The cerebral aneurysm consists of a focal pathological dilatation of the cerebrovasculature, which becomes prone to rupture.
These vascular anomalies are classified by presumed pathogenesis. Saccular or congenital aneurysms constitute 90% of all cerebral aneurysms located in the main branch points of the great arteries.
Dolichoectatic, fusiform or arteriosclerotic aneurysms are elongated expansions of the proximal arteries that account for 7% of all cerebral aneurysms. Infectious or mycotic aneurysms are peripherally located and comprise 0.5% of all cerebral aneurysms.
Other peripheral lesions include neoplastic aneurysms, strange sequelae of embolized tumor fragments, and traumatic aneurysms.
A traumatic injury can also cause the dissection of aneurysms in the proximal vessels. Microaneurysms of small perforating vessels may be the result of hypertension.
Saccular aneurysms are located in the anterior circulation in 85-95% of cases, while dolichoectal aneurysms predominantly affect the vertebrobasilar system.
The location of saccular aneurysms in specific arterial segments frequently varies due to differences in the study populations reported. Multiple saccular aneurysms are observed in 20-30% of patients with cerebral aneurysms.
Saccular aneurysms often rupture in the subarachnoid space, representing 70-80% of spontaneous subarachnoid hemorrhages (SAH).
A ruptured aneurysm can also cause intraparenchymal, intraventricular, or subdural hemorrhage. Giant saccular aneurysms, defined as greater than 25 mm in diameter, account for 3-5% of all intracranial aneurysms.
Although giant aneurysms can cause SAH, these lesions frequently produce mass effects and distal thromboembolism.
Most of these people (60%) die or suffer permanent disability; 50% of the survivors with favorable results experience a considerable neuropsychological dysfunction.
Cerebral vasospasm (i.e., narrowing of the proximal arterial segments) complicates 20-50% of cases and is the leading cause of death and disability associated with aneurysmal SAH.
Signs and symptoms of cerebral aneurysm
The symptoms associated with a cerebral aneurysm (which occurs when a blood vessel widens so that it bulges or swells in the brain, altering the correct blood flow through it and exploding in the form of hemorrhage) are as follows:
– Facial pain
– Alterations in consciousness
– Manifestation of meningeal irritation
– The autonomic disturbances
– Focal neurological complaints
– Visual symptoms
– Respiratory dysfunction
– Cardiovascular instability
– Hormone dysfunction
It is essential to be aware of this type of symptomatology to prevent the formation of cerebral aneurysms. In this regard, specific findings from the physical examination may include prominent scalp veins, signs of congestive heart failure (e.g., Galen’s aneurysm vein), orbital murmurs (e.g., carotid, carotid aneurysms). In contrast, the neurological findings show considerable variability due to differences in the characteristics of the aneurysm. These findings include the following:
SAA aneurysm: may be accompanied by nuchal rigidity, decreased level of consciousness, subhaloid hemorrhages, pupillary abnormalities (i.e., typically dilated), ophthalmoplegia, cranial neuropathies, and other focal deficits.
Giant aneurysms or dolichoectal aneurysms: may cause mass effects and distal thromboembolism with prominent focal deficits; these aneurysms can also produce optic atrophy or other cranial neuropathies or cause compression of the brainstem.
Specific syndromes have been associated with particular aneurysmal locations. For example, aneurysms in the anterior communicating artery, the most common site of aneurysmal SAH (34%), have the following characteristics:
- These aneurysms usually remain silent until they break
- The supra-asthmatic pressure may cause visual field deficit, abulia or akinetic mutism, amnestic syndromes, or hypothalamic dysfunction.
- Neurological deficits in rupture of the aneurysm may reflect intraventricular hemorrhage (79%), intraparenchymal hemorrhage (63%), acute hydrocephalus (25%), or frontal lobe embolisms (20%)
Diagnosis of a cerebral aneurysm
Laboratory studies used in the diagnosis and evaluation of cerebral aneurysms include the following:
– Complete blood count (CBC) with platelets: That includes monitoring the infection, assessing anemia, and identifying the risk of bleeding
– Prothrombin time (PT) / activated partial thromboplastin time (aPTT): which seeks to identify a coagulopathy that increases the risk of hemorrhage
– Serum chemistry, including electrolytes and osmolarity: Whose goal is to obtain baseline studies to control hyponatremia, treat arrhythmogenic abnormalities, evaluate blood glucose and control hyperosmolar therapy for elevated intracranial pressure
– Liver function tests aim to identify liver dysfunction that may complicate the clinical course.
– Arterial blood gases: Through which the oxygenation of the blood is evaluated
The imaging studies used in the treatment of cerebral aneurysms include the following:
– Computed tomography (CT): An aneurysmal SAH can be detected in 90-95% of cases.
– Magnetic resonance imaging (MRI): The fluid-attenuated inversion recovery (FLAIR) sequences are susceptible to SAH, although the comparison of CT with MRI in the detection of SAH is controversial; Dolichoectatic and giant aneurysms are easily identified with an MRI
– Angiography: conventional angiography is the definitive procedure for the detection and characterization of cerebral aneurysms
– Transcranial Doppler Ultrasonography: this modality facilitates the diagnosis of vasospasm and serial monitoring of cerebral blood flow at the patient’s bedside
– Single-photon emission tomography (SPECT), positron emission tomography (PET), Xenon-CT tomography (X): with these techniques, cerebral blood flow studies can show ischemia associated with vasospasm; although these modalities do not, they are routinely used
– Image of the cervical spine: the radiographic evaluation of the cervical spine should be performed on all patients in a coma with a loss of unwarranted consciousness.
– Echocardiography: cardiac sources of embolism, including endocarditis and myxomas, can be seen in cases of infectious or neoplastic aneurysms.
– Lumbar puncture can help establish the diagnosis of SAH without focal signs of massive effects.
An aneurysmal SAH shows hemorrhagic cerebrospinal fluid with a xanthochromia supernatant, although these findings may be absent within the first hours after rupturing the aneurysm.
Effects or consequences of the cerebral aneurysm
One of the consequences of the cerebral aneurysm is aneurysmal subarachnoid hemorrhage (SAH), which is devastating.
About 10% of people with aneurysmal SAH die before receiving medical attention, 25% die within 24 hours, and 40-49% die within three months.