Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of postoperative neuroleptic malignant syndrome is presented. A healthy 23-year-old male underwent a shoulder repair under uneventful fentanyl, halothane, nitrous oxide and oxygen anaesthesia. He received droperidol 5 mg IV and metoclopramide 10 mg IV intraoperatively to prevent postoperative nausea. Postoperatively, the patient developed autonomic instability, fever and generalized muscle rigidity. His level of consciousness was depressed. These findings were consistent with the diagnosis of neuroleptic malignant syndrome. The supportive treatment of the patient included active cooling measures, muscle relaxation and mechanical ventilation. The ability of anti-dopaminergic agents, including metoclopramide and droperidol, to precipitate the neuroleptic malignant syndrome is discussed. Treatment of the neuroleptic malignant syndrome is briefly discussed.
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PMID:Postoperative neuroleptic malignant syndrome. A case report. 366 20

Binding of neurotoxin II Naja naja oxiana derivatives containing one spin label at various positions (Leu 1, Glu 2, Lys 15, Lys 25, Lys 26, His 31, Lys 44 and Lys 46) to purified solubilized acetylcholine receptor protein (AchR) from Torpedo marmorata was studied by EPR techniques. AchR interaction with several dansylated neurotoxin II derivatives was followed by difference fluorescence spectroscopy. A series of neurotoxin II p-azidobenzoyl derivatives were prepared and in three of them modified lysine residues were identified. In combination, spectroscopic data and photolabeling implicate a considerable area of the neurotoxin in association with AchR. Rigidity of the neurotoxin II conformation allowed to regard its binding surface as a mould of the AchR corresponding site and to estimate the minimal size of the latter. Conformation of the long-chain neurotoxins and their binding to AchR are briefly discussed basing on the 1H and 19F NMR studies of neurotoxin I Naja naja oxiana, toxin 3 Naja naja siamensis and its acetylated or trifluoroacetylated derivatives, as well as on Achr interaction with the derivatives spin labeled at Lys 27 and His 71.
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PMID:Interaction surfaces of neurotoxins and acetylcholine receptor. 708 49

We report a right-handed 62-year-old man with early onset familial parkinsonism. The patient was well until 24 years of the age when he noted an onset of resting tremor in his right hand. During the next four years, he noted rigidity, bradykinesia, and difficulty in walking. He was seen in another hospital at 28 years of the age, where he received left pallidotomy. Rigidity on the left side showed marked improvement. He received right pallidotomy at age 30 years. He developed right hemiplegia after this surgery. He was admitted to our hospital in March, 1983 when he was 51 years of the age. He was treated with levodopa but improvement was rather of minor degree. He was transferred to another hospital, but his motor disturbance progressed slowly, and was admitted again to our hospital in November 1990. He had 6 siblings 4 of whom including himself suffered from parkinsonism. No consanguinity was noted in parents. On admission, he appeared chronically ill but the general physical examination was unremarkable. Neurologic examination revealed an alert and mentally sound man. Hasegawa dementia scale was 28.5/32.5. Upward gaze was slightly restricted (3/5). Cranial nerve examination revealed oculogyric crisis, apraxia of eyelid opening, masked face, and small voice. He was able to stand with support; his posture showed left-ward leaning. He had right hemiparesis with moderate weakness. He showed marked bradykinesia and moderate rigidity in his left upper extremity. Fine postural tremor was noted in the left hand. Deep tendon reflexes were diminished in the upper extremities. No Babinski sign was noted. Pain sensation was somewhat diminished on the right side. Results of routine laboratory examination were unremarkable. Cranial CT scan revealed atrophy in the frontal lobe, particularly in the prefrontal area. In addition, MRI revealed T1-and-T2-low signal intensity lesions in the right ventral pallidal region and in the left ventrolateral thalamic-hypothalamic areas. He was treated with 600 mg of levodopa with benserazide and 22.5 mg of bromocriptine with mild to moderate improvement in his bradykinesia and rigidity. He was discharged in January 1991. His clinical course was complicated by intestinal obstruction in October, 1994. He was admitted to another hospital where he was operated on the obstruction on November 5, 1994. The sigmoid colon was markedly dilated but no mass was found. Postoperative course was uneventful until November 18, 1994 when he was found dead in his hospital room shortly after 4 am. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset familial Lewy body-negative parkinsonism. Opinions were divided between Lewy body-positive familial Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed aspiration pneumonia, which appeared to be the cause of his death, in the right lung. Neuropathologic examination revealed loss of malanized neurons in the substantia nigra and the locus coeruleus. In the substantia nigra, neuronal loss was particularly severe in the ventrolateral area. No Lewy bodies were seen. The dorsal motor nucleus of the vagal nerve was well preserved. Stereotaxic lesions involved bilateral thalamic areas. This patient appears to represent a case of autosomal recessive juvenile parkinsonism (AR-JP). Early onset, superb response to levodopa, sleep effect, and easy development of dyskinesias and motor fluctuations characterize AR-JP. The reason why this patient did not show these clinical features is probably bilateral sterotaxic surgeries. Particularly, the second surgery was complicated by right hemiparesis. His siblings who developed parkinsonism showed typical clinical features of AR-JP.
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PMID:[A 62-year-old man with familial parkinsonism with the onset at 24 years of the age]. 870 64

Excessive stimulation of serotonin 5HT1A receptors causes a syndrome of serotonin excess that consists of shivering, muscle rigidity, salivation, confusion, agitation and hyperthermia. The most common cause of this syndrome is an interaction between a monoamine oxidase inhibitor (MAOI) and a specific serotonin reuptake inhibitor. Venlafaxine is a new antidepressant agent that inhibits the reuptake of serotonin and norepinephrine. We report a venlafaxine-MAOI interaction that resulted in the serotonin syndrome in a 23-y-old male who was taking tranylcypromine for depression. He had been well until the morning of presentation when he took 1/2 tab of venlafaxine. Within 2 h he became confused with jerking movements of his extremities, tremors and rigidity. He was brought directly to a hospital where he was found to be agitated and confused with shivering, myoclonic jerks, rigidity, salivation and diaphoresis. His pupils were 7 mm and sluggishly reactive to light. Vital signs were: blood pressure 120/67 mm Hg, heart rate 127/min, respiratory rate 28/min, and temperature 97 F. After 180 mg of diazepam i.v. he remained tremulous with muscle rigidity and clenched jaws. He was intubated for airway protection and because of hypoventilation, and was paralyzed to control muscle rigidity. His subsequent course was remarkable for non-immune thrombocytopenia which resolved. The patient's maximal temperature was 101.2 F and his CPK remained < 500 units/L with no other evidence of rhabdomyolysis. His mental status normalized and he was transferred to a psychiatry ward. This patient survived without sequelae due to the aggressive sedation and neuromuscular paralysis.
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PMID:Serotonin syndrome from venlafaxine-tranylcypromine interaction. 888 41

A 49-year-old man was admitted with the chief complaints of muscle weakness and gait disturbance. His neurological examination was compatible with peripheral neuropathy, and laboratory tests revealed IgA monoclonal gammopathy, increased protein content in the cerebrospinal fluid (CSF) without pleocytosis, and slow motor and sensory nerve conduction velocity. He was diagnosed as having chronic inflammatory demyelinating polyneuropathy with IgA monoclonal gammopathy of undetermined significance. The patient was treated with steroid, and plasmapheresis. He became so restless that antidepressant and haloperidol were administered. Then, he became unresponsive, and developed high fever, sweating, tachycardia, and tremor. Examination of CSF showed increased 3-methoxy-4-hydroxy-phenylglycol and decreased homovanillic acid. He was diagnosed as having neuroleptic malignant syndrome (NMS). However, his muscle tonus was still flaccid in his lower extremities that had been suffered from chronic polyneuropathy. Interestingly, his serum creatine kinase (CK) content was only slightly elevated. We suppose that the pathophysiological location of NMS might be primarily central, and that muscle rigidity and elevation of serum CK might not occur, if the peripheral nerves were completely impaired.
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PMID:[Neuroleptic malignant syndrome in a patient with polyneuropathy: mechanism of muscle rigidity and elevated serum creatine kinase levels]. 1020 83

A 27-year-old robust man, without any medical and surgical history, attempted to commit suicide by consumption of 300 cc (44.1%, 132.3 g) basagran, a readily available herbicide. This poisoning resulted in vomiting, fever, sweating, pipe-like muscle rigidity, sinus tachycardia, drowsiness, leukocytosis, rhabdomyolysis and hepatorenal damage. Emperical treatment with bromocriptine was temporally associated with resolution of above signs and symptoms. His clinical presentations and the effect of bromocriptine may be indicative that basagran poisoning mimicks neuroleptic malignant syndrome.
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PMID:Acute basagran poisoning mimicking neuroleptic malignant syndrome. 1046 61

A 63-year-old man with chronic renal failure who had received hemodialysis three times per week for 4 years developed neuroleptic malignant syndrome 10 days after taking amoxapine. His condition was characterized by muscle rigidity, elevation of body temperature and altered consciousness. Although he was treated with dantrolen and supportive care as well as discontinuation of amoxapine, his condition rapidly deteriorated, resulting in death. Because the pharmacokinetics of drugs, especially those such as antidepressants, in patients with chronic renal failure has not been fully clarified, one should be careful about giving such patients these drugs.
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PMID:A case of neuroleptic malignant syndrome in a patient with hemodialysis. 1071 Feb 50

We reported a 74-year-old male case of progressive supranuclear palsy (PSP) who responded to tandospirone citrate, a serotonin receptor (5-HT1A) agonist. The patient manifested postural instability and gait disturbance at 71 years. Additionally, he showed vertical gaze paresis, regidity of the neck, extremities and trunk, bradykinesia and mild cognitive impairment. A brain MRI revealed moderate atrophy of bilateral frontal/temporal lobes and of midbrain tegmentum one year after the onset. The patient had been diagnosed as PSP and treated with L-DOPA. However, L-DOPA therapy showed only transient response for a few months. His symptoms deteriorated gradually, and he became unable to sit, stand up or walk by himself. Tandospirone citrate was additionally administered at 30 mg/day. Rigidity and bradykinesia were remarkably improved in two weeks after the start of tandospirone treatment. He became able to stand up and walk a short distance with supports in four weeks. Cognitive disturbance was also slightly improved. Tandospirone citrate was effective on our case of PSP, especially on rigidity. Our findings suggest that combination of levodopa and tandospirone citrate is a useful therapy for PSP.
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PMID:[A case of progressive supranuclear palsy improved with tandospirone citrate]. 1148 61

We experienced two cases of malignant hyperthermia (MH) triggered by sevoflurane. Case 1 was a six-year-old girl, 15.8 kg, undergoing strabismus repair. She had flat back, elevated diaphragm and high arched palate. Anesthesia was induced and maintained with sevoflurane and nitrous oxide in oxygen. Her trachea was intubated without the use of muscle relaxant. Thirty minutes after the induction of anesthesia, ETco2 was over 60 mmHg despite hyperventilation. Muscle rigidity of legs and the rise in temperature were noted. MH was diagnosed and dantrolene i.v. was administered. Her maximum esophageal temperature was 40.2 degrees C. ETco2 and temperature returned to baseline values after dantrolene administration. Creatine phosphokinase (CK) level was 252 U.l-1 preoperatively, and 1690 U.l-1 next day. Case 2 was a year-and-9-month-old boy undergoing accessory ear resection. Anesthesia was induced with sevoflurane and nitrous oxide in oxygen. His trachea was intubated with an aid of vecuronium. Forty minutes after administration of sevoflurane his temperature rose to 38.6 degrees C with heart rate 191 bpm and Spo2 93%, and muscle rigidity of legs. MH was diagnosed and dantrolene was administered. His highest temperature was 39.3 degrees C and was reduced promptly after dantrolene. Postoperatively he was noted to have downslanting palpebral fissures, micrognathia, low set ears, and a single crease of the fifth finger and diagnosed as King syndrome which is reported to have association with MH. Both patients had no history of anesthesia nor abnormal family history. Both of them were rescued with dantrolene and recovered without sequelae.
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PMID:[Two pediatric cases of malignant hyperthermia caused by sevoflurane]. 1175 32

A 45-year-old man was admitted to our hospital after taking an intentional overdose of 90 sustained-released lithium tablets (450 mg each). The patient was stabilized with three sessions of hemodialysis. On day 7 of his hospital stay, his serum lithium level was 0.5 mEq/L. On day 10, he developed high fever, tachypnea, muscle rigidity, rhabdomyolysis, acute renal insufficiency, mental confusion, and obtundation. His creatine kinase level was 698 IU/L, serum creatinine 3.5 mg/dl. Late-onset neuroleptic malignant syndrome (NMS) was diagnosed. The patient died after developing acute renal failure and acute respiratory distress syndrome. Clinicians should be aware that lithium may cause NMS independent of other neuroleptic agents.
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PMID:Acute lithium intoxication and neuroleptic malignant syndrome. 1282 Aug 23


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