I. Concept
Lacunar cerebral infarction is a special type of cerebral infarction, based on hypertension and arterial infarction, occlusion of microscopic arteries in the deep brain occurs, causing ischemic softening lesions in brain tissue, and the lesion range is generally 2-20 mm, among which 2-4 mm is the most common.
Clinically, patients are mostly asymptomatic, and about 3/4 of them have no symptoms of focal neurological damage, or only mild inattention, memory loss, mild headache and dizziness, vertigo, and unresponsiveness, etc. The diagnosis of the disease is mainly CT or MRI examination, while multiple lacunar cerebral infarcts can affect brain function, leading to progressive intellectual decline and finally cerebrovascular dementia. Small infarcts with a diameter of 2-20 mm (5-15 mm in some books) are caused by occlusion of a deep penetrating branch of the cerebral artery or its branch arteries.
Those larger than 15mm are giant lacunae, even up to 25mm, and 2 or more are multiple. Infarct foci are mostly located in deep brain, such as cerebral white matter, internal capsule, basal ganglia, thalamus, brainstem and cerebellum, etc. Cranial CT is more suitable for examination 8-11 days after the disease.
Clinical symptoms
Clinical symptoms are generally mild, except for a few, most of them have a slow onset and peak at 12 to 72 hours, and some patients have a history of transient ischemic attacks. Clinical symptoms are related to the size and location of the luminal infarct foci, and the following types are common.
(a) Pure motor stroke: manifests as paralysis of the face, tongue, and limbs to varying degrees without sensory impairment, visual field loss, or aphasia. The lesions are located in the radial crown, internal capsule, basal ganglia, cerebral bridge, and medulla oblongata.
(b) Pure sensory stroke: The patient complains of hemianesthesia, tugging, chills, fever, pins and needles, pain, swelling, becoming larger, smaller or heavy sensation. Examination reveals decreased or absent sensation in one limb or body. Sensory disturbances are occasionally seen to cross the midline affecting the nose, tongue, penis, and anus bilaterally, indicating a thalamic lesion.
(iii) Ataxic mild hemiparesis: It is manifested as pure motor mild hemiparesis and cerebellar ataxia on the opposite side of the lesion, with the lower limbs being the most important, and may also have dysarthria and nystagmus, which is caused by the occlusion of the paramedian artery of the basilar artery and the lesion at the junction of the upper 1/3 and lower 1/3 of the pontine base.
(iv) Sensorimotor stroke: Mostly hemianesthesia followed by mild hemiparesis. It is caused by lacunar infarction of the posterior ventral nucleus of the thalamus with involvement of the posterior limb of the internal capsule.
(v) Dysarthria and clumsiness syndrome: The patient has severe dysarthria, swallowing difficulties, central facial and tongue palsy on one side, mild weakness of the hand on that side with slow and clumsy movements (especially fine movements such as writing are more difficult), inaccurate finger-nose test, unsteady gait, hyperactive tendon reflexes and positive pathological reflexes, the lesion is located at the junction of the upper 1/3 and lower 2/3 of the pontine base, and may also have ipsilateral ataxia.
Treatment
The treatment of this disease is basically the same as cerebral thrombosis, hypertension should be actively treated, especially those who have had lacunar infarction in their medical history need to prevent recurrence, and care should be taken that the pressure should not be too fast and too low.
(I) Acute phase: The principle is to improve the blood circulation in the cerebral ischemic area and promote the recovery of neurological function as early as possible.
1. Relieve cerebral edema: for patients with large and severe infarct area, dehydrating agents or diuretics can be used.
2. Improve microcirculation: use low-molecular dextrose, which can reduce blood viscosity and improve microcirculation.
3. Blood dilution.
① Isovolemic hemodilution therapy: Blood is released through a vein, and an equal amount of fluid is replaced;
②High-volume hemodilution therapy: intravenous injection of fluid without blood to achieve the purpose of volume expansion.
4. Thrombolysis.
①Streptokinase.
②Urokinase.
5. Anticoagulation: To prevent the extension of thrombus and the occurrence of new thrombus.
①Heparin.
②Dicoumarin.
6. Vasodilators: It is generally believed that the effect of vasodilators is not certain, and in severe patients with increased intracranial pressure, the condition can sometimes be aggravated, so early use is not recommended.
7. Other: hyperbaric oxygen therapy, extracorporeal counterpulsation therapy and photometric blood therapy can also be used for this disease.
(B) Recovery period: Continue to strengthen the functional exercise of paralyzed limbs and speech function training, in addition to drugs, can be used with
physical therapy, body therapy and acupuncture, etc.