the time of a stroke, may have some protective effects. Patients with TIA or minor stroke are often treated with aspirin, usually 1 tablet (325 mg) per day, to prevent further episodes of cerebrovascular ischemia. There may be additional benefits to combining aspirin with dipyridamole.

What is the role of ticlopidine and clopidogrel in the management of cerebrovascular disease?
Ticlopidine, like aspirin, acts as a platelet inhibitor and similarly decreases the risk of further cerebrovascular ischemia. Unlike aspirin, it does not affect the cyclo-oxygenase pathway and instead acts by interfering with platelet membrane interactions. Clopidogrel is another antiplatelet agent with similar properties. Their current role is primarily for the prevention of stroke in patients with cerebral ischemia for whom aspirin therapy has failed, has caused intolerable side effects, or is otherwise contraindicated.

What is the main indication for carotid endarterectomy in cerebrovascular disease?
For patients with symptomatic atherosclerotic stenosis of > 70% in the carotid artery, carotid endarterectomy is clearly beneficial, significantly decreasing the risk of ipsilateral stroke.

Discuss the role of carotid endarterectomy in asymptomatic patients.
In asymptomatic patients with atherosclerotic stenosis of the carotids, the role of carotid endarterectomy is less clear. Three large randomized trials done in the early 1990s detected no benefit of endarterectomy in these patients. However, the Asymptomatic Carotid Atherosclerosis Study (ACAS) demonstrated a reduction in cerebral infarction in asymptomatic patients with as little as 60% stenosis, provided perioperative morbidity was kept to a minimum. The benefits were sufficiently modest that not all experts were convinced of the utility of surgery, and considerable individual variation remains among physicians managing such patients. Clearly, any surgical intervention in the treatment of carotid artery stenosis must be used in addition to, not in lieu of, aggressive control of modifiable risk factors.

References
WEB SITES
www.neuroguide.com
www.aan.com (American Academy of Neurology)
www.medmatrix.org
www.internets.com/mednets/sneurolo.htm
www.medwebplus.com/subject/Neurology.html

BIBLIOGRAPHY

• Halley EC: Thrombolysis in the treatment of acute ischemic stroke. Curr Treat Opt Neurol 5: 377-380, 2003.
• Brott T, Bogousslavsky J: Treatment of acute ischemic stroke. N Engl J Med 343:710-722, 2000.
• North American Symptomatic Carotid Endarterectomy Trial Collaborators: Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 339: 1415-1425, 1998.
• Aminoff M: Neurology and General Medicine, 3rd ed. Philadelphia, Churchill-Livingstone, 2001.
• Noseworthy JH (ed): Neurologic Therapeutics. London, Martin Dunitz, 2003.
• Bradley WG, Daroff RB, Fenichel GM, Jankovic J: Neurology in Clinical Practice, 4th ed. Philadelphia, Butterworth-Heinemann, 2004.
• Caplan LR: Stroke: A Clinical Approach, 3rd ed. New York, Butterworth-Heinemann, 2000.
• Samuels MA, Feske S (eds): Office Practice of Neurology, 2nd ed. Boston, Churchill-Livingstone, 2003.
• Johnson RT, Griffin JW: Current Therapy in Neurologic Disease, 6th ed. St. Louis, Mosby, 2002.
• Victor M, Ropper AH: Prinicples of Neurology, 7th ed. New York, McGraw-Hill, 2001.

What is the second step in evaluation of dizziness?
The next step is to determine whether the vertigo is central (due to a brain-stem lesion) or peripheral (due to an ear lesion).

How do you distinguish between central and peripheral vertigo?
Although many accompanying signs and symptoms have been promulgated to differentiate central from peripheral vertigo, none has great sensitivity or specificity. The most useful way to diagnose vertigo is by the company it keeps. Central vertigo is almost always accompanied by other signs of brain-stem dysfunction, such as double vision, weakness or numbness of the face, dysarthria, or dysphagia. Peripheral vertigo may be accompanied by tinnitus or hearing loss, but no other neurologic abnormalities.

Name the common causes of peripheral vertigo and central vertigo.

• Peripheral
• Ménière’s disease
• Vestibular neuronitis
• Local trauma
• Drugs (antibiotics, diuretics)
• Acoustic neuroma
• Benign positional vertigo
• Central
• Stroke
• Multiple sclerosis
• Tumors

How is dizziness best treated?
Nonvertigo dizziness (including near-syncope, anxiety, and ataxia) should be treated by addressing the underlying cause. True vertigo can be treated symptomatically, almost regardless of the cause. Scopolamine has proved to be the best available treatment in comparative trials against other drugs and placebos. Benzodiazepines and antihistamines are of some value, including meclizine (Antivert) and diazepam. Canalith repositioning maneuvers (epley maneuvers) effectively treat benign paroxysmal positional vertigo.

References
WEB SITES
www.neuroguide.com
www.aan.com (American Academy of Neurology)
www.medmatrix.org
www.internets.com/mednets/sneurolo.htm
www.medwebplus.com/subject/Neurology.html

BIBLIOGRAPHY

• Aminoff M: Neurology and General Medicine, 3rd ed. Philadelphia, Churchill-Livingstone, 2001.
• Noseworthy JH (ed): Neurologic Therapeutics. London, Martin Dunitz, 2003.
• Bradley WG, Daroff RB, Fenichel GM, Jankovic J: Neurology in Clinical Practice, 4th ed. Philadelphia, Butterworth-Heinemann, 2004.
• Samuels MA, Feske S (eds): Office Practice of Neurology, 2nd ed. Boston, Churchill-Livingstone, 2003.
• Johnson RT, Griffin JW: Current Therapy in Neurologic Disease, 6th ed. St. Louis, Mosby, 2002.
• Victor M, Ropper AH: Prinicples of Neurology, 7th ed. New York, McGraw-Hill, 2001.

How does spinal cord compression present clinically?
Spinal cord compression causes the classic cord syndrome of a sensory level, bowel and bladder changes, and upper motor neuron weakness with spasticity, hyperreflexia, and a positive Babinski sign. Superficial reflexes, such as abdominal reflexes and the anal wink, may be diminished.

How is spinal cord compression best diagnosed?
The first step is to localize the site of the lesion. Plain x-rays of the spine have a high yield for showing metastatic disease, as evidenced by lytic lesions and erosion of pedicles. Bone scans lack specificity and are generally of low yield. MRI has largely replaced myelography for the definitive documentation of compression.

Summarize the treatment for spinal cord compression.
Surgical intervention is indicated for compression due to cervical spondylosis or mechanical deformation, such as spondylolisthesis. For neoplastic compression, radiation therapy is increasingly favored over surgical decompression, since results are equally good in many studies. Otherwise, surgery may be needed for diagnosis as well as treatment. In either case, high-dose IV steroids, such as 100 mg of dexamethasone daily, may provide additional relief.

KEY POINTS: NEUROLOGY I

• Myopathies cause proximal symmetric weakness without sensory loss and with little change in tone or reflexes.
• Neuromuscular junction diseases cause proximal symmetric weakness that fluctuates (fatigues), without pain or sensory loss.
• Neuropathies usually cause distal weakness, often asymmetric, with atrophy, sensory loss, and pain.
• Most back pain is not caused by a radiculopathy.
• Myelopathies cause a sensory level.

References
WEB SITES
www.neuroguide.com
www.aan.com (American Academy of Neurology)
www.medmatrix.org
www.internets.com/mednets/sneurolo.htm
www.medwebplus.com/subject/Neurology.html

BIBLIOGRAPHY

• Armstrong R: Myelopathies. In Rolak LA (ed): Neurology Secrets. Philadelphia, Hanley & Belfus, 1998, pp 103-111.
• Noseworthy JH (ed): Neurologic Therapeutics. London, Martin Dunitz, 2003.
• Bradley WG, Daroff RB, Fenichel GM, Jankovic J: Neurology in Clinical Practice, 4th ed. Philadelphia, Butterworth-Heinemann, 2004.
• Caplan LR: Stroke: A Clinical Approach, 3rd ed. New York, Butterworth-Heinemann, 2000.
• Samuels MA, Feske S (eds): Office Practice of Neurology, 2nd ed. Boston, Churchill-Livingstone, 2003.
• Johnson RT, Griffin JW: Current Therapy in Neurologic Disease, 6th ed. St. Louis, Mosby, 2002.
• Rolak LA (ed): Neurology Secrets, 4th ed. Philadelphia, Hanley & Belfus, 2005.
• Victor M, Ropper AH: Prinicples of Neurology, 7th ed. New York, McGraw-Hill, 2001.

How should the patient with a radiculopathy be evaluated?
The diagnostic evaluation generally begins with an MRI of the area where the root emerges from the spinal cord, since this is the most common site of disorders causing radiculopathies. If imaging studies are negative, showing no root compression, then nonmechanical causes such as inflammation or infection should be considered.

Discuss the treatment for radiculopathies.
For most mechanical radiculopathies, the recommended treatment consists simply of analgesics, such as aspirin or other NSAIDs. Avoid muscle relaxants and chronic opioid use. There are surprisingly few careful, controlled studies analyzing the value of bed rest, traction, spinal manipulation, or invasive procedures such as acupuncture or trigger point injection. At this time, these methods have no proven benefit in the treatment of radiculopathy.

What is the main indication for surgery in the treatment of a radiculopathy?
Many experts believe that the presence of focal neurologic findings-such as weakness, atrophy, or fasciculations in the muscles affected, an absent reflex, or dermatome sensory loss is a strong indication for surgery. Such hard findings are unlikely to improve spontaneously and may well progress unless pressure on the nerve is relieved.

Is surgery ever appropriate for patients without focal neurologic findings?
This issue is much more controversial. Even in well-chosen patients with clear lesions and no overlying complications (such as litigation or secondary gain), surgery to alleviate pain is effective in only about half the cases. It is therefore often reserved for patients who have “failed medical management,” which is a clinical decision and generally implies persistent, severe pain after an adequate trial of analgesics.

What are the most common causes of back pain?
Only about 20% of back pain is caused by a slipped disk or root compression. There are many other causes, such as arthritis of the facet joints, but most back pain is thought to be musculoskeletal, due to strain placed on the tendons, ligaments, and muscles of the back. Many experts feel that this pain is largely mechanical, secondary to the inherent instability of the lordotic spine required for the human upright posture and aggravated by the problems of obesity, lack of exercise, and other precipitating factors in the modern lifestyle. For most such pain, conservative therapy and patience are indicated.

References
WEB SITES
www.neuroguide.com
www.aan.com (American Academy of Neurology)
www.medmatrix.org
www.internets.com/mednets/sneurolo.htm
www.medwebplus.com/subject/Neurology.html

BIBLIOGRAPHY

• Bigus S, et al: Acute Low Back Problems in Adults [Clinical Practice Guideline 14.] Rockville, MD, Agency for Health Care Policy and Research, 1994. [AHCPR publ no. 95-0643.]
• Van Tulder MW, Koes BW, Bouter LM: Conservative treatment of acute and chronic nonspecific low back pain: A systematic review of randomized controlled trials of the most common interventions. Spine 22: 228-256, 1997.
• Aminoff M: Neurology and General Medicine, 3rd ed. Philadelphia, Churchill-Livingstone, 2001.
• Noseworthy JH (ed): Neurologic Therapeutics. London, Martin Dunitz, 2003.
• Bradley WG, Daroff RB, Fenichel GM, Jankovic J: Neurology in Clinical Practice, 4th ed. Philadelphia, Butterworth-Heinemann, 2004.
• Caplan LR: Stroke: A Clinical Approach, 3rd ed. New York, Butterworth-Heinemann, 2000.
• Samuels MA, Feske S (eds): Office Practice of Neurology, 2nd ed. Boston, Churchill-Livingstone, 2003.
• Johnson RT, Griffin JW: Current Therapy in Neurologic Disease, 6th ed. St. Louis, Mosby, 2002.
• Rolak LA (ed): Neurology Secrets, 4th ed. Philadelphia, Hanley & Belfus, 2005.
• Victor M, Ropper AH: Prinicples of Neurology, 7th ed. New York, McGraw-Hill, 2001.

The evaluation of a patient with a peripheral neuropathy usually begins with which study?
An electromyogram and nerve conduction velocity (EMG/NCV) study. This test applies electrical current directly over the nerves and uses an electrode to record the speed with which the nerves conduct the current. It thus documents the extent and degree of impairment of nerve conduction. The EMG uses a needle electrode within the muscles to record muscle contractions and thus show denervation of the muscles.

Describe the management of a patient with a neuropathy.
Once a neuropathy has been confirmed, work-up for the etiology, requiring evaluation for diabetes, alcoholism, vitamin B12 deficiency, metabolic abnormalities such as thyroid disease or uremia, familial illnesses, toxic exposure, and collagen vascular disease. A spinal tap is seldom needed to detect inflammatory neuropathies. Only rarely is a nerve biopsy required. Many neuropathies improve with treatment of the underlying etiology.

What is the most common entrapment neuropathy?
Carpal tunnel syndrome (CTS), caused by compression of the median nerve at the wrist.

Describe the presentation of CTS.
Most commonly the result of mechanical overuse, CTS usually presents with symptoms of pain and tingling in the hand (especially at night), weakness, and/or numbness. Pain in the hand at night is considered CTS until proved otherwise.

How is CTS diagnosed?
There may be no objective neurologic findings in CTS. As with other peripheral neuropathies, EMG/NCV studies are helpful in making the diagnosis.

How is CTS treated?
Treatment is usually surgical, involving open or endoscopic release at the wrist, although conservative measures (such as wrist splinting) may be sufficient for mild cases.

What is Guillain-Barré syndrome (GBS)?
GBS is an acute inflammatory polyradiculopathy with inflammation of the nerve roots and peripheral nerves. It is presumably autoimmune and often follows viral infections, surgery, pregnancies, and other immune-altering events. It runs a monophasic course, with weakness progressing for several days to weeks, reaching a plateau, and then recovering over a period of several weeks to months.

What are the symptoms of GBS?
GBS causes weakness, often but not always in an ascending pattern (from legs up the trunk to the arms and face). The weakness is hyporeflexive, but there is no significant sensory loss. Rapidly progressive weakness with absent reflexes and no sensory change is almost always GBS. The diagnosis is supported by high CSF protein and slowed nerve conduction velocities on EMG.

Treatment of GBS is based on which of its abnormalities?
Although GBS is presumably autoimmune, no specific antigen or well-defined immune abnormality has been confirmed. Nevertheless, treatment is directed toward an immunologic cause, employing IVIG or plasmapheresis. If done early in the disease, these treatments shorten the overall course. Because autonomic dysfunction frequently complicates the syndrome and because respiration is often impaired by the weakness, patients usually require management in the intensive care unit. Therapy thus focuses on the day-to-day concerns of respirators, vital signs, nutrition, and other aspects of critical care.

References
WEB SITES
www.neuroguide.com
www.aan.com (American Academy of Neurology)
www.medmatrix.org
www.internets.com/mednets/sneurolo.htm
www.medwebplus.com/subject/Neurology.html

BIBLIOGRAPHY

• Zochodne DW: Diabetic neuropathies. Curr Treat Options Neurol 2: 23-29, 2000.
• Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group: Randomized trial of plasma exchange, intravenous immunoglobulin, and combined treatments on Guillain-Barré syndrome. Lancet 349: 225-230, 1997.
• Aminoff M: Neurology and General Medicine, 3rd ed. Philadelphia, Churchill-Livingstone, 2001.
• Noseworthy JH (ed): Neurologic Therapeutics. London, Martin Dunitz, 2003.
• Bradley WG, Daroff RB, Fenichel GM, Jankovic J: Neurology in Clinical Practice, 4th ed. Philadelphia, Butterworth-Heinemann, 2004.
• Samuels MA, Feske S (eds): Office Practice of Neurology, 2nd ed. Boston, Churchill-Livingstone, 2003.
• Johnson RT, Griffin JW: Current Therapy in Neurologic Disease, 6th ed. St. Louis, Mosby, 2002.
• Rolak LA (ed): Neurology Secrets, 4th ed. Philadelphia, Hanley & Belfus, 2005.
• Victor M, Ropper AH: Prinicples of Neurology, 7th ed. New York, McGraw-Hill, 2001