Posttraumatic Hydrocephalus Clinical Presentation

Updated: Feb 03, 2021
  • Author: John J Danko, DO, FAAPMR; Chief Editor: Elizabeth A Moberg-Wolff, MD  more...
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Posttraumatic hydrocephalus (PTH) often has an atypical or nonspecific presentation and therefore may be easily missed. A high level of clinical suspicion is important for diagnosis. [16, 17]

  • If acute, patients may present with coma and other focal neurologic deficits.

  • If chronic, patients may demonstrate a gradual decline in functional status or may show a failure to improve. [6] The decline in performance or functioning may be initially observed by therapists.



A complete neurologic examination should be performed and repeated as necessary to assess for changes over time.

PTH may present as a syndrome of increased intracranial pressure with symptoms of papilledema, focal neurologic deficits, or coma. [6]

Most commonly, PTH presents as noncommunicating hydrocephalus with the following findings [5] :

  • Papilledema resulting from increased intracranial pressure and transmission through the subarachnoid space
  • Cognitive changes, including decreased memory, decreased attention, and irritability


PTH results from TBI, with or without intracerebral hemorrhage. Hemorrhage may be seen in the subdural, subarachnoid, or intraventricular spaces or may arise within brain parenchyma. [18]  Additional, non–trauma-related causes of acquired hydrocephalus include aneurysm rupture, arteriovenous malformation, and hemorrhagic stroke. [19]

A study by Kammersgaard et al indicated that older age and low consciousness level are independent risk factors for the development of PTH during rehabilitation in patients with severe TBI. The study involved 444 patients with severe TBI, 14.2% of whom developed PTH, with 75% of the hydrocephalus cases arising during rehabilitation. [20]

Age may further affect risk factors in that, as indicated in a retrospective study by Ved et al, pediatric patients who have suffered a TBI may have a greater likelihood of PTH in the presence of intraventricular and/or subarachnoid hemorrhages, subdural hematomas, or severe TBI. Previous research has found that risk factors for PTH in adults with TBI include severe TBI, subdural hematomas, and the need for surgery. [21]

A retrospective study by Su et al indicated that in patients who have suffered TBI, independent risk factors for the development of PTH in association with unilateral decompressive craniectomy include age and contralateral subdural hygroma. The investigators noted a 3.6% rise in the PTH development rate for every 1-year increase in age. Subdural hygroma existed in 58.1% of patients with PTH, versus 27% of patients without PTH. [22]

A retrospective study by Di et al reported that other risk factors for the development of PTH in TBI patients who undergo decompressive craniectomy include a Glasgow Coma Scale score of less than 6 on admission, a finding of intraventricular hemorrhage on initial head CT scan, and a requirement for bilateral decompressive craniectomy. [23]

Another study, by Vedantam et al, indicated that in cases of severe TBI treated with decompressive craniectomy, patients with interhemispheric subdural hygromas and of younger age are at greater risk for the development of shunt-dependent PTH. [24]

A retrospective study by Fotakopoulos et al reported that in patients with severe TBI who undergo decompressive craniectomy, craniectomy size, but, in contrast to the Su and Vedantam studies, not patient age, correlates with the incidence of PTH. [25]