Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27-year-old woman had a subacute onset of back pain, dysesthesia and weakness of both arms. Neurological examination revealed bilateral pyramidal signs, paresthesia of both hands and arms, and hypalgesia below T-4. CSF showed no abnormal findings. T2-weighted MR images revealed linear high signal within the cervical and upper thoracic cord, but no syrinx. The signs and symptoms resolved substantially within three months, with the exception of paroxysmal itching localized to the right forearm. At age 30, she experienced an acute onset of back pain, and dysesthesia of both feet. She developed weakness of both legs and urinary retention two days after the onset. Neurological examination showed bilateral pyramidal signs in the lower extremities, hypalgesia below T-4, hypopallesthesia on both legs, but no abnormalities in the upper extremities. CSF contained 8 white cells/mm3, protein 17 mg/dl and glucose 44 mg/dl. Oligoclonal bands were not detected. T1-weighted, proton density, and T2-weighted MR images revealed a syrinx formation within the spinal cord, extending from the level of T-2 to T-5. There was no evidence of spinal tumor. MRI of the brain revealed multiple areas of high signal intensity on T2-weighted image, consistent with multiple sclerosis. The signs and symptoms resolved substantially within two months. The syrinx within the thoracic cord reduced in size after two months and disappeared after three months. Two months after the second episode of myelopathy, she experienced right optic neuritis, resolving substantially within three weeks. This case was diagnosed as definite multiple sclerosis based on the clinical and radiological findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serial magnetic resonance imaging of spinal syrinx formation in a case of multiple sclerosis]. 130 34

Five adult patients (four of them men) had episodic brachioradial pruritus associated with forearm paresthesia and hypalgesia. No cervical, shoulder, or forearm trauma was known. Onset was variable, but two had had the condition for more than ten years. In each, sensory alteration was detectable by pinprick and temperature in the distribution of the posterior cutaneous nerve of the forearm supplying the skin over the proximal portion of the brachioradial muscle. This seems to be a benign neuropathy.
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PMID:Forearm neuropathy and pruritus. 376 25

The effects of epinephrine 1/200,000 as an adjuvant to epidural morphine were investigated in three healthy male volunteers, during 26-h observation sessions. Peak blood concentrations of morphine were 44 +/- 12.9 ng/ml after plain morphine and 13.7 +/- 6.7 ng/ml after epinephrine-morphine. Cutaneous hypalgesia was more intense, faster in onset, and longer in duration after epinephrine-morphine than after plain morphine, and analgesia to ice-water immersion of extremities lasted longer. Adverse side effects of pruritus, nausea, vomiting, and difficulty of micturition were also more intense after epinephrine-morphine, and respiratory sensitivity to CO2 was depressed more severely between 6 and 16 h. The results indicated that epinephrine 1/200,000 reduces vascular absorption of epidural morphine and intensifies all the manifestations of cord and brainstem uptake.
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PMID:Influence of epinephrine as an adjuvant to epidural morphine. 682 60

Ten healthy males between 18 and 33 years received 10 mg morphine sulfate intravenously, or by lumbar epidural injection at two sessions 2-4 weeks apart, in random sequence. The following observations were made at intervals for 22 h. (1) Segmental hypalgesia to ice and pin scratch. (2) Cold pressor response test in hand and foot as an index of analgesia. (3) Time of onset and duration of side effects. (4) Serum concentrations of morphine. Few non-respiratory changes were seen after intravenous morphine. Cold pressor response was unchanged in hand and foot, no segmental hypalgesia or itching occurred, and only one subject complained of nausea. Marked changes occurred after epidural morphine. Cutaneous hypalgesia to ice and pin scratch appeared in the thoracolumbar region all subjects. In six subjects hypalgesia rose to the midthoracic region during the second or third hour and to the trigeminal distribution between the sixth and ninth hour in five subjects. Cold pressor response fell rapidly in the foot during the first 1.5 h after epidural morphine, and a little later cold pressor response also fell in the hand in all subjects, and remained depressed for the duration of the experimental period. Pruritus occurred at three hours in nine of the 10 subjects, nausea at about four hours in six of the subjects, and vomiting at about six hours in five of the subjects. Hypalgesia and side effects were not related to serum concentrations of morphine. These results suggest that lumbar epidural morphine travels cephalad in the cerebrospinal fluid to reach the brain stem and fourth ventricle by the sixth hour.
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PMID:Rostral spread of epidural morphine. 708 27

Ten healthy young male volunteers received in random sequence 10 mg of morphine sulfate intravenously and by lumbar epidural route during two 26-hour study sessions, in order to observe the appearance and resolution of the following side effects: (a) pruritus, (b) nausea, (c) vomiting, (d) urinary dysfunction. With the exception of one subject, who experienced transient (2 hours) nausea, none of the subjects experienced any adverse side effects after the intravenous morphine. However, all subjects experienced some degree of one or more complications, starting 3 hours after the epidural administration: generalized pruritus started at 3.0 +/- 0.3 hours (nine of 10 subjects, mean +/- SD) and lasted 5.3 +/- 4.0 hours. Nausea occurred in six subjects at 4.0 +/- 0.6 hours, and lasted 3.0 +/- 2.1 hours; vomiting occurred at 6.3 +/- 2.0 hours in five of the nauseated subjects. Urinary retention of varying intensity and duration appeared in nine subjects and required pharmacologic intervention in six subjects. Serum levels of unmodified morphine were measured at various times after administration during both sessions and did not correlate with the incidence or temporal appearance of side effects. Serial evaluation of dermatomal level of hypalgesia to ice and pin scratch demonstrated a progressive spread in the rostral direction after epidural morphine; trigeminal areas were affected by 9 hours in five of the 10 subjects. The stereotyped sequence of side effects after 10 mg of morphine by the epidural route can be interpreted to reflect widespread dispersion of morphine throughout the subarachnoid and ventricular cerebrospinal fluid.
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PMID:Nonrespiratory side effects of epidural morphine. 720 Jul 37

In order to determine the effects of spinal cord lesions on nociceptive sensitivity of rodents, methods were developed to assess the speed of operant escape responses to electrocutaneous stimulation (ES). ES was delivered across the dorsal and ventral surfaces of either hindpaw, producing a current path through deep tissues. In order to guide establishment of a range of stimulus intensities for this manner of stimulation, a preliminary human psychophysical experiment was conducted with stimulation between the dorsal and ventral surfaces of a finger. For the human subjects, detection thresholds averaged 0.13 mA, and thresholds for a sharp (but nonpainful) sensation were 0.42 mA. Levels of stimulation between these thresholds for detection and a sharp quality elicited sensations of tingle or itch. Thresholds for reports of pain averaged 0.67 mA. On the basis of these results, intensities of ES ranging from 0.05 to 1.0 mA were presented to the feet of rats that were trained to perform an escape response with one forelimb. Thresholds for escape averaged slightly less than 0.1 mA; responding was consistent at 0.4 mA; and response probability and speed were maximal at approximately 0.8 mA. Thus, the rats responded aversively at intensities below those rated as sharp or painful by the human subjects, but the speed of escape reached a plateau at intensities that were above pain threshold for the human subjects. Unilateral thoracic lesions of the lateral spinal column of rats produced a contralateral hypalgesia. Escape thresholds were elevated, and the speed of escape responses to all intensities was reduced. This effect depended upon interruption of axons in the middle and anterior portions of one lateral column, corresponding to the location of long ascending pathways for nociception, including the spinothalamic tract. The speed of escape responding increased over 20 weeks of postoperative testing of animals with the largest lesions. This confirms results obtained previously from monkeys (by means of a similar paradigm), and corresponds to clinical reports of humans who have received spinal lesions for control of intractable pain. Thus, the location and organization of nociceptive pathways in the spinal cord of rodents appear to be similar to those of primates, and similar adaptations occur following interruption of these pathways.
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PMID:Effects of anterolateral spinal lesions on escape responses of rats to hindpaw stimulation. 750 6

Capsaicin applied topically to human skin produces itching, pricking and burning sensations due to excitation of nociceptors. With repeated application, these positive sensory responses are followed by a prolonged period of hypalgesia that is usually referred to as desensitization, or nociceptor inactivation. Consequently, capsaicin has been recommended as a treatment for a variety of painful syndromes. The precise mechanisms that account for nociceptor desensitization and hypalgesia are unclear. The present study was performed to determine if morphological changes of intracutaneous nerve fibers contribute to desensitization and hypalgesia. Capsaicin (0.075%) was applied topically to the volar forearm four times daily for 3 weeks. At various time intervals tactile, cold, mechanical and heat pain sensations were assessed in the treated and in contralateral untreated areas. Skin blisters and skin biopsies were collected and immunostained for protein gene product (PGP) 9.5 to assess the morphology of cutaneous nerves and to quantify the number of epidermal nerve fibers (ENFs). Capsaicin resulted in reduced sensitivity to all cutaneous stimuli, particularly to noxious heat and mechanical stimuli. This hypalgesia was accompanied by degeneration of epidermal nerve fibers as evidenced by loss of PGP 9.5 immunoreactivity. As early as 3 days following capsaicin application, there was a 74% decrease in the number of nerve fibers in blister specimens. After 3 weeks of capsaicin treatment, the reduction was 79% in blisters and 82% in biopsies. Discontinuation of capsaicin was followed by reinnervation of the epidermis over a 6-week period with a return of all sensations, except cold, to normal levels. We conclude that degeneration of epidermal nerve fibers contributes to the analgesia accredited to capsaicin. Furthermore, our data demonstrate that ENFs contribute to the painful sensations evoked by noxious thermal and mechanical stimuli.
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PMID:Topical capsaicin in humans: parallel loss of epidermal nerve fibers and pain sensation. 1035 1