Brain injuries may be accompanied by a number of late or long-term complications. These secondary brain injuries include cerebral herniations, which may occur under the falx cerebri or through the tentorium. Herniations can cause compression of adjacent brain substance or vessels, with the production of secondary signs and symptoms (Fig. 6-93). Penetrating injuries or fractures can injure nearby large or small vessels, producing thrombosis, embolism, traumatic aneurysm formation, or internal carotid–cavernous sinus fistula. Basal skull fractures involving the dura and arachnoid can cause CSF leaks that show up as CSF rhinorrhea or otorrhea. Local or diffuse brain swelling can compress the cerebral aqueduct or fourth ventricle, producing obstructive hydrocephalus. Subarachnoid hemorrhage may obstruct CSF resorption and cause a late-developing communicating hydrocephalus. Focal cerebral atrophy can occur at sites of infarction, hemorrhage, or trauma. Generalized atrophy can follow diffuse injuries and can be demonstrated by an increased size of sulci, fissures, cisterns, and ventricles.
FIGURE 6-93. Nonenhanced CT scan shows a left MCA infarct with mass effect causing contralateral midline shift (arrow ) corresponding to subfalcine herniation.
Source: Physical Medicine and Rehabilitation – Principles and Practice
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