Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Muscle Rigidity”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources

SCH 58261, a selective adenosine A2A receptor antagonist, decreases the haloperidol-enhanced proenkephalin mRNA expression in the rat striatum.

In the striatum, dopamine D(2) receptors are co-localized with adenosine A(2A) receptors on the GABAergic neurons of the striopallidal pathway. Moreover, blockade of A(2A) receptors has been previously shown to suppress parkinsonian-like symptoms (catalepsy, akinesia, muscle rigidity) in rodent and primate models of Parkinson's disease (PD). Since it is believed that main motor symptoms of PD are due to the overactivity of the GABAergic striopallidal pathway, the aim of the present study was to find out whether SCH 58261, a selective antagonist of the adenosine A(2A) receptors, is capable of counteracting both the catalepsy and the enhancement of proenkephalin (PENK) mRNA expression in the rat striatum, induced by haloperidol administered at 1.5 mg/kg s.c. 3 times, every 3 h. Systemic administration of SCH 58261 (5 mg/kg i.p., 3 times, every 3 h, 10 min before haloperidol), partially decreased the haloperidol-induced catalepsy and the increase in the PENK mRNA expression in both dorsolateral and ventrolateral parts of the striatum at all three examined levels. No such changes were seen in the medial striatum and in the nucleus accumbens. Moreover, SCH 58261 given alone did not influence the level of PENK mRNA in any examined part of the striatum. The present results suggest that similarly to other A(2A) receptor antagonists, SCH 58261 normalizes activity of the striopallidal pathway, enhanced by blockade of dopamine D(2) receptors with haloperidol, which may result in recovery of motor functions.

Analysis of Variance↗

Laminin alpha 2 (merosin)-deficient muscular dystrophy and demyelinating neuropathy in two cats.

We report laminin alpha 2 (merosin) deficiency associated with muscular dystrophy and demyelinating neuropathy in two cats. The cats developed progressive muscle weakness, and atrophy. Either hypotonia or contractures resulted in recumbency, necessitating euthanasia. Muscle biopsies showed dystrophic changes including marked endomysial fibrosis, myofiber necrosis, variability of fiber size, and perimysial lipid accumulation. Immunohistochemistry showed that laminin alpha 2 chain was absent or reduced, while dystrophin and all the components of the dystrophin-associated glycoprotein complex were present and normal. One cat was examined in detail. Motor nerve conduction velocity (MNCV) was decreased, and ultrastructurally the peripheral nerves showed Schwann cell degeneration and demyelination. Brain imaging was not performed, but white matter changes were not apparent in the brain at necropsy. The disease in these cats is similar to primary or secondary merosin (laminin alpha 2)-deficient congenital muscular dystrophy (CMD) in humans and to dystrophia muscularis in mice.

Animals↗

Neuroleptic malignant syndrome.

Neuroleptic malignant syndrome is a rare but potentially fatal reaction associated with neuroleptic drugs. It occurs in about 0.2% of patients treated with neuroleptics. Risk factors include previous episodes, dehydration, agitation, and the rate and route of neuroleptic administration. Although NMS has been reported in patients with diverse psychiatric diagnoses, as well as in normal subjects, patients with organic brain disorders or mood disorders, particularly when receiving lithium, may be at increased risk. Standardized criteria for the diagnosis of NMS have been developed and emphasize the classic findings of hyperthermia, muscle rigidity, mental status changes, and autonomic dysfunction. The syndrome lasts 7 to 10 days in uncomplicated cases receiving oral neuroleptics. Treatment consists primarily of early recognition, discontinuation of triggering drugs, management of fluid balance, temperature reduction, and monitoring for complications. Use of dopamine agonists or dantrolene or both should be considered and may be indicated in more severe, prolonged, or refractory cases. Electroconvulsive therapy has been used successfully in some cases and is particularly useful in the post-NMS patient. As a result of these measures, mortality from NMS has declined in recent years although fatalities still occur. Neuroleptics may be safely reintroduced in the management of the majority of patients recovered from an NMS episode, although a significant risk of recurrence does exist, dependent in part on time elapsed since recovery and dose or potency of neuroleptics used. Data drawn from clinical observations and basic studies support the primary role of an acute reduction in brain dopamine activity in the development of NMS. Additional studies of facilitating cofactors may lead to innovative risk-reduction strategies and the development of safer neuroleptic drugs.

Age Factors↗

Tetany following resuscitation after abruptio placentae.

BACKGROUND: Serum ionized calcium and magnesium are normally decreased during later stages of pregnancy. A further rapid decline may be caused by the rapid infusion of blood bank products in which citrate is used as an anticoagulant/preservative. Tetany, as reported here, may be precipitated by such infusions. CASE: A gravid woman presented in hemorrhagic shock due to abruptio placentae. Rapid infusion of packed red blood cells and fresh frozen plasma precipitated signs of tetany, muscle rigidity, posturing, high airway pressure during mechanical ventilation, etc. Ionized calcium and magnesium blood levels were very low (0.58 mmol/L and 1.0 mg/dL, respectively), but responded to rapid electrolyte administration. CONCLUSION: Binding of calcium and magnesium by citrate may lead to hypo-ionized calcemic and hypomagnesemic tetany after rapid replacement of blood products in the pregnant patient. This consequence is worsened when extreme alkalemia due to respiratory or metabolic causes is also present.

Abruptio Placentae↗

Nursing care of patients with Parkinson's disease.

Nursing interventions for each of the symptoms of Parkinson's disease, muscle rigidity, bradykinesia, tremors at rest and postural reflex abnormalities, are designed to increase the patient's quality of life by minimizing symptoms. Nurses are responsible for planning patient medication schedules to maximize drug effectiveness. Dietary implications include a low-protein regimen for the patient during the day, eliminating foods high in Vitamin B6, high caloric foods, and soft-solid foods offered at frequent feedings. Constipation is addressed by increasing the patient's fiber and fluid intake and by increasing the patient's mobility. Patient mobility is increased when the patient is taught purposeful activities and to concentrate on the way he walks. Communication is facilitated if the patient takes deep breaths before speaking and uses diaphragmatic speech. A telephone receiver which amplifies the patient's voice is also available. Interventions are good only if the patient chooses to implement them; he is the head of the health team planning his care.

Humans↗

Neuroleptic malignant syndrome.

We present the case of a 35-year-old man who developed symptoms of the neuroleptic malignant syndrome (NMS) after taking prescribed, moderately high, therapeutic doses of haloperidol. When brought to the emergency department, he was comatose, hypotensive, and had rigid muscle tone and a core body temperature of 42.2 C. Although initial treatment was supportive, intubation, ventilator support, and further care in the intensive care unit were necessary. Ensuing disseminated intravascular coagulation was treated successfully and the patient was weaned from the ventilator on the third day after admission. He was discharged from the hospital 11 days after admission. Recently recognized drug therapy for NMS, such as bromocriptine mesylate and dantrolene sodium, was not used in this case.

Adult↗

Serotonin syndrome associated with nefazodone and paroxetine.

A 51-year-old woman was brought to the emergency department unresponsive, hyponatremic, and diaphoretic, with muscle rigidity. Her condition improved dramatically after supportive treatment and dantrolene. The patient had received nefazodone for 6 months, but the drug had been discontinued 2 days before admission after a tapering period. One day before admission, paroxetine 20 mg/day was started. A repeat challenge with paroxetine 7 days after discontinuation of nefazodone did not result in recurrence of the patient's symptoms. We believe this to be the first report of serotonin syndrome associated with nefazodone and paroxetine.

Antidepressive Agents, Second-Generation↗

[Clinical aspects and prognostic factors of icterohemorrhagic leptospirosis in adults. Apropos of 249 cases in La Reunion].

Human leptospirosis of the classical and severe icterohemorrhagic type, usually due to the L. icterohaemorrhagiae serogroup, is frequent in La Réunion. In a retrospective study conducted between 1980 and 1984 in 249 adult patients, the mortality rate was 13 p. 100. Our data and those found in the literature indicate that the main cause of death is pneumopathy, followed by profuse haemorrhages, arrhythmias and cardiovascular collapse. Acute renal failure is common and often severe; it facilitates gastrointestinal bleeding and is of poor prognosis, particularly in patients with prolonged anuria, a possible cause of lethal hyperkalaemia. Other factors of unfavourable outcome have been demonstrated statistically; they include disturbances of consciousness, hypoprothrombinaemia, epigastric muscle rigidity, hyperleukocytosis, thrombocytopenia, high aspartate aminotransferase levels and chronic alcoholism. At the moment, pulmonary, cardiac and haemorrhagic complications concur with renal failure to darken the prognosis of these severe forms of leptospirosis.

Adult↗

The importance of the striato-nigro-collicular pathway in the expression of haloperidol-induced tonic electromyographic activity.

Experiments were carried out to investigate the participation of the striatonigral and nigrocollicular GABAergic pathways in the expression of haloperidol-induced tonic electromyographic (EMG) activity of the gastrocnemius-soleus muscle in awake rats. It was shown that bilateral injections of haloperidol (500 ng/0.5 microliter) into the rostral part of the neostriatum induced a tonic EMG activity which could be significantly reduced by a second bilateral injection of muscimol (25 ng/0.5 microliter) into the substantia nigra pars reticulata (SNR) or of bicuculline (50 ng/0.5 microliter) into the intermediate or deep layers of the colliculus superior (CS). These results suggest that the striatonigral and nigrocollicular GABAergic pathways play a critical role in the transmission of haloperidol-induced tonic EMG activity.

Animals↗

Continuous intravenous infusion of naloxone does not change behavioral, cardiovascular, or inflammatory responses to subcutaneous formalin in the rat.

The opioid antagonist, naloxone, produces equivocal effects on the magnitude of nociceptive responses in several animal models of persistent pain, including the formalin test. Hindpaw injection of dilute formalin produces not only inflammation but also phasic (Phase 1) and persistent (Phase 2) behavioral and cardiovascular nociceptive responses in the rat. To test the hypothesis that endogenous opioid systems contribute to the magnitude of responses to intraplantar formalin injection, we evaluated the effects of continuous naloxone administration (0.01-100 mg/kg per h, i.v.) on formalin-evoked hindpaw inflammation, on behavioral indices of pain, flinching and licking pain behavior, and on changes in mean arterial pressure and heart rate. We report that naloxone, at doses less than 100 mg/kg per h, did not change any formalin-evoked response. Although the 100 mg/kg per h dose significantly decreased these responses, it also produced muscle rigidity and profound bradycardia. We conclude that endogenous opioids do not significantly modulate the nociceptive processing induced by subcutaneous formalin.

Animals↗

Cerebrospinal fluid studies in the Rett syndrome: biogenic amines and beta-endorphins.

The etiology of the Rett syndrome (RS) is unknown. Reduced function of biogenic amines has been described. Symptoms of central apnea, hyperventilation, hypothermia, peripheral analgesia, muscle rigidity, myoclonic jerks, hand stereotypy and seizures occur in RS and have been suggested as a result of elevated central beta-endorphins. It was hypothesized that a dysfunctional modulation of endogenous opiate systems and biogenic amines may be present. Cerebrospinal fluid (CSF) from 12 girls with RS was studied for beta-endorphin immunoreactivity, and biogenic amines. Lactates and pyruvate levels were measured. Eleven of the 12 girls had elevated beta-endorphin immunoreactivity in CSF, 4 girls had reduced biogenic amines and 6 girls had elevated pyruvate and lactate levels. Whether the elevated beta-endorphin immunoreactivity is a primary disorder or is a result of secondary feedback mechanisms is unknown. Naltrexone, an antiopioid drug, may reduce symptoms.

Adolescent↗

Neuroleptic malignant syndrome-like state in a patient with Down syndrome and basal ganglia calcification.

We report a case of rhabdomyolysis in a 13-year-old Down syndrome patient with progressive quadriplegia, choreoathetosis and dystonia. Cranial CT demonstrated bilateral basal ganglia calcification. He experienced the sudden onset of high fever, cloudiness of consciousness, muscle rigidity and severe opisthotonus. The diagnosis was made on the basis of the marked increases in serum creatine kinase and myoglobin. There was remarkable elevation of 5-hydroxyindoleacetic acid, homovanillic acid and methoxy-hydroxyphenyl glycol in the cerebrospinal fluid during hyperpyrexia. This case exhibited almost all the diagnostic criteria of the neuroleptic malignant syndrome. It was suggested that abnormalities of monoamines in the central nervous system may be related to the pathologic etiology of this state and rhabdomyolysis.

Adolescent↗

The neuroleptic malignant and serotonin syndromes.

The neuroleptic malignant syndrome and the serotonin syndrome share many clinical features and may exist on a spectrum of the same disorder. The neuroleptic malignant syndrome, however, is an idiosyncratic drug reaction, whereas the serotonin syndrome is an effect of drug toxicity. Both syndromes present with varying degrees of mental status changes and autonomic instability. In general, patients with the neuroleptic malignant syndrome have higher fevers and pronounced extrapyramidal signs with muscle rigidity, whereas patients with the serotonin syndrome have lower fevers, more gastrointestinal dysfunction, and myoclonus. Treatment for both syndromes consists of removing the offending agent and providing intensive supportive care. Syndrome-specific therapies are controversial.

Diagnosis, Differential↗

Emergency department presentations of patients with Parkinson's disease.

Parkinson's disease (PD) is a chronic progressive neurological disorder characterized by tremor, muscle rigidity, slowness of movement (bradykinesia), and gait instability. In early disease, PD is well managed in an office setting, however, as the disease progresses, a variety of syndromes may result in emergency department visits. The scenarios most likely to require an emergent evaluation are severe motor "off" periods with immobility, involuntary movements (dyskinesia), psychosis, acute confusion, panic disorder, and pain. Other less frequent presentations are also discussed. This article uses illustrative cases to provide a framework to discuss emergency department diagnosis and management issues in caring for these patients.

Acute Disease↗

Pediatric tremors.

Explore the source record for details and available documents.

Anti-Dyskinesia Agents↗