Multifocal motor neuropathy (MMN) belongs to the group of rare autoimmimmial peripheral neuropathy characterized by weakness or decrease in asymmetrical movement and muscle atrophy but no sensory abnormalities.
1. Symptoms of multi-drive motor neuron disease
Multi-drive motor neuron disease manifests it quite clearly, specifically as follows:
- Semi-level on-starting with asymmetric weakness.
- Symptoms of lower motor neurone disease (LMN) usually appear in the disease in 2 arms accompanied by weakness of the arms and hands without loss of sensation in other areas.
- Begins as a single-drive neurological disease that affects the distant segmented arm; wrists and hand weakness or may also manifest in the legs.
- Usually people with multi-outlet motor neuron disease begin to feel weak from the hands, progress usually consists of spreading to the opposite arm and then the legs.
- Symptoms of muscle twitching or cramps may appear.
- Muscle atrophy occurs late during multi-drive motor neuron disease.
- Deep tendon reflexes are significantly affected, decreasing in most cases but normally or increasing (but without pathology) in people with the disease.
- Cranial nerves, pharynx muscles, and respiratory muscles are often preserved in multi-drive motor neuron disease.
- Nerve damage in multi-drive motor neuron disease is often varied, with some nerves unaffected, with other cords severely damaged.
- Sensory conduction through the same segment of nerves and cerebral fluid proteins is normal.
2. Diagnosis of multi-drive motor neuron disease
Methods of diagnosis of multi-drive motor neuron disease.
- Progress slowly or gradually, regionally, asymmetrically weak, in the motor nerve distribution of at least two nerves, lasting more than a month. If the symptoms appear only in the distribution of a nerve then only a diagnosis of "possible" disease.
- There are no objective sensory abnormalities except for abnormal vibrations applied at the far head of the lower genus.
Clinical standards that support the diagnosis of the disease:
- Mainly upper genuss;
- Decreased tendon reflexes or inactivation in the affected genus;
- There is no active participation of the cranial nerve;
- Cramps and vibrations of muscle bundles in the affected genus;
- Muscle health response when immunosuppressive treatment;
Differentive diagnosis: similar manifestations but also scattered sensory lesions, called Lewis-Sumner syndrome or multi-drive motor neuron disease and myelin-destroying sensations with multiple drives. There is also motor neuron disease caused by inflammation of the vessels.
- Motor marks on Babinski (+), Hoffman(+);
- Have damaged pharyngeal muscles;
- Decreased sensation is noted heavier than loss of vibration that applies to the head away from the lower genus;
- Symmetrical motor muscle weakness spreads in the first weeks.
3. How to treat multi-drive motor neuron disease?
Currently there are quite a few treatments for multi-drive neuropath disease, some effective treatments are as follows:
3.1. Immunoglobulin Immunoglobulin Treatment
Multi-drive motor neuron disease can be treated with intravenous globulin, which is the leading treatment in the treatment of multi-drive motor neuron disease:
- Plasma replacements may have an enterative effect on Immunoglobulins, which is great for the treatment of short-term multi-drive motor neuron disease but usually they are ineffective and are not recommended for prolonged repetition in treatment. While Immunoglobulin is used in prolonged repeated treatment.
- Most cases of multi-drive motor neuron disease improve quite quickly in terms of muscle strength with Immunoglobulin, but the improvement is generally unsustainable after a few months so immunoglobulin intravenous infusion is usually required every 2-6 weeks.
3.2. Immunosuppressive drugs
In cases of resistance, doctors may consider taking immunosuppressive drugs. However, in some cases, Corticosteroids do not have an effect that even sometimes aggravates the disease.
3.3. Plasma replacement
The treatment of multi-drive motor neuron disease by plasma replacement and Mycophenolate mofetil (Cellcept) has no effect. Cyclophosphamide (Endoxan) and Rituximab can be studied.
Multi-outlet neurological disease has slow progress and defects in patients who are not treated, so before the disease left complications, patients should go to medical centers for examination and treatment.
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