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At least 109 records · Page 6Linked to original sources
PubMed2003

Drug-induced hyperthermia and muscle rigidity: a practical approach.

Body thermoregulation can be violently offset by drugs capable of altering the balance between heat production and dissipation. Such events may rapidly become fatal. The drugs that are involved in the eruption of such syndromes include inhalation anaesthetics, sympathomimetic agents, serotonin antagonists, antipsychotic agents and compounds that exhibit anticholinergic properties. The resultant hyperthermia is frequently accompanied by an intense skeletal muscle hypermetabolic reaction that leads to rapidly evolving rigidity, extensive rhabdomyolysis and hyperkalemia. The differential diagnosis should, however, rule out non-drug-induced causes, such as lethal catatonia, central nervous system infection or tetanus, strychnine poisoning, thyrotoxic storm and pheochromocytoma. Prompt life-saving procedures include aggressive body temperature reduction. Patients with a suspected drug (or non-drug) hypermetabolic reaction should be admitted into an intensive care area for close monitoring and system-oriented supportive treatment. We present six conditions, in decreasing order of gravity and potential lethality, in which hyperthermia plays an essential role, and suggest a clinical approach in such conditions.

Body Temperature Regulation↗
PubMed1998

Respiratory muscle rigidity in a preterm infant after use of fentanyl during Caesarean section.

UNLABELLED: Fentanyl is in many neonatal intensive care units the sedative of choice. One side-effect is, however, the possibility of muscle and/or chest wall rigidity. A pregnant woman with a critical pulmonary valve stenosis had a balloon dilatation at 26 weeks of gestation. She was put on propranolol, but went into a severe cardiac failure. In week 31, she developed pregnancy induced hypertension. Periodically absent diastolic flow in the umbilical cord was demonstrated. A Caesarean section was performed using fentanyl as analgesia. A boy weighing 1440 g, had a 1 min Apgar score of 3 without respiratory movements. Mask ventilation was tried, but chest wall expansion was not achieved despite using high pressures. He was intubated and positive pressure ventilation attempted, with the same result. Despite the use of high pressures up to 60-70 cm H2O, no chest movement could be achieved. An intravenous line was established in order to give naloxone and pancuronium. Just before the drugs were given, chest wall movements were achieved and the heart rate normalized. CONCLUSION: This is the first report on chest wall rigidity in a neonate after administration of fentanyl to the mother during Caesarean section.

Adult↗
PubMed1987

The role of gamma-aminobutyric acid mechanisms of the zona incerta-lateral hypothalamus in the catalepsy and muscle rigidity evoked by morphine.

Picrotoxin or bicuculline were injected bilaterally into the zona incerta-lateral hypothalamus (ZI-LH) of the rat. Each drug (50 ng) inhibited or abolished the catalepsy induced by 20 mg/kg s.c. of morphine. Each drug also strongly inhibited the tonic electromyographic activity (EMG) induced by 10 mg/kg s.c. of morphine in the gastrocnemius soleus muscle (GS). The obtained results demonstrate participation of the ZI-LH in both catalepsy and rigidity induced by a systemic administration of morphine.

Animals↗
PubMed1997

Soft tissue manipulation: neuromuscular and muscle energy techniques.

Muscle rigidity and spasms occur with neurological disease and may contribute to contractures and shortening of muscle fibers that can interfere with motor behaviors, such as ambulation, or activities of daily living, such as combing hair, feeding or dressing. The neuromuscular technique (NMT) and muscle energy technique (MET) are nursing interventions that can reduce pain and muscle rigidity, lengthen muscle fibers and increase range of motion necessary for normal motor behavior. Nurses can use these techniques in patients with acute neurological diseases and those recovering in rehabilitation and long-term care settings. With some neurological diseases, muscle rigidity, increased muscle tone and muscle spasms reduce the range of motion of joints and the quality of movement. These changes often lead to contractures and impairments in performing daily tasks or ambulating, and thus, to loss of independence. Soft tissue manipulation can be used to reduce muscle tension and spasms, reduce pain and enhance the range of motion of joints whose function depends on the involved muscles. Soft tissue manipulation may also improve movement during specific tasks. Although the muscle relaxation achieved with manipulation techniques is primarily short-term, long-term effects occur. This article describes two techniques of soft tissue manipulation, their mechanisms of action, assessment and implementation. A case study is used to illustrate application of the techniques and possible long-term effects.

Aged↗
PubMed1992

[Effect of small doses of L-dopa on synergic tonic reaction in patients with childhood cerebral palsy].

As many as 8 patients aged 8-19 years suffering from infantile cerebral paralysis (ICP) with torsion dystonia, akinetic, rigid, spastic and hypotonically atactic syndromes were examined for the maximum amplitude of EMG activity of the musculus tibialis anterior in voluntary rear flexion of the foot and in Strümpell's tibial synkinesia before treatment and after intake of small doses of L-DOPA (nakom, 62 mg/day). It has been established that the amplitude of voluntary EMG activity and the rate of impulse transmission in efferents of the tibial nerve remained practically unchanged during treatment; in all the cases, the synergic EMG activity, discharges of EMG and prolonged activity decreased; the scope of active movements in the talocrural joint increased by 10-20 degrees. The greatest decrease of synergic EMG activity (by 40%) was recorded in patients with rigid muscle tone, the mean in patients with spastic and spastic -dystonic (by 25-33%), the least one (17%) in muscle hypotonia. It is assumed that voluntary and synergic automatic movements have varying neuromediator supply. The effect of L-DOPA is realized via changes in the function of suprasegmental brain structures regulating polysynaptic postural reflexes with primary action on extensors. The effects of the subcortical nuclei, stem and cerebellar systems are made possible by dopamine neuromediation to a different measure.

Adolescent↗
PubMed2002

Muscle tone facilitation and inhibition after orexin-a (hypocretin-1) microinjections into the medial medulla.

Orexins/hypocretins are synthesized in neurons of the perifornical, dorsomedial, lateral, and posterior hypothalamus. A loss of hypocretin neurons has been found in human narcolepsy, which is characterized by sudden loss of muscle tone, called cataplexy, and sleepiness. The normal functional role of these neurons, however, is unclear. The medioventral medullary region, including gigantocellular reticular nucleus, alpha (GiA) and ventral (GiV) parts, participates in the induction of locomotion and muscle tone facilitation in decerebrate animals and receives moderate orexinergic innervation. In the present study, we have examined the role of orexin-A (OX-A) in muscle tone control using microinjections (50 microM, 0.3 microl) into the GiA and GiV sites in decerebrate rats. OX-A microinjections into GiA sites, previously identified by electrical stimulation as facilitating hindlimb muscle tone bilaterally, produced a bilateral increase of muscle tone in the same muscles. Bilateral lidocaine microinjections (4%, 0.3 microl) into the dorsolateral mesopontine reticular formation decreased muscle rigidity and blocked muscle tone facilitation produced by OX-A microinjections into the GiA sites. The activity of cells related to muscle rigidity, located in the pedunculopontine tegmental nucleus and adjacent reticular formation, was correlated positively with the extent of hindlimb muscle tone facilitation after medullary OX-A microinjections. OX-A microinjections into GiV sites were less effective in muscle tone facilitation, although these sites produced a muscle tone increase during electrical stimulation. In contrast, OX-A microinjections into the gigantocellular nucleus (Gi) sites and dorsal paragigantocellular nucleus (DPGi) sites, previously identified by electrical stimulation as inhibitory points, produced bilateral hindlimb muscle atonia. We propose that the medioventral medullary region is one of the brain stem target for OX-A modulation of muscle tone. Facilitation of muscle tone after OX-A microinjections into this region is linked to activation of intrinsic reticular cells, causing excitation of midbrain and pontine neurons participating in muscle tone facilitation through an ascending pathway. Moreover, our results suggest that OX-A may also regulate the activity of medullary neurons participating in muscle tone suppression. Loss of OX function may, therefore, disturb both muscle tone facilitatory and inhibitory processes at the medullary level.

Anesthetics, Local↗