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PubMedDate not supplied

[Syndrome of the superior oblique muscle rigidity: clinico-anatomical aspects and results of treatment of 8 patients].

Tenectomy of the superior oblique muscle resulted in complete disappearance of Brown's syndrome in 7 out of 8 children operated on. In view of this, it can be a method of choice in treatment of the syndrome. There was the first clinical case of an additional abnormal attachment of the superior oblique muscle tendon to the sclera. In another patient an abnormal marked vascularization of the tendon identified histologically had the appearance of a muscular structure at the site of the tendon seen at the operation.

Age Factors↗
PubMed1988

A new syndrome of axial muscle rigidity associated with etretinate therapy.

We report on three cases of a novel syndrome associated with treatment for psoriasis with the retinoid etretinate. The distinctive features of this syndrome include rigidity that is restricted to the axial muscles, impairment of neck extension greater than flexion, impairment of anteflexion at the waist, severe impairment of lateral flexion at both the waist and the neck, and, in one case, rigidity of proximal lower extremity muscles. Peripheral nerve block extinguished the lower extremity rigidity in one patient, and two patients had a favorable response to Sinemet. One patient had persistence of symptoms and findings 2 years after discontinuation of etretinate. The clinical features of this syndrome are consistent with an effect of etretinate on central, possible catecholaminergic neurons.

Adult↗
PubMed1974

A comparison of the actions of some drugs on decerebrate rigidity, muscle spindle activity and alpha-adrenoceptors.

1 The relative potencies of methotrimeprazine, (+)-methotrimeprazine, (+/-)-10-(3-dimethylamino-2-methylpropyl)-2-valeroyl phenothiazine hydrochloride (M & B 18,706) and (+)-M & B 18,706 in reducing the pressor action of noradrenaline in the spinal cat, reducing intercollicular decerebrate rigidity, and muscle spindle afferent activity have been studied.2 Methotrimeprazine was eight times as potent as (+)-methotrimeprazine in reducing the pressor action of noradrenaline and six times as potent in reducing decerebrate rigidity. M & B 18,706 was also eight times as potent as (+)-M & B 18,706 in reducing the pressor action of noradrenaline and six times as potent in reducing decerebrate rigidity.3 For the above compounds and chlorpromazine there was a significant correlation between the effective doses for the inhibition of the pressor action of noradrenaline and for the reduction of decerebrate rigidity.4 The doses which reduced decerebrate rigidity were similar to those that reduced muscle spindle afferent discharge. It is likely that these drugs reduce decerebrate rigidity by inhibiting fusimotor activity.5 Desipramine increased decerebrate rigidity and increased spindle afferent discharge.6 It is thought that the phenothiazine derivatives studied reduce decerebrate rigidity and spindle afferent discharge by inhibiting receptors for noradrenaline in the central nervous system.

Animals↗
PubMed1987

Mechanographic analysis of muscle rigidity after morphine and haloperidol: a new methodological approach.

The new method described in this study was based on consecutive repeated measurements of the resistance of flexor and extensor muscles of the hind foot of the rat to forced flexions and extensions of the foot. Locomotor movements of the rat were restrained with a metaplex box which had a slot for the hind limb. The control muscle tone measured by this method was constant for more than 2 h, and amounted to approx. 25 g for flexor muscles, and approx. 45 g for extensors. Morphine (2.5, 5, 10, 20 mg/kg) enhanced dose-dependently the resistance of flexor muscles up to approx. 45 g, 70 g, 100 g and 140 g, respectively, and the resistance of extensors of the paw up to approx. 100 g, 140 g, 180 g and 240 g, respectively. Haloperidol (5 and 10 mg/kg) enhanced dose-dependently the resistance of flexor muscles up to approx. 45 g and 70 g, respectively, and that of extensors of the foot up to approx. 75 g and 120 g, respectively. Morphine rigidity, measured as resistance of respective muscles to forced movements, was almost completely inhibited by a consecutive injection of 0.2 mg/kg of naloxone. The new method seems to have considerable advantages in comparison with electromyographical (EMG) or other kinds of mechanographical measurements of the muscle tone.

Animals↗
PubMed2003

Magnesium sulfate for control of muscle rigidity and spasms and avoidance of mechanical ventilation in pediatric tetanus.

OBJECTIVE: To describe the use of intravenous magnesium sulfate for the control of muscle spasms and severe generalized rigidity in a child with moderate to severe tetanus without the need for prolonged deep sedation, mechanical ventilation, or neuromuscular blockade. DESIGN: Case report. SETTING: Pediatric intensive care unit in a tertiary care, university-based children's hospital. INTERVENTIONS: A continuous infusion of magnesium sulfate. MEASUREMENTS AND MAIN RESULTS: We describe a 12-yr-old child with moderate to severe tetanus who was treated with a continuous infusion of magnesium sulfate to control painful muscle spasms and severe generalized rigidity initially refractory to moderate sedation. Muscle spasms and severe generalized rigidity were improved with magnesium sulfate. No adverse effects associated with the use of magnesium sulfate were noted during the monitoring of cardiovascular and respiratory function, reflexes, and serum magnesium concentrations. CONCLUSIONS: An infusion of magnesium sulfate can be utilized to treat muscle spasms and severe generalized rigidity without the need for deep sedation, mechanical ventilation, or neuromuscular blockade. We recommend that magnesium sulfate be considered in the armamentarium of therapeutics utilized to treat muscle spasms and rigidity associated with tetanus, provided the patient's neurologic, cardiovascular, and respiratory status can be closely monitored in the pediatric intensive care unit.

Child↗