Proximal diabetic neuropathy

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Proximal diabetic neuropathy
Classification and external resources
ICD-10 N312
ICD-9 353.5
OMIM 603933
MedlinePlus 000693

Proximal diabetic neuropathy, also known as lumbosacral radioplexus neurophagy, femoral neurophagy and diabetic amyotrophy, is a nerve disorder that results as a complication of diabetes mellitus. It affects the thighs, hips, buttocks and legs. Proximal diabetic neurophagy is a peripheral nerve disease (diabetic neuropathy) characterized by painful muscle wasting and weakness.[1] Diabetic neuropathy is a common complication of diabetes. It is defined as damage to the nerves that allow you to feel the sensation pain. There are a number of ways that diabetes damages the nerves, all of which seem to be related to increased blood sugar levels over a long period of time. Proximal diabetic neuropathy is one of four types of diabetic neuropathy.[2]

Proximal diabetic neuropathy can occur in type 2 and type 1 diabetes mellitus patients however, it is most commonly found in type 2 diabetes patients.[3] Proximal neuropathy is the second most common type of diabetic neuropathy and can be resolved with time and treatment.[4]

Signs & Symptoms[edit]

Symptoms of proximal diabetic neuropathy depend on which nerves are affected. The first symptom is usually pain in the buttocks, hips, thighs or legs. This pain most commonly affects one side of the body and can either start gradually, seemingly minor at first, or can come on all of a sudden. This is followed by intense weakness in the proximal muscles of the lower limbs that can result in patients being unable to go from a sitting to standing position without assistance.[3] This weakness begins unilaterally but can also spread bilaterally.[1]

Proximal diabetic neuropathy is often accompanied by polyneuropathy, a malfunction of many peripheral nerves at the same time, and musclefasciculation, small, involuntary muscle twitches or contractions that are visible under the skin.[1][5][6]

Andy - Leg-1

Causes[edit]

The nerve damage associated with the disease was first thought to be caused by metabolic changes such as endoneurial microvessel disease, which is the degeneration of pericytes due to hyperglycemia, and the reproduction of basement membranes when the pericytes are no longer regulating their cell cycle. The decreased size of the lumen plus the absence of the pericyte, which regulate capillary blood flow and phagocytosis of cellular debris, leads to ischemia. Nerve biopsies have shifted the view toward an immune mechanism that causes Micro Vasculitis, which could eventually lead to ischemia.[7] Experimental treatments using immunosuppressive proteins have provided further corroborative evidence to the immune mechanism theory.[8] Although this disease does occur in patients without diabetes the prevalence is much greater in the diabetic indicating that although hyperglycemia does not directly cause the nerve damage it may play a role [7]

Diagnosis[edit]

Though very difficult to diagnose because of the similarity to other diseases, the causes are often due to neurological lesions on the nerve endings that are created by improper glucose levels in the muscles, resulting in extreme pain and muscle wasting.[9] To definitively diagnose the condition, electrodiagnostic testing can be used. In addition, needle electromyography and nerve conduction testing are often used to support the diagnostic and to rule out other possible conditions.[10]

A
Needle Electromyography Test

Treatment[edit]

Proper management of diabetes mellitus can prevent proximal diabetic neuropathy from ever occurring.

Proximal diabetic neuropathy is very much reversible.[citation needed] This can be done by taking various measures such as:

  • Controlling the blood sugar levels
  • Proper eating habits, medication, physical exercise, good mental health and avoiding harmful habits like drinking, smoking etc. all form a part of the lifestyle to control diabetes.
  • Physical therapy to restore the nerves in the legs is very useful, it brings back feeling in the legs.[citation needed]
  • Medication helps reduce the pain involved in proximal diabetic neuropathy. Most patients take oral medication that is prescribed by a doctor. Common types include antidepressants, opiates or opiate like drugs, and anticonvulsants.[3]

Length of treatment varies with the amount of nerve damage.[4]

The main treatment of diabetic amyotrophy is managing the individual’s diabetes and glycemic levels.[11] Once they have done these two tasks they will notice an improvement. Receiving an IV of a corticosteroid or taking an immunosuppressant drug, will help to relieve pain and start regaining strength.[12][13] While doing any of the treatment options they should also be working with either a physical therapist or occupational therapist to start gaining muscle strength back.[13]

References[edit]

  1. ^ a b c h-b-f.info. (2012) Diabetic proximal neuropathy. Retrieved March 20, 2012, from http://www.h-b-f.info/diabetes_neuropathy_proximal.htm
  2. ^ Nazario, B., Wed MB. (2011). Diabetic neuropathy. Retrieved March 20, 2012, from http://diabetes.webmd.com/diabetes-neuropathy
  3. ^ a b c National Diabetes Information Clearinghouse (NDIC). (2009, February). Diabetic neuropathies: the nerve damage of diabetes. Retrieved March 20, 2012, from http://diabetes.niddk.nih.gov/dm/pubs/neuropathies/#proximalneuropathy
  4. ^ a b Walker, K. A. (2011) Types of diabetic neuropathy. Retrieved March 20, 2012, from http://www.endocrineweb.com/guides/diabetic-neuropathy/types-diabetic-neuropathy
  5. ^ Rubin, M., & Merck Manual. (2008). Polyneuropathy. Retrieved March 20, 2012, from http://www.merckmanuals.com/home/brain_spinal_cord_and_nerve_disorders/peripheral_nerve_disorders/polyneuropathy.html
  6. ^ Medicine Net. (2012). Defenition of Fasciculation. Retrieved March 12, 2012, from http://www.medterms.com/script/main/art.asp?articlekey=13290
  7. ^ a b Dyck P. J., Winderbank, A. J. (2002). Diabetic and non diabetic lumbosacral radiculoplexus neuropathies. New insights into pathophysiology and treatment. Muscle Nerve, 25, 477–491.
  8. ^ Courtney, A. E., McDonnell, G. V., Patterson, V. H. (2001). Human Immunoglobulin for Diabetic Amyotrophy- a Promising Prospect? Postgraduate Medical Journal, 77, 326-328.
  9. ^ Wada, Y., Yanagihara, C., Nishimura, Y., & Oka, N. (2007. A case of diabetic amyotrophy with severe atrophy and weakness of shoulder girdle muscles showing good response to intravenous immune globulin. Diabetes Research & Clinical Practice, 75(1), 107-110
  10. ^ Diabetic Amytrophy. 2014. American Association of Neuromuscular & Electrodiagnostic Medicine. https://aanem.org/Education/Patient-Resources/Disorders/Diabetic-Amyotrophy.aspx
  11. ^ Garland,H. "Diabetic Amyotrophy." National Center for Biotechnology Information. U.S.National Library of Medicine, 26 Nov. 1955. Web. 20 Apr. 2014.
  12. ^ Jaspard, M., and D. Jacobi. "Diabetic Amyotrophy: Favorable Outcome following Corticosteroid Therapy?" Europe PubMed Central. Europe PubMed Central, 2010. Web. 19 Apr. 2014.
  13. ^ a b Serban,A.L.,& Udrea,G.F.(2012). Rheumatic manifestations in diabetic patients. Journal Of Medicine & Life,5(3), 252-257.