Historical Evaluation of Key Signs and Symptoms
A detailed history is the most important part of the evaluation of a patient with cerebrovascular disease. Initial attention should be directed toward identifying and characterizing (1) the patient’s chief complaints or main symptoms; (2) the time of onset and possible precipitating events; (3) the features of the circumstance of onset, including the patient’s activities, the temporal profile of the onset of symptoms, and the rapidity with which the maximal deficit developed (a typical vascular profile involves sudden onset with rapid progression to maximal deficit with all of the affected areas of the body involved from the onset); (4) the presence of focal or generalized neurologic deficit at the onset or alterations of level of consciousness at onset; (5) the presence of headache, vomiting, or seizure activity (focal or generalized); and (6) the chronologic course of neurologic symptoms after onset.
Frequently, the patient may not remember the precise details of the early temporal course and other important historical details. In this case, family members are often the best source of information. The patient should be asked what is specifically meant by certain words that are used to describe symptoms (e.g., “ dizziness,” “headache,” and “poor vision”) because these terms have a wide range of different meanings with different implications for diagnosis and management.
This chapter describes several symptoms that are particularly pertinent to patients with cerebrovascular disorders and addresses their application to the diagnosis of these conditions.
HEADACHE
Sudden severe headache that is described by the patient as “like being hit over the head by a hammer” (or some similar description) is suggestive of subarachnoid hemorrhage. This headache is usually associated with neck stiffness (meningismus) and may be localized to the posterior neck. However, as many as 30% of all subarachnoid hemorrhages present atypically, and a minor subarachnoid hemorrhage, especially in elderly individuals, may not present with severe headache, stiff neck, or catastrophic onset. In these cases, any element of abruptness in a new character of headache should always raise the possibility of subarachnoid or other intracranial hemorrhage.
Localized headache associated with slowly progressive focal neurologic deficit may occur with growing intracranial arteriovenous malformations (which may produce pulsatile tinnitus with or without cranial bruit) or aneurysms. Aneurysms of the internal carotid artery (intracavernous part or near the petrous apex) may produce facial or retro-orbital pain. Aneurysms of the middle cerebral artery (lateral fissure) are sometimes associated with retro-orbital
pain, aneurysms of the posterior cerebral artery are associated with retro-orbital or occipital pain, and aneurysms of the basilar artery may cause hemifacial pain.
pain, aneurysms of the posterior cerebral artery are associated with retro-orbital or occipital pain, and aneurysms of the basilar artery may cause hemifacial pain.
The headache of intracerebral hemorrhage is usually sudden in onset and often associated with a progressive focal neurologic deficit, vomiting, and altered consciousness.
Patients with cerebral infarction uncommonly (20%) have headache at the onset of the episode (more commonly with embolic etiology). Occasionally, a patient with a large cerebral infarction may experience headache (caused by cerebral edema) beginning up to a few days after the onset of stroke. However, this type of headache is usually temporary; more severe or persistent headache warrants further investigation for other underlying causes, such as tumor, abscess, vasculitis, or hemorrhagic infarct. Although few headache syndromes in the setting of cerebral infarction provide aid in localization, a focal supraorbital headache associated with homonymous hemianopia may be caused by an embolus or a thrombosis in the posterior cerebral artery. Transient ischemic attack (TIA) seldom produces prominent headache.
Severe hypertension with diastolic blood pressures of more than 110 mm Hg may be associated with headache, but mild hypertension rarely causes headaches. Severe headache caused by abrupt increase in blood pressure may occur in patients with acute hypertensive encephalopathy (often associated with neurologic deficits resulting from cerebral edema, hemorrhage, or vasospasm).
Headache caused by chronic increased intracranial pressure, as occurs with cerebral tumor, is often present when the patient awakens in the morning and may be brought on with increased Valsalva maneuvers or lowering the head below the level of the heart. In contrast, almost any type of headache may be worsened by Valsalva maneuvers, lowering the head below the level of the heart, or excessive stress or tension.
Headache that is caused by venous circulatory dysfunction (e.g., intracranial venous sinus thrombosis) usually results from increased intracranial pressure and has a tendency to be present when the patient awakens and to be brought on or enhanced by Valsalva maneuvers, supine position, or lowering of the head below the level of the heart. Occasionally, these disorders are associated with central nervous system (CNS) infection and produce fever and headache as a result of meningeal irritation.
The headache of temporal (giant cell) arteritis is characterized by severe, persistent pain associated with enlarged, beaded, tender, erythematous, or pulseless temporal arteries and jaw claudication. Scalp tenderness is characteristic, and it is often difficult for patients to comb their hair. Other associated features include general malaise, polyarthralgias, polymyalgias, fever, and unilateral or bilateral loss of vision. This type of headache usually occurs in patients who are older than 55 years but has also been reported in patients in their 30s. The diagnosis is suggested by a high sedimentation rate (often >100 mm per hour) and confirmed by temporal artery biopsy. Corticosteroid treatment usually produces a dramatic and rapid improvement in headache.
Migraine headaches usually start in adolescence or early adulthood. There is often a positive family history. The headaches are intermittent, sometimes preceded by 15- to 30-minute prodromes such as scintillating scotomata, usually unilateral, throbbing, and associated with nausea, vomiting, or photophobia. The pain usually builds to a peak in less than 1 hour and persists for hours to 1 or 2 days and is exacerbated by noise and bright light. In some patients, the headaches are precipitated by stress; fasting; menses; and certain foods, such as alcohol, chocolate, cured meats, and monosodium glutamate (often used in Chinese food). Often, the headache is relieved with sleep.
Cluster headaches are characterized by recurrent, nocturnal, unilateral, usually retro-orbital searing pains that last 20 to 60 minutes and typically are accompanied by unilateral lacrimation and nasal and conjunctival congestion. These headaches normally occur in men who are older than 20 years and often include an ipsilateral Horner’s syndrome and rhinorrhea during the headache. Episodes are characteristically precipitated by alcohol.
Vascular headaches (Table 2-1) should be distinguished from nonvascular headaches, such as those associated with (1) cerebral trauma (subdural hematoma and posttraumatic headache); (2) infections or tumors of the CNS; (3) contraction, inflammation, or trauma related to cranial or cervical muscles (tension
and muscle contraction headache); (4) paranasal sinus disease; (5) glaucoma; (6) benign intracranial hypertension; and (7) nonspecific headaches related to use of various drugs (e.g., nitrates, indomethacin, or rebound headaches because of overuse of analgesics).
and muscle contraction headache); (4) paranasal sinus disease; (5) glaucoma; (6) benign intracranial hypertension; and (7) nonspecific headaches related to use of various drugs (e.g., nitrates, indomethacin, or rebound headaches because of overuse of analgesics).
TABLE 2-1 Classification of Headache | ||||||||||||||||||||||||||||||||||||||||
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Headache is a very common symptom of subacute (2-14 days) or chronic (>14 days) traumatic subdural hematoma. The headache often fluctuates in severity, with a deep-seated, steady, unilateral, or, less common, generalized presentation, often proceeding to involve alterations of consciousness and focal neurologic dysfunction. The diagnosis is established by computed tomography (CT) or magnetic resonance imaging (MRI) of the head. Posttraumatic headaches may be intermittent, continuous, or chronic (bilateral or, less commonly, unilateral) and are sometimes associated with light-headedness, vertigo, or tinnitus. Posttraumatic dysautonomic cephalalgia is characterized by severe, episodic, throbbing, unilateral headaches accompanied by ipsilateral mydriasis and excessive facial sweating.
Meningitis or encephalitis often produces intense, deep, constant, and increasing headache that is usually generalized and associated with stiff neck, Kernig and Brudzinski signs, and fever. The diagnosis is established by lumbar puncture. Subacute onset, persistent headache over a period of hours or days may also occur in systemic infections, such as influenza, without definite CNS involvement.
Headaches that are associated with brain tumors are usually unilateral and slowly progressive in frequency and severity and have a tendency to occur when the patient awakens in the morning. As the tumor grows, the pain is frequently associated with focal neurologic signs or signs of increased intracranial
pressure. As with other lesions that cause mass effect, the headaches may be brought on by bending over with the head downward or engaging in Valsalva maneuvers (coughing, sneezing, and straining to defecate).
pressure. As with other lesions that cause mass effect, the headaches may be brought on by bending over with the head downward or engaging in Valsalva maneuvers (coughing, sneezing, and straining to defecate).
Tension-type headache (muscle contraction headache) is usually steady; deep; generalized; bilateral; and occipital, frontal, or in a bandlike distribution around the head with associated tightness and tenderness of the neck muscles. It may persist unremittingly for days or weeks and is usually associated with excessive stress or tension, anxiety, insomnia, or depression.
Headache caused by paranasal sinus disease is usually localized over the affected sinuses, often with associated purulent nasal discharge and fever. The diagnosis is established by CT or MRI of the sinuses.
Headache of ocular origin (ocular muscle imbalance, hyperopia, astigmatism, impaired convergence/accommodation, narrow-angle glaucoma, and iridocyclitis) is usually located in the ipsilateral orbit, forehead, or temple and has a steady, aching quality that may follow prolonged, intensive use of the eyes for close work (with glaucoma, the pain is often associated with loss of vision). A careful description of the type of headache and a history of its onset, relationship to use of the eyes, duration, and associated symptoms often suggest the diagnosis, which is established from other eye signs. For example, long-lasting, mild-to-moderate headache that occurs toward the end of a day and is relieved by a few hours of rest or sleep is more likely to be related to an ocular disorder.
Benign intracranial hypertension usually produces intermittent mild or severe headache that may be brought on by Valsalva maneuvers or by bending with the head down and is associated with papilledema. Criteria for this diagnosis include evidence of increased intracranial pressure and absence of clinical or laboratory evidence of a focal brain lesion, an infection, or hydrocephalus.
Low cerebrospinal fluid pressure headache, sometimes called spinal headache (typically occurring after lumbar puncture), is usually generalized and characteristically worsens substantially when the person is sitting or standing. The headache is generally relieved entirely when the person lies down.
DIZZINESS
It is important to determine whether the patient is describing a sensation of self or environmental movement or spinning (i.e., vertigo), a sensation of light-headedness with or without visual graying or postural swaying (i.e., faintness or near-syncope), or something else (such as an unusual head sensation or gait unsteadiness).
Vertigo
Vertigo indicates dysfunction in the peripheral or central components of the vestibular system. Central vertigo results from disorders that affect brainstem or vestibulocerebellar pathways; peripheral vertigo indicates involvement either of the vestibular end organ (e.g., semicircular canals) or of their peripheral neurons, including the vestibular portion of the eighth cranial nerve. A method for categorizing the causes of vertigo is presented in Table 2-2.
Central vertigo is a common part of posterior circulation disturbances such as cerebellar or brainstem infarction, hemorrhage, or vertebrobasilar TIA. In the context of vascular disease, vertigo is almost always associated with other symptoms of brainstem or cerebellar dysfunction. Central vertigo may also be caused by neoplasms of the posterior fossa (often associated with headache or
gait or limb ataxia), demyelinating disease, arteriovenous malformation, brainstem encephalitis, and vertiginous epilepsy (tornado epilepsy) originating in the temporal lobe. Medications such as analgesics, antiarrhythmics, anticonvulsants, antibiotics, loop diuretics, and sedatives may also lead to vertigo.
gait or limb ataxia), demyelinating disease, arteriovenous malformation, brainstem encephalitis, and vertiginous epilepsy (tornado epilepsy) originating in the temporal lobe. Medications such as analgesics, antiarrhythmics, anticonvulsants, antibiotics, loop diuretics, and sedatives may also lead to vertigo.
TABLE 2-2 Causes of Vertigo | ||||||
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Peripheral vertigo may be caused by unilateral or bilateral labyrinthine dysfunction (infection, trauma, ischemia, or toxins), vestibular neuronitis, lesions of the cerebellopontine angle impinging on the eighth cranial nerve (such as acoustic neuroma), Ménière’s disease (recurrent attacks of vertigo associated with hearing loss, tinnitus, and a sensation of ear fullness, which may improve after the attack subsides), or benign positional vertigo (episodic vertigo occurring after changes of head position, which diminishes with repeated attempts to elicit vertigo with the same movement).
Positional vertigo that results from peripheral and central causes may be differentiated on the basis of clinical features, nystagmus characteristics, and findings with Nylen’s maneuver (Table 2-3). Nylen’s maneuver is performed by having the patient lie down abruptly from a sitting position and orient the head approximately 30 degrees below the horizontal plane. The test is repeated with the head positioned to the left, straight, and to the right, with observation for nystagmus and notation of any clinical symptoms.
Light-Headedness (Faintness)
Light-headedness is analogous to feelings that precede syncope (near-syncope) that is caused by generalized cerebral ischemia. True vertigo almost never occurs during the presyncopal state. Presyncopal, stereotyped faintness may be associated with visual graying, heaviness in the lower limbs, and postural swaying. The causes of light-headedness relate to generalized cerebral hypoperfusion and
include postural hypotension, orthostatic hypotension, decreased cardiac output (e.g., cardiac arrhythmias), anemia, or other vasovagal disorders.
include postural hypotension, orthostatic hypotension, decreased cardiac output (e.g., cardiac arrhythmias), anemia, or other vasovagal disorders.
TABLE 2-3 Differentiating Features of Peripheral and Central Vertigo | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Other Causes of Nonvertiginous Dizziness
Other causes include hyperventilation syndrome (often associated with shortness of breath, rapid heartbeat, and a feeling of fear); diabetes mellitus (related to hypoglycemia, autonomic neuropathy, or postural hypotension); and various drugs, such as tricyclic antidepressants, antihypertensives, and tranquilizers.
VISUAL DISTURBANCES
Visual disturbances most often involve visual loss (including blurriness) or diplopia. It is very important to determine whether these symptoms are a result of cerebrovascular disease, a nonvascular neurologic disorder, a primary ocular
disturbance, or something else (e.g., a psychogenic disorder). Visual disturbances can be caused by defects in the retina, optic nerve, chiasm, optic tract, lateral geniculate nucleus, geniculocalcarine tract (optic radiation), and striate cortex of the occipital lobes.
disturbance, or something else (e.g., a psychogenic disorder). Visual disturbances can be caused by defects in the retina, optic nerve, chiasm, optic tract, lateral geniculate nucleus, geniculocalcarine tract (optic radiation), and striate cortex of the occipital lobes.
Many disturbances of vision are caused by primary ocular disease (Table 2-4). For example, astigmatism or macular lesions may produce distortion of the normal shapes of objects (metamorphopsia). Photophobia is usually caused by corneal inflammation; aphakia; iritis; ocular albinism; or certain drugs, such as chloroquine or acetazolamide. Color change (chromatopsia) may result from systemic disturbances (e.g., yellow vision accompanying jaundice), drug use (such as yellow and white vision in digitalis toxicity), chorioretinal lesions, or lenticular changes. Rings that are seen when viewing lights or bright objects may be caused by lens changes, incipient cataract, glaucoma, or corneal edema. Spots or dots before the eyes, which move with movement of the eye, are commonly caused by benign vitreous opacities (floaters). Difficulty seeing in the dark (nyctalopia) may result from congenital retinitis pigmentosa, hereditary optic atrophy, vitamin A deficiency, glaucoma, optic atrophy, cataract, or retinal degeneration.
Visual Field Defects
Symptoms of visual loss include loss of visual acuity, various types of visual field defects (Table 2-5), and unilateral or bilateral visual loss (the clinical approach to evaluating visual acuity and fields is discussed in Chapter 5).
Vascular retinal lesions may cause arcuate, central, or cecocentral scotomata corresponding to the area of vascular supply of the arteriole involved (the patient sees them as wedge-shaped dark spots) (Fig. 2-1). Arcuate scotomata may also be caused by compressive or vascular lesions of the optic disc as a result of glaucoma or by hyaline bodies (drusen) of the disc. Optic neuritis and retrobulbar optic nerve lesions (demyelinating disease; infiltrative, neoplastic, or infectious diseases; degenerative diseases; aneurysm; tumor) often produce cecocentral scotomata. Small, central scotomata in macular disease often cause distorted vision for straight lines (metamorphopsia), a trait that aids in the distinction between macular and optic nerve lesions. Toxic states or nutritional
disorders (tobacco-alcohol amblyopia) may produce relatively symmetric central or cecocentral scotomata. Scintillating scotoma (the patient sees bright, colorless, or colored lights in the field of vision) usually occurs as a part of migraine or epilepsy with occipital lobe involvement. Progressive peripheral constriction of the visual field may be caused by papilledema or perioptic sheath meningioma or may be psychogenic (tunnel vision).
disorders (tobacco-alcohol amblyopia) may produce relatively symmetric central or cecocentral scotomata. Scintillating scotoma (the patient sees bright, colorless, or colored lights in the field of vision) usually occurs as a part of migraine or epilepsy with occipital lobe involvement. Progressive peripheral constriction of the visual field may be caused by papilledema or perioptic sheath meningioma or may be psychogenic (tunnel vision).
TABLE 2-4 Visual Disturbances Caused by Primary Ocular Disorders | ||||||||||||||
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TABLE 2-5 Causes of Visual Field Defects | |||||||||||||||||||||||||||||||
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 FIGURE 2-1. Patterns of visual field defects and localization of deficit. |
Lesions of the optic chiasm (pituitary tumor, craniopharyngioma, sellar meningioma, and suprasellar aneurysm of the circle of Willis) produce bitemporal hemianopias (blindness in the temporal half of the visual fields). Pregeniculate optic tract lesions (infection and tumor) produce homonymous hemianopia associated with optic atrophy and afferent pupillary defects. Lesions of the lateral geniculate nucleus (infection, tumor, and circle of Willis aneurysm) or postgeniculate lesions in the optic radiation (ischemic or hemorrhagic stroke, arteriovenous malformation, and glioma) produce incongruous homonymous hemianopias (field defects in the two eyes are not identical) with normal pupillary reflexes. Congruous homonymous hemianopia (field defects in the two eyes are identical) with normal pupillary reflexes signifies a lesion in the calcarine cortex, usually the result of a cerebrovascular or neoplastic disorder, such as ischemic stroke or glioma.
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