Posttraumatic Hydrocephalus

Posttraumatic Hydrocephalus

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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] :

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.

Pertinent laboratory studies include the following:

The progressive enlargement of the ventricular system shown on repeat computed tomography (CT) scans is the key to the diagnosis of PTH. [6] Magnetic resonance imaging (MRI) is useful in the evaluation of injury to structures in the posterior fossa, including cerebral aqueduct stenosis and cerebellar tonsil herniation. [11]

Another exam, the CSF tap test, is a lumbar puncture (LP) with manometry and CSF removal. Cognitive and physical functions are assessed before and after the removal of 50 mL of CSF. Improvement suggests that shunting may be beneficial.

Shunting is the most common treatment for hydrocephalus. The outcome is typically favorable. A shunt is usually placed from the right ventricle to the peritoneal space. The right side is normally used to avoid injury to the language centers on the left side of the brain. Shunts are most often equipped with reservoirs that are used for transiently increasing output and for testing the patency of flow.

The resumption of rehabilitation is usually prompt after the placement of a ventriculoperitoneal (VP) shunt. [12] Patients are typically observed for 2-3 days postoperatively. They then return to rehabilitation services to complete their brain-injury rehabilitation program. Successful shunting is usually related to more obvious and rapid improvements during rehabilitation efforts. [13]

See also the following related resource in Medscape:

Resource center: Trauma

See also the following related topics in Medscape Drugs & Diseases:

Hydrocephalus [Neurology]

Hydrocephalus [Neurosurgery]

Classification and Complications of Traumatic Brain Injury

Normal Pressure Hydrocephalus [Neurology]

Normal Pressure Hydrocephalus [Radiology]

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 [14] :

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.

United States

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, 15]

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

International

In a multi-year study, Kim and colleagues followed 789 patients who had suffered a TBI, diagnosing PTH in 129 (16.3%) of them. [16] 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]

Bontke CF. Medical complications related to traumatic brain injury. Phys Med Rehabil: State Art Rev. 1989. 3:43-58.

Narayan RJ, Gokaslan ZL, Bontke CF. Neurologic sequelae of head injury. Rosenthal M, ed. Rehabilitation of the Adult and Child With Traumatic Brain Injury. 2nd ed. Philadelphia, Pa: Davis; 1990. 94-106.

Stein S, Schrader P. Neurologic sequelae. Phys Med Rehabil: State Art Rev. 1990. 4:543-57.

Katz RT, Brander V, Sahgal V. Updates on the diagnosis and management of posttraumatic hydrocephalus. Am J Phys Med Rehabil. 1989 Apr. 68(2):91-6. [Medline].

Guyot LL, Michael DB. Post-traumatic hydrocephalus. Neurol Res. 2000 Jan. 22(1):25-8. [Medline].

Groswasser Z, Cohen M, Reider-Groswasser I, et al. Incidence, CT findings and rehabilitation outcome of patients with communicative hydrocephalus following severe head injury. Brain Inj. 1988 Oct-Dec. 2(4):267-72. [Medline].

Mazzini L, Campini R, Angelino E, et al. Posttraumatic hydrocephalus: a clinical, neuroradiologic, and neuropsychologic assessment of long-term outcome. Arch Phys Med Rehabil. 2003 Nov. 84(11):1637-41. [Medline].

Dandy WE, Blackfan KD. Internal hydrocephalus: an experimental, clinical, and pathological study. Am J Dis Child. 1914. 8:406:

Adams RD, Victor M. Disturbances of cerebrospinal fluid and its circulation, including hydrocephalus and meningeal reactions. Principles of Neurology. 4th ed. New York, NY: McGraw-Hill Information Services Co; 1989. 623-35.

Portnoy HD, Chopp M, Branch C, et al. Cerebrospinal fluid pulse waveform as an indicator of cerebral autoregulation. J Neurosurg. 1982 May. 56(5):666-78. [Medline].

Graff-Radford NR. Normal pressure hydrocephalus. Neurol Clin. 2007 Aug. 25(3):809-32, vii-viii. [Medline].

Wu Y, Green NL, Wrensch MR, et al. Ventriculoperitoneal shunt complications in California: 1990 to 2000. Neurosurgery. 2007 Sep. 61(3):557-62; discussion 562-3. [Medline].

Bontke CF, Zasler ND, Boake C. Rehabilitation of the head-injured patient. Narayan RK, Wilberger JE, Povlishock JT, eds. Neurotrauma. New York, NY: McGraw-Hill; 1996. 841-58.

Kaye AH, Laws ER, eds. Brain Tumors: An Encyclopedic Approach. 2nd ed. New York, NY: Churchill Livingstone; 2001. 205.

Mori K, Shimada J, Kurisaka M, et al. Classification of hydrocephalus and outcome of treatment. Brain Dev. 1995 Sep-Oct. 17(5):338-48. [Medline].

Kim SW, Lee SM, Shin H. Clinical Analysis of Post-Traumatic Hydrocephalus. J Korean Neursurg Soc. 2005. 38:211-214.

Long DF. Diagnosis and management of intracranial complications in traumatic brain injury rehabilitation. Horn LJ, Zasler ND, eds. Medical Rehabilitation of Traumatic Brain Injury. Philadelphia, Pa: Hanley & Belfus; 1996. 333-62.

Paoletti P, Pezzotta S, Spanu G. Diagnosis and treatment of post-traumatic hydrocephalus. J Neurosurg Sci. 1983 Jul-Sep. 27(3):171-5. [Medline].

Wostyn P, Audenaert K, De Deyn PP. Alzheimer’s disease-related changes in diseases characterized by elevation of intracranial or intraocular pressure. Clin Neurol Neurosurg. 2008 Feb. 110(2):101-9. [Medline].

Factora R, Luciano M. Normal pressure hydrocephalus: diagnosis and new approaches to treatment. Clin Geriatr Med. 2006 Aug. 22(3):645-57. [Medline].

Tian HL, Xu T, Hu J, et al. Risk factors related to hydrocephalus after traumatic subarachnoid hemorrhage. Surg Neurol. 2007 Aug 16. [Medline].

Kammersgaard LP, Linnemann M, Tibaek M. Hydrocephalus following severe traumatic brain injury in adults. Incidence, timing, and clinical predictors during rehabilitation. NeuroRehabilitation. 2013. 33(3):473-80. [Medline].

Nasel C, Gentzsch S, Heimberger K. Diffusion-weighted magnetic resonance imaging of cerebrospinal fluid in patients with and without communicating hydrocephalus. Acta Radiol. 2007 Sep. 48(7):768-73. [Medline].

Weintraub AH, Gerber DJ, Kowalski RG. Posttraumatic Hydrocephalus as a Confounding Influence on Brain Injury Rehabilitation: Incidence, Clinical Characteristics, and Outcomes. Arch Phys Med Rehabil. 2017 Feb. 98 (2):312-9. [Medline].

Tribl G, Oder W. Outcome after shunt implantation in severe head injury with post-traumatic hydrocephalus. Brain Inj. 2000 Apr. 14(4):345-54. [Medline].

Denes Z, Barsi P, Szel I, Boros E, Fazekas G. Complication during postacute rehabilitation: patients with posttraumatic hydrocephalus. Int J Rehabil Res. 2011 Sep. 34(3):222-6. [Medline].

Linnemann M, Tibaek M, Kammersgaard LP. Hydrocephalus during rehabilitation following severe TBI. Relation to recovery, outcome, and length of stay. NeuroRehabilitation. 2014. 35(4):755-61. [Medline].

Percival H Pangilinan, Jr, MD Associate Professor, Department of Physical Medicine and Rehabilitation, University of Michigan Health System

Percival H Pangilinan, Jr, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Brian M Kelly, DO Professor, Medical Director, Division of Orthotics and Prosthetics, Department of Physical Medicine and Rehabilitation, University of Michigan Medical School; Assistant Program Director, Residency Training Program, University of Michigan Health System

Brian M Kelly, DO is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Joseph E Hornyak, IV, MD, PhD Associate Professor, Department of Physical Medicine and Rehabilitation, University of Michigan Medical School; Consulting Staff, Medical Director of Human Performance Laboratory, Department of Physical Medicine and Rehabilitation, University of Michigan Medical Center

Joseph E Hornyak, IV, MD, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, Association of Academic Physiatrists, American Academy of Cerebral Palsy and Developmental Medicine

Disclosure: Nothing to disclose.

Scott Strum, MD 

Scott Strum, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Kat Kolaski, MD Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine

Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Consuelo T Lorenzo, MD Medical Director, Senior Products, Central North Region, Humana, Inc

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Elizabeth A Moberg-Wolff, MD Medical Director, Pediatric Rehabilitation Medicine Associates

Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Posttraumatic Hydrocephalus

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