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Computed tomography (CT scan): A CT scan may be normal if it is done soon after the onset of symptoms. A CT scan is the best test to look for bleeding in or around your brain. In some hospitals, a perfusion CT scan may be done to see where the blood is flowing and not flowing in your brain.
Magnetic resonance imaging (MRI scan): A special MRI technique (diffusion MRI) may show evidence of an ischemic stroke within minutes of symptom onset. In some hospitals, a perfusion MRI scan may be done to see where the blood is flowing and not flowing in your brain.
Angiogram: a test that looks at the blood vessels that feed the brain. An angiogram will show whether the blood vessel is blocked by a clot, the blood vessel is narrowed, or if there is an abnormality of a blood vessel known as an aneurysm.
Carotid duplex: A carotid duplex is an ultrasound study that assesses whether or not you have atherosclerosis (narrowing) of the carotid arteries. These arteries are the large blood vessels in your neck that feed your brain.
Transcranial Doppler (TCD): Transcranial Doppler is an ultrasound study that assesses whether or not you have atherosclerosis (narrowing) of the blood vessels inside of your brain. It can also be used to see if you have emboli (blood clots) in your blood vessels.
Both computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have been proved to be effective in diagnosing intracranial vascular malformations after ICH. So frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage or to detect a "spot sign".
Intraparenchymal hemorrhage can be recognized on CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain because of edema, and therefore shows up darker on the CT scan.
When due to high blood pressure, they typically occur in the putamen or thalamus (60%), cerebrum (20%), cerebellum (13%) or pons (7%).
An AVM diagnosis is established by neuroimaging studies after a complete neurological and physical examination. Three main techniques are used to visualize the brain and search for AVM: computed tomography (CT), magnetic resonance imaging (MRI), and cerebral angiography. A CT scan of the head is usually performed first when the subject is symptomatic. It can suggest the approximate site of the bleed. MRI is more sensitive than CT in the diagnosis of AVMs and provides better information about the exact location of the malformation. More detailed pictures of the tangle of blood vessels that compose an AVM can be obtained by using radioactive agents injected into the blood stream. If a CT is used in conjunctiangiogram, this is called a computerized tomography angiogram; while, if MRI is used it is called magnetic resonance angiogram. The best images of an AVM are obtained through cerebral angiography. This procedure involves using a catheter, threaded through an artery up to the head, to deliver a contrast agent into the AVM. As the contrast agent flows through the AVM structure, a sequence of X-ray images are obtained.
Diagnostic methods include:
- Angiogram
Due to positive remodeling the plaque build-up shown on angiogram may appear further downstream on the x-ray where the luminal diameter would look normal even though there is severe narrowing at the real site. Because angiograms require x-rays to be visualized the number of times an individual can have it done over a year is limited by the guidelines for the amount of radiation they can be exposed to in a one-year period.
- Magnetic resonance imaging (MRI)
Magnetic resonance imaging has the ability to quantify the plaque anatomy and composition. This allows physicians to determine certain characteristics of the plaque such as how likely it is to break away from the wall and become an embolus. MRI does not use ionizing radiation, so the number of times that it is used on a single person is not a concern; however since it uses strong electric fields those who have metal implants in cannot use this technique.
- Computed tomography (CT)
Multidirectional computed tomography (MDCT) is better than regular CT scans, because it can provide a higher spatial resolution and it has a shorter acquisition time. MDCT uses x-rays to obtain the image; however it can identify the composition of the plaque. Thus it can be determined whether the plaque is calcified plaque and lipid-rich plaque, so the inherent risks can be determined. Subjects are exposed to a substantial amount of radiation with this procedure, so their use is limited.
Intracerebral hemorrhages is a severe condition requiring prompt medical attention. Treatment goals include lifesaving interventions, supportive measures, and control of symptoms. Treatment depends on the location, extent, and cause of the bleeding. Often, treatment can reverse the damage that has been done.
A craniotomy is sometimes done to remove blood, abnormal blood vessels, or a tumor. Medications may be used to reduce swelling, prevent seizures, lower blood pressure, and control pain.
A limitation of the Spetzler-Martin Grading system is that it does not include the following factors: Patient age, hemorrhage, diffuseness of nidus, and arterial supply. In 2010 a new supplemented Spetzler-Martin system (SM-supp, Lawton-Young) was devised adding these variables to the SM system. Under this new system AVMs are classified from grades 1 - 10. It has since been determined to have greater predictive accuracy that Spetzler-Martin grades alone.
There are various neuroimaging investigations that may detect cerebral sinus thrombosis. Cerebral edema and venous infarction may be apparent on any modality, but for the detection of the thrombus itself, the most commonly used tests are computed tomography (CT) and magnetic resonance imaging (MRI), both using various types of radiocontrast to perform a venogram and visualise the veins around the brain.
Computed tomography, with radiocontrast in the venous phase ("CT venography" or CTV), has a detection rate that in some regards exceeds that of MRI. The test involves injection into a vein (usually in the arm) of a radioopaque substance, and time is allowed for the bloodstream to carry it to the cerebral veins - at which point the scan is performed. It has a sensitivity of 75-100% (it detects 75-100% of all clots present), and a specificity of 81-100% (it would be incorrectly positive in 0-19%). In the first two weeks, the "empty delta sign" may be observed (in later stages, this sign may disappear).
Magnetic resonance venography employs the same principles, but uses MRI as a scanning modality. MRI has the advantage of being better at detecting damage to the brain itself as a result of the increased pressure on the obstructed veins, but it is not readily available in many hospitals and the interpretation may be difficult.
Cerebral angiography may demonstrate smaller clots than CT or MRI, and obstructed veins may give the "corkscrew appearance". This, however, requires puncture of the femoral artery with a sheath and advancing a thin tube through the blood vessels to the brain where radiocontrast is injected before X-ray images are obtained. It is therefore only performed if all other tests give unclear results or when other treatments may be administered during the same procedure.
The modality of choice is computed tomography (CT scan) without contrast, of the brain. This has a high sensitivity and will correctly identify over 95 percent of cases—especially on the first day after the onset of bleeding. Magnetic resonance imaging (MRI) may be more sensitive than CT after several days. Within six hours of the onset of symptoms CT picks up 98.7% of cases.
Screening for aneurysms is not performed on a population level; because they are relatively rare, it would not be cost-effective. If someone has two or more first-degree relatives who have had an aneurysmal subarachnoid hemorrhage, screening may be worthwhile.
Autosomal dominant polycystic kidney disease (ADPKD), a hereditary kidney condition, is known to be associated with cerebral aneurysms in 8 percent of cases, but most such aneurysms are small and therefore unlikely to rupture. As a result, screening is only recommended in families with ADPKD where one family member has had a ruptured aneurysm.
An aneurysm may be detected incidentally on brain imaging; this presents a conundrum, as all treatments for cerebral aneurysms are associated with potential complications. The International Study of Unruptured Intracranial Aneurysms (ISUIA) provided prognostic data both in people having previously had a subarachnoid hemorrhage and people who had aneurysms detected by other means. Those having previously had a SAH were more likely to bleed from other aneurysms. In contrast, those having never bled and had small aneurysms (smaller than 10 mm) were very unlikely to have a SAH and were likely to sustain harm from attempts to repair these aneurysms. On the basis of the ISUIA and other studies, it is now recommended that people are considered for preventive treatment only if they have a reasonable life expectancy and have aneurysms that are highly likely to rupture. At the same time, there is only limited evidence that endovascular treatment of unruptured aneurysms is actually beneficial.
A 2004 study suggested that the D-dimer blood test, already in use for the diagnosis of other forms of thrombosis, was abnormal (above 500 μg/l) in 34 out of 35 patients with cerebral sinus thrombosis, giving it a sensitivity of 97.1%, a negative predictive value of 99.6%, a specificity of 91.2%, and a positive predictive value of 55.7%. Furthermore, the level of the D-dimer correlated with the extent of the thrombosis. A subsequent study, however, showed that 10% of patients with confirmed thrombosis had a normal D-dimer, and in those who had presented with only a headache 26% had a normal D-dimer. The study concludes that D-dimer is not useful in the situations where it would make the most difference, namely in lower probability cases.
Diagnosis of cerebrovascular disease is done by (among other diagnoses):
- clinical history
- physical exam
- neurological examination.
It is important to differentiate the symptoms caused by a stroke from those caused by syncope (fainting) which is also a reduction in cerebral blood flow, almost always generalized, but they are usually caused by systemic hypotension of various origins: cardiac arrhythmias, myocardial infarction, hemorrhagic shock, among others.
The aim in cerebral amyloid angiopathy is to treat the symptoms, as there is no current cure. Physical and/or speech therapy may be helpful in the management of this condition.
It is usually associated with amyloid beta.
However, there are other types:
- the "Icelandic type" is associated with Cystatin C
- the "British type" is associated with ITM2B
Research is currently being conducted to determine if there is a link between cerebral amyloid angiopathy and ingestion of excessive quantities of aluminum.
Diagnostic methods for hypertensive encephalopathy include physical examination, blood pressure measurement, blood sampling, ECG, EEG, chest X-ray, urinalysis, arterial blood gas analysis, and imaging of the head (CAT scan and/or MRI). Since decreasing the blood pressure is essential, anti-hypertensive medication is administered without awaiting the results of the laboratory tests. Electroencephalographic examination detects the absence of alpha waves, signifying impaired consciousness. In people with visual disturbances, slow waves are detected in the occipital areas.
Prognostics factors:
Lower Glasgow coma scale score, higher pulse rate, higher respiratory rate and lower arterial oxygen saturation level is prognostic features of in-hospital mortality rate in acute ischemic stroke.
Smith (2015) conducted a study that looked into specific biological markers that correlate to Moyamoya disease. Some of the categories of these biomarkers include phenotypes - conditions commonly related to Moyamoya, radiographical markers for the diagnosis of Moyamoya, and proteins as well as cellular changes that occur in cases of Moyamoya.
Similar to Moyamoya Disease, there are conditions that are closely associated with Moyamoya Syndrome. Some of the more common medical conditions that are closely associated with Moyamoya Syndrome include trisomy 21 (Down's Syndrome), sickle cell disease, and neurofibromatosis type 1. There is also evidence that identifies hyperthyroidism and congenital dwarfing syndromes as two of the more loosely associated syndromes that correlate with the possibility of being diagnosed with Moyamoya Disease later in life.
There is also research that has shown that certain radiographic biomarkers that lead to the diagnosis of Moyamoya Disease have been identified. The specific radiographic markers are now considered an acceptable key component to Moyamoya Disease and have been added to the INternational Classification of Diseases (ICD). These biomarkers of Moyamoya are "stenosis of the distal ICA's up to and including the bifurcation, along with segments of the proximal ACA and MCA...dilated basal collateral vessels must be present" Some other common findings that have not been added to the classification index of those with Moyamoya Disease which are found using radiography involve very distinct changes in the vessels of the brain. These changes include newly formed vessels made to compensate for another change noted, ischemia and cerebrovascular reserve, both found on MRI. Functional changes include evidence of ischemia in vessels of the brain (ICA, ACA, MCA, specifically). It is important to also note that the radiographic biomarkers, in order to be classified as Moyamoya Disease, all findings must be bilateral. If this is not the case and the findings are unilateral, it is diagnosed as Moyamoya Syndrome.
There are also several protein biomarkers that have been linked to the Moyamoya Disease diagnosis. Although the sample size of the studies performed are small due to the rarity of the disease, the findings are indicative of a correlation between the disease and several specific protein biomarkers. Other studies have confirmed the correlation of Moyamoya and adhesion molecule 1 (ICAM-1) being increased as compared to normal vascular function counterparts Furthermore, it has been concluded that the localization of inflammatory cells suggests that the inflammation stimulus iteself may be responsible for the proliferation and occlusion in the ICA, ACA, and MCA found in those with Moyamoya Disease.
Many studies of the mechanical properties of brain edema were conducted in the 2010, most of them based on finite element analysis (FEA), a widely used numerical method in solid mechanics. For example, Gao and Ang used the finite element method to study changes in intracranial pressure during craniotomy operations. A second line of research on the condition looks at thermal conductivity, which is related to tissue water content.
Although the mechanism is not entirely understood, the likelihood of a watershed stroke increases after cardiac surgery. An experiment conducted in a five-year span studied the diagnosis, etiology, and outcome of these postoperative strokes. It was observed that intraoperative decrease in blood pressure may lead to these strokes and patients who have undergone aortic procedures are more likely to have bilateral watershed infarcts. Furthermore, bilateral watershed strokes are associated with poor short-term outcomes and are most reliably observed by diffusion-weighted imaging MRI. Thus future clinical research and practice should focus on the identification of bilateral stroke characteristics. This identification can help discover affected areas and increase correct diagnosis.
Treatment approaches can include osmotherapy using mannitol, diuretics to decrease fluid volume, corticosteroids to suppress the immune system, hypertonic saline, and surgical decompression to allow the brain tissue room to swell without compressive injury.
The natural history of this disorder is not well known. The long term outlook for patients with treated moyamoya seems to be good. While symptoms may seem to improve almost immediately after the in-direct EDAS, EMS, and multiple burr holes surgeries, it will take probably 6–12 months before new vessels can develop to give a sufficient blood supply. With the direct STA-MCA surgery, increased blood supply is immediate.
Once major stroke or bleeding take place, even with treatment, the patient may be left with permanent loss of function so it is very important to treat this condition promptly.
Dr. Michael Scott, MD discusses the success rate for Moyamoya surgery in
AVMs are diagnosed primarily by the following methods:
- Computerized tomography (CT) scan is a noninvasive X-ray to view the anatomical structures within the brain to detect blood in or around the brain. A newer technology called CT angiography involves the injection of contrast into the blood stream to view the arteries of the brain. This type of test provides the best pictures of blood vessels through angiography and soft tissues through CT.
- Magnetic resonance imaging (MRI) scan is a noninvasive test, which uses a magnetic field and radio-frequency waves to give a detailed view of the soft tissues of the brain.
- Magnetic resonance angiography (MRA) – scans created using magnetic resonance imaging to specifically image the blood vessels and structures of the brain. A magnetic resonance angiogram can be an invasive procedure, involving the introduction of contrast dyes (e.g., gadolinium MR contrast agents) into the vasculature of a patient using a catheter inserted into an artery and passed through the blood vessels to the brain. Once the catheter is in place, the contrast dye is injected into the bloodstream and the MR images are taken. Additionally or alternatively, flow-dependent or other contrast-free magnetic resonance imaging techniques can be used to determine the location and other properties of the vasculature.
AVMs can occur in various parts of the body:
- brain (cerebral AV malformation)
- spleen
- lung
- kidney
- spinal cord
- liver
- intercostal space
- iris
- spermatic cord
- extremities – arm, shoulder, etc.
AVMs may occur in isolation or as a part of another disease (for example, Von Hippel-Lindau disease or hereditary hemorrhagic telangiectasia).
AVMs have been shown to be associated with aortic stenosis.
Bleeding from an AVM can be relatively mild or devastating. It can cause severe and less often fatal strokes. If a cerebral AVM is detected before a stroke occurs, usually the arteries feeding blood into the nidus can be closed off to avert the danger. However, interventional therapy may also be relatively risky.
Asymptomatic individuals with intracranial stenosis are typically told to take over the counter platelet inhibitors like aspirin whereas those with symptomatic presentation are prescribed anti-coagulation medications. For asymptomatic persons the idea is to stop the buildup of plaque from continuing. They are not experiencing symptoms; however if more build up occurs it is likely they will. For symptomatic individuals it is necessary to try and reduce the amount of stenosis. The anti-coagulation medications reduce the likelihood of further buildup while also trying to break down the current build up on the surface without an embolism forming. For those with severe stenosis that are at risk for impending stroke endovascular treatment is used. Depending on the individual and the location of the stenosis there are multiple treatments that can be undertaken. These include angioplasty, stent insertion, or bypass the blocked area.
Diagnosis of a cerebral vascular accident begins with a general neurological examination, used to identify specific areas of resulting injury. A CT scan of the brain is then used to identify any cerebral hemorrhaging. An MRI with special sequences called diffusion-weighted MR imaging (DWI), is very sensitive for locating areas of an ischemic based stroke, such as a watershed stroke.
Further diagnosis and evaluation of a stroke includes evaluation of the blood vessels in the neck using either Doppler ultrasound, MR-angiography or CT-angiography, or formal angiography. An echocardiogram may be performed looking for a cardiac source of emboli. Blood tests for risk factors also may be ordered, including cholesterol levels, triglyceride levels, homocysteine levels, and blood coagulation tests.
The clinician should first rule out conditions with similar symptoms, such as subarachnoid hemorrhage, ischemic stroke, pituitary apoplexy, cerebral artery dissection, meningitis, and spontaneous cerebrospinal fluid leak. This may involve a CT scan, lumbar puncture, MRI, and other tests. Posterior reversible encephalopathy syndrome has a similar presentation, and is found in 10–38% of RCVS patients.
RCVS is diagnosed by detecting diffuse reversible cerebral vasoconstriction. Catheter angiography is ideal, but computed tomography angiography and magnetic resonance angiography can identify about 70% of cases. Multiple angiographies may be necessary. Because other diseases (such as atherosclerosis) have similar angiographic presentations, it can only be conclusively diagnosed if vasoconstriction resolves within 12 weeks.