Cerebral vasospasm is the narrowing of blood vessels in the brain, a constriction known as vasoconstriction. This can reduce blood flow to brain tissue. It often arises as a complication following a specific type of brain hemorrhage, and the reduced blood supply can disrupt normal brain function.
How Cerebral Vasospasm Develops
Cerebral vasospasm commonly occurs after a subarachnoid hemorrhage (SAH), which is bleeding into the space surrounding the brain. When an aneurysm ruptures, blood enters this subarachnoid space. This blood irritates and constricts the large arteries at the base of the brain, reducing cerebral blood flow.
Vasospasm begins a few days after the hemorrhage, typically between days 3 and 14, peaking around day 7. Hemoglobin, released from blood clots in the subarachnoid space, initiates this process. Hemoglobin scavenges nitric oxide, which normally helps blood vessels relax. The reduction of nitric oxide causes smooth muscle cells in vessel walls to contract, narrowing the arteries.
This narrowing reduces blood flow, leading to delayed cerebral ischemia (DCI). DCI is a condition where parts of the brain do not receive enough oxygen and nutrients. The severity of vasospasm links to the amount of blood in the subarachnoid cisterns, assessable by computed tomography (CT) scans.
Recognizing the Warning Signs
Recognizing the warning signs of cerebral vasospasm allows for timely intervention. Symptoms vary depending on the affected brain areas and reduced blood flow. These signs develop gradually over hours or days.
Indicators include a worsening headache, which can be more severe than the initial hemorrhage headache. Altered mental status is also observed, presenting as confusion, drowsiness, or a decreased level of consciousness that can progress to a coma.
Patients may exhibit focal neurological deficits, which are problems with specific brain functions. These include weakness or numbness on one side of the body (hemiparesis), difficulties with speech (aphasia), or changes in vision. Seizures can also occur, indicating disruption of brain activity due to inadequate blood supply.
Diagnosing and Treating Cerebral Vasospasm
Diagnosing cerebral vasospasm involves clinical assessment and imaging techniques to evaluate brain blood flow. Transcranial Doppler (TCD) ultrasonography is a non-invasive method measuring blood velocity through cerebral arteries. Increased velocities, exceeding 120 cm/second, indicate vessel narrowing, with velocities above 200 cm/second suggesting severe vasospasm.
Other imaging modalities include CT angiography (CTA) and magnetic resonance angiography (MRA), which provide images of cerebral blood vessels. Digital subtraction angiography (DSA) is the gold standard for visualizing vasospasm, offering detailed views of the cerebral vasculature, though it is an invasive procedure. These tests confirm the presence and severity of vasospasm and rule out other causes of neurological decline.
Treatment strategies aim to restore adequate blood flow to the brain and prevent neurological damage. Medical management begins with the oral calcium channel blocker Nimodipine, administered daily to patients at risk. Maintaining adequate blood pressure and hydration also improves cerebral perfusion.
For severe cases, or when medical management is insufficient, interventional procedures are considered. Induced hypertension, hypervolemia, and hemodilution, known as “Triple-H therapy,” were historically used to augment cerebral blood flow by increasing blood pressure, fluid volume, and reducing blood viscosity. The current focus is euvolemic-induced hypertension, maintaining normal fluid volume while elevating blood pressure.
Endovascular procedures, performed by neurointerventional specialists, include balloon angioplasty and intra-arterial vasodilators. Balloon angioplasty involves inserting a tiny balloon into the narrowed artery and inflating it to widen the vessel, providing a more durable dilation. Intra-arterial vasodilators, such as nicardipine or verapamil, are delivered directly into affected blood vessels to relax arterial walls and improve blood flow. These treatments are reserved for patients whose symptoms do not respond to medical therapy.
Long-Term Effects and Recovery
If cerebral vasospasm is not effectively treated, it can lead to long-term consequences due to prolonged reduced blood flow to the brain. An ischemic stroke is a severe outcome, where brain tissue dies from lack of oxygen. This results in permanent brain damage and lasting neurological deficits, impacting physical and cognitive abilities.
Neurological deficits vary depending on the affected brain area and damage extent. These include persistent weakness or paralysis on one side of the body, speech difficulties, vision impairments, or problems with balance and coordination. Cognitive impairments, such as memory loss, confusion, or personality changes, are also possible.
Recovery after cerebral vasospasm involves comprehensive rehabilitation. This includes physical therapy to regain strength and mobility, occupational therapy to relearn daily living activities, and speech therapy to address communication challenges. The extent of recovery varies among individuals, depending on vasospasm severity, intervention timeliness, and other complications.