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The diagnosis of a vascular lesion rests essentially on recognition of the stroke syndrome; without evidence of this, the diagnosis must always be in doubt The three criteria by which the stroke is identi ed should be re-emphasized: (1) the temporal pro le of the clinical syndrome, (2) evidence of focal brain disease, and (3) the clinical setting De nition of the temporal pro le requires a clear history of the premonitory phenomena, the mode of onset, and the evolution of the neurologic disturbance in relation to the patient s medical status Here, an inadequate history is the most frequent cause of diagnostic error If these data are lacking, the stroke pro le may still be determined by extending the period of observation for a few days or weeks, thus invoking the clinical rule that the physician s best diagnostic tool is a second and third examination There are few categories of neurologic disease whose temporal pro le mimics that of the cerebrovascular disorders Migraine may do so, but the history usually provides the diagnosis A seizure may be followed by a prolonged focal de cit (Todd s paralysis) but is rarely the initial event in a stroke; the setting in which these symptoms occur and their subsequent course clarify the clinical situation Stroke-like episodes appear in the course of certain hereditary metabolic disorders (Fabry disease, homocystinuria, mitochondrial disease) Differentiation is not dif cult because of the associated myopathic and neurologic signs and characteristic metabolic defects Tumor, infection, in ammation, degeneration, and nutritional de ciency are not likely to manifest themselves precipitously, although rarely a brain metastasis produces a focal de cit of abrupt onset (see below) Trauma, of course,
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occurs abruptly but usually offers no problem in diagnosis In multiple sclerosis and other demyelinative diseases, there may be an abrupt onset or exacerbation of symptoms, but for the most part they occur in a different age group and clinical setting Conversely, a stroke-like onset of cerebral symptoms in a young adult should always raise a suspicion of demyelinative disease A stroke developing over a period of several days usually progresses in a stepwise fashion, increments of de cit being added abruptly from time to time A slow, gradual, downhill course over a period of 2 weeks or more indicates that the lesion is probably not vascular but rather neoplastic, demyelinative, infectious (abscess) or granulomatous, or a subdural hematoma In regard to the focal neurologic de cits of cerebrovascular disease, many of the nonvascular diseases may produce symptoms that are much the same, and the diagnosis cannot rest solely on this aspect of the clinical picture Nonetheless, certain combinations of neurologic signs, if they conform to a neurovascular pattern eg, the lateral medullary syndrome mark the disease as vascularocclusive in nature Many thrombotic strokes are preceded by TIAs, which, if recognized, are diagnostic of this form of vascular disease It is essential that TIAs be differentiated from seizures, syncope, panic attacks, neurologic migraine, and attacks of labyrinthine vertigo, since a failure to do so may result in unnecessary arteriographic studies and even a surgical operation With very few exceptions, the presence of blood in the CSF points to a cerebrovascular (rarely spinal vascular) lesion provided that trauma and a traumatic tap can be excluded Headache is common in cerebrovascular disease; it occurs not only with hemorrhage but also with thrombosis, arterial dissections, and rarely with embolism Seizures are almost never the premonitory, rst, or only manifestation of a stroke but can rarely occur in the rst few hours after infarction or intracranial bleeding Brief unconsciousness (5 to 10 min) is rare in stroke, being seen only with basilar artery insuf ciency and as an initial event in ruptured aneurysm or primary intracerebral hemorrhage In the latter case, a depression in the state of consciousness soon reasserts itself and is then progressive Certain neurologic disturbances are hardly ever attributable to stroke eg, diabetes insipidus, fever, bitemporal hemianopia, parkinsonism, generalized myoclonus, repeated falls, and isolated cranial nerve palsies and their presence may be of help in excluding vascular disease Finally, the diagnosis of cerebrovascular disease should always be made on positive data, not by exclusion A few conditions are so often confused with cerebrovascular diseases that they merit further consideration When a history of trauma is absent, the headache, drowsiness, mild confusion, and hemiparesis of subdural hematoma may be ascribed to a small stroke, and the patient may fail to receive immediate surgical therapy In subdural hematoma, the symptoms and signs usually develop gradually over a period of days or weeks The degree of headache, obtundation, and confusion is disproportionately greater than the focal neurologic de cit, which tends to be inde nite and variable until late in the evolution of the hematoma If the patient has fallen and injured his head at the onset of the stroke, it may be impossible to rule out a complicating subdural hematoma on clinical grounds alone, in which case CT scanning and MRI are usually diagnostic The reverse diagnostic error will not be made if one remembers that patients with subdural hematoma rarely exhibit a total hemiplegia, monoplegia, hemianesthesia, homonymous hemianopia, or aphasia If such focal signs are present and particularly
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if they developed suddenly, subdural hematoma is not likely to be the explanation A brain tumor, especially a rapidly growing glioblastoma multiforme or lymphoma, may produce a severe hemiplegia within a week or two Also, the neurologic de cit due to carcinoma metastatic to the cerebrum may evolve rapidly, almost at a stroke-like pace Moreover, in rare cases, the hemiplegia may be preceded by transitory episodes of neurologic de cit, indistinguishable from TIAs However, in both conditions, a detailed history will indicate that the evolution of symptoms was gradual; if it was saltatory, seizures will usually have occurred The chest lm frequently discloses a primary or secondary tumor, and an increased blood sedimentation rate suggests that a concealed systemic disease process is at hand A lack of detailed history may also be responsible for the opposite diagnostic error, ie, mistaking a relatively slowly evolving stroke (usually due to internal carotid artery or basilar occlusion) for a tumor Again, CT scanning and MRI will usually settle the problem A brain abscess or in ammatory necrotic lesion eg, herpes encephalitis or toxoplasmosis may also develop rapidly Dementia of the Alzheimer type is often ascribed, on insuf cient and conceptually incorrect grounds, to the occurrence of multiple small strokes If vascular lesions are responsible, evidence of an apoplectic episode or episodes and of focal neurologic de cit to account for at least part of the syndrome will almost invariably be disclosed by history and examination In the absence of a history of episodic development or of focal neurologic signs, it is unwarranted to attribute senile dementia to cerebrovascular disease in particular to small strokes in silent areas Cerebral arteriosclerosis is another term that has often been used carelessly to explain such mental changes, the implication (incorrect) being that arteriosclerosis itself causes ischemic damage to the nervous system, producing loss of intellectual function but no other neurologic de cit If cerebral arteriosclerosis (atherosclerosis) is actually responsible, there should be evidence of it in the form of strokes at some time in the course of the illness and often in the heart (myocardial infarction, angina pectoris) or legs (intermittent claudication, loss of pulses) Frequently the lesions of both vascular and Alzheimer disease are present, in which case there may be dif culty in determining to what extent each of them is responsible for the neurologic de cit Several studies have shown an increased incidence or an acceleration of Alzheimer dementia if there are concurrent vascular lesions, but further studies are needed to con rm this notion Recurrent seizures as the result of a previous stroke occur in up to 10 percent of cases ( postinfarction epilepsy, page 740) When evidence, by history or examination, of the original stroke is lacking, as it often is, or if the seizures are not observed or leave behind a temporary increase in the neurologic de cit (Todd s paralysis), the diagnosis of another stroke or a tumor may be made in error Miscellaneous conditions occasionally taken to be a stroke are Bell s palsy; Stokes-Adams attacks; a severe attack of labyrinthine vertigo; diabetic ophthalmoplegia; acute ulnar, radial, or peroneal palsy; embolism to a limb; and temporal arteritis associated with blindness Contrariwise, certain manifestations of stroke may be incorrectly interpreted as evidence of some other neurologic disorder In lateral medullary infarction, dysphagia may be the outstanding feature; if the syndrome is not kept in mind, a fruitless radiologic search for a local esophageal or pharyngeal cause may be undertaken Similarly, facial pain or a burning sensation due to involvement of the trigeminal spinal nucleus in lateral medullary stroke may be misattributed to sinus disease Headache, at times severe,
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