Posttraumatic Hydrocephalus

Updated: Apr 22, 2015
  • Author: Percival H Pangilinan, Jr, MD; Chief Editor: Consuelo T Lorenzo, MD  more...
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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]


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 Alzheimer disease. 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.

See also the following related resource in Medscape:

Resource Center Trauma

See also the following related topics in Medscape Reference:

Hydrocephalus [Neurology]

Hydrocephalus [Neurosurgery]

Classification and Complications of Traumatic Brain Injury

Normal Pressure Hydrocephalus [Neurology]

Normal Pressure Hydrocephalus [Radiology]



Normal anatomy and physiology:

In adults, the following features are encountered in posttraumatic hydrocephalus [9] :

  • Normal intracranial pressure (ICP) is approximately 8 mm Hg.
  • The average intracranial volume is about 1700 mL.
  • The average CSF volume is about 104 mL.

By volume, the intracranial contents include the following [11] :

  • Brain parenchyma - About 80%
  • CSF - About 10%
  • Blood - About 10%

CSF is primarily produced in the lateral ventricles by the choroids plexus at a rate of 500 mL/d. The CSF flows down toward the third ventricle through the foramen of Monro and into the fourth ventricle through the cerebral aqueducts. The CSF then exits the ventricular system through the foramen of Magendie (medially) and the foramen of Luschka (laterally) and flows into the perimedullary and perispinal subarachnoid spaces. The CSF continues around the brainstem to the basal and ambient cisterns. It then flows to the lateral and superior surfaces of the cerebral hemispheres, where it is largely absorbed through the arachnoid villi. The total volume of CSF is replaced several times daily.




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The onset of PTH may vary from 2 weeks to years after TBI. Studies cite a wide range of incidence (0.7-50%); part of this variation results from underdiagnosis and atypical presentation, as well as from the fact that different sets of clinical criteria are used to diagnose PTH. [5, 6, 7, 12]

Mazzini and colleagues found that 50% of patients with postacute phase severe TBI had PTH but that only 11% required surgery. [7]


In a multi-year study, Kim and colleagues followed 789 patients who had suffered a TBI, diagnosing PTH in 129 (16.3%) of them. [13] Sixty-four patients with PTH required shunting.


If PTH goes unrecognized or untreated, increased morbidity or mortality following a TBI is more likely. [6, 7]


Race does not appear to be a factor in the development of PTH.


Sex does not appear to be a risk factor in the development of PTH.


Increased age appears to increase the risk of developing PTH. [7]