Cases reported "Diabetic Neuropathies"

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1/45. 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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2/45. 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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3/45. 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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4/45. Neuropathic pain--from mice to men.

    The past decade has seen great progress in understanding the syndrome of neuropathic pain, its causes and in finding new drugs that promise great benefit. For example, an early outcome of the research has been the observation that the new drugs do not blunt normal pain sensation--a pattern beginning to find explanation through the realisation that neural pain circuits rewire themselves, both anatomically and biochemically, after nerve injury. In this article, we discuss a case of a known diabetic patient with intractable pain and the course of management provided by the use of novel tools and devices coming to the fore in this rapidly expanding specialty.
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5/45. Diabetic neuropathy masquerading as glossodynia.

    BACKGROUND: Diabetic neuropathy, or DN, occurs in approximately 50 percent of patients who have type 2 diabetes mellitus, or DM. Oral burning and symptoms consistent with glossodynia (burning mouth syndrome) may occur secondary to DN. CASE DESCRIPTION: A 54-year-old woman reported to a university dental clinic with a chief complaint of oral burning. No clinical signs were evident. Her medical history was positive for type 2 DM. The initial diagnosis was glossodynia, and she was evaluated with relevant blood studies, which indicated that her diabetes was not well-controlled. The patient was referred back to her physician, and her symptoms abated once her diabetic condition was under control. CLINICAL IMPLICATIONS: It is important to consider DN within the differential diagnoses of patients who have symptoms consistent with glossodynia but have no clinical signs. dentists are invaluable in ascertaining underlying systemic disease considerations in patients with oral symptomatology. Cooperation between dentists and physicians often is helpful and necessary in caring for patients who have uncontrolled type 2 DM and oral symptoms.
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6/45. guillain-barre syndrome in patient with Burkitt's lymphoma and type 2 diabetes mellitus.

    Although peripheral neuropathies are commonly observed in patients with non-Hodgkin's malignant lymphomas (NHML), guillain-barre syndrome (GBS) belongs to the occasional complications of lymphoproliferative disorders. It appears in less than 0.3 per cent of NHML. It is worthy of note that in the reported case there occurred three independent risk factors of peripheral neuropathy: Burkitt's lymphoma, chemotherapy and type 2 diabetes mellitus. Based on clinical course, EMG finding and neuropathological examination, in spite of normal cerebrospinal fluid protein content, GBS as a paraneoplastic disorder was diagnosed. It was assumed that chemotherapy and diabetes mellitus conduced to severe neuropathy.
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7/45. Bilateral carpal tunnel syndrome with type 1 diabetes mellitus in childhood.

    The differences between diabetic mono- or polyneuropathy and entrapment neuropathy are most important with respect to choosing treatment alternatives in pediatric patients. A 7-year-old girl with type 1 diabetes mellitus was admitted to our clinic with a complaint of bilateral weakness in her hands. Her clinical findings and electromyography study revealed an entrapment neuropathy of the median nerve at the wrist. She underwent operation by open carpal tunnel release. All symptoms resolved within 6 months after the operation. carpal tunnel syndrome, especially bilateral, is very rare in childhood and it can be treated surgically.
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8/45. Painful diabetic peripheral neuropathy relieved with use of oral topiramate.

    Diabetic peripheral neuropathy affects 5 to 50% of people with diabetes in the united states. It is a progressive disorder that results in a gradual decrease in peripheral sensation and eventually complete loss of sensation. patients with diabetic peripheral neuropathy are challenging to treat because of intolerable adverse medication effects and the development of tolerance to medical treatment. We present the case of a patient with peripheral neuropathy that was unresponsive to usual therapies. She experienced significant relief with the administration of topiramate. Topiramate is an anticonvulsant that is gaining recognition in the treatment of patients with neuropathic pain syndromes.
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9/45. Pain in diabetic neuropathy case study: whole patient management.

    Painful diabetic peripheral neuropathy (DPN) is described as a superficial burning pain associated with other positive and/or negative sensory systems affecting the feet and lower extremities. It is one of the most commonly encountered neuropathic pain syndromes in clinical practice. Presentation may be complicated by multiple symptoms, including allodynia, hyperalgesia, other less well characterized dysesthesias, and serious disruption of social functioning and mood. Peripheral nerve function may deteriorate, which can account for patient reports of diminution of pain after several years of follow-up. Although current understanding holds that the pathogenesis of DPN is multifactorial in nature, long-term studies have shown that rigorous glycemic control is the most relevant factor in clinical intervention and can delay the onset and slow the progression of neuropathy. In addition to glycemic control, other treatment approaches must be examined in order to restore quality of life for patients experiencing painful DPN. Differential diagnosis is required to isolate DPN from other unexplained chronic pain. Neurologic testing in painful DPN is an area of active research and is used to assess the neurologic pathways giving rise to the pain, the degree of neural damage and the degree of subclinical damage. Current treatment options for DPN include mainly antidepressants and anticonvulsants, with other agents such as tramadol, dextromethorphan and memantine being employed or studied. This review article includes a case study of a patient with painful DPN to demonstrate the current management strategies for this neuropathic pain syndrome.
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10/45. Erythromelia, or Mitchell's syndrome--new names for unexplained signs of inflammation in distal symmetrical neuropathy in diabetes.

    BACKGROUND: Two cases are described in which distal symmetrical sensorimotor neuropathy complicating diabetes was associated with episodes of subacute vasodilation of one or other lower limb, and which were otherwise unexplained. The vasodilation was associated with swelling and stiffness, but was painless and self-limiting. INTERPRETATION: It is suggested that this phenomenon results from disordered vasoregulation in diabetic neuropathy, and is linked to the processes which underlie diabetic neuropathic osteoarthropathy (Charcot foot), as well as disorders such as complex regional pain syndrome-1 (CRPS-1, reflex sympathetic dystrophy) and erythromelalgia. CONCLUSIONS: As self-limiting vasodilation may be not uncommon in distal symmetrical neuropathies, but unrecognized because the phenomenon has not been named, the terms 'neuropathic erythromelia' or 'Mitchell's syndrome' are proposed. The adoption of either of these names may lead to earlier diagnosis and prevent inappropriate investigation and treatment.
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