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Peripheral neuropathy is a common side effect of many chemotherapy agents. As many as 60% of patients receiving taxane therapy report symptoms such as numbness, tingling, burning, pain, and, in severe cases, weakness in a stocking and glove pattern. These symptoms are associated with problems in physical mobility and decreased quality of life, yet few articles in the literature discuss collaborative interdisciplinary assessment and treatment of this population. This article describes the care of a patient with diabetes and docetaxel-induced, painful peripheral neuropathy by a multidisciplinary team of nurses, physicians, and physical therapists. Because nurses are often the first clinicians to recognize symptoms of chemotherapy-induced peripheral neuropathy, they provide the essential coordination of care by appropriate medical and rehabilitative services. This case also raises important questions about the relationship between diabetes mellitus and persistent, painful peripheral neuropathy.
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PMID:Case report: painful peripheral neuropathy following treatment with docetaxel for breast cancer. 1585 62

A case manifesting symptoms due to organochlorine toxicity was treated with the fat substitute olestra in his diet. Before treatment, the patient was obese, with severe type 2 diabetes mellitus and mixed hyperlipidemia, chloracne, frequent headaches, and numbness and paraesthesias of his trunk and lower limbs. Earlier attempts at weight loss had been unsuccessful due to worsening of his symptoms. After inclusion of olestra in his diet for 2 years, weight loss was successful without aggravation of his symptoms, and the patient reverted to normoglycemia and normolipidemia. Olestra may have assisted weight loss and amelioration of his diabetes by increasing fecal elimination of organochlorines, rather than by preventing the partitioning of these pollutants into tissues, where they have been reported to exert antimetabolic effects on substrate oxidation.
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PMID:Treatment with a dietary fat substitute decreased Arochlor 1254 contamination in an obese diabetic male. 1593 51

Since 1992 it has been reported that patients with diabetes mellitus recover sensibility and obtain relief of pain from neuropathy symptoms by decompression of lower-extremity peripheral nerves. None of these reports included a series with more than 36 diabetic patients with lower-extremity nerves decompressed, and only recently has a single report appeared of the results of this approach in patients with nondiabetic neuropathy. No previous report has described a change in balance related to restoration of sensibility. A prospective study was conducted of 100 consecutive patients (60 with diabetes and 40 with idiopathic neuropathy) operated on by a single surgeon, other than the originator of this approach, and with the postoperative results reviewed by someone other than these two surgeons. Each patient had neurolysis of the peroneal nerve at the knee and the dorsum of the foot, and the tibial nerve released in the four medial ankle tunnels. After at least 1 year of follow-up, 87% of patients with preoperative numbness reported improved sensation, 92% with preoperative balance problems reported improved balance, and 86% whose pain level was 5 or greater on a visual analog scale from 0 (no pain) to 10 (the most severe pain) before surgery reported an improvement in pain. Decompression of compressed lower-extremity nerves improves sensation and decreases pain, and should be recommended for patients with neuropathy who have failed to improve with traditional medical treatment.
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PMID:Surgical treatment of peripheral neuropathy: outcomes from 100 consecutive decompressions. 1616 62

The medical records of 2239 patients (mean age=73 years) with established peripheral neuropathy (PN) were examined to determine whether treatment with MIRE was, in fact, associated with increased foot sensitivity to the Semmes Weinstein monofilament (SWM) 5.07 and a reduction in neuropathic pain. The PN in 1395 of these patients (62%) was due to diabetes. Prior to treatment with MIRE, of the 10 tested sites (5 on each foot), 7.1+/-2.9 were insensitive to the SWM 5.07, and 2078 patients (93%) exhibited loss of protective sensation defined by Medicare as a loss of sensation at two or more sites on either foot. After treatment, the number of insensate sites on both feet decreased to 2.4+/-2.6, an improvement of 66%. Of the 2078 (93%) patients initially presenting with loss of protective sensation, 1106 (53%) no longer had loss of protective sensation after treatment (P<.0001); 1563 patients (70%) also exhibited neuropathic pain in addition to sensory impairment. Prior to treatment with MIRE, pain measured on the 11-point visual analogue scale (VAS) was 7.2+/-2.2 points, despite the use of a variety of pain-relieving therapeutic agents. After treatment with MIRE, pain was reduced by 4.8+/-2.4 points, a 67% reduction. Therefore, MIRE appears to be associated with significant clinical improvement in foot sensation and, simultaneously, a reduction in neuropathic pain in a large cohort of primarily Medicare aged, community-dwelling patients, initially diagnosed with PN. The quality of life associated with these two outcomes cannot be underappreciated.
J Diabetes Complications
PMID:Improved foot sensitivity and pain reduction in patients with peripheral neuropathy after treatment with monochromatic infrared photo energy--MIRE. 1650 36

Burning mouth syndrome (BMS) has been comparatively recently isolated as the separate nosologic diagnosis. This disease is characterized by the feeling of burning, dryness, numbness, pricking and seldom by pain in the tongue or mouth cavity area (palate, lips, alveoli) without any changes in mucous membrane. Absence of visible causes of the disease complicates its treatment and makes the patients to address the physicians of various profiles, often without any result. All the above stated made the authors to define the etiologic factors of various clinical versions of BMS and to carry out their differential diagnostics along with the development of pathogenetic therapy of BMS. 30 women of 40 to 70 year of age were examined. According to the anamnesis, BMS was developing gradually and in most cases it was associated with the aggravation of the existing disease (hypertension, diabetes mellitus, aggravation of climacteric state) or with deterioration of psycho-emotional sphere due to conflicting situation. The carried out studies enabled the authors to select and divide patients with BMS into groups according to clinical values and the etiologic factors. In most cases diverse clinical versions of the burning mouth syndrome are cause-and-effect expressions of various somatic diseases, the timely determination and adequate therapy of which give the best results in the struggle against BMS.
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PMID:[Role of various etiologic factors in the development of burning mouth syndrome]. 1690 8

We report two cases of heterozygous Fabry disease with severe organ damage. Case 1 was a 47-year-old woman. In April 1977, at the age of 27 years, she had proteinuria and edema around the 26th week of her second pregnancy and was diagnosed as toxicosis of pregnancy. She had proteinuria after the delivery. In 1990, a renal biopsy showed zebra bodies under electron microscopic findings, and the patient was diagnosed as Fabry disease. In 1998, a myocardial biopsy showed identical findings. The patient developed severe hypertension and decreased renal function, and alpha-galactosidase enzyme replacement therapy was initiated. However, despite treatment, she was started on dialysis in 2004. Case 2 was a 40-year-old woman. In March 2003, the patient presented with severe hypertension. The patient had cerebral infarction, cardiac hypertrophy, old myocardial infarction and renal failure without diabetes mellitus, hyperlipidemia and collagen disease. The patient was diagnosed as Fabry disease from persistent numbness and pain in the four extremities, a family history of mortality due to heart disease, and skin biopsy findings. She is currently undergoing enzyme replacement therapy. It is generally known that female Fabry disease patients are asymptomatic or mildly symptomatic, as were the present two patients, but some can have marked organ disorders. Hence, even in female patients, it is necessary to consider Fabry disease as a causative disease of chronic renal failure.
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PMID:[Two cases of heterozygous Fabry disease]. 1691 64

Diabetic neuropathies are a heterogeneous group of disorders that include a wide range of abnormalities. They can be focal or diffuse, proximal or distal, affecting both peripheral and autonomic nervous systems, causing morbidity with significant impact on the quality of life of the person with diabetes, and can result in early death. Distal symmetric polyneuropathy, the most common form of diabetic neuropathy, usually involves small and large nerve fibers. Small-nerve-fiber neuropathy often presents with pain but without objective signs or electrophysiologic evidence of nerve damage, and is recognized as a component of the impaired glucose tolerance and metabolic syndromes. The greatest risk resulting from small-fiber neuropathy is foot ulceration and subsequent gangrene and amputation. Large-nerve-fiber neuropathies produce numbness, ataxia and uncoordination, impairing activities of daily living and causing falls and fractures. A careful history and detailed physical examination are essential for the diagnosis. Symptomatic therapy has become available and newer and better treatment modalities, based on etiologic factors, are being explored with potential for significant impact on morbidity and mortality. Preventive strategies and patient education still remain key factors in reducing complication rates and mortality.
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PMID:Diabetic neuropathies: clinical manifestations and current treatment options. 1693 98

Diabetic neuropathy (DN) is a common severe complication of type 2 diabetes. The symptoms of chronic pain, tingling, and numbness are generally attributed to small fiber dysfunction. However, little is known about the pathology among innervation to distal extremities, where symptoms start earliest and are most severe, and where the innervation density is the highest and includes a wide variety of large fiber sensory endings. Our study assessed the immunochemistry, morphology, and density of the nonvascular innervation in glabrous skin from the hands of aged nondiabetic rhesus monkeys and from age-matched monkeys that had different durations of spontaneously occurring type 2 diabetes. Age-related reductions occurred among all types of innervation, with epidermal C-fiber endings preferentially diminishing earlier than presumptive Adelta-fiber endings. In diabetic monkeys epidermal innervation density diminished faster, became more unevenly distributed, and lost immunodetectable expression of calcitonin gene-related peptide and capsaicin receptors, TrpV1. Pacinian corpuscles also deteriorated. However, during the first few years of hyperglycemia, a surprising hypertrophy occurred among terminal arbors of remaining epidermal endings. Hypertrophy also occurred among Meissner corpuscles and Merkel endings supplied by Abeta fibers. After longer-term hyperglycemia, Meissner corpuscle hypertrophy declined but the number of corpuscles remained higher than in age-matched nondiabetics. However, the diabetic Meissner corpuscles had an abnormal structure and immunochemistry. In contrast, the expanded Merkel innervation was reduced to age-matched nondiabetic levels. These results indicate that transient phases of substantial innervation remodeling occur during the progression of diabetes, with differential increases and decreases occurring among the varieties of innervation.
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PMID:Differential hypertrophy and atrophy among all types of cutaneous innervation in the glabrous skin of the monkey hand during aging and naturally occurring type 2 diabetes. 1727 31

Spinal cord infarction is uncommon and usually presents with sudden onset of paralysis and sensory disturbances. A variety of causes are described, but rarely with multiple factors involved. We report a case of a 63-year-old man with a history of diabetes mellitus, hypertension, and osteoarthritis who presented with acute onset of chest pain, numbness, and weakness associated with episodic hypotension. He had incomplete tetraplegia and was areflexic without spasticity. Pain and temperature sensations were impaired below the C7 dermatome and absent below the T4 dermatome bilaterally. Proprioception and vibration sensations were diminished on the right below the C6 dermatome. Magnetic resonance imaging showed spinal cord infarction affecting C6-T3 segments, and severe cervical and lumbar spine degenerative changes. This case illustrates an unusual presenting symptom of spinal infarction, the need to identify multiple risk factors for spinal cord infarction, and the importance of optimal preventive therapy in patients at risk.
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PMID:Spinal cord infarction with multiple etiologic factors. 1735 58

Peripheral neuropathy is a common medical problem with numerous aetiologies. Unfortunately, for the majority of cases there is no available medical solution for the underlying cause, and the only option is to try to treat the resulting symptoms. Treatment options exist when neuropathy results in positive symptoms such as pain, but there is a significant lack of treatments for negative symptoms such as numbness and weakness. Systemic application of growth factor peptides has shown promise in protecting nerves from neuropathic insults in preclinical animal studies, but translation into human trials has been problematic and disappointing. Significant advancements have been made in the past few years in utilising gene therapy approaches to treat peripheral neuropathy by expressing neuroprotective gene products either systemically or in specific nervous tissues. For example, plasmids expressing vascular endothelial growth factor injected into muscle, or herpes-simplex-virus-based vectors expressing neurotrophin gene products delivered to dorsal root ganglion neurons, have been used to protect peripheral nerve function in animal models of diabetes-associated peripheral neuropathy. Many published studies support the feasibility of this approach, although several questions still need to be addressed as gene therapy to treat peripheral neuropathy moves out of the laboratory and into the clinic.
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PMID:The therapeutic potential of gene transfer for the treatment of peripheral neuropathies. 1736 56


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