Hydrocephalus is “an active distention of the ventricular system of the brain related to inadequate passage of cerebrospinal fluid (CSF) from its point of production within the ventricular system to its point of absorption into the systemic circulation.” It is broadly categorized as communicating or non-communicating. It is caused by:
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Excess CSF production
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Obstruction of CSF flow in the ventricles or subarachnoid space
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Decrease in absorption via the arachnoid granulations
Hydrocephalus ex vacuo is a compensatory enlargement of CSF space including cerebral ventricles and subarachnoid spaces in response to brain parenchyma loss.
Pathophysiology
The choroid plexus produces 80% of CSF, and 20% is produced by the transependymal flow of fluid to the ventricles from parenchyma.
CSF circulates from the lateral ventricles foramina of Monro, third ventricle aqueduct of Sylvius fourth ventricle foramina of Luschka and Magendie subarachnoid space ( Fig. 26.1 ).
It is reabsorbed by arachnoid granulations in the dural venous sinuses.
The underlying pathophysiology of posttraumatic hydrocephalus is primarily caused by a disruption of CSF flow.
Communicating or nonobstructive hydrocephalus is caused by impaired reabsorption of CSF at the arachnoid granulations after infection, inflammation, or hemorrhage. These processes cause scarring and fibrosis of the subarachnoid space, impairing re-absorption leading to enlargement of the ventricles.
The dysfunction of the arachnoid villa is thought to be caused by subarachnoid blood; its metabolic products including hemoglobin, iron, and transforming growth factor-ß1 (TGF-β1) released from platelets. TGF-β1 and thrombin cause mechanical blockage and fibrosis of the arachnoid granulations, preventing CSF absorption and outward CSF flow from the subarachnoid space to the venous circulation. , Additionally, iron and thrombin cause ciliary dysfunction and destruction and ependymal cell damage in the ventricles impairing CSF circulation and causing hydrocephalus. ,
Noncommunicating or obstructive hydrocephalus is caused by a blockage preventing the flow of CSF to the subarachnoid space. The obstruction can happen anywhere along the pathway of CSF flow, including the foramen of Monro, aqueduct of Sylvius, fourth ventricle, or the foramen of Luschka or Magendie. This causes accumulation of CSF proximal to the blockage, leading to increased ventricle size and increased CSF pressure.
There are emerging hydrodynamic models looking at the role of pulsatile pressure and flow of CSF in the pathophysiology of hydrocephalus. These concepts are challenging the current theories of hydrocephalus.
Incidence
Within 2 months after moderate to severe traumatic brain injury (TBI), 70% of patients develop ventriculomegaly caused by any etiology. Studies excluding other causes of hydrocephalus, such as atrophy, have shown an incidence of posttraumatic hydrocephalus (PTH) ranging from 3.7% to 45%. Variation may be caused by underdiagnosis and differences in diagnosing criteria. In patients with decompressive craniectomy, a metaanalysis of retrospective studies determined that the rate of PTH is 6.3% to 54%, similar to that reported by De Bonis et al. (0.7%–51.4%).
In the postacute period, patients may be diagnosed with hydrocephalus up to 8 weeks into their rehabilitation stay, with most diagnosed earlier. In some cases, patients may be diagnosed even a year after their injury.
Presentation
The classic triad of symptoms present in a patient with hydrocephalus include incontinence, ataxia, and confusion—also known as wet, wild, and wobbly . The gait abnormality can be described as magnetic and resembles the type of ambulation noted in those with frontal lobe or subcortical injury. The cognitive deficits may manifest as impaired memory and confusion.
In PTH, the presentation is often subtler. As described by Ivanhoe, “patients may present with abulia, emotional lability, perseveration, mutism, apraxia, or change in bladder or bowel function not related to infection .” The citation for this quote is the same as that following- It is Clinicians must be wary of a decline in function, plateau in improvement, or less improvement than expected as potential signs of PTH. Additional symptoms include headache, nausea, increased spasticity, epileptic seizures, aggressiveness and parkinsonian features such as bradykinesia, rigidity, and postural instability. , , ,
The most telling findings on physical examination are the characteristic gait of hydrocephalus (wide based, unsteady, small steps), papilledema, focal neurological findings, and an abducens nerve palsy presenting as a mild decrease in lateral horizontal eye movement. The lateral rectus palsy has been described as a component of Parinaud’s syndrome, in which dilation of the third ventricle causes a downward compression on the collicular plate of the midbrain.
In patients with severe TBI, diagnosis of PTH may be more difficult. A combination of radiographic imaging, CSF dynamics, and clinical deterioration during rehabilitation are used to assist the diagnosis of PTH.
PTH has been shown to prevent and delay recovery after TBI and impair outcomes. With CSF diversion, significant clinical improvement has been reported both acutely and long term, with positive impact seen in the Glasgow Outcome Scale, Functional Independence Measure (FIM), Disability Rating Scale (DRS), and Neurobehavioral Rating Scale at follow-up. ,
Risk factors
Risk factors for subsequent development of PTH include , , , :
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Older age
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Traumatic subarachnoid hemorrhage and intraventricular hemorrhage (Fisher grades III or IV)
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Posterior circulation bleeds
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More severe injury
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Longer posttraumatic amnesia
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Lower GCS scores
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Vegetative state
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Length of coma greater than or equal to 1 week
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Lower FIM scores on admission to rehabilitation
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Decompressive craniectomy defects
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Larger craniectomy defects
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Superior craniectomy edges closer to midline
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Bilateral craniectomy defects
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Extracranial herniation or subdural hygroma after decompressive craniectomy
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Evaluation
Evaluation of suspected PTH typically begins with radiographic evaluation consisting of a standard magnetic resonance imaging (MRI) or computed tomography (CT) scan of the brain. Visualization of the brain is important in identifying ventriculomegaly, distinguishing hydrocephalus from hydrocephalus ex vacuo, and assessing shunt function. Multiple methods exist to standardize evaluation, including the Evans index, which is a marker of ventricular enlargement, or the enlargement of the anterior horns of the lateral ventricles, temporal horns, and third ventricle, and periventricular interstitial edema in the presence of normal or absent sulci ( Fig. 26.2 ).
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