Several other circumstances influence the early prognosis in cerebral infarction. In the case of very large infarcts in the middle cerebral artery territory, swelling of the infarcted tissue may occur, followed by displacement of central structures, transtentorial herniation, and death of the patient after several days. This can at times be anticipated by the sheer volume of the infarct and is usually evident on the CT or MRI scan within a day of the stroke. Smaller infarcts of the inferior surface of the cerebellum may also cause a fatal herniation into the foramen magnum. Milder degrees of swelling and increased intracranial pressure in both of these strokes may progress as gauged by imaging studies for 2 to 3 days but do not prove fatal. (See earlier under “Treatment of Brain Swelling [Edema] and Raised Intracranial Pressure After Ischemic Stroke.”)
In extensive brainstem infarction associated with deep coma caused by basilar artery occlusion, the early mortality rate approaches 40 percent but some of this is self-fulfilling as support is sometimes withdrawn. In any type of stroke, if coma or stupor is present from the beginning, survival is largely determined by success in keeping the airway clear, preventing aspiration pneumonia, controlling brain swelling, and maintaining fluid and electrolyte balance, as described further on. With smaller thrombotic infarcts, the mortality is 3 to 6 percent, much of it from myocardial infarction and aspiration pneumonia.
As for the eventual prognosis of the neurologic deficits, some improvement is the rule. The patient with a lacunar infarct usually fares well but may take months to improve to the maximum extent. With other small infarcts, recovery may start within a day or two, and restoration may be complete or nearly complete within a week. In cases of severe deficit, there may be little significant recovery; after months of assiduous efforts at rehabilitation, the patient may remain bereft of speech and understanding, with the upper extremity still useless and the lower extremity serving only as an uncertain prop during attempts to walk. Between these two extremes there is every gradation of recovery. Measurement of central motor conduction by magnetic stimulation has been somewhat predictive of motor recovery but is not widely used for clinical work. If clinical recovery does not begin in 1 or 2 weeks, the outlook is poorer for both motor and language functions. Constructional apraxia, uninhibited anger (with left and rarely with right temporal lesions), nonsensical logorrhea and placidity, unawareness of the paralysis and neglect (with nondominant parietal lesions), and confusion and delirium (with nondominant temporal lesions) all tend to diminish and may disappear within a few weeks. A hemianopia that has not cleared in a few weeks will usually be permanent, although reading and color discrimination may continue to improve. In lateral medullary infarction, difficulty in swallowing may be protracted, lasting 8 weeks or longer, yet relatively normal function is finally restored in nearly every instance. Aphasia, dysarthria, cerebellar ataxia, and walking may improve for a year or longer, but for all practical purposes it may be said that whatever motor and language deficits remain after 5 to 6 months will be permanent.