The following page will outline and describe ischemic lacunar stroke. It will explain how and why an ischemic lacunar stroke begins, as well as places in the brain where ischemic lacunar stroke occurs. Additionally, this page will discusssymptoms of lacunar stroke syndrome (LACS) and how they affect the human body as well as potential ischemic lacunar stroke treatment. Here at LacunarStroke.ca, we sincerely hope our website broadens your knowledge of ischemic lacunar stroke.Internal Link
Ischemic lacunar stroke commonly referred to, as “lacunar stroke” is a type of ischemic stroke, which accounts for up to 25% of all suffered ischemic strokes. To avoid confusion, for the remainder of the page, when referring to ischemic lacunar stroke, we will be abbreviating the term to “lacunar stroke”.
Prior to any in-depth explanation of lacunar stroke, it is imperative that one familiarizes themselves with the intricacies of ischemic stroke.
Explained in simple terms, an ischemic stroke commences when a mass of semisolid or gelatinous coagulated blood forms in the brain. This coagulation of blood is referred to as a blood clot. Within the brain, blood clots are detrimental, as they have the ability to block the distribution of oxygenated blood throughout the body. The result of this blockage is defined as hemostasis. Hemostasis refers to the process in which blood loss occurs within a damaged blood vessel, and resultantly is repaired. Juvenilely put, blood flow completely ceases.
The result of the cessation of blood within the damaged blood vessel is detrimental, resulting in deadly consequences, such as the deprivation of oxygen and nutrients to the brain. In addition to this deprivation, carbon dioxide and other harmful waste cannot be removed from the body adequately, due to the circulatory system’s inability to properly function being halted by the blockage in the damaged blood vessel.
There are two types of ischemic stroke, a thrombotic ischemic stroke and an embolic ischemic stroke. A thrombotic ischemic stroke occurs when a blood clot forms within in the brain and remains there, causing a thrombotic ischemic stroke. Contrastingly, an embolic ischemic stroke refers to the process in which a blood clot, formed outside the brain loosens and travels to the brain, and consequently causes a blockage, which results in an embolic ischemic stroke.
Dependent on the type of ischemic stroke, whether embolic or thrombotic, the type of blood clot or thrombosis causing the stroke is different. These blood clots are defined as a thrombus or embolus.
The difference between thrombi and emboli, are size and movement. An embolus, which causes embolic ischemic stroke, commences when a small particle moves freely within a vein or artery (blood vessels). These particles will collide and coagulate over time, eventually forming a clot. Embolic clots consist of a variety of material, including blood cells, gas bubbles and foreign material within a blood vessel.
On the contrary, the term thrombus refers to a blood clot that remains stationary throughout the process of coagulation. Once formed, the thrombus is referred to as a thrombosis in situ.
Lacunar stroke, briefly addressed above, refers to a specific type of ischemic stroke. A lacunar stroke, or lacunar infarct (LACI), occurs when one of the penetrating cerebral arteries, one that provides blood to the deep structures of the brain undergoes occlusion. Deep structures of the brain that are commonly affected by lacunar stroke include, but are not limited to the thalamus and basal ganglia. Lacunar strokes occurring within this section of the brain are referred to as a thalamic lacunar stroke/lacunar thalamic stroke or basal ganglia lacunar stroke.
As the terms thalamus and basal ganglia are crucially important to the understanding of lacunar stroke/lacunar infarct (LACI) and lacunar stroke syndrome (LACS), they will appear frequently throughout LacunarStroke.ca. This is because of a basal ganglia lacunar stroke or a thalamic lacunar stroke/lacunar thalamic stroke occurs within these regions.
The thalamus refers to either of two distinct masses of gray matter within the brain. These masses reside within the third ventricle of the human brain, between the hemispheres. The prime function of the thalamus is the relaying of sensory information within the brain. Additionally, the thalamus serves as the primary center of pain perception within the brain. A thalamic lacunar stroke/lacunar thalamic stroke may irreparably damage the thalamus. A thalamic lacunar stroke/lacunar thalamic stroke occurs when a thrombosis in situ forms within the thalamus.
The basal ganglia are comprised of several subcortical nuclei with varying origins. Specifically, these nuclei exist within vertebral species. Articulately interconnected, the basal ganglia’s nuclei strongly bond with the brainstem, cerebral cortex and thalamus, among other important elements of the brain. A basal ganglia lacunar stroke may irreparably damage the basal ganglia. A basal ganglia lacunar stroke occurs when a thrombosis in situ forms within the basal ganglia.
Referring to the causation of lacunar stroke, you are already aware that arterial occlusion is at fault. Occlusion refers to the process in which a blood vessel, whether an artery or vein, closes. Pertaining to lacunar stroke, two proposed mechanisms; lipohyalinosis and microatheromacause occlusions within the brain.
The first mechanism, lipohyalinosis is a small vessel disease within the brain. Scientifically defined, lipohyalinosis characterizes the thickening of the walls of blood vessels, which results in their luminal diameters being reduced. The term luminal refers to the interior space of a tubular structure, like a blood vessel. Simply, it refers to the area in which blood flows.
A strong factor contributing to the commencement of lipohyalinosis is hypertension. Hypertension is the medical term for high blood pressure. Hypertension is dangerous and increases the risk of stroke within an individual. It is common and easily detectable, affecting the majority of people in different severities at some point in their lives.
The second mechanism, microatheroma, refers to the accumulation of degenerative materials within the inner layer (tunica intima) of arterial walls. These materials consist (almost entirely) of arterial debris (containing lipids, fatty acids, traces of calcium and varying amounts of connective tissue of fibrous origin), and macrophage cells. Microphage cells are a specific type of white blood cell whose main purpose is to engulf and digest the debris of other cells, foreign substance, microbial bodies, cancerous cells and anything else that does not appear healthy.
This accumulation of material causes swelling within the arterial walls, which may intrude through the channel of the artery, ultimately restricting blood flow. Over time, this swelling progresses, in both size and thickness, and may lead to arterial rupturing. This rupturing will result in a showering of debris, and an accumulation of platelets and clots over the area of the rupture. Consequently, this may close the lumen of the artery, resulting in a lacunar infarction.
A prime cause of microatheroma is atherosclerosis. Atherosclerosis, also known as arteriosclerotic vascular disease or ASVD, refers to the thickening of an arterial wall. This thickening is resultant of the invasion and accumulation of white blood cells, as well as the freeing of intimal smooth muscle cells creating a fibrous fatty plaque.
There are a variety of additional factors that increase the risk of suffering a lacunar stroke. The chances of succumbing to lacunar stroke increase with age. People with hypertension, atherosclerosis, diabetes mellitus or pre-existing heart conditions are at greater risk to suffer a lacunar infarct. If you are of African American or Hispanic descent, you are at greater risk of suffering a lacunar infarct. Pregnancy also has the ability to increase risk of lacunar stroke.
There are a variety of lifestyle factors that increase the risk of suffering lacunar stroke. They include, but are not limited to high alcohol intake, smoking, poor diet and nutrition, drug abuse and the use of specific contraceptive technologies, such as birth control pills.
Lacunar Stroke Syndrome comprises of symptomatic manifestations that result when a blood clot or thrombosis exists, but has not been diagnosed. There are a variety of methods used to determine if a person is suffering from lacunar stroke syndrome (LACS). These methods often use pathognomonic signs that are associated with one of the five types of lacunar stroke syndrome (LACS). Correctly identifying these pathognomonic signs is crucial to attaining a proper differential diagnosis. The term differential diagnosis within the realm of stroke is commonly referred to as “stroke DDX” or the “DDX of stroke”. This term pertains to ensuring that the correct condition was identified. For example, seizure being chosen over lacunar stroke in this particular case would be an incorrect differential diagnosis.
Depending on the symptom, its occurrence may be sudden, fluctuating or progressive. The classic five symptoms of lacunar stroke syndrome (LACS) are as follows: Pure motor stroke/pure motor hemiparesis, ataxic hemiparesis, dysarthria or clumsy hand syndrome (they are sometimes considered different symptomatic manifestations), pure sensory stroke and mixed sensorimotor stroke.
Pure motor stroke/pure motor hemiparesis is characterized by hemiparesis or hemiplegia, which commonly affect the arms, legs or face on the contralateral side (side opposite of infarct). Hemiparesis refers to the medical phenomenon in which a person succumbs to weakness in entirety on a specific side of the body. Hemiplegia refers to partial, or in its most severe form, full paralysis on a specific side of the body. Locations of infarction that may cause a pure motor stroke/pure motor hemiparesis are the posterior limb of the internal capsule, corona radiata and basis pontis.
The next symptomatic manifestation, ataxic hemiparesis refers to symptoms affecting a person’s cerebellar and motor abilities. These symptoms include weakness and clumsiness on the contralateral side of the body. Ataxic hemiparesis affects the leg more than the arm. Symptom length of ataxic hemiparesis varies from hours to days. Common infarction locations resulting in ataxic hemiparesis include, but are not limited to the posterior limb of the internal capsule, basis pontis and corona radiata.
The succeeding symptomatic manifestation is dysarthria and clumsy hand syndrome. The most common symptoms are dysarthria and clumsiness/weakness of the hand. Dysarthria is different from dextral clumsiness/weakness, as it refers to nonsensical or unclear speech articulation. This is why dysarthria and clumsy hand syndrome are sometimes referred to as separate lacunar stroke syndrome (LACS) symptomatic manifestations. For this condition, infarctions may occur within the basis pontis, anterior limb of the internal capsule, corona radiata, basal ganglia, thalamus and cerebral peduncle. The occurrence of a thalamic lacunar stroke/lacunar thalamic stroke or a basal ganglia lacunar stroke commonly causes dysarthria and clumsy hand syndrome amongst sufferers.
Pure sensory stroke refers to the symptomatic manifestation where impermanent or constant numbness, burning, tingling or other unpleasantness affects one side of the body. The infarcts that cause pure sensory stroke are those sustained within the contralateral thalamus, internal capsule, corona radiata and midbrain. The occurrence of a thalamic lacunar stroke/lacunar thalamic stroke commonly causes pure sensory stroke amongst sufferers.
The symptomatic manifestation of mixed sensorimotor stroke refers to the phenomenon in which sensory impairment occurs whether affecting sight, smell, taste or another sense and/or the presence of hemiparesis or hemiplegia on the contralateral side of the infarct. Infarcts causing mixed sensorimotor stroke occur within the thalamus and the adjacent posterior internal capsule, as well as the lateral pons. The occurrence of a thalamic lacunar stroke/lacunar thalamic stroke commonly causes mixed sensorimotor stroke among sufferers.
Since lacunar stroke is a type of ischemic stroke, there are a variety of existing medications that can help prevent or manage a lacunar stroke. They include anticoagulants, antiplatelets and thrombolytics. Each drug aids with lacunar stroke treatment in its own way. Anticoagulants are designed to halt blood coagulation. Anticoagulants help prevent stroke. Next, antiplatelets also focus on the prevention of stroke. They do so by stopping the coagulation of platelets within the blood. Lastly, thrombolytics aid lacunar stroke treatment though stroke management. They do so by dissolving an existing clot through a process called thrombolysis.