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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Paclitaxel (TXL) and docetaxel (TXT), especially TXL, cause neurotoxicity manifested as polyneuropathy. In clinical practice, detailed knowledge of the symptoms and effect on quality of life (QOL) of neurotoxicity is crucially important both for diagnosis of neuropathy and for management of patients treated with taxanes. In this review, we summarize the symptoms of neurotoxicity caused by taxanes, and highlight the importance of QOL assessment in breast cancer patients treated with taxanes. The most common feature of taxane neurotoxicity is a predominant sensory distal neuropathy, and the incidence and severity of the neuropathic manifestations appear to be related to dose level and cumulative dose. A mixture of paresthesias and dysesthesias is often prominent, and the complaints include burning dysesthesia, numbness, tingling, and shooting pains, typically in a stocking-glove distribution. In contrast to sensory disturbances, motor neuropathy is not well recognized, and is believed to be much less common than sensory neuropathy. Weakness is usually mild, and distal motor neuropathy caused by taxanes rarely affects patients' activities of daily living. The effect of neurotoxicity on QOL is not fully understood, as no study has specifically assessed QOL in terms of neurotoxicity. There is therefore a clear need to collect more detailed data about QOL using well validated, reliable instruments. This will enable us to provide the information that patients require when treatment decisions are being made, and will help in the pursuit of the ameliorative interventions.
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PMID:Neurotoxicity of taxanes: symptoms and quality of life assessment. 1471

Adverse health effects of fungal bioaerosols on occupants of water-damaged homes and other buildings have been reported. Recently, it has been suggested that mold exposure causes neurological injury. The authors investigated neurological antibodies and neurophysiological abnormalities in patients exposed to molds at home who developed symptoms of peripheral neuropathy (i.e., numbness, tingling, tremors, and muscle weakness in the extremities). Serum samples were collected and analyzed with the enzyme-linked immunosorbent assay (ELISA) technique for antibodies to myelin basic protein, myelin-associated glycoprotein, ganglioside GM1, sulfatide, myelin oligodendrocyte glycoprotein, alpha-B-crystallin, chondroitin sulfate, tubulin, and neurofilament. Antibodies to molds and mycotoxins were also determined with ELISA, as reported previously. Neurophysiologic evaluations for latency, amplitude, and velocity were performed on 4 motor nerves (median, ulnar, peroneal, and tibial), and for latency and amplitude on 3 sensory nerves (median, ulnar, and sural). Patients with documented, measured exposure to molds had elevated titers of antibodies (immunoglobulin [Ig]A, IgM, and IgG) to neural-specific antigens. Nerve conduction studies revealed 4 patient groupings: (1) mixed sensory-motor polyneuropathy (n = 55, abnormal), (2) motor neuropathy (n = 17, abnormal), (3) sensory neuropathy (n = 27, abnormal), and (4) those with symptoms but no neurophysiological abnormalities (n = 20, normal controls). All groups showed significantly increased autoantibody titers for all isotypes (IgA, IgM, and IgG) of antibodies to neural antigens when compared with 500 healthy controls. Groups 1 through 3 also exhibited abnormal neurophysiologic findings. The authors concluded that exposure to molds in water-damaged buildings increased the risk for development of neural autoantibodies, peripheral neuropathy, and neurophysiologic abnormalities in exposed individuals.
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PMID:Neural autoantibodies and neurophysiologic abnormalities in patients exposed to molds in water-damaged buildings. 1525 25

2 patients, men aged 60 and 65 years, presented with symptoms of chronic sensory polyneuropathy. Symptoms in the first patient were bilateral numbness in the hands and leg pain and, in the second patient, painful tingling in the legs. Pyridoxine (vitamin B6) toxicity due to daily use of multivitamin supplements was diagnosed. The patients were taking 24 and 40 mg per day, respectively. Neurotoxic syndromes due to pyridoxine overdose have been described before in patients taking high-dose vitamin B. These patients mostly developed progressive sersory neuronopathy with sensory ataxia. Chronic sensory polyneuropathy has not been associated with the use of vitamin supplements, which have previously been considered harmless. Both patients recovered after discontinuation of supplement intake.
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PMID:[Sensory disturbances caused by multivitamin preparations]. 1649

A 45 year-old Japanese woman developed numbness and tingling of both hands and feet. Electrophysiological examination revealed sensorimotor polyneuropathy. She was diagnosed as suffering from sarcoidosis on the basis of the pathological findings from dermal biopsy. Steroid therapy effectively improved the clinical symptoms. Although sarcoid neuropathy is rare, this case suggests sensorimotor polyneuropathy is an important symptom of sarcoidosis and can represent the initial clinical manifestation of the disease.
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PMID:Sensorimotor polyneuropathy as an initial clinical manifestation of sarcoidosis. 1702 53

The combination of pegylated interferon (Peg-IFN) and ribavirin is the standard of care for chronic hepatitis C virus (HCV) infection treatment. In general, common side effects related to this combination therapy are mild and are very well tolerated. However, peripheral neuropathy including demyelinating polyneuropathy related to Peg-IFN is extremely rare. We present the first case of an acute inflammatory demyelinating polyneuropathy (AIDP) associated with Peg-IFN-alpha 2a (Pegasys) after 16 wk of a combination therapy with Pegasys and ribavirin in a 65-year-old woman with chronic HCV infection. She developed tingling, numbness, and weakness of her upper and lower extremities and was hospitalized for acute neurological deficits. Her clinical course, neurological findings, an electromyogram (EMG), nerve conductions studies (NCS), muscle biopsy, and a sural nerve biopsy were all consistent with AIDP likely related to Pegasys use. The patient recovered completely with the use of intravenous immunoglobulin (IVIG) including physical therapy and neurological rehabilitation. It is very important that gastroenterologists and/or hepatologists recognize this rare neurological complication related to Peg-IFN treatment very early, since it requires a prompt discontinuation of therapy including an immediate referral to a neurologist for the confirmation of diagnosis, management, and the prevention of long-term neurological deficits.
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PMID:Acute inflammatory demyelinating polyneuropathy associated with pegylated interferon alpha 2a therapy for chronic hepatitis C virus infection. 1818 75

Polyneuropathy related to decreased levels of Vitamin B6 are well known. In contrast, the association between elevated levels of pyridoxine and neuropathy is not well described. This study is a retrospective review of patients in our neuromuscular clinic that were found to have elevated B6 levels. Twenty-six patients were found to have elevated serum B6 levels. The mean B6 level was 68.8 ng/ml. Twenty patients (76.9%) reported daily vitamin use. Twenty-one patients (80.8%) reported only sensory complaints. The most common symptoms reported were numbness (96%), burning pain (49.9%), tingling (57.7%), balance difficulties (30.7%), and weakness (7.8%). Nine (out of 26) had an abnormal EMG/NCS. Eight patients had an abnormal quantitative sensory study. We conclude that elevated pyridoxine levels should be considered in the differential diagnosis of any sensory or sensorimotor polyneuropathy.
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PMID:Elevated B6 levels and peripheral neuropathies. 1875 31

In the fall of 2007, the Minnesota Department of Health was notified of 11 cases of an unexplained neurological illness, all linked to a pork processing plant, Quality Pork Processors, Inc., in Austin, MN. The cluster of workers had been experiencing similar symptoms, including fatigue, pain, numbness, and tingling in their extremities as well as weakness. The symptoms were described as more sensory than motor, and all patients had evidence of polyradiculoneuropathy with signs of nerve root irritation. An epidemiological investigation revealed that the only commonality between cases was their exposure to a pork brain extraction procedure involving compressed air. As relatives of the cases remained asymptomatic and all cultures for known pathogens were negative, the etiology of the syndrome seemed not to be infectious. Clinically, the syndrome was most akin to chronic inflammatory demyelinating polyneuropathy. Laboratory tests corroborated the clinical findings, revealing inflammation of peripheral nerves and nerve roots; however, these cases also had features clinically distinct from chronic inflammatory demyelinating polyneuropathy as well as laboratory testing revealing a novel immunoglobulin G immunostaining pattern. This suggested that the observed inflammation was the result of 1 or more unidentified antigens. This syndrome was ultimately dubbed progressive inflammatory neuropathy and was theorized to be an autoimmune reaction to aerosolized porcine neural tissue. Since the investigation's outset, 18 cases of progressive inflammatory neuropathy have been identified at the Minnesota pork processing plant, with 5 similar cases at an Indiana plant and 1 case at a Nebraskan plant. The plants in which cases have been identified have since stopped the use of compressed air in removing pork brains. All cases have stabilized or improved, with some requiring immunosuppressive and analgesic treatment. The study of progressive inflammatory neuropathy is ongoing, and the details of this investigation highlight the value of epidemiological principles in the identification and containment of outbreaks while researchers attempt to uncover the unique pathophysiology and potential etiology of the illness. Mt Sinai J Med 76:442-447, 2009. (c) 2009 Mount Sinai School of Medicine.
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PMID:Outbreak of progressive inflammatory neuropathy following exposure to aerosolized porcine neural tissue. 1978 53

A patient developed numbness and tingling in distal extremities with subsequent weakness. Evaluation revealed B12 deficiency. She had evidence of myelopathy on imaging studies and polyneuropathy on electrodiagnostic testing. Treatment with B12 caused remittance of symptoms and resolution/improvement of abnormalities found on the imaging and electrodiagnostic studies. This case demonstrates that early intervention with B12 supplementation can cause reversal of both central and peripheral nervous system dysfunction.
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PMID:Recovery of neurologic dysfunction with early intervention of vitamin B12. 2051 8

Complaints of sensory loss and (painful) tingling in a stocking distribution are not uncommon in primary care. These symptoms are especially troublesome while getting asleep. Characteristically, ankle tendon reflexes and vibration perception are diminished. These are the hallmarks of distal-symmetric sensory polyneuropathy (PNP), with diabetes mellitus being the most common cause in our patient population. PNP presents itself only after years of suboptimal glycemic control in diabetes type 1. In patients with type 2, symptoms of PNP can precede formal diagnosis of diabetes! In this mini-review we present an algorithm for diagnosis and management of PNP's in general practice.
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PMID:[Polyneuropathies--short and sweet]. 2057 99

In the industrialized world, polyneuropathy induced by diabetes mellitus (DM) is one of the most prevalent forms of neuropathy. Diabetic neuropathy can result from a direct toxic effect of glucose on nerve cells. Additionally, the damage of the nerve structures (central and peripheral) is accompanied by a microvascular dysfunction, which damages the vasa nervorum. More than 80% of the patients with DM-induced polyneuropathy have a distal and symmetric presentation. The initial symptoms are: signs of diminished sensation, burning feet, which may occur particularly during the night and worsen when touched, and tingling sensation in the feet. Attacks of shooting pain may also occur. Proper control of DM is mandatory. Based on the recently published National Institute for Health and Clinical Excellence guidelines, treatment of painful diabetic neuropathy should start with duloxetine or amitriptyline if duloxetine is contraindicated. If pain relief is inadequate, monotherapy with amitriptyline or pregabalin, or combination therapy with amitriptyline and pregabalin should be considered. If pain relief is still insufficient, tramadol instead of or in combination with a second-line agent should be considered. In patients who are unable to take oral medication, topical lidocaine can be considered for localized pain. There are currently four studies showing that spinal cord stimulation can potentially provide pain alleviation for the longer term in patients with painful diabetic polyneuropathy. Complications are mainly implant related, though infections also occur. The available evidence (2 C+) justifies spinal cord stimulation to be considered, preferably study related.
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PMID:Evidence-based interventional pain medicine according to clinical diagnoses. 18. Painful diabetic polyneuropathy. 2119 15


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