I was diagnosed in may with diabetes. Within two weeks I was in horrible pain with extreme weakness and fatigue. Think the oral mess threw me into this, or maybe just a coincidence? Anyway after 3months of doctors having no clue what was wrong, a neurologist diagnosed diabetic amyotrophy. Said all we can do is wait for my body to heal itself. Anybody been through this? I am terrified, can’t work because I fall even with a walker. My legs just turn to jelly with no warning and I’m on the ground.Some web info I read said 18 months?!
Hi Mamahentx, welcome to TuD. I am not familiar with amyotrophy, this is first time I’ve heard of it.
But I searched this site and found there are previous discussions that may help you out. Try a search.
The reason why diabetic amyotrophy can appear so soon after onset of diabetes is that it can be caused by auto-immunity rather than high blood sugar. When I was first diagnosed with type 1, I participated in a study of nervous system health with a number of other newly-diagnosed patients, and it was found that we all had marked slowing of nerve conduction velocities, which is a distinct sign of a damaged nervous system. That was also probably also the result of diabetic auto-immunity rather than diabetic hyperglycemia, since I had only had excessive urine and thirst for a day or two before I began taking insulin, so the fact that my nervous system was already measurably damaged points to something other than hyperglycemia.
This study sheds some light on the condition and the causal factors involved:
Fortschr Neurol Psychiatr
Diabetic somatic polyneuropathy. Pathogenesis, clinical manifestations and therapeutic concepts.
Hilz MJ, et al.
“Diabetic polyneuropathy is the most frequent neuropathy in western countries. In Germany, there are 3.5 to 4 million diabetic patients. Diagnosis should rule out other polyneuropathies and assess two out of the five diagnostic criteria: neuropathic symptoms, neuropathic deficits, pathological nerve conduction studies, pathological quantitative sensory testing and pathological quantitative autonomic testing. So far, the pathophysiology of diabetic neuropathy remains to be fully understood. Among the various pathophysiological concepts are the Sorbitol-Myo-Inositol hypothesis attributing Myo-Inositol depletion to the accumulation of Sorbitol and Fructose, the concept of deficiency of essential fatty acids with reduced availability of gamma-linolenic-acid and prostanoids, the pseudohypoxia- and hypoxia-hypothesis attributing endothelial and axonal dysfunction and structural lesions to increased oxidative stress and free radical production. Obviously, the hyperglycemia induced generation of advanced glycation end products (AGEs) also contributes to structural dysfunctions and lesions. Elevated levels of circulating immune complexes and activated T-lymphocytes as well the identification of autoantibodies against vagus nerve or sympathetic ganglia support the concept of an immune mediated neuropathy. The reduction of neurotrophic factors such as nerve growth factor, neurotrophin-3 or insulin-like growth factors also seems to further diabetic neuropathy. The symmetrical, distally pronounced and predominantly sensory neuropathy is far more frequent than the symmetrical neuropathy with predominant motor weakness or the asymmetrical neuropathy. The painless neuropathy manifests with impaired light touch sensation, position sense, vibratory perception and diminished or absent ankle deep tendon reflexes. The painful sensory diabetic neuropathy primarily affects small nerve fibers and accounts for decreased temperature perception and paresthesias. The proximal, diabetic amyotrophy evolves subacutely or acutely, induces motor weakness of the proximal thigh and buttock muscles and is painful. Cranial nerve III-neuropathy is also painful and has an acute onset. Truncal radiculopathy follows the distribution of truncal roots and frequently causes intense pain. Autonomic neuropathy occurs with and without somatic neuropathy. The most important therapy is to attempt optimal blood glucose control, to reduce body weight and hyperlipidemia. Symptomatic therapy includes alpha-lipoic acid treatment, as the antioxidant seems to improve neuropathic symptoms. Aldose reductase inhibitors might reduce sorbitol and fructose production and normalize myo-inositol levels. However, there are no aldose reductase inhibitors available in Europe as yet. Evening primrose oil, containing gamma-linolenic acid, might improve nerve conduction velocities, temperature perception, muscle strength, tendon reflexes and sensory function. Substitution of nerve growth factor showed promising results in pilot studies but failed in a large-scale multicenter study.” (I edited out a long discussion of various pain control medications which can be used to treat the condition.)
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Day by day! Doctors say it will turn around and heal itself in 18 to 24 months. I’m six months in…and trying to stay on my feet and off the floor…thanks for asking.