Definition

The term “stroke” usually refers either to a cerebral infarction or to a non-traumatic cerebral hemorrhage. Although it will vary depending on the population you are seeing (ethnicity, age, comorbidities), the ratio of infarcts to hemorrhages is about 4 to 1. As will be described in more detail in Chapter 3, cerebral infarcts can be caused by a number of pathological processes, but all end with an occlusion of a cerebral artery or vein. If the arterial occlusion results in a reduction of blood flow insufficient to cause death of tissue (infarction), it is termed “ischemia.”

As will be described in more detail in Chapter 12, non-traumatic cerebral hemorrhages are caused by a number of pathological processes which all lead to bleeding into the brain parenchyma and ventricles. Bleeding into the subarachnoid space (Chapter 13) is usually caused by a ruptured aneurysm or vascular malformation. Other types of brain bleeding, for example into the subdural or epidural space, are usually traumatic and are not considered in this book.

Presentation

When taking the history, the most characteristic aspect of a cerebral infarct or hemorrhage is the abrupt onset, so be sure to get the exact flavor of the onset. It is also imperative to determine as precisely as possible the time of onset. The symptoms most often stay the same or improve somewhat over the next few hours, but may worsen in a smooth or stuttering course. Ischemic strokes (but not hemorrhages) may rapidly resolve, but even if they resolve completely, they may recur after minutes to hours. The second characteristic historical aspect of cerebral infarcts is that the symptoms will usually fit the distribution of a single vascular territory. This is also the most important characteristic of the neurological exam in a patient with an infarct. Therefore, patients with an infarct will present with symptoms and signs in the middle, anterior, or posterior cerebral arteries, a penetrating artery (producing a “lacunar” syndrome), or the vertebral or basilar artery (see below).

Parenchymal hemorrhages also occur in characteristic locations, and usually show the same symptom complex and signs as cerebral infarcts except that early decrease in level of consciousness, nausea and vomiting, headache, and accelerated hypertension are more common with hemorrhages.

Subarachnoid hemorrhages classically present as a bursting, very severe headache (“the worst headache of my life”), and are often accompanied by stiff neck, decreased consciousness, nausea, and vomiting. Focal neurological signs are often absent; if present, they usually signify associated bleeding into the parenchyma.

Signs and symptoms characteristic of the various arterial territories are:

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  Middle cerebral – contralateral loss of strength and sensation in the face, arm, and to a lesser extent leg. Aphasia if dominant hemisphere, neglect if non-dominant.

  
  
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  Anterior cerebral – contralateral loss of strength and sensation in the leg and to a lesser extent arm.

  
  
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  Posterior cerebral – contralateral visual-field deficit. Possibly confusion and aphasia if dominant hemisphere.

  
  
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  Penetrating (lacunar syndrome) – contralateral weakness or sensory loss (usually not both) in face, arm, and leg. No aphasia, neglect, or visual loss. Possibly ataxia, dysarthria.

  
  
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  Vertebral (or posterior inferior cerebellar) – ataxia, dysarthria, dysphagia, ipsilateral sensory loss on the face, and contralateral sensory loss below the neck.

  
  
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  Basilar – various combinations of limb ataxia, dysarthria, dysphagia, facial and limb weakness and sensory loss (may be bilateral), pupillary asymmetry, disconjugate gaze, visual-field loss, decreased responsiveness.