Learn more about "Parkinson's syndrome of lower limbs"

Vascular Parkinsonism (VaP) is often referred to as "lower limb Parkinsonism" or "lower body Parkinsonism."

It is a more common type of secondary Parkinson's syndrome. It develops on the basis of cerebrovascular disease and its related pathological factors. It is a group of Parkinson's syndromes with clinical manifestations such as pyramidal tract signs, ataxia and non-motor symptoms (including urinary incontinence, cognitive dysfunction and mental symptoms).

1. Typical clinical manifestations of VaP: bilaterally symmetrical gait disorders, often with "freezing" and difficulty starting. The patient's upper limb functions are generally normal, and resting tremor is rare.

The most important non-motor symptoms are: cognitive dysfunction and urinary incontinence. In addition, sleep disorders, constipation, fatigue and other symptoms may also occur.

2. Diagnostic criteria for VaP

① The presence of Parkinson's syndrome, that is, bradykinesia and one of the following symptoms: resting tremor, muscle rigidity, and unstable postural balance (excluding those caused by primary visual, vestibular, cerebellar and proprioceptive abnormalities);

② The patient has manifestations of cerebrovascular disease, which may be manifestations of brain imaging or focal symptoms and signs caused by stroke;

③ There must be a correlation between the above conditions ① and ②, that is, acute onset after stroke or gradual onset of Parkinson's syndrome within 1 year;

④ Rule out Parkinson's syndrome caused by repeated craniocerebral trauma, encephalitis, frontal lobe tumors or communicating hydrocephalus, use of antipsychotic drugs, etc.

3. VaP classification

At present, VaP is generally divided into two types:

Hemiparkinsonism after stroke and "lower body parkinsonism" with insidious onset.

① Hemiparkinsonism after stroke: The affected area of ​​the stroke is clear, and the lesion is located in the lateral part of the globus pallidus or the substantia nigra compacta, causing enhanced motor output function in the basal ganglia; or the lesion is located in the ventral posterolateral nucleus of the thalamus, or a large area of ​​frontal lobe infarction leads to decreased function of the thalamocortical pathway. The patient mainly manifests hypokinesia and rigidity of the contralateral limbs.

② "Lower body Parkinson's syndrome" with hidden onset: The onset is often hidden, and can be manifested as subcortical white matter damage. Patients may experience gait disorders or cognitive dysfunction in both lower limbs in the early stages.

4. Drug treatment of VaP

Western medicine treatment for VaP can be divided into the treatment of Parkinson's syndrome, the control of stroke and its risk factors, and the treatment of cognitive dysfunction.

① Commonly used drugs for Parkinson's syndrome include anticholinergics, amantadine, compound levodopa, dopamine receptor (DR) agonists, monoamine oxidase type B (MAO-B) inhibitors, catechol-O-methyltransferase (COMT) inhibitors and selective adenosine A2A receptor antagonists, etc. However, for Parkinson's syndrome caused by white matter lesions, the effect of drugs for the treatment of Parkinson's syndrome, including dopaminergic drugs, is often poor.

②The control of stroke and its risk factors and the treatment of cognitive impairment should follow the relevant guidelines of my country for acute management and secondary prevention of cerebrovascular disease.

Currently, there is a lack of research on the prevention and treatment of VaP by antiplatelet drugs such as aspirin. Studies have shown that among statins, simvastatin can delay the progression of severe white matter lesions, but more research is needed on the efficacy of other statins on VaP.

Whether active intervention in the risk factors of various vascular events can delay the progression of VaP remains to be studied.

③Cognitive dysfunction may occur in the early stage of VaP, and its treatment can be based on the treatment principles of vascular cognitive impairment, using cholinesterase inhibitors such as donepezil, galantamine, rivastigmine, as well as memantine, nimodipine, mitochondrial protective agents and other neuroactivators.