Posttraumatic Hydrocephalus

Posttraumatic hydrocephalus (PTH) is a frequent and serious complication that follows a traumatic brain injury (TBI).^{[1, 2, 3]} Its incidence varies greatly from study to study, largely based on different criteria for its diagnosis. However, PTH could greatly impact morbidity following a TBI and could result in increased mortality if it is not recognized and treated.
PTH may result from 1 or a combination of pathophysiologic factors. It can be caused by the overproduction of cerebrospinal fluid (CSF), the blockage of normal CSF flow, or insufficient absorption that results in excessive accumulation of CSF around the brain. Ultimately, PTH is caused by an imbalance that occurs between CSF production and absorption.^[4]
PTH may present as normal pressure hydrocephalus (NPH) or as a syndrome of increased intracranial pressure.^[5] Because of differences in prognosis and treatment, PTH needs to be distinguished from cerebral atrophy (ie, hydrocephalus ex vacuo) and ventricular enlargement caused by a failure of brain development. If PTH goes unrecognized or untreated, increased morbidity or mortality following a TBI is more likely.^{[6, 7]}

Classification

Dandy and Blackfan introduced the classification of hydrocephalus as either noncommunicating or communicating.^[8] In noncommunicating hydrocephalus (also called obstructive hydrocephalus), CSF accumulates in the ventricles because of CSF flow blockage. As a result, the ventricles enlarge and the hemispheres expand. The following sites are prone to the obstruction of CSF flow^[9] :

• Foramen of Monro
• Third ventricle
• Aqueduct of Sylvius
• Fourth ventricle
• Foramen of Luschka
• Foramen of Magendie

Conversely, in communicating hydrocephalus (also referred to as nonobstructive hydrocephalus), full communication between the ventricles and the subarachnoid space exists. Impaired CSF absorption may cause communicating hydrocephalus. The apparent mechanism is partial occlusion of the arachnoid villi, perhaps by blood and inflammatory mediators. Severe skull fractures, hemorrhage, and meningitis may predispose patients to this variant of PTH.^[9] Portnoy proposed that PTH develops as a result of increased dural sinus pressure, causing decreased CSF outflow.^[10]
NPH, a form of communicating hydrocephalus, may result from subarachnoid hemorrhage caused by an aneurysm rupture or a TBI, encephalopathy, or . NPH often presents as the classic triad of a progressive gait disorder, impairment of mental function, and urinary incontinence.^[9] In NPH, ventricles enlarge despite normal or even slightly reduced intracranial pressure, and they continue to press against brain parenchyma.
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