The blood supply to the striatum comes primarily from the internal carotid artery, middle cerebral artery (MCA), anterior cerebral artery, and anterior choroidal artery, followed by posterior communicating arteries and posterior choroidal arteries, which are constantly distributed within a small area. Heubner's artery is located in the anterior cerebral artery region. The lateral small branch supplies the forearm of the inner capsule and the lateral part of the caudate nucleus, the medial small branch supplies the anterior nucleus and the caudate nucleus, and the short central artery branch of the anterior cerebral artery supplies the caudate nucleus. In the medial anterior aspect of the head, the medial branch of the middle cerebral artery, within 10 mm of the MCA, is emitted at a right angle. About 2-3 short and thin protrusions pass through the sac nucleus through the inner sac to the caudate nucleus. The lateral group comprises about 4-6 long and thick, fan-shaped branches that pass through the lenticular nucleus through the inner capsule to the caudate nucleus. The internal choroidal artery of the internal carotid artery is divided into sections 1-4, three of which are located 2 mm from the distal end of the posterior communicating artery, emitting 1-3 cortical branches, each of which has 2-3 branches, which eventually generate the striate cystic artery. One reaches the globus pallidus, and the other runs into the posterior limb of the internal capsule, reaching the radiation. In the striatum, the body of the caudate nucleus is supplied by the lenticulostriate artery. The anterior and lateral parts of the caudate nucleus are supplied by Heubner's artery, the inner side is supplied by the short central artery, and the caudate nucleus is supplied by the anterior and posterior choroid. The anterior part of the nucleus returns to the artery, the middle part becomes the lenticulostriate artery, and the posterior part is supplied by the choroidal artery.
The concept of perforating lesions was first proposed by Caplan et al. in 19892. They believed that deep and small infarcts may be caused by small perforating arteries due to occlusion by tiny atherosclerotic plaques. These tiny arteries are prone to hypertension, which presents as glassy degeneration. These perforating arteries, such as the lenticulostriate artery or the para-aortic artery, usually branch vertically from the main artery. Damage to the vascular endothelium caused by rapid blood flow can lead to the formation of local atherosclerotic plaques. Therefore, effective imaging methods can help identify relevant pathophysiological changes and provide valuable information for the clinician. In their studies, von Morze et al. and Cho et al.3,4 used 7T MR imaging systems to reveal the lenticulostriate artery by MRA and found that non-invasive evaluation of the lenticulostriate artery can be achieved, but the 7T MR system has not yet been applied in clinical practice. However, the images of lenticulostriate arteries based on the 3T MR imaging system and the 3D-HRVWI sequence obtained in this study were satisfactory, suggesting a potential for clinical application.
The overall incidence of striatum infarction was 5%, and most patients in the acute phase developed severe neurological deficits. Acute large striatum cystic infarction usually presents with similar symptoms and signs as infarcts in the cortex, which may manifest as aphasia and go unnoticed. There are many speculations about the development of cortical symptoms in these subcortical deep gray area infarctions. The cortical region has a connecting loop in the deep gray matter nucleus, and this part of the infarction leads to cortical disorders, which may be caused by cortical damage itself, or the functional activity of the corresponding cortical region may be weakened due to the distance effect.
There are four main mechanisms leading to striatum sac infarction2,5: 1. occlusion of the proximal middle cerebral artery; 2. the presence of a T-shaped thrombus at the end of the internal carotid artery; 3. occlusion of the external carotid artery and deep nucleus infarction caused by embolic or hemodynamic damage at the proximal end of the middle cerebral artery; or 4. atherosclerotic lesions at the middle cerebral artery, complicated by in situ thrombosis or other abnormal middle cerebral artery conditions, such as a dissection or vasculitis. There may be good collateral circulation in the cortical region, and due to the lack of collateral circulation in the basal ganglia, the embolus can reach the middle cerebral artery and cause an embolic event.
Although the lacunar infarction caused by a single perforating artery is small, the resulting neurological deficit can be severe. In addition, while a single lacunar infarction rarely causes serious consequences such as coma, a new infarct can continue to develop due to diffuse cerebral arteriolar lesions, resulting in multiple lacunar infarctions. The accumulation and superposition of such lacunar brain damage is bound to cause a wider range of brain dysfunction, and may even lead to vascular dementia. Recent studies6 suggest that not all lacunar infarctions that were confirmed clinically or via imaging are caused by cerebral small vessel disease, and the etiology also includes atherosclerotic lesions.
According to the available literature3, 7-9, a reduction in the number of lenticulostriate arteries is a common manifestation of an infarction of the lenticulostriate artery blood supply area. On the one hand, this conforms to the pathophysiological changes, and confirms the blood supply changes caused by the occlusion of the lenticulostriate arteries. The pathophysiological process of infarction in the area provides strong evidence for the etiology of the infarct involving the lenticulostriate arteries. On the other hand, it has also been confirmed that the HRVWI sequence can reach the lenticulostriate area through the lenticulostriate arteries, as shown by the minimum density projection method (which meets the requirements of vascular imaging), but this is limited by technical conditions such as the imaging resolution of the wall, which may also cause low sensitivity or poor image quality for imaging of the lenticulostriate arteries.
The present study found that the number of lenticulostriate arteries on the lesion side was increased. This may be related to three factors: 1. The bilateral distribution of the lenticulostriate artery itself is asymmetrical; 2. The striatum infarction area is larger than shown in the images, but the secondary pathophysiological changes are still unclear. Whether there are new or newly opened lenticulostriate arteries therefore still needs further study; 3. The original lenticulostriate arteries are dilated and developed as compensatory vessels, while the corresponding lenticulostriate arteries on the normal side are too small to see. Among the 35 patients, six also had deeper lenticulostriate arteries on the lesion side than on the normal side. A study with a larger sample size is needed to clarify the clinical and physiological significance of these changes in lenticulostriate arteries.