Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Motor memory and the sense of effort have been investigated in a man with a complete large fibre sensory neuropathy for over 16 years. The perceptions of pain, heat, cold and muscular fatigue remained but he was without perceptions of light touch and proprioception below the neck. 2. The subject was able to discriminate weights held in the hand with an accuracy only slightly worse than control subjects (20 g in 200 g) when forearm movement and visual inspection were allowed. With eyes shut however he could only distinguish a weight of 200 g from 400 g. It is concluded that a crude sense of effort remains which may have a peripheral origin. 3. A limited motor memory was also present, which allowed him to maintain a posture or continue a simple repetitive movement. No novel movement was possible without visual feedback. 4. Differences in movement ability between this subject and others with similar if less pure sensory neuropathies are ascribed to rehabilitation.
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PMID:The perceptions of force and of movement in a man without large myelinated sensory afferents below the neck. 152 22

Oxaliplatin, or trans-1-diaminocyclohexane-platinum, was tested in a phase I study. A total of 44 patients received 116 courses with dose escalation from 45 to 200 mg/m2. Neither renal nor hematologic toxicities were observed at doses up to 200 mg/m2. Gastrointestinal toxicity was practically constant and often of grade 3-4 on the WHO scale (53% of patients). The dose-limiting toxicity was a peculiar sensory neuropathy; the first neurologic phenomena appeared at a dose of 135 mg/m2 and continued thereafter, occurring after 75% of the courses with mild to moderate intensity (WHO grade 1-2 after 67% of the courses). Neurotoxicity was cumulative and six patients developed grade 3 disabling neuropathy after a cumulative dose of 500 mg/m2, with walking and handwriting difficulties being slowly regressive in three cases. A peculiar symptom was the influence of temperature, with exacerbation of parethesias when patients touched cold surfaces. Nerve-conduction studies carried out in six cases showed a predominantly sensory neuropathy with axonal degeneration. No other toxicities were observed, although audiograms were not systematically done. We observed four partial responses that lasted 6-13 months in patients with oesophageal (2 cases), lung (1), and urothelial cancer (1); two of these patients had been pretreated with cisplatin. Since neurologic side effects occur very frequently and may produce a long-lasting sensory neuropathy, for phase II studies we recommend a starting dose of 135 mg/m2, with a careful neurologic survey.
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PMID:Phase I study of oxaliplatin in patients with advanced cancer. 229 16

Eleven patients with Welander distal myopathy were subjected to detailed sensory testing including measurements of perception thresholds for vibration and temperature in both hands and feet. The threshold values were compared with normal, age-corrected values and also with data from an age-matched control group consisting of patients with antecedent poliomyelitis with the same degree of paresis. The screening examination indicated impaired thermal sensibility in all 11 patients and impairment for at least one other sensory modality in 9 patients. In comparison with age-corrected normal values, the measured warm-cold difference limen was abnormal in the feet of 9 patients and the vibratory threshold at least at one test point in 6 patients. When compared with the data from the paretic controls, the thermal abnormality was significant with regard to warm and cold thresholds, the warm-cold difference limen and the heat pain threshold. The vibration threshold abnormality was significant in the feet. It is concluded that sensibility impairment is present in Welander's myopathy indicating a peripheral sensory neuropathy involving both unmyelinated (C-fibers) and myelinated fibers.
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PMID:Sensory involvement in distal myopathy (Welander). 368 36

The etiology of trigeminal sensory neuropathy remains obscure. In a recent case, a relationship to herpes simplex virus might be inferred. A woman, aged 63 years, had at least ten episodes of "cold sore," always at the same site on her upper lip. After a typical prodromal burning, she expected a cold sore to appear, but a trigeminal sensory neuropathy began instead, starting at the site where the cold sores had always appeared.
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PMID:Trigeminal sensory neuropathy. 661 95

A patient with a chronic, large fibre sensory neuropathy had an immunoglobulin M lambda monoclonal paraprotein reactive at titres in excess of 1/10(5) with NeuNAc(alpha 2-8)NeuNAc(alpha 2-3)Gal configured disialosyl groups present on the gangliosides GD1b, GT1b, GQ1b, and GD3. The paraprotein showed weaker reactivity with GD1a, GM3, and LM1 but no reactivity with GM2, GM1, or asialo-GM1. In addition, the paraprotein had cold agglutinating activity with anti-Pr2 specificity, Pr2 being an antigenic determinant on membrane glycoproteins or glycolipids in erythrocytes or both. A large fibre sensory neuropathy with monoclonal anti-disialosyl antibodies is an increasingly recognised form of paraproteinaemic neuropathy.
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PMID:Peripheral neuropathy associated with monoclonal IgM anti-Pr2 cold agglutinins. 769 74

Sensory aspects of uremic neuropathy were studied in 36 patients using clinical assessment and quantitative sensory tests (QST). The outstanding abnormality in sensory quality was perception of heat in response to low temperature stimuli. This paradoxical heat sensation was found in the foot in 42% (15) of patients, far beyond the normal prevalence of 10%. Paradoxical sensation was positively related to cold hypoesthesia (P = 0.0004) suggesting disinhibition as a possible mechanism. Paradoxical heat sensation also positively related to creatinine level (P = 0.0012). Pruritus was present in 20 patients (56%), intensity not related to any biochemical or clinical parameter. Signs of sensory polyneuropathy (PNP), based on at least two abnormal parameters in the clinical assessment or QST, were found in 39% of patients (14), of whom 11 had paradoxical heat sensation. Thus, in 4 patients (11%), this sensory aberration preceded other signs for PNP. Paradoxical heat sensation seems to be a common and often early expression of the sensory neuropathy in uremia.
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PMID:Paradoxical heat sensation in uremic polyneuropathy. 778 67

Fingertip skin blood flow was measured by laser Doppler flowmetry (as LDflux) under environmental conditions promoting vasodilation in Scottish patients with diabetes mellitus and Indian patients with leprosy. The reflex control of fingertip blood flow was assessed by measuring the reduction in LDflux induced by deep inspiratory gasp (IG) and cold challenge (CC) of immersing the contralateral hand in cold water. The uncomplicated diabetic patients showed normal vasomotor reflexes and an increased, though non significant, LDflux level (p < 0.06). The patients with diabetic neuropathy had resting LDflux levels significantly less than the uncomplicated group and also had substantial impairment of both IG and CC reflexes. Those with retinopathy (but no clinically apparent neuropathy) had LDflux within the normal range, but they showed minor evidence of impairment of the vasomotor reflexes. The uncomplicated newly registered leprosy patients had reduced LDflux and substantial impairment of CC reflexes. These changes were more marked in newly registered leprosy patients with clinical evidence of neuropathy. Leprosy patients with long-standing neuropathy requiring orthopaedic treatment had LDfluxes so greatly reduced that measurement of vasomotor reflexes was not practicable. The CC reflex was more severely affected than the IG reflex and more frequently absent in leprosy patients, possibly because of associated sensory neuropathy affecting the afferent limb of this response. Thus laser Doppler flowmetry can detect impairment of reflex control of fingertip blood flow in both diabetes mellitus and leprosy, but there are functional differences in the pattern of autonomic impairment between the diseases, suggesting differences in the pathogenesis of nerve damage.
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PMID:Vasomotor reflexes in the fingertip skin of patients with type 1 diabetes mellitus and leprosy. 840 Aug 18

Patients with obstructed defaecation (OD) perform major defaecatory efforts that lead progressively to pudendal motor neuropathy. Anorectal sensory function in these patients and its possible influence in the pathogenesis of the disease have been little studied. In the present paper we investigated anorectal sensitivity to electric and thermal stimuli in patients with OD, and studied the possible existence of pudendal sensory neuropathy associated to their known pudendal motor neuropathy. Forty subjects were divided into two groups: 21 healthy controls (11 females and 10 males; mean age 51.8 +/- 11 years, range 33-67) and 19 patients with OD (18 females and 1 male; mean age 48 +/- 15 years, range 20-71). The patients with OD suffered constipation and an obstruction sensation upon defaecating, even in the case of soft stools. Clinical perineometry, manometry, pudendal motor latency studies, external anal sphincter single fibre electromyography and the evaluation of sensitivity to electric and thermal stimuli were carried out in all cases. All pudendal motor function parameters showed statistically significant differences between the two groups. In the controls the electrical sensitivity threshold was minimal in the mid anal canal, where sensory receptor presence is greater. Sensitivity was significantly higher in the upper and lower anal canal regions (P < 0.05), and much higher in the rectum (P < 0.001). A similar sensory profile was recorded in the patients with OD, though with significantly higher thresholds at all points with respect to the controls. The thermal stimulus thresholds in the lower and middle anal canal were significantly smaller than in the upper canal region and rectum, and the thresholds were again higher among the patients with OD than among the controls. In all cases the thresholds for heat were lower than for cold stimuli. In both groups the motor function parameters were correlated with the sensory function variables, and the latter between themselves. Patients with OD presented sensory deterioration at all points studied in the anal canal and rectum. Sensory pudendal neuropathy was found to be associated with the pudental motor neuropathy.
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PMID:Anorectal sensitivity in patients with obstructed defaecation. 873 29

Oxaliplatin, a new third-generation platinum complex, is active in the treatment of colorectal and advanced ovarian cancers, both as monotherapy and in combination therapy. It has demonstrated a very good safety profile, characterized by low haematotoxicity, and moderate and manageable gastrointestinal toxicity. No significant renal or ototoxicities have been observed. Oxaliplatin induces a peripheral sensory neuropathy which is characterized by distal and perioral dysaesthesia, and is induced or exacerbated by the cold; in general, it is regressive between cycles of treatment. This dose-limiting toxicity is cumulative, but reversible within a few months of discontinuation of treatment in the majority of cases. In a cohort study of 490 patients with advanced colorectal cancer included in an extended access programme, more than 2700 cycles of oxaliplatin plus 5-fluorouracil (5-FU) were administered. The overall safety profile of oxaliplatin was shown to be very favourable. Oxaliplatin and cisplatin, each in combination with cyclophosphamide, have a similar efficacy in the treatment of advanced ovarian cancer, but oxaliplatin was better tolerated than cisplatin in terms of haematological, gastrointestinal, neurosensory and renal toxicities. The safety profile of oxaliplatin makes it an ideal candidate for combination therapy.
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PMID:Oxaliplatin in practice. 964 12

We assessed the cutaneous silent period (CSP) in 24 patients with Fabry disease with small-fiber sensory neuropathy and 12 normal subjects to test the hypothesis that small-diameter afferents are responsible for producing the CSP. Sensory nerve conduction studies and quantitative sensory testing for cold and vibration detection thresholds were also measured. Overall, Fabry patients had impaired thermal, but not vibration, detection thresholds, with greatest impairment in the feet. In the upper extremity, CSP latencies, duration, and suppression of electromyographic activity (EMG) did not differ. In the lower extremity, patients had reduced suppression of EMG during the CSP compared to normal controls. CSP durations exhibited a bimodal distribution in patients, including a subset of seven patients with durations shorter than all controls. This subset had profound loss of thermal sensation in the feet, but this was also true of some patients who had normal CSPs. Patients with shortened CSPs had modestly elevated vibration thresholds and reduced sensory potentials in comparison to patients with normal CSPs. Reduced CSPs in Fabry patients are associated with, but not entirely explained by, the severity of small-fiber neuropathy as measured by quantitative sensory testing. The possibility that large-diameter fibers provide a minor contribution to producing the CSP should be considered.
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PMID:Cutaneous silent periods in patients with Fabry disease. 1091 53


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