Cerebral aneurysm refers to a dilation of an intracranial blood vessel. It may exert a local mass effect, and it may also rupture and cause cerebral hemorrhage.
Presentation
The majority of CA is small and does not provoke any symptoms until rupture. Such vascular anomalies may be detected if neuroimaging is performed due to any other reasons.
With regards to symptomatic CA, there may be non-specific symptoms indicating an intracranial lesion, possibly also prompting the suspicion of an increase of intracranial pressure. Patients may claim headaches and facial pain, present decreased levels of consciousness and/or an altered mental state. Ophthalmoplegia and visual impairment (consisting in blurred vision, diplopia and a restricted field of vision) are common and may be triggered by aneurysms located in the anterior or posterior communicating artery or the terminus of the internal carotid artery, among others. Cranial nerve palsies distinct from those of the optical, oculomotor, abducens and trochlear nerves as well as specific neurological deficits may also be observed. For instance, functional deficits of the lower cranial nerves may be seen in patients suffering from vertebrobasilar aneurysm. Cardiovascular or respiratory symptoms indicate compression of the brainstem, and in rare cases, endocrinologic disorders may dominate the clinical picture of CA.
Additionally, symptoms typically associated with hydrocephalus and meningitis may be observed. Nausea and vomiting and neck stiffness are signs of those diseases, and this also applies to some of the aforementioned pathological conditions.
Entire Body System
- Malaise
They also result in nausea, vomiting, photophobia, malaise, or, less commonly, neck pain. Sentinel bleeds precede aneurysm rupture by a few hours to a few months, with a reported mean of two weeks prior to discovery of the SAH. [case.edu]
For example, in the case of an aneurysm caused by vasculitis, or blood vessel inflammation, a person may experience fever, malaise, or weight loss. [medicalnewstoday.com]
- Collapse
At approximately 8:30 pm on January 5, the patient grasped his head, cried out, and collapsed leading to emergency transfer to the nearest hospital. [ajnr.org]
- Unconsciousness
If you receive a general anesthetic, you will be unconscious for the entire procedure, and you will be monitored by an anesthesiologist. [radiologyinfo.org]
Gastrointestinal
- Nausea
A 54-year-old woman presented to the ED after an episode where she had noticed a "bad smell" and sensations of nausea and dizziness. [ncbi.nlm.nih.gov]
Symptoms of a brain aneurysm Symptoms may include: Severe sudden headache Nausea and vomiting Loss of consciousness Stiff neck Fever Sensitivity to light Testing to diagnose a brain aneurysm Your doctor will perform a CT scan of the head to look for blood [upmc.com]
They also result in nausea, vomiting, photophobia, malaise, or, less commonly, neck pain. Sentinel bleeds precede aneurysm rupture by a few hours to a few months, with a reported mean of two weeks prior to discovery of the SAH. [case.edu]
Before an aneurysm ruptures, the individual may experience such symptoms as a sudden and usually severe headache ("worst headache of my life"), nausea, vision impairment, vomiting, and loss of consciousness, or the individual may be asymptomatic experiencing [ucdenver.edu]
Other symptoms of an aneurysm rupture may include: Confusion, no energy, sleepiness, stupor, or coma Eyelid drooping Headaches with nausea or vomiting Muscle weakness or difficulty moving any part of the body Numbness or decreased sensation in any part [medlineplus.gov]
Eyes
- Eye Pain
The symptoms of an unruptured cerebral aneurysm may include: Headaches Dizziness Eye pain Vision deficits The first evidence of a cerebral aneurysm may be a subarachnoid hemorrhage (SAH), due to rupture of the aneurysm. [neurosciences.uvahealth.com]
The symptoms of an unruptured brain aneurysm include the following: Headaches (rare, if unruptured) Eye pain Vision changes Diminished eye movement The first evidence of a brain aneurysm is most often a subarachnoid hemorrhage (SAH), due to rupture of [hopkinsmedicine.org]
Symptoms may include: Double vision Loss of vision Headaches Eye pain Neck pain Stiff neck Ringing in the ears A sudden, severe headache is one symptom of an aneurysm that has ruptured. [medlineplus.gov]
- Visual Impairment
Symptoms CA may not cause any symptoms at all, or they may merely lead to unspecific complaints like headaches, facial pain and visual impairment. Decreased levels of consciousness or an altered mental state may be observed. [symptoma.com]
- Visual Impairment
Symptoms CA may not cause any symptoms at all, or they may merely lead to unspecific complaints like headaches, facial pain and visual impairment. Decreased levels of consciousness or an altered mental state may be observed. [symptoma.com]
Neurologic
- Headache
A 67-year-old woman developed a sudden onset headache and left hemiparesis. Emergency medical technicians found that she was conscious, but had left hemiparesis. [ncbi.nlm.nih.gov]
This may cause a severe headache that a person may describe as "the worst headache of my life." It may be called a thunderclap or sentinel headache. [medlineplus.gov]
Migraine headache, meningitis, tumor, and stroke all may cause neurologic symptoms. [medicinenet.com]
- Confusion
Confusion or mild impairment in alertness also may be noted. • Seizures: are present in 25% of aneurysmal SAH cases, with most events occurring within 24 hours of onset. 11. • Autonomic disturbances: Subarachnoid accumulation of products of blood degradation [slideshare.net]
“My manager later told me I kept repeating, ‘I’m confused’ and asking, ‘What time is it?’” LaDel says. “I don’t remember any of that.” [uihc.org]
Ruptured aneurysm symptoms may include: A drooping eyelid A sudden, very severe headache Blurred or double vision Confusion Loss of consciousness Nausea and/or vomiting Seizures Sensitivity to light Stiff neck Intact aneurysms typically do not have symptoms [baptisthealth.com]
Call 911 for any of the following: You have any of the following signs of a stroke: Numbness or drooping on one side of your face Weakness in an arm or leg Confusion or difficulty speaking Dizziness, a severe headache, or vision loss You lose consciousness [drugs.com]
Other symptoms of an aneurysm rupture may include: Confusion, no energy, sleepiness, stupor, or coma Eyelid drooping Headaches with nausea or vomiting Muscle weakness or difficulty moving any part of the body Numbness or decreased sensation in any part [medlineplus.gov]
- Intracranial Hemorrhage
NCA from cardiac myxoma were probably multiple and rarely associated with intracranial hemorrhage, while the majority of NCA from choriocarcinoma and other tumors were single and presented with intracranial hemorrhage. [ncbi.nlm.nih.gov]
hemorrhage or intracranial hemorrhages; giant aneurysms (>2.5 cm in diameter) may compress adjacent structures, including the oculomotor nerve. [fpnotebook.com]
General Neurosurgery and Emergency Care Intracranial Hemorrhage Spinal Cord Injury Spine Fractures Traumatic Brain Injury SPINE Cervical, Thoracic, and Lumbar Degenerative Spine Disease Degenerative Disc Disease Foraminal Stenosis Herniated Disc Radiculopathy [vaneurosurgeons.com]
[…] brain; rupture results in subarachnoid hemorrhage or intracranial hemorrhages; giant aneurysms (>2.5 cm in diameter) may compress adjacent structures, including the oculomotor nerve. [icd10data.com]
Noncontrast MRI with susceptibility-weighted sequences is likely to be as sensitive as noncontrast head CT scans in the detection of intracranial hemorrhage. [5] Diffuse, severe SAH is seldom helpful in identifying the specific site of the aneurysm. [emedicine.com]
- Cranial Neuropathy
[…] deficits Giant aneurysms or dolichoectatic aneurysms: May cause mass effects and distal thromboembolism with prominent focal deficits; these aneurysms may also result in optic atrophy or other cranial neuropathies or cause brainstem compression. [emedicine.com]
neuropathies (12 percent of aneurysms) Chronic symptomatology (32 percent) which included headache (51%) Visual deficits (29 percent) Weakness (11 percent) and Facial pain (nine percent) The management of both ruptured and un-ruptured cerebral aneurysms [aans.org]
- Vertigo
Abstract A 43-year-old male with a history of bioprosthetic aortic valve replacement and tricuspid valve annuloplasty presented with vertigo and was found to have an acute infarct in the left superior cerebellum, as well as a left-middle cerebral artery [ncbi.nlm.nih.gov]
Dizziness and vertigo 840 26.2. Meniere s disease 842 26.3. Facial nerve palsy 844 26.4. Hearing loss 848 26.5. References 849 27. Head trauma 850 27.1. Transfer of trauma patients 854 27.2. Management in E/R 855 27.3. Neuromonitoring 866 27.4. [worldcat.org]
Workup
With decreasing frequency, CA are detected in the anterior communicating artery, the terminus of the internal carotid artery, the posterior communicating artery and the anterior choroidal artery [8], and neuroimaging allows for their visualization, for the assessment of size, morphology and precise location. Angiography, carried out by means of 3D digital subtraction, computed tomography or magnetic resonance imaging, is generally indicated. The sensitivity of all techniques exceeds 95%. For a long time, 3D digital subtraction angiography has been the gold standard in CA diagnostics, but this approach is increasingly replaced by digital subtraction computed tomography angiography. Acquisition times and limited accessibility of the patient argue against magnetic resonance imaging. In any case, cerebral hemorrhages may not permit angiography to be realized within a reasonable time frame [7]. Of note, it is not uncommon to detect multiple CA.
In order to assess the general condition of the patient, laboratory analyses of blood samples and measurement of coagulation times should be realized.
Treatment
CA may be treated either conservatively or surgically, and a variety of factors should be considered before deciding for either of both options [9]. In detail, the following aspects should be taken into account:
- Age of the patient
- Medical history and individual risk factors, e.g., hypertension and ethnicity
- Clinical presentation and current quality of life
- Comorbidities, especially if associated with a reduced life expectancy
- Size, morphology and location of CA
- Detection of aneurysm growth
There is a risk inherent to surgery, although it may vary depending on the site of the aneurysm. In case of small, non-growing CA, the overall risk of rupture is low, and may indeed be lower than the aforementioned risk associated with a surgical intervention to repair the vasculopathy.
Conservative treatment basically consists in observation and regular follow-ups. With regards to drug therapy, corticosteroids, diuretics like mannitol and fibrinolytics have been applied in case of CA. Evidence supporting their efficacy is scarce and thus, their application is matter of ongoing debate. Thromboembolism due to CA may have detrimental consequences, though, and thus, at least the use of fibrinolytics is often recommended. Furthermore, control of hypertension by application of calcium channel blockers or alternative anti-hypertensive drugs should be pursued, and patients prone to seizures benefit from anticonvulsants.
Endovascular repair of CA presumably bears lower risks of recurrence than surgical clipping. Endovascular CA treatment comprises coiling of the respective bulge, while a clip encloses the neck of an aneurysm and thus isolates it from circulation. Relapses may be associated with incomplete clipping of aneurysms [10]. Of note, blood pressure should be maintained in the upper physiological ranges after such interventions, since the risk of vasospasms and subsequent ischemia is rather high. Generally, vasospasms develop within three weeks after surgery.
Prognosis
CA are potentially life-threatening and death may occur due to cerebral hemorrhage and/or compression of brain structures. CA rupture is associated with particularly high mortality rates and large aneurysms are most likely to rupture. However, the prevalence of small CA by far exceeds that of large CA and thus, the majority of cerebral hemorrhages is indeed caused by small aneurysms. Besides size, aneurysm growth, a medical history of cerebral hemorrhages and vertebrobasilar aneurysms have been identified as prognostic factors of CA rupture [5]. In sum, about one in four patients presenting with ruptured CA dies within 24 hours, a further 50% within one month [8].
Etiology
CA may be congenital or acquired, whereby the latter are much more common than the former. In fact, a review of the available literature only reveals a few isolated case reports of congenital CA [1]. Furthermore, a patient may be genetically predisposed for aneurysms and thus have a higher risk of developing this condition throughout life. The fact that familial accumulation of CA has been registered supports this statement. Hereditary connective tissue disorders like Marfan syndrome, for instance, may be associated with an increased elasticity of arteries and remodeling processes that progressively weaken the arterial wall. Nevertheless, most CA develop due to an unfavorable combination of acquired pathologies like atherosclerosis or vasculitis, and hypertension. Here, release of pro-inflammatory mediators and endogenous or bacterial proteinases provokes structural alterations of the vessel's wall, causes loss of flexibility and resistance [2]. Bacteremia - in itself a complication of primary diseases like endocarditis - may be the trigger for these events. Depending on the severity of vascular lesions, single entities may or may not lead to CA formation. Increased blood pressure augments the mechanical stress on affected arteries and veins, and thus, favors further dilation of the aneurysm and possible rupture. Further pathologies that may lead to CA are metastasizing neoplasms [3], head trauma and sickle cell disease. Smoking as well as abuse of alcohol and illicit drugs have been shown to be enhancing etiologic factors.
Epidemiology
It has been estimated that 2 to 5% of the overall population are affected by CA [4], whereby rising tendencies are primarily ascribed to improved diagnostics. Fortunately, the incidence of CA rupture is much lower. According to a recent retrospective study, 1 to 2% of CA rupture per year [5]. Interestingly, prevalence of CA and incidence of cerebral hemorrhage due to CA vary with geographical location. Finnish people seem to be particularly susceptible to fatal rupture of CA [6]. Often, women are reported to be more frequently affected by CA and rupture, but according to the cited study, this does not apply to all populations. The overall incidence of CA increases with age, and pediatric patients usually suffer from congenital disorders predisposing for aneurysm development [7].
Pathophysiology
Similar to aneurysms in other parts of the body, CA are focal, pathological dilations of blood vessels. In most cases, they have a regular, round to oval shape, and such aneurysms are generally referred to as saccular or berry aneurysms. They may be connected to the respective vessel through a narrow or wide neck, and this distinction is of importance with regards to the choice of therapy. Wide-necked aneurysms are absolute contraindications of endovascular coiling since the coil may prolapse into the vessel, which would cause an obstruction of blood flow.
The greatest risk associated with CA is that of rupture. Such an event generally leads to subarachnoid hemorrhage, but blood may also accumulate in subdural, intraventricular or intraparenchymal spaces. Both the initial lesion of the vessel's wall as well as the eventual rupture have been classified as inflammatory events [2]. Due to an often unknown cause, pro-inflammatory cytokines and matrix metalloproteinases are released. They stimulate smooth muscle cell apoptosis and degradation of the extracellular matrix of the vessel's wall, which results in a focal weak spot. Because of ongoing pressure, this spot may dilate. Thus, the aneurysm grows, and the presence of a CA causes turbulences, favors thrombus formation and further degradation of the vessel's wall. Over the course of this iterative process, the CA may grow, and the pressure on adjacent tissue and the probability of rupture increases.
As has been indicated before, formation of blood clots within an aneurysm may occur and may lead to thromboembolism in peripheral organs, e.g., in coronary or renal arteries.
Prevention
No specific measures can be recommended to prevent CA. Since early mortality is high and symptoms associated with CA may be rather non-specific, complete workups are of utmost importance to improve the patient's prognosis. In case an aneurysm is detected and treated, regular follow-ups are recommended to recognize aneurysm growth, CA rupture and possible recurrences.
Summary
In general, the term aneurysm describes a pathological dilation of a blood vessel. An aneurysm results from anomalies in the vessel's wall that renders it less resistant to the pressure it is constantly exposed to. Because the arterial blood pressure is higher than the venous blood pressure, aneurysms most commonly affect arteries. Virtually any blood vessel in the human body may dilate, and depending on its precise location, the corresponding bulge may compress adjacent structures. In case of cerebral aneurysm (CA), i.e., dilation of an intracranial blood vessel, pressure-induced lesions of adjacent tissues may have detrimental, life-threatening effects. Moreover, an aneurysm may rupture and the ensuing hemorrhage may add to the local mass effect or provoke hemodynamical failure. The former is of great importance in CA, the latter rather applies to aortic aneurysm and lesions of other major vessels.
Estimated prevalence rates of up to 5% of the general population may be surprising, but there is an explanation for the apparent contradiction between a high prevalence of CA and a low incidence of severe complications due to cerebral hemorrhage: The majority of CA measure less than a few millimeters in diameter and affected individuals remain asymptomatic. The risk of rupture and potentially fatal hemorrhages positively correlates with aneurysm size, but there is no cut-off value that would exclude the possibility of CA rupture.
According to the aforementioned epidemiological data, a specific treatment may or may not be indicated. Drug therapy has proven to be little helpful, and both endovascular coiling and surgical clipping are associated with considerable risks. Guidelines have been developed to aid the treating physician in their choice for either therapeutic approach.
The term intracranial aneurysm is often used synonymously to CA.
Patient Information
An aneurysm is a focal, pathological dilation of a blood vessel. Virtually all vessels may be affected, and if an aneurysm is encountered intracranially, it is referred to as cerebral aneurysm (CA).
Causes
Most CA develop due to an unfavorable combination of acquired pathologies like atherosclerosis, inflammation of blood vessels and hypertension. During an inflammatory reaction, mediators and enzymes are released that degrade the vessel's wall. It thus loses flexibility and resistance and eventually succumbs to blood pressure.
In some cases, CA may be congenital.
Symptoms
CA may not cause any symptoms at all, or they may merely lead to unspecific complaints like headaches, facial pain and visual impairment. Decreased levels of consciousness or an altered mental state may be observed. In some cases, neurological deficits may be registered.
Diagnosis
Angiography, i.e., visualization of blood vessels, is the diagnostic approach of choice. There are distinct techniques that may be applied to depict intracranial vessels, and in fact, some CA may be detected on images obtained for unrelated reasons.
Treatment
Patients incidentially diagnosed with small, non-growing CA may not need any specific therapy. Their condition should be monitored, though, and it is important they comply with regular follow-ups.
With regards to those patients presenting CA-associated symptoms, large, growing aneurysms or vasculopathies at risk of rupture, there are essentially two therapeutic options: Endovascular coiling or surgical clipping. Coils may be placed inside an aneurysm without the need for open surgery, but this technique may not be feasible in case of wide-necked CA. On the other hand, a clip may be placed on the neck of the aneurysm and isolate it from circulation.
References
- Hill TR. Two Cases of Leaking Congenital Intracranial Aneurysm. Ligature of Internal Carotid Artery. Proc R Soc Med. 1938; 31(3):215-218.
- Chalouhi N, Hoh BL, Hasan D. Review of cerebral aneurysm formation, growth, and rupture. Stroke. 2013; 44(12):3613-3622.
- Zheng J, Zhang J. Neoplastic cerebral aneurysm from metastatic tumor: a systematic review of clinical and treatment characteristics. Clin Neurol Neurosurg. 2015; 128:107-111.
- Arning A, Jeibmann A, Kohnemann S, et al. ADAMTS genes and the risk of cerebral aneurysm. J Neurosurg. 2016:1-6.
- Ishibashi T, Murayama Y, Urashima M, et al. Unruptured intracranial aneurysms: incidence of rupture and risk factors. Stroke. 2009; 40(1):313-316.
- Ingall T, Asplund K, Mahonen M, Bonita R. A multinational comparison of subarachnoid hemorrhage epidemiology in the WHO MONICA stroke study. Stroke. 2000; 31(5):1054-1061.
- Hülsmann S, Moskopp D, Wassmann H. Management of a ruptured cerebral aneurysm in infancy. Report of a case of a ten-month-old boy. Neurosurg Rev. 1998; 21(2-3):161-166.
- Grasso G, Perra G. Surgical management of ruptured small cerebral aneurysm: Outcome and surgical notes. Surg Neurol Int. 2015; 6:185.
- Etminan N, Brown RD Jr, Beseoglu K, et al. The unruptured intracranial aneurysm treatment score: a multidisciplinary consensus. Neurology. 2015; 85(10):881-9.
- Rothemeyer S, Lefeuvre D, Taylor A. Recurrent or new symptomatic cerebral aneurysm after previous treatment. Interv Neuroradiol. 2005; 11(4):341-348.