Small-vessel stroke (lacunar infarction)

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Small-vessel stroke (lacunar infarction)

The term "lacunar infarction" describe atherosclerosis and thrombosis lipogialinoznoe damage with blocked arteries penetrating branches of the circle of Willis, middle cerebral artery trunk, as well as vertebrates and the main arteries of the brain.

View of the base of the brain arteries, blockage which can lead to lacunar infarcts (lacunar disease of the brain).

Small-vessel stroke (lacunar infarction) causes

The trunk of the middle cerebral artery, as well as the arteries, forming the Willis' artery (A1 segment of anterior cerebral artery, anterior and posterior communicating artery, prekommunalnye segments posterior cerebral arteries), the main and vertebral arteries all together give the branch diameter 100-400 mm, perforating the deep gray and white matter of the cerebrum and brain stem. Each of these small branches may be subject to a thrombosis in atherothrombotic lesion in its early (branches of the basilar artery lesion or the trunk of the middle cerebral artery) or lipogialinoznom thinning of its walls more remote from the beginning of localization. Thrombosis of these branches develop infarcts of small size (less than 2 cm), which is referred to as gaps. In many cases they are even smaller - 3-4 mm. There is no doubt that a risk factor for such a small vessel lesions is arterial hypertension. The share of lacunar infarcts of the brain accounts for 10 % of cases of ischemic stroke.


Small-vessel stroke (lacunar infarction) clinical symptoms

Clinical manifestations observed during the development gaps, referred to as lacunar syndromes. Often lacunar infarctions of the brain accompanied by lacunar transient ischemic attack (TIA). Transient ischemic attack (TIA) can be observed by the patient several times a day and last only a few minutes.

The development of cerebral infarction (ischemic stroke) may be accompanied by sporadic or progressive over several days, neurologic deficit. After a few hours or days after the development of cerebral infarction (ischemic stroke), the patient's condition is improving, although some patients become disabled. Recovery of the patient over a period of several weeks to months may be full or remains minimal residual neurological deficit.

Known neurological manifestations of many lacunar syndromes. Some of these neurological syndromes requires confirmation. In the lacunar disease the most common neurological syndromes following:

  1. Pure motor hemiparesis with myocardial in rear thigh of the internal capsule or basis of the pons. In this case almost always involves face, arm, leg, foot and toes. Muscle weakness may be intermittent during transient ischemic attack (TIA), gradually increasing or sudden. Muscle weakness may progress to paralysis (plegia), and then often regress. In many cases, these syndromes recovery is complete;
  2. Syndromes with purely sensitive to impairments in thalamic infarctions gemitipu;
  3. True atactic hemiparesis myocardial near the base of the pons and dysarthria with clumsiness in the hand or arm due to a heart attack at the base of the pons or the knee of the internal capsule;
  4. Pure motor hemiparesis with "motor aphasia" due to thrombotic occlusion of the artery branches lentikulostriarnoy lenticular nucleus and the striatum, which supplies blood knee and thigh anterior internal capsule with adjoining white substance radiate crown.

Prior to the start of treatment for hypertension multiple gaps often cause patients the development of pseudobulbar palsy with emotional lability, the state of lethargy, abulia, and bilateral pyramidal signs. Currently, the syndrome is rare.

There are other lacunar syndromes have been associated with arterial pathology observed:

  1. Pseudobulbar syndrome with loss of ability to produce speech sounds (anarthria) due to bilateral infarcts in the internal capsule, may develop in lesions of lenticular nucleus and the striatum.
  2. Syndromes caused by narrowing of the lumen (occlusion) penetrating branches of the underlying plot the posterior cerebral artery (listed above).
  3. Syndromes observed in a possible narrowing of the lumen (occlusion) penetrating arteries originating from the basilar artery. These lacunar syndromes include ataxia and paresis of the ipsilateral lower extremity, pure motor hemiparesis with paralysis of horizontal gaze, and hemiparesis with paralysis cross abducens (VI cranial).
  4. Syndromes of the damage of downstream branches of the basilar artery include sudden nuclear ophthalmoplegia, horizontal gaze palsy and appendicular cerebellar ataxia.
  5. Syndromes that develop in the possible narrowing of the lumen (occluded) branches of the vertebral artery, pure motor hemiparesis include (in this case remain intact muscles of the face) due to the involvement of the pyramid of the medulla oblongata, as well as lesions of the lateral parts of the syndrome of the pons and the medulla, accompanied by dizziness, vomiting, weakness facial muscles, Horner syndrome, ipsilateral numbness in the area of ??innervation of the trigeminal nerve and contralateral loss of sensitivity due to the damage of the way spinotalamicheskogo syndrome (partial lesion of the lateral medulla oblongata).


Small-vessel stroke (lacunar infarction) diagnosis

Computed tomography (CT) scan of the brain can detect most of the supratentorial lacunar infarcts. Magnetic resonance imaging (MRI) brain reveals how clearly supra- and subtentorial infarcts (lacunae size of 7 mm or more), as well as the distribution of cortical gray matter in the surface of a small infarct in the white matter of the brain. This spread is mainly due to embolism, but no narrowing of the lumen (occlusion) of small penetrating vessels. Therefore, in such situations should not be diagnosing lacunar infarctions.

On brain MRI shows lacunar infarctions in the basal ganglia (top) and white matter of the brain parenchyma (bottom).

Many strokes are larger than 2 cm, combined not only with pure motor hemiparesis in the literature incorrectly called lacunae. They are too big to be the result of occlusion of a single penetrating branch. This is probably embolic infarctions, in which computed tomography (CT) scan of the brain is not able to demonstrate the involvement of the cortical surface. The diagnosis of lacunar infarctions should be placed only when the value of a heart attack is less than 2 cm and its location can be explained by the occlusion of small penetrating branches of one of the major arteries of the base of the brain. Larger deep infarcts in the white matter of the pool I of the middle cerebral artery, probably due to embolism.

Electroencephalography (EEG) is usually normal in contrast to that for heart attacks, affecting the cerebral cortex. If the EEG study, shortly after the onset of symptoms received normal results, this gives reason to think of the deep white matter infarction in the brain.


Small-vessel stroke (lacunar infarction) treatment

The best treatment for lesions of small-vessel - is prevention, namely, careful control of hypertension. However, the drop in blood pressure during the stroke contribute to increasing neurological symptoms. Decrease in blood pressure begin after the patient is stabilized neurological symptoms.

The effectiveness of anticoagulants and antiplatelet agents in patients with lacunary transient ischemic attack (TIA) and fluctuating stroke is not clear. According to some experts, thalamic lacunae caused lipogialinozom may be combined with minor bleeding (haemorrhage). At autopsy in such infarctions sometimes show hemosiderin macrophages.

The possibility of using heparin in this state as questionable. But, on the other hand, some patients with fluctuating hemiparesis atherothrombotic lesions in the area of the basilar artery branches or outgoing trunk of the middle cerebral artery and arteries of lenticular nuclei in the striatum when administered heparin may show improvement.

Patients with lacunar stroke showed no long-term anticoagulant treatment. At the same time it is necessary to carefully monitor blood pressure in order to prevent the progression of vascular lesions in patients with hypertension, a history of his disease.

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