Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Distal sensory polyneuropathy (DSP) is the most frequent neurological complication of HIV infection. Neuropathic symptoms vary from mild paresthesias to severe pain that respond only partially to symptomatic treatment. Forty-five subjects with human immunodeficiency virus (HIV)-associated symptomatic DSP (SDSP) were enrolled in a randomized, multicenter, 16-week placebo-controlled study of memantine, an N-methyl-D-aspartate (NMDA) uncompetitive antagonist. Although memantine was well tolerated, no trend toward clinical benefit was observed. Results were similar to those of other pilot studies of memantine for neuropathic pain unrelated to HIV, suggesting that memantine is ineffective for the symptomatic treatment of HIV-associated SDSP.
 ...
PMID:A placebo-controlled study of memantine for the treatment of human immunodeficiency virus-associated sensory neuropathy. 1696 23

A 57-year-old man had progressive paresthesias ascending from both legs together with paraparesis. Distal paresthesias of the upper extremities developed earlier than segmental sensory impairments. At transfer to our hospital, a neurological examination detected bilateral lower limb weakness predominant in the distal part; severe glove and stocking paresthesias in addition to superficial sensory impairment below the Th8 level; and micturition problems. T2-weighted thoracolumbar MRI showed a hyperintense spinal cord lesion between Th5 and L1. At the L4 level, a spinal arteriogram showed enlarged and tortuous vessels extending from the lumbar artery which drains to the spinal vein. These findings led to the diagnosis of spinal dural arteriovenous fistula. Anatomical substrates for this sensory impairment may be produced by development from the side to forward parts of lesions in the outer circumference of the anterior funiculi, resulting in the dominating sensory impairment in the distal parts of the upper extremities. Physicians need to be aware of patients who have polyneuropathy-like sensory impairment without segmental sensory signs, and must consider the possibility of spinal dural arteriovenous fistula.
 ...
PMID:[Case of spinal thoracic-lumbar dural arteriovenous fistula with polyneuropathy type sensory impairment]. 1698 6

Accumulating evidence over the past decade indicates that synthetic retinoids may be capable of affecting both growth and differentiation of nervous tissue. Our aim was to substantiate possible side-effects of oral isotretinoin therapy on peripheral nerve functions, both neurologically and neurophysiologically. We performed neurological examination and electroneuromyographic studies on 18 patients with various skin diseases before, at the third month, and at the end of isotretinoin treatment. Abnormal neurophysiological findings in this study point towards a typical distal, length-dependent and predominantly sensory polyneuropathy. Clinicians should be aware of possible neurological sensorial symptoms during isotretinoin therapy. In our opinion, electroneuromyographic investigation should be performed on all patients reporting symptoms (e.g. paresthesia, numbness, sensory loss) before and during oral isotretinoin treatment. The precise clinical significance of the isotretinoin-induced neurophysiological alterations reported here remains to be determined in further studies.
 ...
PMID:Effects of oral isotretinoin therapy on peripheral nerve functions: a preliminary study. 1943 30

Numerous clinical forms of CIDP have been described, but pain is generally considered a rare or secondary sign. We describe here the clinical, electrophysiological and neuropathological characteristics of five patients with CIDP and pain as the main presenting symptom, and their course with treatment. Between January 2003 and December 2004, we selected five patients with prominent or isolated pain among 27 patients diagnosed with CIDP. All patients were subjected to clinical and electrophysiological examinations, and had a complete laboratory work up to exclude other causes of neuropathy. In view of the atypical clinical presentation, all five patients underwent nerve biopsy. There were two men and three women. The mean age at onset of neuropathy was 70+/-7.39 years. All patients initially presented with pain in the lower limbs associated with modest motor impairment (1 case), distal paresthesia (4 cases), cramps (1 case) and fatigue (2 cases). CSF was normal in three cases. On electrophysiological examination, three patients had nerve conduction abnormalities with subtle or clear signs of demyelination: three (case 1, 2 and 4) fulfilled the criteria of Rotta et al. and two (case 2 and 4) the criteria of both Nicolas et al and the INCAT group. Patients were all given symptomatic treatment and four patients received an immunomodulatory treatment, which was constantly effective. Pain may be a major and disabling symptom in patients with CIDP, so this diagnosis has to be considered in patients referred for a painful polyneuropathy. Moreover, immunomodulatory treatment has to be considered in such patients as symptomatic therapy may be ineffective.
 ...
PMID:Pain as the presenting symptom of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). 1728 85

Transthyretin familial amyloid polyneuropathies (TTR-FAPs) are autosomal dominant neuropathies of fatal outcome within 10 years after inaugural symptoms. Late diagnosis in patients who present as nonfamilial cases delays adequate management and genetic counseling. Clinical data of the 90 patients who presented as nonfamilial cases of the 300 patients of our cohort of patients with TTR-FAP were reviewed. They were 21 women and 69 men with a mean age at onset of 61 (extremes: 38 to 78 years) and 17 different mutations of the TTR gene including Val30Met (38 cases), Ser77Tyr (16 cases), Ile107Val (15 cases), and Ser77Phe (5 cases). Initial manifestations included mainly limb paresthesias (49 patients) or pain (17 patients). Walking difficulty and weakness (five patients) and cardiac or gastrointestinal manifestations (five patients), were less common at onset. Mean interval to diagnosis was 4 years (range 1 to 10 years); 18 cases were mistaken for chronic inflammatory demyelinating polyneuropathy, which was the most common diagnostic error. At referral a length-dependent sensory loss affected the lower limbs in 2, all four limbs in 20, and four limbs and anterior trunk in 77 patients. All sensations were affected in 60 patients (67%), while small fiber dysfunction predominated in the others. Severe dysautonomia affected 80 patients (90%), with postural hypotension in 52, gastrointestinal dysfunction in 50, impotence in 58 of 69 men, and sphincter disturbance in 31. Twelve patients required a cardiac pacemaker. Nerve biopsy was diagnostic in 54 of 65 patients and salivary gland biopsy in 20 of 30. Decreased nerve conduction velocity, increased CSF protein, negative biopsy findings, and false immunolabeling of amyloid deposits were the main causes of diagnostic errors. We conclude that DNA testing, which is the most reliable test for TTR-FAP, should be performed in patients with a progressive length-dependent small fiber polyneuropathy of unknown origin, especially when associated with autonomic dysfunction.
 ...
PMID:Diagnostic pitfalls in sporadic transthyretin familial amyloid polyneuropathy (TTR-FAP). 1842 77

Peripheral nerve disorders are frequent complications of HIV disease. Distal symmetrical polyneuropathy (DSP) is the most common peripheral nerve disorder associated with HIV and occurs in over one third of infected patients but may occur in up to 67% if asymptomatic patients are included. Risk factors for DSP include increased age, advanced HIV disease, and history of "d-drugs" or other neurotoxic drugs. The primary manifestations of polyneuropathy are slowly progressive numbness and paresthesias, with burning sensations in the feet usually in a symmetrical pattern. The etiology of HIV-associated DSP is unknown, although neurotoxic effects of cytokines, toxicity of HIV proteins, and mitochondrial damage have been implicated. The current treatment for HIV-associated DSP is symptomatic, with pain modifying medications, including anti-inflammatory agents, opioids, antidepressants, antiepileptics, topical anesthetics, and capsaicin. Sustained virologic control may improve DSP. Novel therapies such as -acetyl-l-carnitine or neurotrophic factors are being studied for treatment of DSP.
 ...
PMID:Managing HIV peripheral neuropathy. 1788 96

Paraesthesia in the legs can have numerous causes. In addition to the restless legs syndrome, other primary causes include venous insufficiency in the leg, propriospinal myoclonus, nocturnal leg cramps, peripheral polyneuropathy that affects mostly the legs or neuroleptic drug-induced akathisia. Through detailed questioning of the patient, restless legs syndrome can be specifically distinguished from the other named differential diagnoses.
 ...
PMID:[Paraesthesia in the legs]. 1798 22

Acute peripheral neuropathy caused by a disulfiram overdose is very rare and there is no report of it leading to vocal fold palsy. A 49-year-old woman was transferred to our department because of quadriparesis, lancinating pain, sensory loss, and paresthesia of the distal limbs. One month previously, she had taken a single high dose of disulfiram (130 tablets of ALCOHOL STOP TAB, Shin-Poong Pharm. Co., Ansan, Korea) in a suicide attempt. She was not an alcoholic. For the first few days after ingestion, she was in a confused state and had mild to moderate ataxia and giddiness. She noticed hoarseness and distally accentuated motor and sensory dysfunction after she had recovered from this state. A nerve conduction study was consistent with severe sensorimotor axonal polyneuropathy. Laryngeal electromyography (thyroarytenoid muscle) showed ample denervation potentials. Laryngoscopy revealed asymmetric vocal fold movements during phonation. Her vocal change and weakness began to improve spontaneously about 3 weeks after transfer. This was a case of acute palsy of the recurrent laryngeal nerve and superimposed severe acute sensorimotor axonal polyneuropathy caused by high-dose disulfiram intoxication.
 ...
PMID:Acute vocal fold palsy after acute disulfiram intoxication. 1802 25

Neuropathy in rheumatoid arthritis (RA) may result secondary to entrapment, vasculitis, and drug toxicity. We aimed to study clinical and electrophysiological neuropathy and pathological changes in sural nerve in patients with RA. One hundred eight patients of RA, fulfilling American College of Rheumatology 1987 criteria (mean age, 45.83 years; M/F 1:3, 80.3% seropositive) were examined clinically and electrophysiologically for evidence of peripheral neuropathy. Sural nerve biopsies were performed in the involved cases. In all RA patient medications, disease activity, results of blood tests, and X-rays of affected joints were recorded. Twenty-three patients complained of paresthesias in the extremities. Vibration sensations were decreased in 9, and tendon reflexes were decreased or absent in 28 patients. Sixty-two (57.4%) patients had electrophysiologic evidence of neuropathy. Of these 53 (85.5%) patients had pure sensory or sensory motor axonal neuropathy (mononeuritis multiplex, n = 7), while 9 (14.5%) had demyelinating neuropathy (chronic inflammatory demyelinating polyneuropathy, n = 1). Carpal tunnel syndrome was seen in 11 (10.1%) patients (associated with neuropathy in 6). Of 23 sural nerve biopsies available, perineurial thickening (n = 5, amyloid deposits n = 4), perivascular lymphomononuclear cell infiltrate (n = 4), loss of myelin fibers (n = 2), and necrotizing vasculitis (n = 1) were found. Clinically, however, seven patients had evidence of cutaneous vasculitis. Comparing the clinical characteristics of the patients with or without electrophysiological neuropathy, absence of deep tendon jerks (p < 0.005) and presence of extra articular manifestations (p < 0.01) were conspicuous in the neuropathic group. There was no relation of neuropathy with the duration of RA, seropositivity, joint erosions, joint deformities, prior disease-modifying anti-rheumatic drugs or glucocorticoid intake, and 28-joint disease activity score. Neuropathy in RA was mostly subclinical and predominantly axonal. Pathologically, neuropathy secondary to amyloid infiltration was second only to vasculitic neuropathy. Absence of deep tendon jerks and presence of vasculitis were more commonly observed in patients with neuropathy.
 ...
PMID:A clinical, electrophysiological, and pathological study of neuropathy in rheumatoid arthritis. 1808 7

A 67-year-old man affected by moderate weight loss, acral paresthesia and plantar burning sensation was admitted to our department. Electromyographic (EMG) and electroneurographic (ENG) studies confirmed a peripheral, asymmetrical, motor-sensorial polyneuropathy (PPN). Hematological data and bone marrow biopsy discovered a non-secerning multiple myeloma (MM). All other probable causes of peripheral neuropathy could be excluded, and the possible relationship between nerve damage and neoplasia was confirmed. Furthermore, all possibilities of association of MM with PPn, namely the osteosclerotic variant, the Crow-Fukase syndrome, and the amyloid one have been evaluated. The only finding of osteolytic bone areas by radiology, the absence of organomegaly, diabetes mellitus, skin alterations, and of amyloid deposition in muscles and nerves, exclude the possible connection of the case to any of the listed possibilities. On the other hand, some clinical aspects differ, in part, to others described in the literature. In conclusion, the association between PPN and MM as the result of multiform clinical variants could be considered.
 ...
PMID:Peripheral neuropathy and multiple myeloma in aging: a case report. 1864 92


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>