Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 64-year-old woman, with history of hypertension and arteriosclerosis, developed left painful ophthalmoplegia in July, 1988. Neurological examination proved abnormality of the third cranial nerve innervation, otherwise normal. No systemic illness was present. With corticosteroid therapy, the symptoms regressed and completely disappeared in 3 months. In January, 1990, right painful ophthalmoplegia appeared. Neurological examination revealed involvement of right sixth nerve and first branch of the right fifth nerve. With corticosteroid therapy, the symptoms completely regressed in several weeks. In April, 1990, she developed severe pain in the right side of the face. The facial pain disappeared rapidly with corticosteroid therapy, but reappeared following quit of steroid. She complained of severe pain of the right face, the territory of first and second branch of the right fifth nerve, but neurological examination was negative. With corticosteroid therapy, the pain disappeared remaining with mild tingling sensation on the right face, but during the tapering of corticosteroid in August, a severe peripheral type right facial palsy developed. Corticosteroid therapy resumed and the facial palsy regressed almost completely in ten days. Our case suggests that THS might be a variant of so-called recurrent cranial neuropathy.
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PMID:[A case of recurrent cranial neuropathy presenting as recurrent Tolosa-Hunt syndrome]. 180 72

Cylindrical spirals (CS) have been reported in muscle biopsies from five individual cases, as well as in two belonging to one family where there was another affected member, clinically associated with cramps, pain, stiffness and/or weakness. Here we studied muscle biopsies of a 70-yr-old mother and her 52-yr-old son, the latter with an associated neuropathy, both with late clinical onset in whose family at least 10 other members, spanning five generations, were diversely affected by muscular weakness, gait disorders, motor impairment and/or scoliosis, featuring an autosomal dominant trait with variable expression. CS as the main pathological findings were observed by light microscopy mostly in type 2 fibres, consisting of subsarcolemmal or intermyofibrillar granular and/or rod-like clusters, bluish with haematoxylin, bright red with Gomori's modified trichrome, non- or lightly reactive with PAS, faintly coloured with NADH-TR, non-reactive with SDH or ATPase, strongly stained with non-specific esterase and myoadenylate deaminase. Ultrastructurally, CS appeared as concentrically wrapped lamellae 1-2 microns in diameter. On occasion CS merged into tubular vesicular structures strongly resembling tubular aggregates (TA). Dilation of terminal cisternae (TC) in their proximity supports an origin from the sarcoplasmic reticulum (SR). Variable gene expression possibly explains both the highly diverse clinical compromise and time of onset.
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PMID:Autosomal dominant neuromuscular disease with cylindrical spirals. 182 55

Ninety cases of chronic perineal pain of neurological origin are reported. Alcock's canal syndrome, consecutive to damage of the pudendal nerve in the ischiorectal fossa, is the most frequent of these neuralgias. It is characterized by burning pain or paraesthesia increased in sitting position and relieved by standing up. The specific treatment is CT-guided infiltrations of the pudendal nerve. Other neurological causes are spinal cord lesions (notably tumours of the conus medullaris), sacral meningoradiculitis (perineal herpes zoster), plexitis and pudendal nerve neuritis. In some cases the responsibility of perineal stretching neuropathy may be considered. In all patients, electrophysiological exploration of the perineum (detection of perineal floor muscles, sacral latency, somatosensory and motor evoked potentials of the pudendal nerve) are necessary to confirm the aetiological diagnosis and guide neurological investigations.
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PMID:[Perineal neuralgia]. 182 7

A 22-year old unmarried healthy woman was admitted to the Swedish department with low fever, tiredness, SR 75 mm, positive uricult, but no urinary tract symptoms. Urinary tract infection was suspected and treatment was started with norfloxacin. Nevertheless, the urine culture proved to be negative. A few weeks later she had increasing trouble with stiff knee and shoulder joints and the left foot became swollen. The subfebrile status continued, and tonsillitis was suspected and diagnosed. V-penicillin and cefaklor treatment was applied. She was transferred to the infectious diseases ware, where fever was confirmed with leukocytosis (19 x 1 billion/1), C-reactive protein at 66 (normal value 10) mcg/ml, pronounced blood pressure increase (160/130 mm Hg), anemic signs, and pathological liver status with increased transaminases (ASAT 6.3-10.4 and ALAT 8.,8-16 ukat/1). ALP increased slightly to 6 ukat/1. The symptoms of weight loss indisposition, and muscles and joints aches, especially in foot ache continued. Collagen disease was suspected, and she was transferred to the internal medicine department. She regularly had tachycardia and high blood pressure. She had to use crutches for mobility because of the pain. S-albumin was 32 (normal 36- 50) g/l and S-hepatoglobin was 2.7 (normal value .4-1.8) g.l. Various others tests were normal. Ulnaris neuropathy was suspected on the left hand. Intensive blood pressure reducing combination treatment was started with 200 mg x 1 of metoprolol, 10 mg x 2 nifedipin, and 20 mg x 1 enalapril. The Desolett oral contraceptive (containing 30 mcg of ethinyl estradiol and 150 mcg of desogestrel) she had been taking for a few months were discontinued. Quick improvement of clinical and laboratory parameters followed. SR and leukocytosis became normal. The values of ALP, ASAT, and ALAT became normal some days later. She was discharged shortly thereafter, and blood pressure medication was gradually discontinued. In the 1940s there were reports about the hepatotoxic effects of synthetic estrogens followed by carbohydrate, lipid, and protein metabolism alterations. Jaundice has also been reported, and the Swedes have an ethnic susceptibility to it. The global incidence rate is 1/10.000 vs. 1/100 and 1/4000 in Sweden induced by high-dose OCs containing more than 50 mcg ethinyl estradiol, but with low-dose OCs this rate is much lower. Both estrogens and gestagens can increase blood pressure. A 1969 study reported that 22 young women developed arthritis, arthralgia, and myalgia after taking pills for 3- 12 months. Rheumatic symptoms were also recorded with pill use. Thus, it is very likely that OCs were responsible for the patient's symptoms, especially since her status rapidly improved after discontinuing them.
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PMID:[Were the severe adverse effects on several organs and the marked blood pressure increase caused by oral contraceptives?]. 182 62

The symptoms of cardiovascular autonomic dysfunction may be subtle and occur late in the course of diabetes. They include abnormal exercise-induced cardiovascular performance, postural hypotension, and cardiac denervation syndrome. Autonomic nervous system testing involves an evaluation of the responses of complex reflex pathways. Some of the most commonly used and validated cardiovascular autonomic tests are RR-variation, the Valsalva manoeuvre, and postural testing. Sinus arrhythmia during breathing is termed RR-variation. In diabetic patients with autonomic neuropathy the magnitude of the RR-variation is decreased. Abnormal exercise-induced cardiovascular performance has been observed in diabetic subjects with abnormal RR-variation due to autonomic neuropathy. The Valsalva manoeuvre consists of forced expiration against a standardized resistance for a specified period of time. The reflex bradycardia that follows the Valsalva period in normal subjects is lacking in diabetic patients with clinical evidence of autonomic neuropathy. Postural hypotension in diabetics may be due to neuropathy or to a variety of secondary causes. An algorithm is presented to facilitate assessment of diabetic patients with postural symptoms. Treatment of postural hypotension should be directed primarily to the correction of secondary causes, in the absence of which the symptoms can be controlled by mechanical measures, plasma volume expansion, and vasoconstriction. Cardiac denervation syndrome may result in denervation supersensitivity and afferent (pain) nerve dysfunction. The RR-variation is a sensitive indicator of impairment of cardiac autonomic innervation and is a simple method for identifying asymptomatic patients at risk for painless ischaemia. Formal cardiovascular stress testing may be prudent before initiating an exercise programme in such individuals.
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PMID:Cardiovascular autonomic dysfunction: diagnosis and prognosis. 182 67

Type II (noninsulin-dependent) diabetes (NIDDM) can be preceded by a relatively long period of disturbed glucose metabolism. Therefore, the prevalence of neuropathy and its possible relationship to metabolic abnormalities were investigated in 95 newly diagnosed type II diabetics (upper age limit was set at 55 years) with a mean age of 49.7 years (men/women ratio 1:1). The study program was as follows: Detailed history, clinical investigation of peripheral nerves, sensory assessment to touch and pain (pinprick), vibration sensation using established techniques, and motor nerve conduction velocities (MNCV) of the fibular (peroneal) and ulnar nerves. Three cardiovascular autonomic function tests were performed: the Valsalva maneuver, standing (ratio between RR-intervalmax: RR-intervalmin), and deep breathing (maximum/minimum heart rate). Vascular diseases were diagnosed using a conventional 12-lead resting electrocardiogram (ECG) and impedance measurement of the lower extremities. The results were as follows: abnormal vibration sensation in 80.0%, abnormalities of MNCV in 15.7%, abnormal sensations to touch or pinprick in 14.7%, and loss of reflexes in 13.6%. If peripheral neuropathy was defined as having at least three of the four abnormalities plus neuropathic symptoms, the prevalence was 6.3% (6 of 95 patients). Abnormalities of the three cardiovascular autonomic function tests were much less prevalent in type II diabetic patients (2.1-7.3%). In conclusion, the study showed that peripheral and autonomic neuropathy is not common at diagnosis in middle-aged type II diabetic patients without signs of microvascular or macrovascular complications.
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PMID:Prevalence of peripheral and autonomic neuropathy in newly diagnosed type II (noninsulin-dependent) diabetes. 183 Mar 12

A trigger point is frequently found over the iliac crest at 7 to 8 cm from the midline in low-back-pain syndromes. Previously, this was described as either a painful insertion site of the iliolumbar ligament or pain in the distribution of the cutaneous dorsal ramus of the first or second lumbar nerve. The authors performed 37 dissections, and they report their anatomic findings. The iliac insertion of the iliolumbar ligament is inaccessible to palpation, being shielded by the iliac crest. The dorsal rami of L1 or L2 nerve roots, however, cross the crest at 7 cm from the midline, and this distance closely correlates with the dorsal projection of the iliolumbar ligament insertion. These rami are superficial and dorsal to the crest, easily accessible to palpation. In two of the 37 dissections performed, some rami were found to be narrowed as they crossed through an osteofibrous orifice over the crest, thus being susceptible to an entrapment neuropathy. The authors conclude that the trigger point sometimes localized over the iliac crest at 7 cm from the midline likely corresponds to elicited pain from a cutaneous dorsal ramus originating from the thoracolumbar junction rather than from the iliac insertion of the iliolumbar ligament.
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PMID:Trigger point of the posterior iliac crest: painful iliolumbar ligament insertion or cutaneous dorsal ramus pain? An anatomic study. 183 38

A 60 year-old Japanese man having a 20-year history of diabetes mellitus presented with truncal neuropathy. The severe pain, especially its nocturnal exacerbation, prevented him from sleeping and eating, resulting in rapid emaciation. However, he recovered from the condition with oral mexiletine, which dramatically controlled the pain.
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PMID:Relief of severe diabetic truncal pain with mexiletine. 183 66

Three cases of nerve compression causing lumbosciatic pain and/or cruralgia due to hematoma secondary to coagulopathies of varying etiology are described. The cases involved a multiple nerve root syndrome of the cauda equina due to extradural hematoma in coagulopathy resulting from the administration of dicumarol drugs, a neuropathy of the crural nerve caused by hematoma of the iliopsoas muscle in hemophilia B, and a neuropathy of the sciatic nerve caused by hematoma in the gluteus and thigh in coagulopathy resulting from the administration of dicumarol drugs. In all three of the cases the clinical picture resembled that of lumbar disc herniation, but a careful evaluation of each patient's history, objective picture, and laboratory and radiological testing allowed us to make a correct diagnosis. Medical therapy is based on the correction of the coagulopathy by means of suitable drugs or hemoderivates. Surgical treatment is reserved for the most severe cases.
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PMID:Lumbosciatic pain and coagulopathies. 184 97

Diabetic femoral neuropathy is an uncommon, unpleasant and sometimes disabling condition, on account of both pain and muscular atrophy, whose long-term prognosis has not previously been documented. We have reviewed a group of 27 patients up to 14 years (median 62 months) after diagnosis; 18 of these were re-examined after an average of nearly 4 years (median 45 months). The condition was more common in non-insulin-dependent diabetics (88 per cent), in men (59 per cent) and in older patients (median age at diagnosis 64 years). The neuropathy was bilateral (10 cases) or unilateral (17 cases); five patients with unilateral neuropathy developed femoral neuropathy on the opposite side, usually within a few weeks of the first episode. Recovery was apparent after 3 months and usually complete by 18 months; only two of the 27 patients had severe relapses. No patients remained disabled, although there were minor residual symptoms and signs in half of the patients (2 cm reduction in thigh circumference and diminished reflexes). The outlook for femoral neuropathy, even in its most severe form, is therefore very good: residual features are demonstrable but do not cause symptoms, and relapses after the first few weeks are very rare.
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PMID:The natural history of diabetic femoral neuropathy. 185 54


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