Stroke: An Introduction to Diagnosis

designs. Typically the overall conception or "Gestalt" will be most severely disrupted and they may omit features on the left side as part of a neglect syndrome (Figure 2). Neglect and visuospatial dysfunction may persist long after the acute stroke, leading to a propensity for getting lost and hazardous driving as patients fail to attend to left sided stimuli. Table 3 Clinical Features of Large Vessel Distribution and Lacunar Infarctions in the Posterior Circulation Large Vessel Lacunar Lateral medullary infarction Ataxic hemiparesis Vertigo, nausea & vomiting Dysequilibrium with falling to side of lesion Diplopia (skew deviation) Dysarthria Dysphagia Ipsilateral Horner's syndrome Ipsilateral reduction in corneal reflex Diminished sensation pinprick & temperature, ipsilateral face Diminished sensation pinprick & temperature, contralateral body Failure of ipsilateral palate to elevate Ipsilateral ataxia, dyssynergia, dysmetria, on finger to nose maneuver Top of the basilar infarction Unilateral or bilateral visual impairment Impairment in memory acquisition Lethargy, stupor or coma Arm > leg hemiparesis Basilar thrombosis Step by step progression of bilateral deficits Supraand infranuclear deficits in ocular motility Bilateral motor dysfunction Lethargy, stupor or coma Large vessel posterior circulation infarcts. There are three common types of large vessel distribution posterior circulation infarcts: lateral medullary (Wallenberg) infarction (usually due to vertebral artery thrombosis), top of the basilar embolism, and basilar thrombosis (5) (Table 3). Lateral medullary infarction is variously associated with vertigo, nausea, vomiting, dysequilibrium with falling to the side of the lesion, diplopia, dysarthria, dysphagia, ipsilateral abnormalities on the exam that may include a Horner's syndrome, reduction of the corneal reflex, diminution in sensation for pinprick and temperature over the face, failure of elevation of the palate when the patient vocalizes, and ataxia on finger to nose maneuver, and contralateral diminution in sensation for pinprick and temperature over the hemibody. There should be no lethargy, visual impairment, weakness, reflex changes or alteration in higher cortical function. Top of the basilar embolism is most commonly characterized by the sudden development of persistent unilateral, less often bilateral, visual impairment due to posterior cerebral artery distribution infarction. Patients often report impairment in vision in the contralateral eye when actually it is the contralateral field. There may be associated recent memory impairment (due to compromised hippocampal blood