Cases reported "Diabetic Neuropathies"

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1/242. An unusual manifestation of diabetes mellitus.

    MEDICAL history: Type 2 diabetes mellitus for five years; unexplained 35-lb weight loss three years ago; Bell's palsy on right side many years ago. MEDICATIONS: glipizide, 10 mg/day. family history: Father died of leukemia at age 65; mother has kidney stones; no diabetes or neuromuscular disease. SOCIAL history: insurance salesman; heterosexual, promiscuous, uses condoms; smokes (25 pack years); does not drink. physical examination: Well-nourished, well developed, not in acute distress; had difficulty rising from a sitting position because of right lower extremity weakness. blood pressure, 154/74; pulse, 88; temperature, 36.6 degrees C; respiratory rate, 16. head, eyes, ears, nose, and throat: normal. neck: normal. heart: S4. Lungs: clear. abdomen: mildly obese. extremities: no cyanosis, clubbing, or edema; atrophy and weakness of right thigh and both calves; wide-based gait; able to walk on toes but not heels. Neurologic responses: cranial nerves intact; deep tendon reflexes, 1 symmetrically; plantar reflexes, flexor bilaterally. skin: macular rash in sun-exposed areas. LABORATORY FINDINGS: Hemoglobin, 13.2 gm/dL; mean corpuscular volume, 80 micron 3; white blood cell count, 7,200/mm3 (normal differential); platelet count, 137,000/mm3. serum: electrolytes, normal; blood urea nitrogen, 18 mg/dL; creatinine, 0.8 mg/dL; glucose, 308 mg/dL; total protein, albumin, liver enzymes, and creatine kinase, normal. urine: 1 glucose. Venereal disease test: nonreactive; hiv test: negative. DIFFERENTIAL diagnosis: dermatomyositis; heavy-metal poisoning; diabetic amyotrophy. HOSPITAL COURSE: The patient was given 50 mg/day of oral amitriptyline to alleviate the painful paresthesias and was switched to 20 U/day of subcutaneously injected neutral protamine Hagedorn (NPH) insulin to normalize the blood glucose level. Histologic studies of skin and muscle showed sun damage and neuropathic changes, respectively. There was no evidence of vasculitis. Screening for heavy-metal toxins produced negative results.
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ranking = 1
keywords = nerve
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2/242. I-123 MIBG cardiac imaging in diabetic neuropathy before and after epalrestat therapy.

    I-123 metaiodobenzylguanidine (MIBG) scintigraphy is a new method to evaluate cardiac sympathetic nerve disturbance in patients with diabetes mellitus. Epalrestat specifically inhibits aldose reductase and improves diabetic neuropathy. The authors report a case of improvement in cardiac sympathetic dysfunction using MIBG scintigraphy with epalrestat therapy. In this case, epalrestat effectively reversed diabetic neuropathy, and MIBG scintigraphy was useful to evaluate the effect of epalrestat.
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ranking = 3206.3076714269
keywords = neuropathy, nerve
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3/242. Treatment of neuropathic pain in a patient with diabetic neuropathy using transcutaneous electrical nerve stimulation applied to the skin of the lumbar region.

    BACKGROUND AND PURPOSE: Diabetic neuropathy can produce severe pain. The purpose of this case report is to describe the alteration of pain in a patient with severe, painful diabetic neuropathy following application of transcutaneous electrical nerve stimulation (TENS) to the low back. CASE DESCRIPTION: The patient was a 73-year-old woman with pain in the left lower extremity over the lateral aspect of the hip and the entire leg below the knee. The pain prevented sound sleep. The intensity of pain was assessed with a visual analog scale. INTERVENTION: The TENS (80 Hz) was delivered 1 to 2 hours a day and during the entire night through electrodes placed on the lumbar area of the back. OUTCOMES: Following 20 minutes of TENS on the first day of treatment, the patient reported a 38% reduction in intensity of pain. After 17 days, the patient reported no pain following 20 minutes of TENS and that she could sleep through the night. Application of TENS to the skin of the lumbar area may be an effective treatment for the pain of diabetic neuropathy.
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ranking = 3744.5256166647
keywords = neuropathy, nerve
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4/242. Proximal diabetic neuropathy presenting with respiratory weakness.

    A patient is described with proximal diabetic neuropathy presenting with respiratory weakness. A 50 year old man developed progressive shortness of breath over 2 months. He also had weakness of hip flexion. phrenic nerve responses were absent, and spontaneous activity was seen in the intercostal and lumbar paraspinal muscles with long duration neurogenic MUPs and reduced recruitment in the diaphragm. Without treatment, the patient began to improve with resolution of his proximal leg weakness and breathing difficulties. Proximal diabetic neuropathy is another cause of neuromuscular respiratory weakness.
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ranking = 3206.3076714269
keywords = neuropathy, nerve
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5/242. Prerenal azotemia in a diabetic patient with hyporeninemic hypoaldosteronism and autonomic neuropathy.

    patients with hyporeninemic hypoaldosteronism show mild to moderate renal insufficiency, with a creatinine clearance of 20-75 ml/min, and asymptomatic hyperkalemia. A low degree of sodium wasting and mild hyperchloremic metabolic acidosis are also usually present. However, severe sodium wasting and volume depletion are not typically seen unless the patient is placed on severe sodium restriction or has some other cause of extrarenal sodium loss. In fact, acute renal failure has not been reported in such patients. We describe a diabetic patient with hyporeninemic hypoaldosteronism and autonomic neuropathy who developed recurrent episodes of acute renal failure due to prerenal azotemia during acute exacerbations of diarrhoea. In our case, despite significant hypovolemia, the renin-aldosterone axis was markedly suppressed, implying that sympathetic tone played a decisive role in renin regulation.
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ranking = 2671.089726189
keywords = neuropathy
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6/242. Diabetic neuropathic pain in a leg amputated 44 years previously.

    The mechanism of neuropathic pain in the diabetic limb is far from clear. phantom limb pain likewise is of obscure aetiology. The development of typical pain in an absent leg in a patient with diabetes many years after the amputation stimulates thought as to the mechanism, not only of neuropathic pain, but also of phantom limb pain. A 58-year-old man was diagnosed with type 2 diabetes 44 years after having undergone left below knee amputation for congenital AV malformation, at the age of 13. Eight months before the diagnosis of diabetes he began to complain of pain in the leg on the amputated side-pain very similar to that described in typical diabetic neuropathy. This was followed by similar pain in the right leg. MR scan of the spine revealed a small syringohydromyelia of the thoracic cord in addition to a prolapse of disc at L(5)/S(1) level on the left side, which was first noted 5 years previously. There were no other features of S(1) compression. The typical neuropathic character of the pain involving both the amputated and the intact limbs that developed with the diagnosis of type 2 diabetes suggest that the neuropathic pain may originate from centres higher than peripheral nerves.
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ranking = 552.96008905558
keywords = neuropathy, peripheral, peripheral nerve, nerve
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7/242. Following the clues to neuropathic pain. Distribution and other leads reveal the cause and the treatment approach.

    Neuropathic pain can seem enigmatic at first because it can last indefinitely and often a cause is not evident. However, heightened awareness of typical characteristics, such as the following, makes identification fairly easy: The presence of certain accompanying conditions (e.g., diabetes, hiv or herpes zoster infection, multiple sclerosis) Pain described as shooting, stabbing, lancinating, burning, or searing Pain worse at night Pain following anatomic nerve distribution Pain in a numb or insensate site The presence of allodynia Neuropathic pain responds poorly to standard pain therapies and usually requires specialized medications (e.g., anticonvulsants, tricyclic antidepressants, opioid analgesics) for optimal control. Successful pain control is enhanced with use of a systematic approach consisting of disease modification, local or regional measures, and systemic therapy.
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keywords = nerve
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8/242. Diabetic neuropathic cachexia: the importance of positive recognition and early nutritional support.

    We report on a patient with acute painful diabetic neuropathy in whom abdominal pain and severe weight loss mimicked neoplastic disease. Positive recognition of the diabetic neuropathic cachexia syndrome might have avoided extensive invasive investigation. Intensive enteral nutritional support was associated with prompt resolution.
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ranking = 534.21794523781
keywords = neuropathy
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9/242. Reversible tetraplegia due to polyneuropathy in a diabetic patient with hyperosmolar non-ketotic coma.

    critical illness polyneuromypathy has not previously been reported as a complication of diabetic coma. We describe a patient with hyperosmolar non-ketotic coma (HONK) complicating gram-negative sepsis in whom persistent coma and profound tetraplegia caused considerable concern. Although, initially, it was feared that the patient had suffered a central neurological complication such as stroke or cerebral oedema, a diagnosis of critical illness motor syndrome (CIMS) was subsequently confirmed neurophysiologically. Profound limb weakness associated with HONK is not necessarily due to a catastrophic cerebral event, rather it may be a result of CIMS, which has an excellent prognosis for full neurological recovery.
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ranking = 2136.8717809512
keywords = neuropathy
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10/242. The spectrum of chronic inflammatory demyelinating polyneuropathy.

    research criteria for the diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP) were proposed by an Ad Hoc Subcommittee of the American Academy of neurology (AAN) in 1991, and since then these criteria have been widely used in clinical studies. We have been impressed by the frequent finding of electrophysiological changes of a demyelinating neuropathy in patients whose clinical presentation does not conform to the usually accepted clinical phenotype of CIDP. To determine the clinical spectrum of CIDP, we conducted a retrospective review of patients of the peripheral electrophysiology laboratory of the University of Miami-Jackson Memorial Medical Center. Diagnostic criteria for acquired demyelination of an individual nerve were adapted from the AAN research criteria for the diagnosis of CIDP (1991). patients were accepted for inclusion when such evidence was demonstrated in at least one motor nerve or at least two sensory nerves. We then reviewed the clinical phenotype and the underlying etiology of the neuropathy in these cases. Eighty-seven patients, 63 male and 24 female, age of onset 4-84 (mean 49.3) years, met these inclusion criteria. Forty-seven patients (54%) had distinct features outside the usual clinical presentation of CIDP. Of these, 15 (17%) had predominantly distal features, 13 (15%) had exclusively sensory polyneuropathy; seven (8%) had markedly asymmetric disease, seven (8%) had associated CNS demyelination, four (5%) had predominant cranial nerve involvement, and one (1%) had only the restless legs syndrome. An associated medical condition that may have been responsible for the acquired demyelinating neuropathy was present in 60% of the patients. We conclude that spectrum of CIDP is broader than would be indicated by the strict application of the AAN research criteria, and that many of the cases meeting more liberal criteria frequently respond to immunosuppressive therapy.
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ranking = 4825.3770133204
keywords = neuropathy, peripheral, nerve
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