Ventricular Enlargement after TBI—Shunt or No Shunt

Abstract

A large number of brain trauma patients develop ventricular enlargement. The incidence varies from 30% to 86% of patients examined up to 12 months after trauma, and it has been proposed as an index of severity of brain damage [1]. The management of ventriculomegaly following severe traumatic brain injury (TBI) still is controversial because it is difficult to determine whether posttraumatic ventricular dilatation is related to an atrophic process or to a true hydrocephalus. The incidence of postraumatic hydrocephalus (PTH) has been reported as low as 0.7% [2] and as high as 29% [3]. The diagnosis of true hydrocephalus is not always simple. Several variations of the syndrome are seen in the clinical and radiological settings. PTH can present acutely, with progressive coma, the patients can present signs of increased intracranial pressure with disturbance of consciousness and neurological deficits or subacutely, with a history of a gradual decline in daily functioning or in a failure to improve. PTH can present as a normal pressure hydrocephalus (NPH) syndrome with the so called “classical” clinical NPH triade mental deterioration, gait disorder and bladder dysfunction. This “classical” triade of NPH is not classical at all in TBI patients as these patients have so many postraumatic neurological deficits and the classical triade may be misinterpreted.