• The brain is anesthetic. This means that most causes of head pain do not arise from the brain itself but rather from surrounding structures, such as blood vessels or periosteum. Since most headaches are not caused by brain disease, most are benign.
• The more severe the headache, the more benign the disease. The exception to this rule is intracranial hemorrhage, but, in general, most severe headaches are due to self-limited causes.
• Eye problems and sinus disease seldom cause headaches. Patients tend to blame their headaches on eye strain or sinusitis, but, in fact, these are rare causes.

List the common types of headache.

• Common migraine (without aura)
• Classic migraine (with aura)
• Tension headaches

What are the less common types of headaches?
Other less common or rare types of headaches include cluster headaches and headaches from brain tumor, meningeal irritation, and temporal arteritis.

Which serious diseases capable of causing permanent neurologic dysfunction can present as headaches?
Most processes causing headache are benign, but some are serious. Examples include:

• Primary brain tumor
• Metastatic brain tumor
• Abscess
• Subdural hematoma
• Intracerebral hemorrhage
• Subarachnoid hemorrhage
• Meningitis
• Temporal artery disease
• Hypertension
• Hydrocephalus
• Glaucoma

What clinical features are seen with increased intracranial pressure (ICP)?
Because the brain is completely surrounded by the hard bony skull, any increase in ICP can impair brain function. The most sensitive indicator of increased ICP is an altered mental status, and it is usually the first symptom to change as the pressure rises. With increased pressure, the brain can herniate downward through the foramen magnum, compressing and destroying the brain stem. Herniation can be recognized by the development of brain-stem signs as the top of the brain stem (midbrain) becomes impaired. In addition to altered mental status, these signs include dilatation of one or both pupils (“blown pupil”), hyperventilation, and focal neurologic signs such as hemiparesis. Herniation can progress to coma and death.

What basic principle underlies all techniques of lowering ICP?
Lowering ICP requires reduction of the intracranial contents to make room for the mass lesion and increased pressure. The intracranial contents consist essentially of the brain, CSF filling the ventricles, and blood within the blood vessels.

List four specific techniques for lowering ICP.

• Lowering blood pressure lowers the ICP and can be accomplished with a diuretic such as furosemide.
• Incubation and hyperventilation cause vasospasm that reduces the blood volume intracranially.
• Steroids can reduce swelling secondary to vasogenic edema. They may take hours or days to work and have little value acutely.
• Shunting can be used in emergency situations to remove CSF and to lower ICP.

How does intracranial hemorrhage present?
Intracranial hemorrhage causes the abrupt onset of an extremely severe headache. Patients report that it is “the worst headache in my life.” Approximately half of these patients die at the time of the bleed. The remainder usually present to an emergency department with an altered mental status but may not have significant focal neurologic findings.

What causes intracranial hemorrhage?
The bleeding may result from the rupture of a vessel outside the brain (subarachnoid hemorrhage) or inside the brain (intracerebral hematoma). Subarachnoid hemorrhage is usually due to the rupture of a small intracranial aneurysm, called a berry aneurysm, often located on the anterior communicating artery, middle cerebral artery, or their branches.

What is temporal arteritis?
Temporal arteritis is a giant cell arteritis, which is a systemic illness with generalized symptoms such as fevers, myalgias, arthralgias (polymyalgia rheumatica), anemia, and elevated liver function tests. The headache is a mild-to-moderate diffuse pain, not necessarily confined to the temples or frontal region of the head. The disease should be suspected in elderly people, over age 55, who develop new headaches.

How is temporal arteritis diagnosed?
The erythrocyte sedimentation rate (ESR) is usually very elevated, >100 mm/min, and is a good screening test. The confirmatory test is a temporal artery biopsy showing granulomatous arteries.

How is temporal arteritis treated?
High-dose steroids for a period of 1-2 years are often required, sometimes in doses of 60 mg/day of prednisone equivalent or more. Approximately 15% of patients, if left untreated, develop significant visual loss.

What are migraine headaches?
Migraine headaches are paroxysmal, intermittent headaches occurring on an average of once a month and lasting from 4-12 hours or more. Migraines typically begin in the teenage years, sometimes even in childhood, and diminish in both frequency and intensity of attacks in later adulthood. About half of all patients with migraine have a family history of the problem.

What are the common symptoms of migraines?

• About one third of patients have hemicranial pain, but in two thirds of patients the headache is diffuse over the entire head.
• Some patients have a preceding aura for 20-40 minutes before the headache. This often consists of visual changes, such as flashing lights.
• Gastrointestinal disturbances are very common, including nausea, vomiting, and anorexia. If the patient can eat during the headache, it is probably not migraine!
• Photophobia and phonophobia.
• Mood changes.
• Visual or sensory loss.

What causes migraine headaches?
The cause is not entirely understood. Probably low serotonin levels in the brain trigger certain brainstem neurons to fire, which alters cerebral function and blood flow. The nausea, neurologic deficits, and head pain result from low brain serotonin levels, aggravated by concomitant vascular changes.

What is the best treatment for a migraine headache?
For symptomatic relief from mild to moderate migraines, simple analgesics or NSAIDs such as aspirin or naproxen may be sufficient. For more severe attacks, triptans are the drugs of choice. Sumatriptan, a 5-hydroxytryptamine receptor agonist, was the first triptan to be used, but multiple other triptans are now available in various routes of administration. Patients should be warned of the flushing, sweating, and chest tightness that can occur as side effects.

When is prophylactic therapy indicated for migraine headaches?
For patients having frequent headaches (2-3/month or more) or for the occasional patient whose headache is complicated by persistent neurologic deficits, prophylactic treatment may be indicated.

Which drugs may be used for prophylaxis of migraine headaches?

• Amitriptyline, a tricyclic compound. Doses of 100 mg/day or more may be necessary. Many other tricyclics are not effective.
• Propranolol, a beta-adrenergic blocking agent. Again, doses of 100 mg/day or more may be needed. Most other beta-adrenergic blockers are not effective.
• Calcium channel blockers. Both nifedipine and verapamil are useful.
• Anticonvulsants, especially valproic acid, are sometimes effective.

Describe the clinical features of tension headaches.
Tension headaches are diffuse headaches, often described as a band around the head, usually bifrontal but sometimes occipital. Unlike migraine, these headaches are usually not paroxysmal but are constant and chronic. Like migraine, they are more common in women and generally begin early in life. About half of the patients have a family history. Usually, there are no associated neurologic symptoms (such as visual changes) or nausea and vomiting.

What causes tension headaches?
The cause is not known. There is no convincing evidence that they are due to psychological factors or emotional stress, nor do sound data show that they are related to muscle contraction. Some of them may be transformed migraines.

How should tension headaches be treated?
Amitriptyline, up to 75-150 mg/day, works independently of its antidepressant effects. NSAIDs are useful for common headaches but are seldom successful in chronic persistent tension headache. Muscle relaxants are not effective.

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

1. Ferrari MD: Migraine. Lancet 351:1051-1093, 1998.
2. Aminoff M: Neurology and General Medicine, 3rd ed. Philadelphia, Churchill-Livingstone, 2001.
3. Noseworthy JH (ed): Neurologic Therapeutics. London, Martin Dunitz, 2003.
4. Bradley WG, Daroff RB, Fenichel GM, Jankovic J: Neurology in Clinical Practice, 4th ed. Philadelphia, Butterworth-Heinemann, 2004.
5. Caplan LR: Stroke: A Clinical Approach, 3rd ed. New York, Butterworth-Heinemann, 2000.
6. Samuels MA, Feske S (eds): Office Practice of Neurology, 2nd ed. Boston, Churchill-Livingstone, 2003.
7. Johnson RT, Griffin JW: Current Therapy in Neurologic Disease, 6th ed. St. Louis, Mosby, 2002.
8. Victor M, Ropper AH: Prinicples of Neurology, 7th ed. New York, McGraw-Hill, 2001.

List the four cardinal features of Parkinson’s disease.

• Tremor
• Rigidity
• Bradykinesia (slowness of movement)
• Postural instability

Describe the tremor of Parkinson’s disease.
The tremor is usually a to-and-fro, pronation-supination, resting tremor that diminishes with voluntary movement. It is coarse and slow and most prominent in the hands and head.

Describe the rigidity of Parkinson’s disease.
The rigidity is associated with a diffuse increase in muscular tone and sometimes a “cog-wheeling” property to the joints when passively moved.

How does bradykinesia manifest in Parkinson’s disease?
Patients exhibit a paucity or lack of movement and tend to show minimal axial expression. They often sit quite immobile, almost like statues.

What is the differential diagnosis of Parkinson’s disease?
A few conditions can cause parkinsonism, a symptom complex that mimics idiopathic Parkinson’s disease. The most common examples are the neuroleptic drugs. Similar symptoms also can be mimicked by multiple strokes, hydrocephalus, and degenerative conditions such as Alzheimer’s disease.

How is Parkinson’s disease treated?
The best treatment is a combination of levodopa plus carbidopa (Sinemet). The main cause for the symptoms of Parkinson’s disease is a deficiency of dopamine within the pathway running from the substantia nigra to the basal ganglia. Since dopamine cannot be given directly (because it does not cross the blood-brain barrier), it is given as levodopa. Other dopamine agonists are sometimes used to supplement Sinemet. Anticholinergic agents, which suppress the overactive cholinergic system and bring it into balance with the diminished dopamine system, can also alleviate symptoms.

What are the important types of tremors other than the resting tremor of Parkinson’s disease?
Essential tremor. This rapid, fine tremor involving the head and arms becomes more noticeable with sustained postures or intentional movement. A family history, with an autosomal dominant inheritance, is seen in about half the cases. Treatment may include a beta blocker (propranolol, 80 mg/day) or primidone (starting at 50 mg/day).
Cerebellar tremor. Damage to the cerebellum disturbs motor control by causing a tremor. The tremor is absent at rest and appears only with intentional or voluntary movements. It is a slow, coarse, dyssynergic tremor. Other evidence of cerebellar dysfunction may be present. Pharmacologic treatment is generally unsatisfactory.

What are dystonias?
Dystonias, as the name suggests, are disorders of muscle tone that result in involuntary, sustained muscle contractions. They can lead to abnormal posturing or unique repetitive movements. Examples include spasmodic torticollis, blepharospasm, and oromandibular dystonia.

How are dystonias treated?
Relief can often be obtained by injecting the muscles with botulinum toxin (Botox).

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

1. Lambert D, Waters CH: Essential tremor. Curr Treat Options Neurol 1: 6-13, 1999.
2. Aminoff M: Neurology and General Medicine, 3rd ed. Philadelphia, Churchill-Livingstone, 2001.
3. Noseworthy JH (ed): Neurologic Therapeutics. London, Martin Dunitz, 2003.
4. Bradley WG, Daroff RB, Fenichel GM, Jankovic J: Neurology in Clinical Practice, 4th ed. Philadelphia, Butterworth-Heinemann, 2004.
5. Caplan LR: Stroke: A Clinical Approach, 3rd ed. New York, Butterworth-Heinemann, 2000.
6. Samuels MA, Feske S (eds): Office Practice of Neurology, 2nd ed. Boston, Churchill-Livingstone, 2003.
7. Johnson RT, Griffin JW: Current Therapy in Neurologic Disease, 6th ed. St. Louis, Mosby, 2002.
8. Victor M, Ropper AH: Prinicples of Neurology, 7th ed. New York, McGraw-Hill, 2001.

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

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