Inflammatory polyneuropathy in the setting of diabetes mellitus (original) (raw)
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Diabetic Neuropathy: A Position Statement by the American Diabetes Association
Diabetes Care
Table 1-Classification for diabetic neuropathies Diabetic neuropathies A. Diffuse neuropathy DSPN c Primarily small-fiber neuropathy c Primarily large-fiber neuropathy c Mixed small-and large-fiber neuropathy (most common) Autonomic Cardiovascular c Reduced HRV c Resting tachycardia c Orthostatic hypotension c Sudden death (malignant arrhythmia) Gastrointestinal c Diabetic gastroparesis (gastropathy) c Diabetic enteropathy (diarrhea) c Colonic hypomotility (constipation) Urogenital c Diabetic cystopathy (neurogenic bladder) c Erectile dysfunction c Female sexual dysfunction Sudomotor dysfunction c Distal hypohydrosis/anhidrosis, c Gustatory sweating Hypoglycemia unawareness Abnormal pupillary function B. Mononeuropathy (mononeuritis multiplex) (atypical forms) Isolated cranial or peripheral nerve (e.g., CN III, ulnar, median, femoral, peroneal) Mononeuritis multiplex (if confluent may resemble polyneuropathy) C. Radiculopathy or polyradiculopathy (atypical forms) Radiculoplexus neuropathy (a.k.a. lumbosacral polyradiculopathy, proximal motor amyotrophy) Thoracic radiculopathy Nondiabetic neuropathies common in diabetes Pressure palsies Chronic inflammatory demyelinating polyneuropathy Radiculoplexus neuropathy Acute painful small-fiber neuropathies (treatment-induced) care.diabetesjournals.org Pop-Busui and Associates 137 Exercise intolerance Constipation c May alternate with explosive diarrhea care.diabetesjournals.org Pop-Busui and Associates 145
JPMA. The Journal of the Pakistan Medical Association, 2014
To conclude, diabetes is associated with a variety of chronic and acute neuropathies, the commonest form being distal symmetric polyneuropathy. Performing an annual screening through a good neurological history and clinical examination and using a sensitive screening tool can facilitate an early diagnosis. More sensitive and quantitative measures of detecting early peripheral nerve injury including skin biopsy for intra-epidermal and dermal nerve fiber density and confocal corneal microscopy, hold promise to identify neuropathy patients early in their disease course.
Diabetic neuropathy: a clinical and neuropathological study of 107 patients
Neurology research international, 2010
One hundred seven patients were retrospectively studied from 1992 to 2002 with diabetic neuropathy that underwent peripheral nerve biopsy. Nerve biopsy revealed the underlying histopathology, including cell and humoral-mediated immunological lesions in the majority of patients. When combined with clinical and laboratory studies, nerve biopsy has the potential to assist in the selection of patients who may benefit from immunomodulatory therapy.
Diabetic polyneuropathy in the elderly
Acta Neurologica Scandinavica, 2009
Objective-To assess the prevalence and the risk factors of diabetic polyneuropathy in representative samples of elderly individuals. Patients-4191 subjects 55 years and older from two areas of Italy were screened by their general practitioners (GPs) and those positive for neuropathic symptoms were subjected to a standard clinical examination. Methods-The screening questionnaire included a list of clinical conditions possibly causing polyneuropathy, including diabetes. In patients with diabetes, the date of diagnosis, the most recent fasting and post-prandial blood glucose value and glycosylated hemoglobin were sought. Probable polyneuropathy was diagnosed through impairment of 2 or 3 nerve functions (strength, sensation, tendon reflexes) in the extremities with symmetrical and distal distribution. Results-The sample included 347 patients with diabetes (8.3 Yo). Sixty-six of them (19%0) had symptoms and signs consistent with probable polyneuropathy (overall prevalence 1.6%). The disease prevailed in women and in subjects aged 75 years and older. Diabetic patients with polyneuropathy had a longer disease course (lQ0.02) and high mean fasting (P<O.OOl) and post-prandial (P<0.02) blood glucose. Conclusion-Diabetic polyneuropathy in the elderly is a fairly common clinical condition prevailing in women and in subjects 75 years and older. Risk factors for polyneuropathy include prolonged disease duration and high I mean fasting and post-prandial blood glucose. Estimates of the prevalence of diabetic polyneuropathy vary widely in different studies (1-10). This may be related to factors including the small sample size in most series, the use of different diagnostic criteria, the differing populations at risk, and the different methods of patient selection. The elderly are at greater risk of polyneuropathy because many neurologic abnormalities, including signs of peripheral nerve involvement, are
Study of 50 Cases of Neuropathy in Type II Diabetes Mellitus
International Journal of Scientific Research, 2012
INTRODUCTION: Diabetes mellitus (DM) is a group of common metabolic disorders that share the phenotype of hyperglycemia; caused by complex interaction of genetics, environmental factors, and lifestyle choices and classified on the basis of a pathogenic process leading to hyperglycemia. Long standing diabetes mellitus is usually complicated by some form of neuropathy which may be symmetrical or asymmetrical. It may be rapidly reversible, persistent, focal or mixed.DM is associated with several types of polyneuropathy: distal symmetric sensory or sensorimotor polyneuropathy, autonomic neuropathy, diabetic neuropathic cachexia, polyradiculoneuropathies, cranial neuropathies, and other mononeuropathies. Risk factors for the development of neuropathy include longstanding, poorly controlled DM and the presence of retinopathy and nephropathy.1,2AIMS & OBJECTIVES: (1). To study clinical presentation of diabetic neuropathy in type 2 DM. (2). To study biochemical parameters in diabetic neuropathy. CONCLUSION: In our study it is evident that DM neuropathy affects more commonly in males (62%) than females (38%). The most common form of diabetic neuropathy is distal symmetric polyneuropathy.1 In our study; 62% patients have sensory, 38% sensory motor and 52% have autonomic neuropathy. It is also in linear relationship with duration of diabetes mellitus and level of blood glucose; more the duration of DM II and more level of blood glucose, more chances of developing neuropathy.
Diabetes/Metabolism Research and Reviews, 2011
Prior to a joint meeting of the Neurodiab Association and International Symposium on Diabetic Neuropathy held in Toronto, Ontario, Canada, 13‐18 October 2009, Solomon Tesfaye, Sheffield, UK, convened a panel of neuromuscular experts to provide an update on polyneuropathies associated with diabetes (Toronto Consensus Panels on DPNs, 2009). Herein, we provide definitions of typical and atypical diabetic polyneuropathies (DPNs), diagnostic criteria, and approaches to diagnose sensorimotor polyneuropathy as well as to estimate severity. Diabetic sensorimotor polyneuropathy (DSPN), or typical DPN, usually develops on long‐standing hyperglycaemia, consequent metabolic derangements and microvessel alterations. It is frequently associated with microvessel retinal and kidney disease—but other causes must be excluded. By contrast, atypical DPNs are intercurrent painful and autonomic small‐fibre polyneuropathies. Recognizing that there is a need to detect and estimate severity of DSPN validly ...
Neurologic Clinics, 2013
Diabetic neuropathies consist of a variety of syndromes resulting from different types of damage to peripheral or cranial nerves. Although distal symmetric polyneuropathy is most common type of diabetic neuropathy, there are many other subtypes of diabetic neuropathies which have been defined since the 1800's. Included in these descriptions are patients with proximal diabetic, truncal, cranial, median, and ulnar neuropathies. Various theories have been proposed for the pathogenesis of these neuropathies. The treatment of most of these requires tight and stable glycemic control. Spontaneous recovery is seen in most of these conditions with diabetic control Immunotherapies have been tried in some of these conditions but are quite controversial.
Diabetic polyneuropathy (DPN) is defined as peripheral nerve dysfunction. There are three main alterations involved in the pathologic changes of DPN: inflammation, oxidative stress, and mitochondrial dysfunction. Inflammation induces activation of nuclear factor kappa B, activator protein 1, and mitogen-activated protein kinases. Oxidative stress induced by hyperglycemia is mediated by several identified pathways: polyol, hexosamine, protein kinase C, advanced glycosylation end-products, and glycolysis. In addition, mitochondrial dysfunction accounts for most of the production of reactive oxygen and nitrosative species. These free radicals cause lipid peroxidation, protein modification, and nucleic acid damage, to finally induce axonal degeneration and segmental demyelination. The prevalence of DPN ranges from 2.4% to 78.8% worldwide, depending on the diagnostic method and the population assessed (hospital-based or outpatients). Risk factors include age, male gender, duration of diabetes, uncontrolled glycaemia, height, overweight and obesity, and insulin treatment. Several diagnostic methods have been developed, and composite scores combined with nerve conduction studies are the most reliable to identify early DPN. Treatment should be directed to improve etiologic factors besides reducing symptoms; several approaches have been evaluated to reduce neuropathic impairments and improve nerve conduction, such as oral antidiabetics, statins, and antioxidants (alpha-lipoic acid, ubiquinone, and flavonoids).
Journal of Neurology, Neurosurgery & Psychiatry, 1999
Objective-To quantify the progression of diabetic polyradiculoneuropathy-a condition in which immune factors have been implicated-after immunotherapy. Methods-The study evaluated 15 consecutive patients with this condition. All patients were older than 40. Four had type I diabetes and six were women. The duration of pre-existing diabetes varied from 2 to 20 years. The clinical presentation was dominated by painful progressive motor weakness, with or without exacerbation of sensory symptoms. The weakness involved all limbs, but was often asymmetric. Results-Electrophysiological testing showed a predominantly axonal polyneuropathy, with more recent denervating polyradiculopathy. Analysis of CSF showed increased protein in 14 and oligoclonal bands in five. Quantitative autonomic tests showed abnormalities in all patients. Sural nerve biopsy was performed in 14 patients; all showed fibre loss and segmental demyelination, four had occasional onion bulbs, and 10 showed various inflammatory infiltrates. After immunomodulating therapy, there was no further deterioration and clinical improvement occurred in all patients. Sweat responses, cardiovascular reflexes, and sural nerve fibre density correlated best with functional outcome. There was no significant diVerence between plasmapheresis and intravenous gammaglobulin. Conclusion-Immunotherapy may improve this condition, but only certain variables correlate with rapid therapeutic response.