The brain relies on a constant blood supply to function properly, and this supply comes from a complex network of blood vessels. Among these, lenticulostriate arteries are noteworthy due to their small size and deep location. These vessels deliver oxygen and nutrients to specific deep brain regions, supporting various neurological processes.
What Are Lenticulostriate Arteries?
Lenticulostriate arteries are small, penetrating arteries that emerge primarily from the initial segment of the middle cerebral artery (M1 segment), and sometimes from the anterior cerebral artery (A1 segment). They are categorized into medial and lateral groups based on their origin. These arteries have a narrow diameter, typically ranging from 0.10 mm to 1.28 mm, and a long course as they penetrate deep into brain tissue. After originating, they pass through the anterior perforated substance to reach their target brain areas.
Their Role in Brain Function
These small arteries supply blood to several deep-seated brain structures, including the basal ganglia and the internal capsule. The basal ganglia, located at the base of the brain, are involved in the control of voluntary motor movements, procedural learning, routine behaviors, and emotion. Components such as the putamen, caudate nucleus, and globus pallidus receive blood from these arteries, supporting their diverse functions.
The internal capsule, another region supplied by lenticulostriate arteries, contains major motor and sensory pathways that connect the brain’s outer layer (cortex) with the brainstem and spinal cord. The lateral lenticulostriate arteries supply the posterior striatum, lateral globus pallidus, and various parts of the internal capsule, including the anterior limb, genu, and posterior limb. The functioning of these areas, which depends on blood supply from lenticulostriate arteries, is necessary for coordinated movement, sensation, and cognitive processes.
Conditions Related to Lenticulostriate Arteries
The small diameter and deep penetration of lenticulostriate arteries make them susceptible to damage, particularly from hypertension. High blood pressure is a significant risk factor, leading to structural changes in these vessels, such as thickening of the arterial walls (lipohyalinosis) and fibrinoid deposition. These changes can narrow the arterial lumens, restricting blood flow and increasing vascular resistance.
Occlusion of these arteries often results in lacunar infarcts, a type of ischemic stroke characterized by small, deep lesions in the brain. These infarcts are typically 15 to 20 mm in size and are most frequently caused by intrinsic thrombi within the vessels, often due to chronic hypertension. Symptoms of a lacunar stroke can include sudden weakness or paralysis on one side of the face and body, slurred speech, or loss of coordination, depending on the affected area within the basal ganglia or internal capsule.
Beyond ischemic events, lenticulostriate arteries are also implicated in intraparenchymal hemorrhages, which are bleeds within the brain tissue. Hypertension is associated with these hemorrhages, particularly those involving the basal ganglia. Damage to these arteries can also contribute to cerebral small vessel disease, which may lead to cognitive decline. The lack of significant collateral circulation makes the territories supplied by these arteries vulnerable to damage.