|Classification and external resources|
Arteries beneath brain
Lacunar stroke or lacunar infarct (LACI) is a type of stroke that results from occlusion of one of the penetrating arteries that provides blood to the brain's deep structures. Patients who present with symptoms of a lacunar stroke, but who have not yet had diagnostic imaging performed may be described as suffering from Lacunar Stroke Syndrome (LACS).
Much of the current knowledge of lacunar strokes comes from C. M. Fisher's cadaver dissections of post-mortem stroke patients. He observed "lacunes" (Latin for 'lake') of empty fluid left in the deep brain structures after occlusion of 200-800 μm penetrating arteries and connected them with 5 classic syndromes. These syndromes are still noted today, though lacunar infarcts are diagnosed based on clinical judgment and radiologic imaging.
It is estimated that lacunar infarcts account for 25% of all ischemic strokes, with an annual incidence of approximately 15 per 100,000 people. They may be more frequent in men and in African Americans, Mexican Americans, and Hong Kong Chinese.
Lacunes are caused by occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery. The corresponding lesions occur in the deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%). They less commonly occur in the deep cerebral white matter, the anterior limb of the internal capsule, and the cerebellum.
The two proposed mechanisms are microatheroma and lipohyalinosis. At the beginning, lipohyalinosis was thought to be the main small vessel pathology, but microatheroma now is thought to be the most common mechanism of arterial occlusion (or stenosis). Occasionally, atheroma in the parent artery blocks the orifice of the penetrating artery (luminal atheroma), or atheroma involves the origin of the penetrating artery (junctional atheroma). Alternatively, hypoperfusion is believed to be the mechanism when there is stenosis of the penetrating artery. When no evidence of small vessel disease is found on histologic examination, an embolic cause is assumed, either artery-to-artery embolism or cardioembolism. In one recent series, 25% of patients with clinical radiologically defined lacunes had a potential cardiac cause for their strokes.
Advanced age, chronic hypertension, smoking and diabetes mellitus are risk factors. It is unclear whether there is an association with alcohol consumption, elevated cholesterol, or history of prior of stroke. Lacunar strokes may result from carotid artery pathology or microemboli from the heart as in atrial fibrillation. Patients often recover well, but if there is enough white matter disease from lacunar pathology, one can see a subcortical dementia such as Binswanger disease.
Each of the 5 classical lacunar syndromes has a relatively distinct symptom complex. Symptoms may occur suddenly, progressively, or in a fluctuating (eg, the capsular warning syndrome) manner. Occasionally, cortical infarcts and intracranial hemorrhages can mimic lacunar infarcts, but true cortical infarct signs (such as aphasia, neglect, and visual field defects) are always absent. The 5 classic syndromes are as follows.
|Name||Location of infarct||Presentation|
|Pure motor stroke/hemiparesis (most common lacunar syndrome: 33-50%)||posterior limb of the internal capsule, or the basis pontis||It is marked by hemiparesis or hemiplegia that typically affects the face, arm, or leg of one side. Dysarthria, dysphagia, and transient sensory symptoms may also be present.|
|Ataxic hemiparesis (second most frequent lacunar syndrome)||posterior limb of the internal capsule, basis pontis, and corona radiata.||It displays a combination of cerebellar and motor symptoms, including weakness and clumsiness, on the ipsilateral side of the body. It usually affects the leg more than it does the arm; hence, it is known also as homolateral ataxia and crural paresis. The onset of symptoms is often over hours or days.|
|Dysarthria/clumsy hand (sometimes considered a variant of ataxic hemiparesis, but usually still is classified as a separate lacunar syndrome)||basis pontis||The main symptoms are dysarthria and clumsiness (ie, weakness) of the hand, which often are most prominent when the patient is writing.|
|Pure sensory stroke||contralateral thalamus (VPL)||Marked by persistent or transient numbness, tingling, pain, burning, or another unpleasant sensation on one side of the body.|
|Mixed sensorimotor stroke||thalamus and adjacent posterior internal capsule||This lacunar syndrome involves hemiparesis or hemiplegia with ipsilateral sensory impairment|
Typically, tissue plasminogen activator may be administered within three hours of stroke onset if the patient is without contraindications (ie. a bleeding diathesis such as recent major surgery or cancer with brain metastases). High dose aspirin can be given within 48 hours. For long term prevention of recurrence, medical regimens are typically aimed towards correcting the underlying risk factors for lacunar infarcts such as hypertension, diabetes mellitus and cigarette smoking. Blood thinners such as heparin and warfarin have shown no benefit over aspirin with regards to five year survival.
Patients who suffer lacunar strokes have a greater chance of surviving beyond thirty days (96%) than those with other types of stroke (85%), and better survival beyond a year (87% versus 65-70%). Between 70% and 80% are functionally independent at 1 year, compared with fewer than 50% otherwise.
Lacunar: A carpentry Term: Pertaining to lacuna. In architecture, a ceiling or undersurface of a cornice formed of sunken compartments.