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episodes of vertigo, diplopia, numbness, impaired vision in one or both visual elds, and dysarthria These TIA syndromes are described more fully further on Such attacks last from a few minutes to several hours; in most instances the duration is less than 10 min Those of several hours duration have a different connotation, since they are usually due to demonstrable embolism The nal stroke may be preceded by one or two attacks or a hundred or more brief TIAs, and the stroke may follow the onset of the attacks by hours, days, or less frequently by weeks or months When there are no prodromal ischemic attacks, one must use other criteria to establish the diagnosis of atherosclerotic thrombosis The thrombotic stroke, whether or not it is preceded by warning attacks, nally develops in one of several ways Most often there is a single episode but the whole illness evolves over a few hours or less More characteristic is a stuttering or intermittent progression of neurologic de cits extending over several hours or a day or longer This is a starkly different pro le from the abrupt onset of a complete stroke syndrome that characterizes the embolic mechanism discussed further on Again, in thrombosis a partial stroke may occur and even recede temporarily for several hours, after which there is rapid progression to the completed stroke or several eeting episodes may be followed by a longer one and, hours or a day or two later, by a major stroke Several parts of the body may be affected at once or only one part, such as a limb or one side of the face, the other parts becoming involved serially in step-like fashion until the stroke is fully developed Sometimes the de cit is episodic; spells of weakness or involuntary movement of a hand or arm or dimness of vision, lasting 5 to 10 min, occur spontaneously or are brought on by standing or walking Each of the transient attacks and the abrupt episodes of progression reproduces the pro le of the stroke in miniature The principle of intermittency seems to characterize the thrombotic process from beginning to end As frequent as the modes of onset outlined above, and most characteristic of atherothrombotic events, is the occurrence of the stroke during sleep; the patient awakens paralyzed, either during the night or in the morning Unaware of any dif culty, he may arise and fall helplessly to the oor with the rst step This is the story in fully 60 percent of our patients with thrombotic strokes and in a smaller number with embolic ones as well Most deceptive of all are the relatively few patients in whom the neurologic disorder has evolved over several days or even longer, in a slow, gradual fashion ( slow stroke ) One s rst impulse is to make a diagnosis of brain tumor, abscess, or subdural hematoma This error can usually be avoided by a careful analysis of the course of the illness, which will disclose an uneven, saltatory progression; if the clinical data are incomplete, observation for a few days makes the stroke pro le more apparent Actually there are a few cases and these are usually instances of pure motor hemiplegia in which the evolution of a thrombotic stroke is evenly progressive over a period of days In addition to these several modes of evolution of atherothrombotic stroke, thrombotic stenosis or occlusion of certain large vessels may lead instead to the generation of embolic fragments (artery-to-artery embolus), thereby precipitating a new stroke in a region distal to the occlusion This is most likely to occur during the period of clinical uctuation and active thrombus formation The most common occurrence of artery-to-artery embolism is with carotid artery thrombosis, the embolus passing to branches of the ipsilateral middle or anterior cerebral artery With atherothrombotic blockage of the vertebral or lower basilar artery, the embolus orig-.

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inates in the occluded vessel but then proceeds to lodge in the posterior cerebral artery or the top of the basilar artery In most of the cases of this nature that we have observed, there are additional telltale signs of slight pontine strokes (dysarthria, diplopia, see page 702), presumably from the transient occlusion of the mouths of several small penetrating arteries as the embolus moves upward ( stop-and-go or traveling embolus syndrome) Arterial thrombosis is not usually accompanied by headache, but lateralized cranial pain occurs in some cases Usually the pain is located on one side of the head in carotid occlusion, at the back of the head, or simultaneously in forehead and occiput in basilar occlusion, and behind the ipsilateral ear or above the eyebrow in vertebral occlusion The headache is less severe and more regional than that of intracerebral or subarachnoid hemorrhage, and there is no stiffness of the neck The mechanism is unclear; presumably it is related to the disease process or distention of the vessel wall, since it may antedate the other manifestations of the stroke by days or even weeks As mentioned in the introductory section, hypertension is more often present than not in patients with atherothrombotic infarction Diabetes mellitus is common also, or the patient is a smoker or hyperlipidemic Often there is evidence of vascular disease in other parts of the body: a history of coronary occlusion or angina pectoris, an electrocardiographic (ECG) abnormality re ecting a previous myocardial infarction or left ventricular hypertrophy, intermittent claudication, or an absence of one or several pulses in the lower limbs The retinal arteries may show uniform or focal narrowing, increase and irregularity of the light re ex, and arteriovenous nicking, but these ndings correlate with hypertension rather than atherosclerosis The patient is more often elderly but may be in the fourth decade of life or even younger Laboratory Findings These have been discussed at various points in the preceding pages and need only be recapitulated brie y In the laboratory investigation of atherothrombotic infarction, one may employ noninvasive techniques Ultrasonography will reveal with fair accuracy the cervical and intracranial segments of the internal carotid and vertebrobasilar arteries MRI is more sensitive to ischemic brain damage than is the CT scan While the latter reveals hemorrhage immediately after it occurs, softened tissue cannot be seen until several days have elapsed On the other hand, MRI reveals ischemic damage within a few hours, in both white and gray matter, and diffusion-weighted MRI techniques do so even earlier The various MRI sequences are able to distinguish with reasonable clarity the age of cerebral infarction; the features that signify acute, subacute, and older strokes are summarized in Table 34-6 and discussed in Chap 2 By MRA, one can see all the major cervical and intracranial arteries and may detect the irregular lumen or occlusion of atherosclerosis and even embolic occlusions in more distal vessels (Fig 34-17) This method has to a large extent replaced conventional angiography, which is reserved for cases in which the diagnosis is in doubt (eg, suspected angiitis) or when surgical intervention or long-term anticoagulant therapy is contemplated Lumbar puncture is now performed infrequently in patients with stroke Cerebral thrombosis does not cause blood to enter the CSF The CSF protein is sometimes slightly elevated (usually 50 to 80 mg/dL); rarely is it in excess of 100 mg/dL A small number of polymorphonuclear leukocytes (3 to 8/mm3) is not exceptional in the rst few days; very rarely, and for unexplained reasons, a brisk, transient pleocytosis (400 to 1000 polymorphonuclear leu-.

T2-weighted Proton (spin) Density Fluid-attenuated inversion recovery (FLAIR) Diffusion-weighted image (DWI) Susceptibility sequence Short tau inversion recovery (STIR)

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