Clinical History

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One of the first questions to address in the history is whether the problem involves neurovascular dysfunction. The clinical hallmark of many forms of neurovascular dysfunction is an acute focal change in neurological status. Therefore, an event that has an indistinct onset or course may not involve the neurovascular system. There are two exceptions to consider. One is the indistinct time of onset of symptoms in an individual who awakens with the neurological dysfunction. The other is a stuttering or waxing or waning course that can be seen in some patients with cerebral arterial thrombosis. In most instances of neurovascular dysfunction, the neurological deficit is maximum from its onset, with the involved body parts being simultaneously affected. The diagnosis of neurovascular dysfunction is weakened if there is a series of events in which neurological deficits accumulate, or if there is a march of symptoms from one area to another. Focal seizures can usually be differentiated by obtaining a history of associated involuntary motor activity and a march of symptoms. A gradual onset of symptoms with accumulation of deficits over time would suggest the possibility of a space-occupying lesion. It would be distinctly unusual for neurovascular dysfunction to present with positive neurological phenomena such as visual hallucinations or scintillating visual symptoms. Fleeting positive visual phenomenon would be more consistent with migraine. Isolated vertigo may be more consistent with a labyrinthine disorder. Hypoglycemia should be considered in the diabetic with transient paresis or aphasia, particularly if there is associated altered consciousness or confusion.

Specific details need to be sought in the history to adequately evaluate the possible underlying type and mechanism of neurovascular dysfunction. It is important to review any cerebrovascular risk factors with the patient, including a history of cardiac disorders, hypertension, hematological abnormalities, hyperlipidemia, diabetes, tobacco use, alcohol or drug use, migraine, oral contraceptive use, and a personal history or family history of TIA or stroke. Information should be obtained about use of medications such as oral anticoagulants or antiplatelet agents

and the use of illicit drugs. Patients may have other medical illnesses associated with stroke, including connective tissue diseases, malignancies, and hypercoaguable states. Rarely, a preceding or concurrent infection may predispose to stroke. A history of recent trauma should be sought in patients with symptoms of carotid or vertebral dissection. A history of posterior circulation symptoms with arm exercise may suggest subclavian steal.

It is often difficult to differentiate an ischemic infarction from a hemorrhage. Some historical features that suggest a hemorrhage would be an altered level of consciousness or a seizure at the onset, prominent nausea and vomiting, or a severe headache. However, onset headaches can also be present in 17 percent of patients with ischemic infarction.^ A carotid dissection may present with pain involving the neck, ipsilateral head, or the periorbital region.

While it is difficult to distinguish cardiogenic stroke from other causes based on the neurological profile, historical features that may suggest a cardioembolic cause are an abrupt onset with a maximum deficit at the onset, a history of infarctions in more than one vascular territory, or systemic emboli to the limbs or other organs.

Patients noting monocular visual loss or having complaints of a speech disorder suggestive of aphasia most likely have carotid distribution ischemia. Complaints of binocular visual loss, vertigo, balance difficulties, gait instability, bilateral or alternating weakness or altered sensation, swallowing difficulties, or diplopia suggest ischemia in the vertebrobasilar distribution. Etiologies other than vertebrobasilar ischemia should be considered with isolated vertigo, diplopia, or dysarthria. Localization of the neurovascular dysfunction to the cortical or subcortical region may be possible based on historical features. Patients with complaints of any degree of altered consciousness may have cortical or combined subcortical and cortical ischemia. Loss of vision in one field or forced eye deviation usually implies a cortical or combined cortical and subcortical localization. A history of weakness or sensory loss affecting the face, arm, and leg equally usually implies a subcortical or brain stem localization. Complaints of severe dysarthria are often indicative of a subcortical or combined cortical and subcortical infarction.


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