SARS-CoV-2, the virus responsible for COVID-19, has generated concern regarding its potential for long-term complications beyond the respiratory system. Among the neurological manifestations reported, the question of whether COVID-19 can cause hydrocephalus is a specific scientific inquiry. Hydrocephalus is defined by the abnormal buildup of cerebrospinal fluid (CSF) within the brain’s ventricles. This excess fluid widens these cavities, putting harmful pressure on the surrounding brain tissue. This article examines the current evidence and proposed biological pathways linking SARS-CoV-2 infection to the onset of hydrocephalus.
Understanding Hydrocephalus
Hydrocephalus results from an imbalance in the production, flow, or absorption of cerebrospinal fluid (CSF), leading to ventricular enlargement. CSF is a clear fluid that surrounds the brain and spinal cord, cushioning the central nervous system and removing metabolic waste products. It is primarily produced by the choroid plexus within the ventricles and reabsorbed into the bloodstream through arachnoid villi.
The body continuously produces and cycles CSF. An obstruction in the narrow passageways between the ventricles causes noncommunicating hydrocephalus. Alternatively, a problem with CSF reabsorption outside the ventricles, often related to inflammation, results in communicating hydrocephalus. This condition can occur at any age due to various factors, including brain tumors, congenital malformations, head trauma, and central nervous system infections like meningitis.
Current Evidence Linking COVID-19 and Hydrocephalus
The link between COVID-19 and hydrocephalus is established primarily through clinical case reports and small observational studies, suggesting it is a rare complication. Hydrocephalus has been observed both during the acute phase of severe SARS-CoV-2 infection and as a delayed, post-acute sequela. In many documented adult cases, the diagnosis was made concurrently with the acute COVID-19 diagnosis.
The onset is not limited to severe respiratory illness; cases have been reported in patients with only mild COVID-19 symptoms, including the development of Normal Pressure Hydrocephalus (NPH). The infection also appears capable of triggering the sudden worsening of neurological symptoms in individuals with pre-existing, stable NPH. These observations suggest the virus or its systemic effects can disrupt CSF dynamics.
A primary indirect pathway involves the hypercoagulable state associated with COVID-19, which can lead to Cerebral Venous Sinus Thrombosis (CVST). CVST, the formation of a blood clot in the brain’s venous sinuses, impairs the drainage of blood and the reabsorption of CSF, leading to communicating hydrocephalus. This thrombotic complication has been reported in young, otherwise healthy patients, sometimes masking the underlying hydrocephalus with symptoms of intracranial hypertension.
Proposed Mechanisms of Viral Impact
The primary hypothesis linking SARS-CoV-2 to hydrocephalus centers on neuroinflammation. The systemic inflammatory response, often called a cytokine storm, can cause swelling and damage to the brain’s ventricular lining (ependymitis). This inflammation can impair the normal flow of CSF, leading to an obstructive form of hydrocephalus.
The virus may also exert effects through the angiotensin-converting enzyme 2 (ACE2) receptor, the entry point for SARS-CoV-2. ACE2 receptors are expressed in central nervous system cells, including those in the choroid plexus, which produces CSF. Direct viral infection of these cells could potentially alter fluid production or damage the ependymal cells lining the ventricles, disrupting CSF flow.
A third proposed mechanism relates to the virus’s impact on the neurovasculature. COVID-19 causes endothelial dysfunction, affecting the inner lining of blood vessels. This damage, combined with the pro-thrombotic state, facilitates the formation of microthrombi and larger clots like CVST, which indirectly impair CSF drainage. While direct viral neurotropism remains debated, the indirect effects of inflammation and vascular damage are strongly implicated in the observed neurological complications.
Age-Specific Considerations
Hydrocephalus presents unique concerns across different age groups affected by SARS-CoV-2 infection. In adults, documented cases are generally linked to post-infectious inflammation or thrombotic complications resulting from systemic disease. The worsening of NPH in older adults is often attributed to the inflammatory surge from COVID-19 acting as a precipitating factor in an already vulnerable CSF system.
The possibility of vertical transmission, where the virus passes from a pregnant mother to the fetus, raises concerns for congenital hydrocephalus. Although rare, vertical transmission is documented, particularly with severe maternal infection. Fetal exposure to the virus, especially during the first trimester, may increase the risk of congenital birth defects due to disruption of fetal brain development.
In rare instances of in utero infection, damage to the developing fetal brain, such as cystic encephalomalacia or severe parenchymal atrophy, could lead to secondary hydrocephalus. The mechanism of injury in the developing brain is distinct, involving direct viral damage to forming structures, rather than the inflammatory or thrombotic events seen in adult cases.