Cerebral Vascular Disease Flashcards
Cerebral vascular disease (CVD)
CVD is a broad category of heterogenous diseases. Refers to any pathological process to the blood vessels that results in brain abnormality. It affects the function of large cerebral blood vessels (sudden neurobehavioral changes) and small cerebral blood vessels (chronic cognitive and behavioural decline). The most common forms of CVD are large artery ischemic stroke, hemorrhage, small vessel disease, and the co-occurrence of CVD and AD.
Vascular cognitive impairment (VCI)
VCI is the cognitive and behavioural phenotype reflected by CVD. It is heterogenous and complex with no specific cognitive or behavioural pattern. The most common form of VCI is a subcortical type: cerebral small vessels disease.
Stroke
Sudden, focal loss of neurologic function.
Ischemic stroke
The result of a lack of blood flow due to vessel blockage or vessel damage. They account for approximately 80% to 85% of stroke events. Ischemic strokes may be further divided into embolic or thrombotic events. An embolism is thrombotic or other intravessel material brought to a place of blockage by blood flow. For example, a cardioembolic stroke refers to a blocked brain vessel caused by thrombi formed at or near the heart, often associated with atrial fibrillation, that are transported via the arterial system to the brain. By contrast, a thrombotic ischemic stroke is caused by a buildup of intravessel material at the site of the blockage, often in a previously stenosed (narrowed) area.
Transient ischemic attack (TIA)
An event caused by either an embolic or a thrombotic event and is defined by its duration time rather than the severity of its symptoms. Ischemic attacks that last 24 hours or less are arbitrarily defined as TIAs, thought most TIAs last fewer than 15 minutes before symptom recovery is achieved. By definition, TIAs do not result in permanent brain lesions. TIAs increase risk for subsequent stroke; approximately 5% of persons who experience a TIA will experience a stroke within a year.
Silent stroke
A nonclinical event discovered serendipitously at a later time, usually as a lesion on computed tomography (CT) or magnetic resonance imaging (MRI). One could say that silent strokes are neither silent nor strokes. They are not strokes because of the lack of a clinical event, and they are not silent because of their potent risk for subsequent stroke, cognitive impairment, and dementia.
Hemorrhagic stroke
Accounts for the remaining 15% to 20% of stroke events. Cerebral hemorrhages may be further divided into intracerebral and subarachnoid events. Cause of a hemorrhagic stroke is a burst vessel.
Spontaneous intracerebral hematomas (SICH)
Type of a hemorrhagic stroke. Occurs in the absence of other trauma. Hypertension is by far the leading cause of SICH, followed by arteriovenous malformations (AVMs) and aneurysms. Hemorrhages may also occur after an ischemic stroke, especially after an embolic event. They often occur from the bleeding of small vessels, which form a hematoma, and in more severe cases may leak into the ventricles and/or subarachnoid space.
Subarachnoid hemorrhages (SAH)
Hemorrhages that originate in the subarachnoid space most often are secondary to the rupture of a saccular aneurysm at the branching or bifurcation points of large arteries in or around the Circle of Willis on the ventral surface of the brain. SAH may lead may lead to delayed ischemia caused by vasospasm, or a constriction of the blood vessels. The onset of vasospasm may occur several days after the hemorrhagic event, with peak frequency at about 5 to 7 days post SAH.
Cerebral small vessel disease (CSVD)
Refers primarily to subcortical gray and/or white patter pathology associated with distal penetrating arterioles most often branching from the middle, posterior or basilar arteries. CSVD includes both focal arteriolar occlusion (lacunar infarction) and more diffuse white matter pathology, seen as nonspecific white matter hyperintensities (WMH) on T-2 weighted and fluid attenuated inversion recovery (FLAIR) MRI sequences. Small vessel disease is also associated with brain atrophy, which in turn may be independently associated with cognitive impairment.
Lacunar infarcts
Lacunar infarcts are small noncortical infarcts caused by occlusion of a single penetrating branch of a large cerebral artery. They are most often located in basal ganglia structures, in the thalamus, and in the area of internal capsule or deep hemispheric white matter and may be associated with focal syndromes, such as a pure motor or pure sensory loss event, the cooccurrence of dysarthria, ad a ‘clumsy hand’ or hemiparesis.
Multiple bilateral lacunar infarctions
Associated with etat lacunaire, a syndrome marked by cognitive impairment, incontinence, dysarthria, and gait disturbance.
WMHs (white matter hyperintensities)
They are ubiquitous in elderly patients, with greater than 90% of community samples showing hyperintensities on MRI. They may reflect different pathologic processes but are most often thought to be related to chronic, incomplete ischemia (perhaps venular based) in addition to incomplete arteriole occlusion. Axial T2 or FLAIR MRI often show periventricular ‘caps’ and ‘bands’ of WMH.
Two additioal types of small vessel disease
Microhemorrhages (cerebral microbleeds and lobar microbleeds) and microinfarcts (cerebral microinfarcts)
Cerebral microbleeds
Most often identified via gradient echo MRI sequences (T2*). Their etiology may depend o their location. Linkages between cerebral microhemorrhages and cognitive impairmet are tenuous, though they are established risk factors for subsequent stroke and cognitive decline.
