Also known as Parkinson's disease, it is a degenerative disorder of the central nervous system that primarily occurs in middle-aged and older individuals. The main pathological changes occur in the substantia nigra and striatum, where a reduction in dopamine secretion leads to tremors, increased muscle tone, and movement disorders.

bubble_chart Diagnosis

1. Medical History and Symptoms:

Primary tremor Bi disease with unknown cause. Parkinsonian syndrome is often associated with cerebral arteriosclerosis, traumatic brain injury, CO poisoning, and poisoning from antipsychotic drugs (phenothiazines, monoamine oxidase inhibitors, tricyclics). The onset is usually gradual and progressively worsens, with main symptoms including tremor, increased muscle tone, and movement disorders. The medical history should inquire about the aforementioned conditions.

2. Physical Examination Findings:

1. Tremor:

Initially appears in the distal upper limbs (fingers) and gradually spreads to the lower limbs. The typical rhythmic finger tremor resembles a "pill-rolling motion." In the early stage, it is a resting tremor, but in advanced stages, it may become persistent. It worsens with emotional agitation and stops during sleep.

2. Rigidity:

Increased muscle tone in both flexor and extensor muscles of the limbs, presenting as "lead-pipe" or "cogwheel" rigidity. Involvement of facial muscles results in an expressionless, mask-like face.

3. Movement Disorders:

Difficulty in performing fine motor tasks due to rigidity in the limbs and hands. In severe cases, sitting up or turning over in bed becomes challenging, along with difficulties in putting on shoes, tying laces, or buttoning clothes, leading to loss of self-care ability. Gait disturbances are particularly prominent. Early manifestations include dragging of the lower limbs while walking and lack of arm movement. As the condition progresses, steps become smaller and slower, with difficulty initiating movement. Once walking begins, the patient may take very small, rapid steps forward, accelerating uncontrollably and struggling to stop or turn, known as "festinating gait."

3. Auxiliary Examinations:

1. Lumbar puncture CSF examination shows reduced levels of dopamine metabolites (vanillylmandelic acid) and serotonin metabolites (5-hydroxyindoleacetic acid).

2. Urinary dopamine and its metabolites are also decreased.

3. Some patients may show ischemic degenerative changes in the basal ganglia region on head CT or MRI.

bubble_chart Treatment Measures

1. Drug Therapy:

Can alleviate symptoms and slow disease progression, but cannot alter the course of the disease.

1. Anticholinergic drugs: Inhibit the effect of acetylcholine, thereby relatively enhancing the effect of the neurotransmitter dopamine. Examples include Artane 2mg 3 times/day or scopolamine 0.2mg 3 times/day, often causing side effects such as dry mouth, dilated pupils, and constipation.

2. Dopamine Replacement Therapy: Supplements the deficiency of the neurotransmitter dopamine, restoring balance to the acetylcholine-dopamine system. Typically, levodopa, which can cross the lipid membrane barrier, is used at 0.25mg 3 times/day, gradually increasing the dose until the optimal therapeutic effect with minimal side effects is achieved.

3. Compound levodopa and compound levodopa sustained-release formulations (such as Madopar and Sinemet).

4. Dopamine Receptor Agonists: Bromocriptine starting at 0.625mg, gradually increasing but not exceeding 30mg per day. Pergolide starting at 0.025mg, increasing by 1/4 tablet (1mg) every 2 days until satisfactory results are achieved.

2. Surgical Treatment:

Microelectrode-guided pallidotomy and thalamotomy.

3. Gene Therapy:

Transplantation of myoblasts transfected with the TH gene can increase dopamine neurotransmitter levels by 50%, significantly improving clinical symptoms with promising prospects. TH (tyrosine hydroxylase transplantation).