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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of meningeal carcinomatosis associated with cerebral metastases from an adrenal neuroblastoma is described. The clinical picture was ushered-in by bilateral sciatic pain in a 50 years old female and was followed by rapidly progressive sensory-motor deficits of the arms and legs, leading to flaccid quadriplegia associated with paralysis of cranial nerves and episodes of mental confusion. Death occurred 4 months alter, in cardiac failure. At autopsy, a bilateral tumor of the adrenal glands was found. No metastases were detected anywhere except in the central nervous system. Histology identified the tumor as a neuroblastoma; meningeal carcinomatosis, radicular infiltration by tumor cells and parenchimal metastases were found in the central nervous system. Neuroblastoma is typically a tumor of childhood, only 13% of them being found in adult's according to Russell and Rubinstein. Meningeal metastases from adrenal neuroblastoma have not hitherto been reported in the literature. In our opinion, the most likely mode of spread of tumor cells to the central nervous system was hematogenous because of the presence of small multiple intraparenchimal metastases; however, possible spread through the perineural lymphatics, as proposed by others, cannot be excluded, due to the prominent localization of tumor cells at spinal roots level. The main differential diagnostic problems (paraneoplastic neuropathy (Wyburn-Mason) and infectious subacute or chronic meningitis) are discussed. The authors stress the emportance of complete cerebro-spinal fluid examination including a careful search for tumor cells.
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PMID:[Meningeal carcinomatosis: clinical and anatomical study of a case of suprarenal neuroblastoma (author's transl)]. 6

Two patients had acute, self-limiting, unilateral brachial plexus neuropathy in association with desensitizing subcutaneous injections of extracts of dusts and molds. Diminution of pain and return of function of the affected limb followed a short course of prednisone therapy, although a beneficial effect of the steroid cannot be considered proved. There is a large variety of antigenic substances already known to produce neuropathy following intramuscular injection; desensitizing antiallergy injections should be added to this list.
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PMID:Brachial plexus neuropathy. Association with desensitizing antiallergy injections. 17 Apr 30

The clinical, electrophysiological and pathological changes in 3 patients with recurrent attacks of non-traumatic brachial plexus neuropathy have been described. Two had recurrent attacks and a dominant family history of similar attacks, together with evidence of lesser degrees of nerve involvement outside the brachial plexus. In one patient the attacks were moderately painful, while in the other there was little or no pain. Only one showed undue slowing of motor nerve conduction during ischaemia, but in both cases the sural nerves had the changes of tomaculous neuropathy, with many sausage-shaped swellings of the myelin sheaths, and extensive segmental demyelination and remyelination. The third patient had two attacks of acute brachial plexus neuropathy which were both extremely painful. The clinical features were compatible with a diagnosis of neuralgic amuotrophy. In the second attack, there was vagus nerve involvement and the sural nerve showed evidence of healed extensive segmental demyelination. The various syndromes presenting with acute non-traumatic brachial plexus neuropathy are reviewed, and a tentative nonsological classification advanced. Most patients fall into the category of acute, painful paralysis with amyotrophy, with no family history and no evidence of lesions outside the brachial plexus. It is suggested that the term "neuralgic amyotrophy" be restricted to this group. Patients with features outside this clinical picture probably suffer from other disease entities presenting with brachial plexus neuropathy. The familial cases constitute one or more aetioliogical subgroups, differing from neuralgic amyotrophy in the frequency of recurrences, the relative freedom from pain in the attacks, the frequency of nerve lesions outside the brachial plexus, and of hypotelorism. Individual attacks of acute brachial plexus neuropathy, however, may be identical in patients with the different diseases, and further pathological and biochemical studies are awaited to aid in nosology.
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PMID:Recurrent brachial plexus neuropathy. 17 Oct 26

A case of 21 year old male with neuropathy caused by renal insufficiency was present. He had taken bromate (mixed powder of potassium bromate and sodium bromate) for the purpose of suicide and suffered from acute renal insufficiency and hard of hearing. Renal dysfunction improved gradually by peritoneal dialysis and hemodialysis. However, on the 32th day after the onset, burning pain appeared in the bilateral feets. Following this, he began to complain of the disturbances of superficial and deep sensory below the ankle jerks and the weakness of his toes. Considering the clinical features, we supposed that the disturbance of the peripheral nerve was caused by uremia due to taking bromate. N. suralis was biopsied on the 80th day after the onset and examined electron microscopically. Electroscopical findings was as follows. Degeneration of the Schwann cells and irregularity or destruction of the myelin sheaths were observed. The axoplasm of the myelinated nerve fiber were relatively preserved as compared with the changes of the myelin sheaths. In the unmyelinated nerve fibers, cavity formations were observed. The findings of regeneration were not observed. From the electron microscopical findings, we speculate that the changes of the Schwann cells and the myelin sheaths are primary resulting from the disturbance of the metabolism of the Schwann cells. We speculate that anemia and hypoproteinemia caused by bromate disturbed regeneration.
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PMID:[Peripheral nerve disease associated with acute renal failure due to bromate poisoning]. 19 41

Pain, tactile, vibration and temperature sensitivity, and also electroexcitability of individual nerves were determined. Neuropathy incidence was almost the same among males and females. There was found no association between neuropathy and excessive weight of the patients and the type of treatment. The frequency of affection increased with the advance of age and was maximum (40.4%) in patients aged from 55 to 64 years. The frequency of neuropathy proved to depend on the duration of diabetes. Sensitivity was chiefly distributed by distal and polyneuritic type. Affection of the lower limbs occurred in all the cases. Improvement after the treatment was noted in 69.3% of patients; however, in 13.5% of cases only it was objective in character. The irritative-pain syndrome was the one which yielded to the treatment best. Analysis of the results demonstrated the treatment to be more affective in younger persons with a lesser duration and severity of diabetes. The duration of partial remission constituted from 3 to 13 months. This pointed to the necessity of prophylactic therapeutic courses.
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PMID:[Diabetic peripheral polyneuropathy]. 19 65

The maximum sensory conduction velocity was measured along the articular branch of the suprascapular nerve. The potential was evoked by stimulating in the perception area of the nerve above the glenohumeral joint and recorded by an electrode near the suprascapular nerve in the supraclavicular fossa. The maximum conduction velocity averaged 42 m/s, SD 4.6 m/s (20 normal subjects); it decreased slightly with age. When correcting for the error in distance arising from the measurement by obstetric calipers (20%), the maximum conduction velocity averaged 50 m/s. The peak-to-peak amplitude of the main component of the sensory potential was 0.8 muV, SD 0.5 muV. In one of seven patients with a pain syndrome in the shoulder secondary to a brachial plexus neuropathy the velocity and the amplitude of the sensory potential was diminished. In five other patients with pain in the region of the shoulder the conduction velocity was normal but the amplitude was diminished.
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PMID:Conduction along the articular branch of the suprascapular nerve. 21 24

Review of the various drugs in current clinical use showed that over 50 of them may cause a purely sensory or mixed sensorimotor neuropathy. These include antimicrobials, such as isoniazid, ethambutol, ethionamide, nitrofurantoin, and metronidazole; antineoplastic agents, particularly vinca alkaloids; cardiovascular drugs, such as perhexiline and hydrallazine; hypnotics and psychotropics, notable methaqualone; antirheumatics, such as gold, indomethacin, and chloroquine; anticonvulsants, particularly phenytoin; and other drugs, including disulfiram, calcium carbimide, and dapsone. Patients receiving drug treatment who complain of paraesthesie, pain, muscle cramps, or other abnormal sensations and those without symptoms who are receiving drugs that are known or suspected to be neurotoxic should undergo neurological examination and studies of motor and sensory nerve conduction. This will allow the incidence of drug-induced peripheral neuropathy to be determined more precisely.
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PMID:Drug-induced peripheral neuropathies. 21 31

Neurologic alteration in 36 patients who had received either a sagittal split osteotomy, an intraoral vertical ramus osteotomy, or a mandibular vestibuloplasty was evaluated by questionnaire, detailed neurosensory examination, and personality testing. Subjective sensory alteration was reported by 69.4% of the entire group; neurosensory examination showed demonstrable neuropathy in 54% of the 72 nerve divisions that were examined, with the greatest incidence, 84.6%, in the group that had received sagittal split osteotomies. Personality testing indicated that dysesthetic patients experienced greater degrees of neuroticism and depression than did patients without pain.
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PMID:Analysis of postsurgical neurologic alteration in the trigeminal nerve. 22 Apr

A case of angioimmunoblastic lymphadenopathy with dysproteinaemia complicated by a subacute peripheral neuropathy is described. Clinically the neuropathy was mainly motor, but pain and paraesthesiae in the legs were also present. Sural nerve biopsy indicated decreased numbers of myelinated fibres, mainly the largest, without actual signs of degeneration or regeneration. However, the occurrence of denervation bands indicated that degeneration had led to loss of myelinated fibres.
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PMID:Peripheral neuropathy in angioimmunoblastic lymphadenopathy with dysproteinaemia. 22 48

The records of 31 patients with primary systemic amyloidosis and peripheral neuropathy seen during a 17-year period were analyzed to define the natural history of the neuropathy. Patients tended to be older men with a painful, distal, symmetrical sensorimotor neuropathy and prominent autonomic features. Loss of pain and temperature sensation was frequently more striking than loss of mechanoreception. Renal, cardiac, hematological, and gastrointestinal dysfunction often overshadowed the neuropathy. Clinical, neurophysiological, and histopathological studies pointed to axonal degeneration with predominant but not exclusive involvement of small myelinated and unmyelinated fibers. The neuropathy was progressive in all patients with or without treatment, but death was typically due to supervening medical complications.
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PMID:The natural history of peripheral neuropathy in primary systemic amyloidosis. 22 87


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