Vascular Parkinson's Syndrome

Introduction to vascular Parkinson's syndrome Some diseases or factors can produce clinical symptoms similar to Parkinson's disease (PD), such as infection, drugs (dopamine receptor blockers, etc.), poisons (MPTP, carbon monoxide, manganese, etc.), vascular (multiple cerebral infarction) And caused by brain trauma, etc., clinically known as Parkinson's syndrome (Parkinsonism). Some scholars also refer to Parkinson's disease (PD) together with the above-mentioned clinical symptoms of Parkinson's disease as Parkinsonism. Vascular Parkinsinism (VP), caused by cerebrovascular disease, such as multiple lacunar infarction, basal ganglia, amyloid angiopathy, and subcortical leukoencephalopathy, clinical manifestations similar to PD . basic knowledge The proportion of illness: 0.0325% Susceptible people: the elderly Mode of infection: non-infectious Complications: Hypertension, Hyperlipidemia, Diabetes, Arrhythmia, Congenital heart disease

Causes of vascular Parkinson's syndrome

(1) Causes of the disease

The disease often occurs suddenly after an acute stroke or systemic hypoxemia, but also gradually appears after multiple strokes. The course of the disease progresses stepwise, and the symptoms are asymmetrical when onset.

(two) pathogenesis

Murrow et al reported a group of cases, the clinical manifestations of Parkinson's syndrome, autopsy showed caudate nucleus, internal capsule, globus pallidus, putamen and midbrain and other basal ganglia with extensive lacunar infarction, and the bilateral black matter is normal. Pathological data further confirmed the existence of VP. The pathological data of a case of VP was reported in China. The case had hypertension and diabetes for several years. There were multiple strokes in the clinic, and typical Parkinson's syndrome appeared later. The main clinical manifestations were Slow movement, mask face, increased tonic muscle tension, difficulty in action, panic gait, but no static tremor, accompanied by bilateral pyramidal tract signs, pseudobulbar palsy and mental decline, via Madopar Poor treatment, autopsy found bilateral ventricle enlargement, bilateral basal ganglia with multiple lacunar infarction, microscopic view of the double frontal and occipital lobe, basal ganglia, midbrain, cerebral bridge with multiple old and fresh infarction In the foci, the mesothelioma pigment neurons were normal, and there were no lesions in the blue spot. Therefore, it was confirmed that the patient's Parkinson's syndrome was caused by the infarction of the basal ganglia, and there was no doubt in the diagnosis of VP. This further confirms the presence of VP and therefore suggests that VP can exist as an independent syndrome.

Recently, the Yamanouchi study found that most patients with VP have extensive damage in the brain, especially the white matter of the frontal lobe, while the basal nucleus damage is relatively light, so it is speculated that VP may be closely related to the damage of the anterior white matter of the frontal lobe. Twenty-four patients with VP confirmed by autopsy and 30 patients with Parkinson's disease of the same age group, 22 patients with the same age group of Binswanger disease (BD) without Parkinson's syndrome and the same age group were pathologically. In the study, it was confirmed that the number of pigmented neurons, the number of pigmented neurons and the number of decolorized neurons in the substantia nigra of VP group, BD group and normal control group were not significantly different. The number of pigmented neurons in the substantia nigra of PD group, coloring and decolorizing neurons The total number was significantly lower than that of VP group, BD group and normal control group. The white matter degeneration degree of patients with BD group was more serious than that of VP group. The number of oligocytic cells and the number of astrocytes in front of frontal lobe were reflected as a reflection. The objective index of the degree of white matter degeneration also showed that the BD group and the normal control group were lower than the VP group. At present, it has not been found that the nucleus pituitary infarction can be denied evidence of VP, but VP patients are widespread. The white matter of the frontal lobe is damaged, while the lesion of the basal ganglia is relatively mild, suggesting that the white matter damage in the frontal lobes may be more closely related to VP.

Vascular Parkinson's Syndrome Prevention

The prevention of this disease focuses on the risk factors of cardiovascular and cerebrovascular diseases, early treatment of cardiovascular and cerebrovascular diseases, anticoagulation, antiplatelet adhesion or aggregating drugs under the guidance of physicians, which may be beneficial to reduce the incidence of vascular Parkinson's syndrome. .

Complications of vascular Parkinson's syndrome Complications hypertension hyperlipidemia diabetes arrhythmia congenital heart disease

Patients with a history of acute stroke or risk factors such as hypertension, hyperlipidemia, diabetes, arterial embolism or arrhythmia, congenital heart disease, intracranial and extravascular atherosclerosis, and the presence of the above diseases Clinical manifestations.

Symptoms of vascular Parkinson's syndrome Common symptoms Two hands shaking, gait, gait, hypertensive mask, face, dementia, pseudobulbar, meditation, small gait, ankylosing muscle tone

Vascular Parkinson's Syndrome (VP) is mainly characterized by bilateral lower extremity dyskinesia. The typical symptom is magnetic foot reaction (very difficult to start), but walking is almost normal or short gait during activity, no history of acute stroke. Or neuroimaging changes, clinical manifestations similar to senile gait disorders, often accompanied by pyramidal tract signs and dementia.

The clinical symptoms from the initial symptoms of VP to the long-term course of disease are still different from those of PD. The asymmetry of Parkinson's disease (PD) is increased in myotonic muscle tone, frequent resting tremor, and PD. The drug has a good response and lack of pyramidal tract signs, etc., can be distinguished from VP.

Yamanouchi compared the clinical features of 24 patients with typical VP and 30 patients with PD. As an initial symptom, static tremor was only 1 (4%) in the VP group and 14 in the PD group. 47%), there was a significant difference between the two (P < 0.001). As the disease progressed, 4 patients with VP developed tremor (17%), 3 of which were static and 22 of PD patients had tremor (73). %), 20 of them were static tremor (P<0.01). In patients with VP and PD, myotonic muscle tension increased, asymmetric muscle rigidity, and dementia were significant. In addition, more than half of VP patients had pyramidal tracts. Sign, pseudo-medullary palsy.

The main clinical features of pathologically confirmed VP patients are:

1 onset can be urgent, can be concealed onset; can also be acute or subacute onset.

2 more without static tremor.

3 tonic muscle tension increased.

4 asymmetrical limb rigidity.

5 moves slowly.

6 gait panic.

7 expression is dull, showing a "mask face."

More than half of the patients had pyramidal tract signs and pseudobulbar palsy.

Dementia also occurred in 9VP patients.

10VP patients may have varying degrees of spontaneous remission.

Examination of vascular Parkinson's syndrome

Laboratory tests are non-specific, blood routine, biochemical, routine examination of cerebrospinal fluid is normal, or associated with other diseases that coexist (such as diabetes).

Head MRI shows vascular damage in the cortex or white matter, such as lacunar infarction, mainly located in the watershed area, basal ganglia, etc., and there are lesions such as leukoaraiosis in the white matter of the frontal lobe, and the volume of white matter or gray matter lesion is larger than The brain tissue volume is 0.6%.

Diagnosis and identification of vascular Parkinson's syndrome

When distinguishing between VP and PD clinically, the symptoms should be carefully analyzed, and comprehensive judgment should be made from all aspects except symptoms.

1. Basic basis: The clinical diagnosis of VP should be comprehensively analyzed from medical history, symptoms, signs, imaging examinations, drug efficacy evaluation, etc., and Parkinson's syndrome caused by other causes should be excluded, and VP and PD should be excluded. In the case of PD, it has been confirmed that PD can be complicated by cerebral infarction, especially in the striatum. Although some PD patients have vascular damage to the basal ganglia and cerebral white matter, all the lesions are mild.

Since the application of MRI in clinical practice, it has important clinical value in the diagnosis of VP. Zijlmans and other studies have found that the volume of subcortical white matter or gray matter lesions is significantly larger than that of PD group or VP patients with acute onset or occult onset. In patients with hypertension, the damage of brain tissue volume can be regarded as a critical point. The lesion volume of subcortical white matter or gray matter in VP patients often exceeds 0.6% of the volume of brain tissue. At the same time, clinically insidious onset In VP patients, the vascular damage is mainly diffusely located in the watershed area, and the vascular damage of acute onset VP patients is mainly located in the subcortical gray matter (striatum, globus pallidus, thalamus), regardless of which type of VP patients, There is no change in its substantia nigra.

2. Diagnostic criteria: According to the above, the clinical diagnostic indicators of VP can be summarized as follows:

(1) History: Most VP patients have a history of hypertension, a history of diabetes, or a history of hypertension and diabetes.

(2) History of stroke: Many patients have a history of recurrent stroke before onset.

(3) Symptoms and signs: In addition to hypertonic increase in muscle tone, asymmetry of limb rigidity, panic gait, sluggish expression, dementia and other signs and symptoms of Parkinson's syndrome, patients do not have static tremors, often accompanied by Pyramid bundle sign, pseudobulbar palsy.

(4) Imaging examination: MRI of the skull shows vascular damage of cortex or white matter, such as lacunar infarction, mainly located in the watershed area, basal nucleus and so on.

(5) Levodopa treatment is not effective.

(6) Clinical symptoms and signs of VP patients may have spontaneous relief.

(7) Parkinson's syndrome caused by drugs, poisons, trauma, infection, hydrocephalus and some degenerative diseases should be excluded.

(8) Parkinson's disease and the coexistence of PD and VP should be excluded.

According to the above points, the clinical diagnosis can be VP, but the final diagnosis still needs pathological confirmation.

In addition to the identification of PD and PSP, this disease should also be distinguished from early positive pressure hydrocephalus, especially in the late stage of the disease. The latter CT and MRI examinations show that the whole ventricle system is enlarged and there is positive pressure hydrocephalus. Change and so on.

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