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Giant axonal neuropathy is a rare, autosomal recessive [1] neurological disorder that causes disorganization of neurofilaments.Neurofilaments form a structural framework that helps to define the shape and size of neurons and are essential for normal nerve function.
There is currently no known pharmacological treatment to hereditary motor and sensory neuropathy. However, the majority of people with these diseases are able to walk and be self-sufficient. [3] Some methods of relief for the disease include physical therapy, stretching, braces, and sometimes orthopedic surgery.
Acute motor axonal neuropathy (AMAN) is a variant of Guillain–Barré syndrome. It is characterized by acute paralysis and loss of reflexes without sensory loss. Pathologically , there is motor axonal degeneration with antibody-mediated attacks of motor nerves and nodes of Ranvier .
Infantile neuroaxonal dystrophy (INAD) is a rare pervasive developmental disorder that primarily affects the nervous system.Individuals with infantile neuroaxonal dystrophy typically do not have any symptoms at birth, but between the ages of about 6 and 18 months they begin to experience delays in acquiring new motor and intellectual skills, such as crawling or beginning to speak.
In many cases, symptoms are mild enough to go unnoticed. The time period between episodes is known to vary between individuals. HNPP has not been found to alter the lifespan, although in some cases a decline in quality of life is noticed. Some sufferers (10–15%) report various pains growing in severity with progression of the disease. [1]
If diagnosed early, initiation of early treatment to prevent loss of nerve axons is recommended. However, many individuals are left with residual numbness, weakness, tremors, fatigue and other symptoms which can lead to long-term morbidity and diminished quality of life. [2]
Wallerian degeneration is an active process of degeneration that results when a nerve fiber is cut or crushed and the part of the axon distal to the injury (which in most cases is farther from the neuron's cell body) degenerates. [1]
This condition was discovered in 1991 by Hahn et al., when they described two Chinese-Canadian siblings of the opposite sex. The male had difficulties releasing his grip, childhood-onset neuromyotonia and muscle stiffness, progressive motor neuropathy, finger cramping while and after writing, involuntary twitches of the finger, thigh and forearm muscles, foot drop-associated gait problems ...