Motor neuron repair therapy

Damage to motor neurons is quite common in our daily life. For example, accidental injuries or some chronic progressive degenerative diseases often lead to damage to motor neurons and disability in patients. In addition, this disease is sometimes prone to misdiagnosis during examination. Therefore, it is necessary to have a good examination and regular treatment. Let us learn about the methods of motor neuron repair and treatment.

Motor neuron repair therapy

1. Anti-excitotoxicity treatment

The excitatory amino acid toxicity theory holds that patients with ALS have impaired high-affinity glutamate transport. Due to transport disorders, extracellular glutamate cannot be cleared, which increases toxicity and causes cell damage. The glutamate inhibitor "Rilutek" can block glutamatergic neurotransmission by inhibiting glutamate release presynaptically and interfering with the efficacy of excitatory amino acids postsynaptically. It can also block voltage-dependent sodium channels and guanine nucleotide cyclase associated with second messengers.

2. Eliminate free radicals

The free radical theory is based on the isolation of the gene encoding Cu/Zn superoxide dismutase 1 in patients with familial ALS. Therefore, some scholars are actively conducting research and recommending the use of large doses of vitamins, namely, adding 800 to 1,000 mg of vitamin E, 500 mg of vitamin C, 1,000 U of vitamin A and 1 tablet of complex vitamin B every day. Acetylcysteine ​​is a free radical scavenger and a direct and indirect precursor of glutathione, the main antioxidant ion system in cells. After one year of treatment, the mortality rate of MND, the first symptom of the spinal cord, decreased.

3. Immunotherapy

Although evidence of autoimmunity increases year by year, the effectiveness of immunotherapy is still uncertain. Multifocal motor neuropathy, which mimics ALS, responds well to high-dose cyclophosphamide and intravenous immunoglobulin. However, high-dose cyclophosphamide treatment did not change the course of ALS, suggesting that suppressing T-cell-independent B-cell responses has no benefit in preventing ALS progression. Pathological antibodies are present in axons and neuronal cell bodies and can initiate immune responses to diseases, but secondary damage is unrelated to the attacking antibodies. Therefore, ALS is only effective if it is treated in its early stages.

4. After protective treatment

Neurotrophic factor therapy is a protective treatment. Ciliary neurotrophic factor promotes the survival of rat and human motor neurons in tissue culture and slows the progression of motor neuron degeneration in progressive MND models.

5. Bromocriptine for ALS

Recently, Tak ahashi used positron emission scanning to find that the absorption rate of 62-fluorodopa in the striatum of ALS patients was significantly negatively correlated with the course of the disease (P < 0.01). He believed that ALS had a defect in dopamine function and had the same cause and pathogenesis as Parkinson's disease and Alzheimer's disease, and that ALS could be divided into benign and malignant types. The central D2 dopamine receptor agonist bromocriptine has been widely used in the treatment of Parkinson's disease and has a definite effect in improving symptoms.

6. Antidepressant treatment

Most patients may express despair, anger, and irritability. In the later stages, most people develop hostility not only towards their spouses and friends, but also towards their doctors. Antidepressants and anti-anxiety drugs should be used promptly. Commonly used drugs include amitriptyline 25-150 mg/d, paroxetine 20 mg/d, and fluoxetine 20 mg/d, which have smaller side effects.