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Hereditary neuropathy with liability to pressure palsy (HNPP) is a peripheral neuropathy, a condition that affects the nerves. [4] Pressure on the nerves can cause tingling sensations, numbness, pain, weakness, muscle atrophy and even paralysis of the affected area. In normal individuals, these symptoms disappear quickly, but in sufferers of ...
Patients with hereditary motor and sensory neuropathies are diagnosed through a physical evaluation that looks for muscle atrophy, weakness, and sensory responses. [3] In addition to this, electromyography and motor nerve conduction tests can help clinicians decide what type of motor and sensory neuropathy it is and how severe the disease is.
According to Lopate, et al., methylprednisolone is a viable treatment for chronic inflammatory demyelinative polyneuropathy (which can also be treated with intravenous immunoglobulin). The authors also indicate that prednisone has greater adverse effects in such treatment, as opposed to intermittent (high-doses) of the aforementioned medication.
Peripheral neuropathy may be classified according to the number and distribution of nerves affected (mononeuropathy, mononeuritis multiplex, or polyneuropathy), the type of nerve fiber predominantly affected (motor, sensory, autonomic), or the process affecting the nerves; e.g., inflammation (), compression (compression neuropathy), chemotherapy (chemotherapy-induced peripheral neuropathy).
Sensory neuronopathy is thought to involve 40% of neuropathies in Sjogren's syndrome and 5% of all cases of Sjogren's overall, it is usually subacute in onset. Other immune mediated causes of sensory neuronopathy include systemic lupus erythematosus, autoimmune hepatitis and celiac disease. [4] Toxin exposure can also lead to sensory ...
Furthermore, serine-enriched diet reduced the levels of the metabolites and improved sensory and motor performance of the mice. A small-scale clinical trial also showed similar results. These studies demonstrated that an altered substrate selectivity of the mutant SPT is the key to the pathophysiology of HSAN IA.
Dejerine–Sottas disease, also known as, Dejerine–Sottas syndrome, [3] hereditary motor and sensory polyneuropathy type III, and Charcot–Marie–Tooth disease type 3, is a hereditary neurological disorder characterized by damage to the peripheral nerves, demyelination, and resulting progressive muscle wasting and somatosensory loss.
The symptoms include poor balance and difficulty walking. Chronic cough and difficulty swallowing may also be present. Clinical findings include ataxia, sensory neuropathy, and absence of the vestibulo-ocular reflex. The syndrome was initially described in 2004. [1]
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