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Neurology

NEUROLOGY
Alzheimers Disease
Cerebrovascular Diseases
Depression
Approach to the Patient with Dizziness and Vertigo
Approach to the Patient with Headache
Approach to the Patient with Impairment of Consciousness
Multiple Sclerosis
Parkinson’s Disease
Approach to Disorders of the Peripheral Nervous System
Approach to the Patient with Seizures
Approach to the Elderly Patient with Acute Change in Mental Status
Approach to the Elderly Patient with Urinary Incontinence

ALZHEIMER’S DISEASE
DEFINITION
Dementia is a progressive decline in intellectual function and clear consciousness. Alzheimer’s disease (AD), the most common cause, is a heterogeneous neurodegenerative illness that produces progressive memory loss, changes in behavior and personality, psychotic symptoms, and impairments in insight, judgment, and executive abilities.
DIFFERENTIAL DIAGNOSIS
Late-life dementia can be caused by conditions other than AD, including ischemic vascular dementia, Parkinson dementia, Pick’s disease, frontotemporal dementia, and dementia with Lewy bodies.
EPIDEMIOLOGY, ETIOLOGY, AND PATHOPHYSIOLOGY
The prevalence of AD is about 3% among persons between 65 and 74 years of age. This figure climbs to 47% among persons older than 85 years. The pathologic features of AD are extensive neuron loss, numerous amyloid plaques, and abundant neurofibrillary tangles in vulnerable regions of the brain. Risk factors include age, the presence of an ApoE e4 allele, female sex, a history of head trauma, and having a first-degree relative with AD-like dementia. A small number of patients have an autosomal dominant form of AD.
CLINICAL FEATURES AND DIAGNOSIS
AD is characterized by the insidious onset of memory failure. Symptoms most commonly begin between the ages of 70 and 85 years but can occur as early as 40 years of age and as late as 90 years. During the first several years, patients may have difficulty with problem solving and word finding. They often have subtle personality and behavioral changes. As they withdraw from social situations, they may have symptoms that mimic mild depression. Although they may be aware that their memory is failing, persons with AD usually do not appreciate the extent of the problem. It is almost always a family member who brings the patient to medical attention.
A key diagnostic feature is documentation of memory loss as the earliest manifestation of the illness. Elements that strengthen the diagnosis include a family history of similar late-life dementia, normal results of routine blood studies (including those for thyroid disease and vitamin B12 deficiency), the presence of one or more ApoE e4 alleles, an elevated cerebrospinal fluid t level, and magnetic resonance images that is either normal for age or shows mild generalized cortical atrophy. Findings that cast doubt on the diagnosis include the following: parkinsonism (slow gait, decreased arm swing, en bloc turning), early prominence of language impairment or confusion, symptoms or signs of frontal lobe involvement (disinhibition, perseveration, delusions, or hallucinations) within the first several years, the finding of any focal neurologic signs at examination, and seizures or myoclonus early in the course.
Diagnostic criteria are used to place patients into one of three categories—definite AD, probable AD, and possible AD. A diagnosis of probable AD requires (a) dementia with onset between 40 and 90 years of age, (b) cognitive deficits in two or more areas, (c) progressive memory and cognitive deterioration, (d) no other illness that could account for the dementia, and (e) no disturbance of consciousness. A definite diagnosis requires neuropathologic examination and the clinical criteria for probable AD.
PROGNOSIS AND MANAGEMENT
AD lasts 6 to 12 years on average. There are several components of treatment. First is education of the primary caregiver about the illness, the need for long-range planning, and how to maintain an appropriate living environment. Donepezil has become the standard symptomatic treatment. Its benefits are modest and do not occur for all patients. High-dose vitamin E (a-tocopherol) has been adopted as the standard disease-slowing treatment. Therapy for the behavioral, psychotic, and mood changes is accomplished through the gentle and short-term use of psychotropic, anti-anxiety, and hypnotic medications.
Chapter 466
CEREBROVASCULAR DISEASES
DEFINITIONS
Ischemic cerebrovascular events may be divided into three categories. Transient ischemic attacks (TIAs) are ischemic episodes of focal cerebral dysfunction that last less than 24 hours, usually only a few minutes, and are followed by complete recovery. Modern imaging techniques can depict evidence of cerebral infarction in a high percentage of cases. Therefore, TIAs, especially those of long duration, are best considered small strokes with transient signs and symptoms. Stroke in evolution describes signs and symptoms that worsen while the patient is being observed. Completed stroke denotes a relatively stable neurologic deficit caused by cerebral infarction. Lacunar infarctions are subcortical strokes almost always associated with hypertension.
ETIOLOGY AND PATHOPHYSIOLOGY
Transient ischemic attacks: The cause usually can be limited to one of three broad categories—vascular, cardiologic, or hematologic. The most common mechanism is probably platelet embolization from atherosclerotic extracranial or intracranial cerebral arteries.
Ischemic cerebral infarction: The cause is a reduction in blood flow below the level necessary to maintain tissue viability. Atherosclerotic disease of large arteries is the main cause and can trigger stroke either through occlusion at the site of atherosclerosis (thrombotic stroke) or through embolization to the cerebral vasculature (embolic stroke). Hypertension is the most important risk factor. Others include diabetes mellitus, hyperlipidemia, smoking, family history of vascular disease, and use of oral contraceptives. The extent of infarction is determined by the effectiveness of collateral circulation, possible vasospasm, development of brain edema, hemorrhage from damaged arterioles, and systemic factors such as hyperglycemia and hyperviscosity.
Hypertensive vascular syndromes: Lacunar infarction and hypertensive hemorrhage are caused by hypertensive damage to small arteries deep in the brain. If cases of trauma and ruptured saccular aneurysm or arteriovenous malformation are excluded, the classic type of intracerebral hemorrhage is almost always caused by hypertension.
CLINICAL FEATURES
Transient ischemic attacks: The most common presentation in the carotid artery territory is sudden onset of weakness, paralysis, or clumsiness in one or both extremities on the same side. Sensory symptoms also may be present. If the TIA involves the hemisphere dominant for language function, dysphasia is present. A transient loss of vision in one eye or part of one visual field may occur. In vertebrobasilar TIAs, the most common symptom is a motor defect such as weakness, clumsiness, or paralysis of any combination of extremities with or without sensory changes. The patient may have an unsteady gait, dysequilibrium, and vertigo. Diplopia or loss of vision (varying from complete blindness to partial blindness in homonymous fields) may occur.
The differential diagnosis includes classic migraine with scotoma, hemiplegic migraine, focal convulsive events, Ménière’s disease, and peripheral vestibulopathy. Unlike TIAs, migrainous phenomena generally worsen gradually over several minutes. Headache may accompany TIAs but is generally brief and not severe. Focal seizures generally progress from the distal to the proximal portions of an extremity and may produce persistent neurologic deficits. Isolated vertigo without other motor and sensory symptoms rarely can be attributed to a TIA.
Ischemic cerebral infarction:
Middle cerebral artery: Infarction of the cortex supplied by the superior and inferior divisions of the middle cerebral artery causes contralateral hemiplegia (involving the face, hand, and arm, but sparing the leg), hemisensory deficit, homonymous hemianopsia, and if the dominant hemisphere is affected, both expressive and receptive aphasia. Occlusion of the superior division of the middle cerebral artery produces greater weakness and sensory loss in the face and arm than in the leg, with no visual field defect. If the dominant hemisphere is involved, expressive (Broca’s) aphasia is present with impaired speaking, naming, and writing ability but relative preservation of comprehension. With occlusion of the inferior division, contralateral sensory loss predominates, and weakness may be minimal or absent. If the dominant hemisphere is involved, receptive (Wernicke’s) aphasia is present with impaired comprehension and fluent speech output with jargon and paraphrasia.
Anterior and posterior cerebral arteries: Involvement of the former produces weakness, clumsiness, and sensory loss affecting mainly the contralateral leg and foot. Occlusion of the latter causes contralateral homonymous hemianopsia and may cause transient disturbance of memory due to infarction of the medial temporal lobe.
Basilar artery: Emboli tend to affect the distal portion, whereas atheromatous occlusion affects the proximal and middle portions. Distal vessel effects include loss of consciousness, unilateral or bilateral palsies of the third cranial nerve, and hemiplegia or quadriplegia with decerebrate or decorticate posturing. Consequences of occlusion of the proximal and middle segments include hemiplegia or quadriplegia and unilateral damage to the sixth cranial nerve or nucleus that causes impairment of horizontal eye movement.
Vertebral artery: Unilateral occlusion causes severe vertigo, nausea and vomiting, nystagmus, and loss of pain and temperature sensation in the ipsilateral face. Damage to the inferior cerebellar peduncle causes ipsilateral ataxia and Horner’s syndrome and loss of pain and temperature sensation in the contralateral part of the body. Damage to the ninth and tenth cranial nerves causes hiccups and dysphagia.
Cerebellar infarction: Manifestations include difficulty standing and walking, headache, nausea, vomiting, dizziness, clumsiness, and slurred speech. With progression, most patients have lateral gaze palsy, nystagmus toward the side of the lesion, facial palsy, impaired cognitive function, or depressed consciousness.
Hypertensive vascular syndromes: Lacunar infarctions are the most common cerebrovascular lesions and occur most frequently in the deep nuclei of the brain, the pons, and the posterior limb of the internal capsule. Many are not recognized clinically. The onset usually is gradual, developing over several hours or days. Headache and alterations in consciousness are absent. The four major syndromes are (a) pure motor hemiparesis, with weakness of the face, arm, and leg but no associated sensory, visual or cortical deficits; (b) pure sensory stroke of the face, arm, and leg; (c) homolateral ataxia and crural (distal leg) paresis characterized by weakness of one leg, especially the toes and ankle, with Babinski’s sign and striking incoordination of the ipsilateral arm and leg; and (d) lacunar state, a syndrome in which lability of affect, dementia, small-stepped rigid gait, dysarthria, incontinence, and bilateral long-tract signs are present.
Hypertensive hemorrhage most often occurs among persons older than 50 years. It occurs without warning while the patient is awake and often during exertion. Headache may be severe but is absent or trivial in one-half of cases. Vomiting is common; in thrombotic or embolic strokes it is rare. Blood pressure almost always remains elevated after onset. Once hemorrhage has occurred, the patient’s condition worsens steadily over a period of minutes to days until the neurologic deficit stabilizes or the patient dies. Because much of the deficit is caused by compression rather than destruction, return of function as swelling subsides can be dramatic. Pontine hemorrhage produces coma, pinpoint pupils, impaired horizontal eye movements, quadriparesis, and hyperthermia. Deep cerebral hemorrhage occurs most commonly in the putamen and thalamus. The motor deficit is more severe in the former and the sensory defect more prominent in the latter. Either may be associated with aphasia if there is pressure on cortical speech areas. Cerebellar hemorrhage is sudden without loss of consciousness. Within several minutes, the patient cannot stand or walk and must vomit repeatedly. Headache and dizziness occur in about 50% of cases. Almost 90% of patients become comatose within 24 hours.
ANCILLARY STUDIES AND DIAGNOSTIC TESTS
Transient ischemic attacks: The evaluation is directed at detection of vascular disease. Risk factor assessment should be performed (see earlier). Abnormalities in the vascular system can be detected noninvasively with Doppler ultrasonography or magnetic resonance angiography, although cerebral angiography remains the most definitive test. Transesophageal echocardiography can help identify intracardiac thrombus or lesions such as patent foramen ovale. Testing for hypercoagulable states (such as factor V Leiden and deficiencies of protein C, protein S, and antithrombin III) may be indicated.
Ischemic cerebral infarction: The evaluation is similar to that described earlier. Computed tomography (CT) or magnetic resonance imaging (MRI) of the brain should be performed as soon as possible to rule out cerebral hemorrhage and tumor. In many instances, the CT findings are normal even when the patient has a severe clinical deficit. For these patients, immediate MRI or additional CT performed within 24 to 48 hours will reveal the area of infarction. Cerebral arteriography is not needed unless vasculitis or a cerebral aneurysm is suspected. Ultrasound evaluation of the cervical and intracranial vessels may be used to define the site of occlusion. In patients without evidence of atherosclerotic disease of the cervical carotid arteries, a thorough search should be made for a cardiac source of emboli.
Hypertensive vascular syndromes: Associated hypertension is present. The diagnosis is made clinically and with imaging studies.
MANAGEMENT
Transient ischemic attacks: Risk factor modification is mandatory. Studies of heparin or warfarin therapy have demonstrated little benefit except among patients with a hypercoagulable state or TIAs due to cardiac-origin emboli. Antiplatelet drugs such as aspirin (one to four 325-mg tablets daily) have been shown to reduce the incidence of TIAs and stroke. Clopidigrel or ticlopidine, antiplatelet agents more potent than aspirin, can be used to treat patients with recurrent TIAs taking aspirin who are not candidates for surgery. Carotid endarterectomy is the treatment of choice of patients with TIAs in the carotid distribution who have ipsilateral high-grade stenosis (greater than 60%) without complete occlusion.
Ischemic cerebral infarction: All patients with acute ischemic stroke who are seen within 3 hours of the time of symptom onset and have no evidence of hemorrhage on CT should be evaluated for treatment with tissue plasminogen activator, a thrombolytic agent. In a recent trial, thrombolytic therapy under these circumstances produced a 12% increase in the number of patients with a good clinical outcome 3 months after the stroke but also resulted in a 6% incidence of cerebral hemorrhage, almost one-half of them fatal. Anticoagulation with heparin may be used to treat patients with acute ischemic cardioembolic strokes. Its use to manage ischemic strokes is controversial owing to the increased risk of intracranial hemorrhage. The mainstay of treatment is good nursing care to prevent pneumonia and deep venous thrombosis in paralyzed or paretic limbs. Medical care is focused on the judicious management of hypertension, arrhythmias, and cardiac failure. Seizures, if present, should be controlled to prevent further cerebral damage.
There is extreme variation in outcome from stroke. The overall mortality rate is about 25% in the first month and approaches 50% at 5 years. Neurologic complications account for most deaths in the first week; later deaths usually are caused by heart disease and intercurrent infection. Most patients show some improvement after 14 to 21 days when the cerebral edema of infarction has resolved. In general, 50% of the potential recovery is attained 1 month from onset, 75% at 3 months, 90% at 6 months, and 100% at 1 year. Rehabilitation should begin early (days after onset).
Hypertensive vascular syndromes: Lacunar stroke syndromes are self-limited and relatively benign. Anticoagulation is not needed and may actually be dangerous because lacunar infarction often is associated with microhemorrhages. The prognosis for almost complete recovery is good; the likelihood of future lacunar strokes is reduced with adequate control of blood pressure. Cerebellar hematoma is managed by means of early surgical decompression, which may be life saving and often leads to complete reversal of the neurologic deficits. Surgery is not indicated for pontine or deep cerebral hypertensive hemorrhage, unless a large superficial hemorrhage has caused midline shift and herniation. There is no effective medical treatment. Glucocorticoids and dehydrating agents have given only temporary benefit. Attempts to lower blood pressure may compromise cerebral blood flow, but continued hypertension may cause cerebral edema. It seems reasonable to lower blood pressure carefully to normal levels with initial small doses of the less potent antihypertensive agents.
Chapter 432
DEPRESSION
DEFINITION
Depression is an affective syndrome occurring in unipolar or bipolar forms.
EPIDEMIOLOGY
The incidence of depression is 1% among men and 3% among women. The age at first episode of major depression has steadily decreased, with the mean age now 40 years for both sexes. Concomitant psychiatric conditions are common, including anxiety disorders and alcohol and substance abuse.
ETIOLOGY AND PATHOPHYSIOLOGY
Depression is two to three times more frequent among first-degree relatives of patients with depression. No cause of the disorder is known. Theories include (a) excessive activity of the hypothalamic-pituitary-adrenal axis; (b) disturbed functioning of catecholamines; (c) sleep and circadian rhythm disruptions; and (d) left frontal hypometabolism.
CLINICAL FEATURES AND DIAGNOSIS
Major depression is characterized by at least 2 weeks of a sad mood or loss of interest. The patient also must have four of the following symptoms (remembered with the mnemonic SIG E CAPS): sleep disturbance (usually early morning awakening); loss of interest; guilt or worthlessness; energy loss; impairment of concentration; change in appetite, usually a decrease; psychomotor agitation or retardation; suicidal or death wishes. Depressed patients may report irritability, deny sadness, or have vague somatic symptoms. No laboratory tests exist to confirm the diagnosis.
Major depression can be subcategorized as (a) atypical with hypersomnia, appetite increase, and hypersensitivity to rejection; (b) with psychosis (presence of auditory hallucinations and delusions); (c) postpartum, occurring within 4 weeks of delivery; and (d) pseudodementia (abrupt cognitive decline associated with depressive symptoms, primarily among the elderly). Dysthymic disorder is similar to major depression but the symptoms are less severe and are intermitently present for 2 or more years. In adjustment disorder, symptoms of depression or anxiety develop after exposure to an identifiable precipitating stressor. These symptoms typically disappear when the stressor is gone. Seasonal affective disorder is characterized by development of depressive symptoms (often the atypical symptoms described earlier) in fall or winter and a return to baseline in spring and summer. Bipolar disorder is characterized by one or more manic episodes, which consist of an elevated, expansive, or irritable mood and three of four of the following: grandiosity, decreases in sleep, excessive talking, racing thoughts, distractibility, and excessive involvement in pleasurable activities that have high potential for negative consequences, such as spending sprees.
PROGNOSIS AND MANAGEMENT
Suicide risk must be assessed for each patient. As many as 15% of depressed patients die by suicide. Women are three to four times more likely to make an attempt, but men are three times more likely to be successful. Suicide risk factors include psychosis, absence of social support, chronic medical illness, substance abuse, particularly of alcohol, and an organized plan with little chance of rescue.
Various antidepressants are equally effective, response rates averaging 70%. Patients must be informed that antidepressants are not immediately effective and must be taken daily for at least 2 to 3 weeks before symptoms improve. Drug selection is based on side effect profile and potential drug-drug interactions. Selective serotonin reuptake inhibitors are currently the best initial choice for most patients. The starting dose for fluoxetine or paroxetine is 20 mg per day (maximum 40 mg per day) and for sertraline is 50 mg per day (maximum 200 mg per day).
For patients was have not responded to maximum dosages after 4 to 6 weeks, treatment alternatives include a change to a different agent (e.g., a tricyclic agent such as desipramine or nortriptyline or an agent such as bupropion or venlafaxine), augmentation with lithium or thyroid hormone, consultation with a psychiatrist, or electroconvulsive therapy (ECT). ECT is the most effective therapy for major depression. Once a patient’s symptoms have responded, anti-depressants should be continued for 4 to 9 months at the same dose. Maintenance treatment for several years or longer is indicated for patients with age at onset younger than 20 years and a family history of bipolar disease, two previous severe episodes with early recurrence, or three or more previous episodes. Patients with bipolar disease can be treated with lithium, sodium valproate, and carbamazepine. Monotherapy with antidepressants may cause a conversion to mania.
Chapter 39
APPROACH TO THE PATIENT WITH DIZZINESS AND VERTIGO
PRESENTATION AND PATHOPHYSIOLOGY
“Dizziness” encompanses a variety of symptoms. A feeling of light-headedness or impending fainting may suggest hypotension and a cardiovascular cause. Vertigo is an illusion of motion of self or of the environment. Patients may describe sensations of spinning or tumbling. Vertigo is caused by an acute imbalance in the vestibular inputs from the two labyrinths or in their central connections. Patients with symmetric vestibular lesions (e.g., aminoglycoside toxicity) and those with a slowly developing unilateral lesion (e.g., schwannoma) may not have vertigo. Dysequilibrium is a feeling of imbalance while standing or walking. It may occur among patients with sensory deficits (e.g., blurred vision or bilateral vestibular less), cerebellar disease, or efferent motor disorders such as Parkinson’s disease or stroke. Dizziness that cannot be further characterized often accompanies anxiety, phobias, and panic attacks.
HISTORY AND PHYSICAL EXAMINATION OF A PATIENT WITH THE VERTIGO
The first issue is whether symptoms are acute or chronic and whether they have occurred more than once. If vertigo is episodic, the duration of episodes is important. Brief (less than 1 minute) episodes of vertigo precipitated by a change in the attitude of the head with respect to gravity are typical of benign paroxysmal positional vertigo (BPPV). Vertigo lasting for several minutes up to an hour suggests transient ischemic attacks (TIAs). Longer episodes can be caused by migraine, Ménière’s disease, labyrinthitis, or central nervous system infarction. Associated hearing lose, tinnitus, or ear fullness suggests a peripheral vestibular cause, whereas symptoms of brain stem or cerebellar dysfunction implicate a central cause. In general, symptoms provoked by head movements or changes in head position with respect to gravity are the hallmark of a disturbance in the peripheral vestibular system.
A complete neurologic examination must be performed with particular attention to eye movements (nystagmus), hearing, other cranial nerves, coordination, gait, and balance. The eyes must be examined in the absence of visual fixation, which may suppress spontaneous nystagmus. This may be done either with Frenzel lenses or by looking for movement of the optic disc during direct ophthalmoscopy with the opposite eye occluded. Positioning maneuvers may help identify BPPV.
DIAGNOSTIC TESTS
Every patient with vestibular symptoms should undergo an audiogram. Low-frequency hearing loss is characteristic of Ménière’s disease. Unilateral hearing loss raises the possibility of a tumor involving the vestibulocochlear nerve, such as vestibular schwannoma. Magnetic resonance imaging of the posterior fossa should be ordered whenever symptoms or signs suggest a brain stem or cerebellar lesion. Patients believed to have TIAs should undergo magnetic resonance angiography of the head and neck and additional evaluation for stroke as indicated. Specific vestibular tests, including electronystagmography with caloric or rotatory chair testing and posturography, are helpful to a minority of patients.
SELECTED DISORDERS
BPPV is the most common cause of recurrent vertigo. It occurs when calcium carbonate crystals are released from the otolithic membranes and aggregate in a semicircular canal (usually the posterior canal). Many patients can identify a preceding event, such as an episode of labyrinthitis, trauma, or a prolonged period of having the head back. Symptoms are produced when a change in head position, such as looking up or rolling over in bed, causes the debris to move. The resultant shift of endolymph produces vertigo. Symptoms are usually worse in the morning. BPPV is diagnosed with the Dix-Hallpike maneuver. With the head turned 45 degrees to one side, the patient is moved rapidly from a seated to a supine position with the head hanging down. After a latency of several seconds, the patient experiences vertigo and nystagmus; the upper poles of the eyes beat toward the affected (down) ear. Fatiguing of nystagmus occurs with repeated maneuvers. BPPV is managed with a particle repositioning maneuver.
Vestibular migraine is a common cause of recurrent vertigo. Treatment consists of the usual migraine prophylactic agents. Ménière’s disease is attributed to endolymphatic hydrops, which increases pressure in the inner ear. Attacks may be difficult to differentiate from vestibular migraine, but characteristic additional features include aural fullness, fluctuating hearing loss in the affected ear, and a low-pitched tinnitus. Evaluation should include screening for syphilis and autoimmune disorders. Treatment is aimed at reducing hydrops and includes a low sodium diet and diuretics. Vestibular suppressants may be helpful during an attack. Refractory cases can be managed with surgical labyrinthectomy.
Labyrinthitis and vestibular neuritis often are attributed to viral infection of the vestibular nerve or labyrinth. Severe vertigo, nausea, and vomiting appear suddenly and improve over several days. Central compensatory mechanisms produce further improvement over several weeks to months. Important differential diagnoses are labyrinthine and cerebellar infarction or hemorrhage. Treatment includes vestibular suppressants and antiemetics.
MANAGEMENT
In general, treatment is directed at the specific diagnosis, described earlier. Vestibular suppressant and antiemetic medications, such as diazepam, lorazepam, promethazine, and meclizine, can be useful in the initial phase of an acute vestibular syndrome (e.g., labyrinthitis) and in the management of recurrent attacks of vertigo that last at least several hours. Brief episodes of vertigo, such as those that occur with BPPV, are not amenable to such treatment. Chronic prophylactic vestibular suppression may be appropriate when attacks are frequent; however, prolonged use after an acute vestibular lesion may impede central adaptation and should be avoided. Vestibular rehabilitation may be beneficial in the management of both acute and chronic vestibular disorders.
Chapter 422
APPROACH TO THE PATIENT WITH HEADACHE
PATHOPHYSIOLOGY
Receptors responsible for pain registration are present in the proximal parts of the cerebral and dural arteries, the large veins and venous sinuses, and the extracranial arteries. Distention or displacement of these vessels by inflammation, an aneurysm, a hematoma, a tumor, or ventricular dilatation from obstruction of cerebrospinal pathways causes headache. Migraine and cluster headaches are accompanied by vascular dilatation that contributes to the headache. Pain also may be caused by irritation of the meninges, cranial nerves, or occipital nerves. Some forms of tension headache are associated with overcontraction of muscles.
DIFFERENTIAL DIAGNOSIS
See also History and Physical Examination.
Migraine: Migraine is an episodic cerebral disturbance (aura), headache, or both with intervening periods of relative freedom from headache and without evidence of primary structural abnormality. The headache is usually severe, unilateral, and associated with nausea, vomiting, and photophobia. About one-third of patients have some attacks in which an aura (visual changes, paresthesia, or speech disturbance) precedes the headache by 5 to 60 minutes. Migraine is common (20% of women of reproductive age), and women are affected twice as often as men. Many patients can identify triggers such as noise, perfume, stress, relaxation after stress, particular foods, ingestion of alcohol or other vasodilators, physical exertion, or menses.
Cluster headache: Cluster headache has a prevalence about 3% of that of migraine and tends to recur in bouts or clusters that last weeks or months and are separated by months or years of freedom. During a bout, patients (85% of whom are men) each day or night have one or more attacks of severe pain in and around the eye or adjacent areas of the head and face; these attacks last from 10 minutes to hours at a time. The ipsilateral eye usually becomes red and waters; there is ipsilateral nasal congestion or rhinorrhea. Ocular Horner’s syndrome may be present.
Tension headache: This term is applied to the sensation of tightness around the head or pressure at the top of the head that may recur daily in its chronic form. It affects women more commonly than men and may start at any age.
Pain arising from extracranial structures: Temporal arteritis occurs among women more than men and primarily affects persons older than 50 years. It is an immune disorder of the arterial wall associated with a giant cell arteritis. The scalp arteries are most commonly involved but involvement of the ophthalmic arteries may produce sudden blindness. There is an association with polymyalgia rheumatica. The diagnosis is supported when the erythrocyte sedimentation rate (ESR) is greater than 40 mm per hour. Results of temporal artery biopsy confirm the diagnosis; treatment with glucocorticoids should be started before the biopsy if suspicion is high, in order to minimize the risk of blindness. Other extracranial disorders include acute angle-closure glaucoma, sinusitis, dental infection, temporomandibular joint syndrome, occipital neuralgia, and disorders of the cervical spine affecting the C2 and C3 nerve roots.
Pain arising from the cranial nerves: Headache can be caused by excessive stimulation of peripheral branches of the first division of the trigeminal nerve by exposure to cold air, food, or drinks. Herpes zoster or trigeminal neuralgia also cause pain in the distribution of the trigeminal nerve, commonly the first division.
Pain of intracranial origin: Headache is a symptom of many intracranial and systemic disorders and can be caused by meningeal irritation or displacement or dilatation of pain-sensitive blood vessels. Investigation determines whether the patient needs neurosurgical or medical management. Benign intracranial hypertension (pseudotumor cerebri) is chiefly a disorder of overweight young women with menstrual abnormalities. They have symptoms and signs of raised intracranial pressure (headache, vomiting, transient obscuring of vision, and papilledema) with no obvious systemic or local cause. Computed tomography demonstrates small ventricles, and results of lumbar puncture confirm the elevation in cerebrospinal fluid (CSF) pressure.
HISTORY AND PHYSICAL EXAMINATION
Acute headache may be accompanied by neck rigidity when there is meningeal irritation and by elevated temperature when there is systemic infection or meningitis. Aggravation of the headache by jarring, coughing, sneezing, or bending forward suggests an intracranial origin. Drowsiness, changes in mental status, seizures, or any neurologic deficits also increase the likelihood of intracranial abnormality.

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