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 51-year-old woman with no history of any familial neurological diseases initially presented with numbness in her extremities, slowing of movements, comprehension deficit, memory disturbance, dyscalculia, muscle rigidity, hyperreflexia, Parkinsonian gait, increasing disorientation, left-right disturbance, finger agnosia, alexia, acalculia, apraxia, aspontaneity, euphoria, gait disturbance, aphasia, echolalia, and in the terminal stage, mutism, contracture of lower extremities and cachexia. She died of bronchopneumonia at the age of 55. The brain showed widespread cerebral lesions, consisting of nerve cell loss and neurofibrillary tangles in the frontal, parietal and occipital cortex, demyelination and gliosis in the frontal, parietal and occipital subcortical white matter in addition to the typical pathological findings of progressive supranuclear palsy (PSP): severe neuronal loss with gliosis and neurofibrillary tangles (NFTs) in the subthalamic nucleus, globus pallidus and substantia nigra. In conclusion, we present a case of PSP with unusual clinical features (extrapyramidal signs, frontal and parietal lobe syndromes without ophthalmoplegia) and neuropathologically widespread cerebral lesions in addition to the typical pathological findings of PSP. The differential diagnosis of PSP and Alzheimer's disease and other degenerative disorders is discussed.
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PMID:Progressive supranuclear palsy with widespread cerebral lesions. 147 14

Neuroleptic malignant syndrome is a potentially lethal side effect of neuroleptic drugs, characterized by fever, muscle rigidity, autonomic dysfunction, and altered consciousness. A 50-year-old female hospitalized three times in the past for psychiatric treatment was admitted to Umayabashi Hospital for treatment of a relapse of a schizophrenic psychosis. She had received 50 mg of chlorpromazine and one tablet of Vegetamin-A (chlorpromazine 25 mg, promethazine 12.5 mg, phenobarbital 40 mg). Approximately 24-36 hours later, the patient became febrile and lost consciousness, and eight days later, acute renal failure occurred with muscle rigidity. She was transported to Maebashi Red Cross Hospital to receive hemodialysis. On admission, the laboratory studies showed high levels of serum creatine phosphokinase, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, creatinine and blood urea nitrogen. She underwent hemodialysis for treatment of acute renal failure and recovered from it after 16 sessions of hemodialysis.
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PMID:[A case of neuroleptic malignant syndrome with acute renal failure]. 148 75

Symptoms of Parkinsonism, most likely induced by an oral contraceptive, were greatly reduced by combined therapy of nicergoline and bromocriptine. A 38-year-old housewife had taken an oral contraceptive, which contained .05 mg of ethinyl estradiol and .5mg of norgestrel per tablet, for 7 years, when she presented took the following symptoms: she stumbled easily, took short, quick dancing/skating steps without arm movement, and found it increasingly difficult to keep slippers on while walking. In the afternoons she experienced extreme fatigue and rigidity in her lower limbs. After a while, languor spread to other parts of her body as well, and she was examined on April 5, 1991. The patient's face was mask-like, and her body was bent forward with her forearms flexed. She showed frozen gait and lowered initiation in her movement. Muscle rigidity was found in both upper and lower extremities, and especially on the right side. A brain MRI showed lacunar infraction with small patches of high signal intensities in the white matter of the bilateral frontal lobes and high signal intensities in the left periventricular white matter. Urine was normal; blood cholesterol and iron were slightly raised. Hormonal examinations showed lowered LH, FSH, progesterone and 24-hr 17-KGS. CT was normal. She was ordered to stop taking pills and to take nicergoline and bromocriptine, which greatly reduced these symptoms except during the first menstruation following the treatment. When mask-like facial expressions, demarche a petit pas, and languor in her lower extremities did not recur during the next menstruation, bromocriptine treatment was discontinued. Four months later nicergoline therapy was also discontinued.
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PMID:[A case of parkinsonism induced by an oral contraceptive]. 156 36

A 47-year-old woman with diabetic gastroparesis, on treatment with domperidone, a dopamine-receptor antagonist, was admitted to the hospital in coma, with high blood pressure and nonreactive pupils. She then developed high fever. Her condition progressively worsened for two days, when muscle rigidity was noted and creatine phosphokinase was greater than 2000 U/liter. A diagnosis of neuroleptic malignant syndrome was made, and the patient was given dantrolene with prompt and complete resolution of all signs and symptoms. Subsequent inquiry revealed a distant past history of positive muscle biopsy for malignant hyperthermia, obtained after the diagnosis had been made in a family member. This case suggests that domperidone may induce neuroleptic malignant syndrome and that patients with malignant hyperthermia are at increased risk for this complication.
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PMID:Neuroleptic malignant syndrome induced by domperidone. 158 2

A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid (CSF) lactic acidosis was reported. A 44-year-old Japanese woman noted tarry stool on July 2, 1988 and was treated with metoclopramide and cimetidine for nausea and vomiting. Hydroxyzine pamoate was also administered for insomnia at 3:10 am and she became comatose with muscle rigidity at 3:40-4:30 am on July 3. Tachycardia and high fever (39.5 degrees C) were evident at 8:00 am on July 4. She was transferred to the Kyushu University Hospital. On admission, serum creatine kinase was elevated to 1640 IU/1; MM fraction was 100%. She was diagnosed as malignant syndrome. Cerebrospinal fluid was normocellular with protein 38 mg/dl and glucose 122 mg/dl. Cerebrospinal fluid lactate increased markedly to 3.43 mmol/l, CSF pH was 7.264, HCO3- 14.4 mEq/l, indicating CSF metabolic acidosis. She became afebrile after the 10th hospital day, and gradually but completely recovered within a month. She was discharged on August 16, 1988. The anti-dopaminergic activity of metoclopramide was considered to be primarily responsible for the development of malignant syndrome in this case. Cerebrospinal fluid lactic acidosis seemed to reflect hyperpyrexia or malignant syndrome induced derangement of the brain metabolism.
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PMID:[A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid lactic acidosis]. 188 79

The patient was a 64-year-old woman who showed muscle weakness and tremor of upper extremities and gait disturbance at the age of 62 years. The symptoms progressed and she was admitted to our hospital. Neurological examination revealed muscle weakness, muscle atrophy and fasciculation bilaterally in the upper extremities. The deep tendon reflexes were reduced in the upper extremities and increased in the lower extremities, but Babinski's sign was not present. There was mild hand tremor at rest (right greater than left). Muscle rigidity was also evident. Her gait was small-stepped and her trunk was bent forward. She showed hypomimia, but no dementia was detected. She died of respiratory failure 7 months after admission. The duration of the illness was about 2 years. At autopsy, macroscopic examination showed depigmentation of the substantia nigra and locus ceruleus, and atrophy of the anterior roots of the spinal cord. Microscopic examination revealed a few senile plaques in the temporal cortex. In the substantia nigra, the number of melanin-containing cells was decreased in its central parts. A few Lewy bodies were found in some of the remaining neurons, and melanin pigment migrated into the parenchyma. In the locus ceruleus and dorsal motor nucleus of vagus, abundant Lewy bodies and mild astrocytosis were seen. A few Lewy bodies were also seen in the nucleus raphe, nucleus basalis of Meynert and hypothalamic nuclei. Severe neuronal loss of the anterior horn cells was observed in the cervical segment, and to a lesser degree, in the lumbo-sacral segments. segments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Motor neuron disease with Parkinson's disease--case report]. 208 32

Two cases of tetanus are presented, and the diagnosis, clinical features, and management of tetanus are reviewed. The first patient, an 86-year-old woman, had marked muscle rigidity but was able to breathe spontaneously. A dark eschar with purulent drainage was noted on her left foot, but Clostridium tetani was not isolated. She was placed in a semidark room and was treated with penicillin G; tetanus immune globulin (TIG) 5000 units i.m.; tetanus toxoid 0.5 mL i.m.; diazepam, chlorpromazine, and morphine for sedation, muscle relaxation, and analgesia; ranitidine for stress ulcer prophylaxis; heparin for prevention of deep-vein thrombosis; and peripheral-vein nutrition. Her condition improved gradually, and she was discharged to a rehabilitation institute after 32 days. The second patient, a 46-year-old woman, experienced progressive descending paralysis and required ventilatory support. She had a periodontal abscess, but cultures of the drainage were negative. She was placed in a semidark room and treated with erythromycin, TIG, tetanus toxoid, diazepam, pancuronium bromide, morphine, ranitidine, and heparin. Autonomic instability occurred during the second and third weeks, but cardiac output was maintained without treatment. The patient was extubated after five weeks, and was transferred out of the intensive-care in the following week. The diagnosis of tetanus is based primarily on characteristic findings of muscle rigidity and reflex spasms; cultures for C. tetani are of limited value. A history of trauma or injury is common. Pulmonary infections and cardiovascular instability are the most common complications. Therapy consists of ventilatory support; control of neuromuscular symptoms with benzodiazepines, narcotics, and neuromuscular blockers; antibiotic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of tetanus. 331 65

We present an autopsied case of striatonigral degeneration (SND) combined with olivopontocerebellar atrophy (OPCA) with subcortical dementia and hallucinatory state. A Japanese woman without a remarkable family history showed hand tremor at the age of 35 years, followed by bradykinesia, muscle rigidity, orthostatic hypotension, neurogenic bladder and pyramidal signs. No obvious cerebellar symptoms were found. Various antiparkinsonian drugs were administered, but were not markedly effective for the parkinsonism. She developed a mild dementia characterized by mild memory disturbance with preservation of orientation, slowing of thought processes, emotional lability toward sadness, impaired ability to manipulate acquired knowledge and poor calculating, and by the absence of aphasia, apraxia and agnosia. The features in this patient were consistent with those seen in subcortical dementia. She also had auditory hallucinations. MRI revealed hypointense T2 signals in the putamina and substantia nigra. T1-weighted MRI demonstrated atrophy of both the pons and cerebellum in addition to atrophy of the putamina and substantia nigra. EEG showed slowing of background activity. She died of cardiac failure at the age of 47. Autopsy disclosed brain stem tegmental atrophy, SND, OPCA and many glial cytoplasmic inclusions in the central nervous system, but well-preserved cerebrum. We discuss the relationship between the psychiatric symptoms and pathologic findings of brain stem tegmentum.
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PMID:Striatonigral degeneration combined with olivopontocerebellar atrophy with subcortical dementia and hallucinatory state. 755 Jun 4

We report a 71-year-old woman with progressive gait disturbance and dementia. The patient was well until 61 years of age (1980) when she noted a gradual onset of gait disturbance. A year later, she noted slurring of the speech and forgetfulness. In 1982, she noted difficulty in looking down and progression of her gait disturbance. In 1983, she became unable to walk alone unless supported. She was admitted to our service in 1984; neurological examination at that time revealed moderate dementia, limitation in the vertical gaze, slurred speech, and wide based ataxic gait. She was discharged for out patient follow up. Cranial CT scan in 1989 revealed cortical, brain stem, and cerebellar atrophies. On March 10, 1990, she fell down and hit her head. She developed headache on April 1, vomited on April 8, and was admitted to our service again. On admission, she was somnolent, she was unable to follow an object to any direction; oculocephalic response was elicited to horizontal directions, however, it was difficult to induce in the vertical direction. Rigidity was noted in the extremities except in the left lower extremity. Rapid alternating movement was difficult and dysmetria was noted in the finger-to nose test. Deep reflexes were exaggerated without clonus; the plantar response was extensor bilaterally. Cranial CT scan revealed bilateral subdural hematoma. She was treated with intravenous infusion of glycerol, and she became alert after this treatment; however, she was markedly demented. She was unable to walk alone. She was discharged to home, but she showed progressive loss of activities, and became bed ridden in December 1992. In January of 1993, she developed fever, dyspnea, and disturbance of consciousness, and was admitted again on January 26, 1993. On admission, her blood pressure was 70 mmHg by palpation and body temperature 38.5 degrees C. The lungs were clear. On neurologic examination, she was semicomatose; the optic fundi were unremarkable; only incomplete eye movements elicited by the oculocephalic reflex. She was passive supine in position; some spontaneous movements were observed in the extremities. Lead-pipe rigidity was noted in both upper extremities, but the muscle tone was decreased in the lower extremities. No abnormal involuntary movements were seen. Deep reflexes were exaggerated except for the ankle jerk which was diminished bilaterally. The plantar response was extensor on both sides.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 71-year-old woman with progressive gait disturbance and dementia]. 766 34

A case of isolated ACTH deficiency accompanying transient primary hypothyroidism was reported along with a review of literature on isolated ACTH deficiency in Japan with special reference to its association with thyroid function. Our case, a 56-year-old woman, developed somnolence and hypoglycemia due to isolated ACTH deficiency. She also had the features of hypothyroidism, namely mounding phenomenon, muscle rigidity, increased plasma myogenic enzymes and cold intolerance. Both free T3 and free T4 were decreased, and basal as well as TRH-stimulated TSH levels were abnormally high. Plasma thyroglobulin was increased and no anti-thyroid antibodies were detected. All thyroid related physical and biochemical abnormalities disappeared after hydrocortisone replacement. A review of the literature on 103 cases disclosed that more than half the cases with isolated ACTH deficiency had a high plasma level of TSH, basal and/or TRH-induced, while the antithyroid antibodies were reported to be positive in only 13 cases. In more than 70% of such cases, the abnormality in the pituitary-thyroid axis was transient and was reversed by glucocorticoid replacement. Our case and cases in the literature indicate that the interference of thyroid hormone synthesis and/or secretion by glucocorticoid deficiency per se is the major cause of thyroid dysfunction rather than associated autoimmune thyroid disease.
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PMID:Thyroid dysfunction in isolated adrenocorticotropic hormone (ACTH) deficiency: case report and literature review. 792 Sep 2


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