Sensorimotor neuropathy damages motor and sensory nerves, often caused by diabetes. Diagnosis includes neurological exams, blood tests, and nerve conduction tests. Treatment focuses on underlying conditions, but damage from metabolic disorders or inherited conditions is often irreversible. Polyneuropathy can also cause autonomic involvement, threatening basic functions. Causes include toxins, diabetes, alcoholism, and vitamin B deficiency. Guillain-Barre syndrome is a severe and rare polyneuropathy that can lead to paralysis, but many patients make a full recovery.
A neuropathy is any disease of neurons. Neuropathies outside the brain and spinal cord are collectively referred to as peripheral neuropathies. The term “sensorimotor neuropathy” refers to a peripheral neuropathy that damages motor nerves, which control muscles, and sensory nerves, which carry touch, temperature, pain and pressure information from the body to the brain. Sensorimotor neuropathy can be caused by an infection along with inflammation, metabolic disorders, and inherited conditions, but is most commonly a complication of diabetes.
The diagnosis of sensorimotor neuropathy begins with a neurological exam and usually includes an electromyogram and a nerve conduction velocity test to measure how fast nerves carry electrical current. Blood tests are essential to determine if a metabolic disorder is present and to check blood sugar if the patient is not a known diabetic. Treatments usually focus on the underlying condition, although pain medications and anti-inflammatory agents may also be given. The success of treatment varies depending on the cause: neuropathies due to metabolic problems or inflammation are much more manageable than genetically inherited ones.
Diabetic sensorimotor neuropathy is a common side effect of diabetes and can cause loss of sensation, lack of muscle control, muscle weakness and muscle wasting, as well as frequent injuries because patients cannot feel one of their limbs. Diabetics who have high blood sugar might have excessive intracellular glucose within their peripheral neurons and it gets converted into other sugars which impairs nerve structure and function. Intracellular glucose can also bind to proteins in the cell and prevent them from performing their normal functions, and destruction of blood vessels that supply peripheral nerves deprives neurons of oxygen, leading to cell death. Treatment requires better management of blood sugar levels, but the damage is often irreversible, and foot amputations often occur.
Sensorimotor polyneuropathy involves the systematic loss of sensation and muscle control throughout the body. Those affected by this form of nerve damage are particularly at risk of injuring nerves in the knees, elbows, and other joints from prolonged pressure, and must change positions frequently to prevent injury. Polyneuropathies sometimes cause not only sensorimotor neuropathy but also damage to the autonomic nervous system. Autonomic involvement threatens basic functions such as breathing, bladder control and digestion.
Metabolic disturbances from toxins, diabetes, advanced alcoholism, or severe vitamin B deficiency are common causes of polyneuropathy and can be identified quickly with the right tests. However, some sensorimotor neuropathies result from inflammation that removes myelin from the nerve cell, the neuron’s protective sheath that allows for rapid electrical conduction from cell to cell. This is the case with Guillain-Barre syndrome, a severe and rare polyneuropathy that leads to paralysis. Although it requires hospitalization with respiratory support and filtration of antibodies in the bloodstream to reduce inflammation, many patients make a full recovery. The rate of permanent sensorimotor impairment is less than 10%.
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