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PubMed1986

Detachable cast pylon technique for rigid dressings on below-knee amputee patients.

The attachment of a pylon and prosthetic foot to a postoperative rigid dressing can be beneficial in the management of a below-the-knee amputation. Recently, a rigid, removable dressing has been used to allow easy inspection of the stump during healing. The removal of the pylon and prosthetic foot at night, preventing unsupervised ambulation, is accomplished by a disconnecting mechanism, which is permanently attached to the end of the rigid removable dressing. This disconnecting mechanism adds to the bulk and weight of the rigid dressing, increasing the shear force on the stump. We are introducing the detachable cast pylon technique, in which a fabricated sleeve attached to the pylon is easily and completely attached and detached from a rigid dressing. It is lightweight, less bulky, easily fabricated, and inexpensive. It offers a quick disconnect system for either the Otto-Bock attachment plate or uniquely with PVC tubing. In addition, this technique affords consistency in shaping the stump, as the same rigid dressing can be used for both rest and training. Its intent is for in-hospital use or when ambulation is restricted to supervised situations.

Acetaminophen↗
PubMed1982

[Experimental study on plates of various stiffness--on their effects on the bones and rigidity in fracture immobilization].

Recently, there has been a tendency to use larger plates such as an AO compression plate in the operative treatment of fractures. However, it was found that the rigid plate fixation for a long period greatly have an effect on the cortex and bone strength. In this regards, the author studied the influences on the cortex and bone strength after long fixation with three types of plates which have large differences in stiffness. Moreover, the rigidity of fracture immobilization was investigated for each plate. The experimental results in mature rabbits as experimental animals showed that the least thinning of the cortex was obtained by use of high density polyethylene (HDP) plate with lowest rigidity and bone strength decreased with increasing rigidity of the plate. However, the fracture site fixed with a HDP plate showed malunion. On the other hand, a carbon fiber polybutylene-telephthalate composite (CFP) plate which has the elastic modulus almost corresponding to that of the tibiofibular bone of a rabbit had less influences on the bone cortex as compared to a stainless steel plate with highest rigidity. Therefore, a CFP plate had less influences on the bone and gave a moderate rigidity in fracture immobilization.

Animals↗
PubMed1996

Determinants of satisfactory rigidity after intracavernosal injection with prostaglandin E1 in men with erectile failure.

The study examines the erectile response of intracavernosal injection with increasing doses of prostaglandin E1 (PGE) and papaverine/phentolamine (PP) in 516 men with erectile failure. The response was correlated to age, the duration of erectile failure, the quality of spontaneous erections, tobacco consumption and medicine use. In addition, the erectile response was related to penile brachial index (PBI) the free testosterone index and various hormonal parameters. Over 60% of the subjects obtained satisfactory rigidity of at least 30 min duration with 7-15 micrograms PGE. A further 15% (PGE non-responders at the doses tested) obtained rigidity with PP. The average dose necessary to achieve rigidity was 8.8 micrograms for PGE and 0.94 ml (papaverine: 15 mg/ml; phentolamine 0.5 mg/ml) for PP. The average duration of rigidity was 2.2 h and 2.3 h for PGE and PP, respectively. Tobacco consumption, the duration of erectile failure and the age of the subject did not influence the response to intracavernosal injection. Moreover the PBI, the free testosterone index or libido of the subject, did not appear to be generally important for obtaining satisfactory rigidity. In contrast, chronic medication, especially antihypertensive drugs, was associated with significantly higher numbers of poor responders, a shorter duration of erection in the responders and higher doses of PGE necessary to achieve a satisfactory response. The combination of increasing age and antihypertensive medication was predictive for a poor intracavernosal response. In general, a reduced incidence of morning erections was predictive of a weaker response to PGE. The proportion of men with a PBI lower than 0.75 increased with age. These subjects more often took chronic medication, had a lower frequency of morning erections and exhibited a significantly weaker reaction to PGE than subjects with higher PBI. In summary, a large number of men with erectile failure can obtain satisfactory rigidity with intracavernosal injection. In men taking antihypertensive medication, especially in higher age groups, the dose of the intracavernosal medication had to be increased. A reduced sensitivity to intracavernosal medication could be predicted from a lower PBI and a reduced frequency of spontaneous erections.

Adrenergic alpha-Antagonists↗
PubMed1998

Rigid external distraction: its application in cleft maxillary deformities.

Patients with severe maxillary hypoplasia secondary to congenital facial clefting present numerous challenging problems for the reconstructive surgeon. Traditional surgical/orthodontic approaches for these patients often fall short of expectations, especially for achieving normal facial aesthetics and proportions. The purpose of this paper is to present our clinical experience and cephalometric results with the use of rigid external distraction for the treatment of patients with severe maxillary deficiency. Eighteen consecutive orofacial cleft patients with severe maxillary hypoplasia were treated with maxillary distraction osteogenesis. Criteria for patient selection included severe maxillary hypoplasia with negative overjet of 8 mm or greater, patients with normal mandibular morphology, and patients with full primary dentition or older. There were 10 unilateral cleft lip and palate patients, 6 bilateral cleft lip and palate patients, and 2 patients with severe congenital facial clefting. A maxillary splint was prepared for each patient, and all patients underwent a high Le Fort I maxillary osteotomy. All surgery was performed on either an outpatient or a 23-hour admission basis. No patient required blood transfusions or intermaxillary fixation. Two types of mechanical distraction were utilized in this series. In group 1 (n = 14), the patients underwent rigid external distraction with an external distraction device. In group 2 (n = 4), patients underwent face mask distraction with elastics. There was no surgical morbidity in any of the patients. For the patients in the rigid external distraction group, the mean effective horizontal advancement of the maxilla was 11.7 mm. All of these patients had correction of their negative overjet. For patients in the face mask distraction group, the results were disappointing. The mean effective advancement of the maxilla in this group was only 5.2 mm. In all face mask distraction patients, the initial maxillary hypoplasia was undercorrected. Maxillary distraction osteogenesis with rigid external distraction permits full correction of the midfacial deficiency, including both the skeletal and soft-tissue deficiencies. Rigid external distraction in patients with severe maxillary hypoplasia allows full correction of the deformity through treatment of the affected region only. It offers the distinct advantage of correcting these severe deformities through a minimal procedure. Rigid external distraction has dramatically improved our treatment results for patients with severe cleft maxillary hypoplasia.

Adolescent↗
PubMed1991

Short-latency autogenic inhibition in patients with Parkinsonian rigidity.

The spinal Ib interneuron efficacy has been compared in 11 control subjects and 19 patients with parkinsonian rigidity. In normal subjects, gastrocnemius medialis nerve stimulation induces an inhibition of the soleus H reflex for 3 to 8 msec with a peak at 5 msec of 83.72 +/- 7.28% of the control value of H reflex. In parkinsonian patients, inhibition is reduced or even replaced by facilitation, which also peaks at 5 msec. The departures from normal values correlate with rigidity intensity assessed by the Webster scale. Increase in rigidity is associated, first, with a reduction of inhibition and, from a score of 2 or more, with facilitation replacing the normal inhibition. In addition to providing an electrophysiological index of rigidity, reduction in autogenic inhibition might be one of the neurophysiological mechanisms underlying rigidity. In association with the known hyperactivity of the Ia inhibitory interneuron in Parkinson's disease, reduction of activity of Ib interneuron could be explained by an increased activity in the reticularis gigantocellularis nucleus; its efferent tracts both inhibit Ib interneurons and activate Ia interneurons.

Aged↗
PubMed1998

Depression in classic versus akinetic-rigid Parkinson's disease.

We examined the prevalence of major depression and dysthymia in 78 patients with the classic variant of Parkinson's disease (PD) (that is, tremor plus rigidity and/or bradykinesia), and in 34 patients with the akinetic-rigid variant. Although the prevalence of dysthymia was similar in both groups (classic PD, 31%; and akinetic-rigid PD, 32%), patients with akinetic-rigid PD had a significantly higher prevalence of major depression (38% versus 15%, respectively; p < 0.01). A stepwise regression analysis demonstrated that bradykinesia was the extrapyramidal sign with the highest correlation with Hamilton depression scale scores. Our findings demonstrate a significant association between major depression and the akinetic-rigid type of PD.

Aged↗
PubMed1991

Structure-activity studies of neurotensin on muscular rigidity and tremors induced by 6-hydroxydopamine lesions in the posterolateral hypothalamus of the rat.

It has previously been reported that intracerebroventricular administration of neurotensin (30 micrograms) reduced muscular rigidity and tremors, induced by a neurochemical lesion with 6-hydroxydopamine in the posterolateral hypothalamus of rats. In the present study, the effects of two fragments (NT1-10 and NT8-13) and two analogues ([D-Tyr11]-NT and [Ala11]-NT) of neurotensin on the grasping time (index of muscle rigidity) and tremors in 6-hydroxydopamine-lesioned rats are reported. Intracerebroventricular administration with 120 micrograms of NT1-10 and [Ala11]-NT had no effect on the muscle rigidity and tremors induced by the neurochemical lesion. The administration of NT8-13 60 micrograms) significantly attenuated both behavioural responses. The analogue [D-Tyr11]-NT produced a much greater attenuation of the muscle rigidity and tremors. The dose of 1.8 micrograms of [D-Tyr11]-NT significantly reduced the grasping time, while the number of tremors was attenuated with the threshold dose of 0.9 micrograms. Together, these results suggest that the effects of neurotensin on muscle rigidity and tremors, induced by pretreatment with 6-hydroxydopamine injected into the posterolateral hypothalamus, were not caused by non-specific effects but largely depended on the carboxy terminal of the peptide. The tyrosine residue in position 11 of the molecule plays a critical role in the action of neurotensin, as shown with the high potency and duration of action of the analogue [D-Tyr11]-NT. As previously suggested, the greater effect with [D-Tyr11]-NT may be due to greater resistance of the analogue to enzymatic degradation because of the incorporation of the D-Tyr amino acid, in position 11 of neurotensin.

Animals↗
PubMed1987

The neostriatal inhibition of catalepsy, but not of muscle rigidity, evoked from the substantia nigra pars reticulata.

The effects of a bilateral blockade of neo- and palleostriatal GABAergic mechanisms on catalepsy and muscle rigidity resulting from picrotoxin injection into the substantia nigra pars reticulata (SNR) were studied. The catalepsy and rigidity were induced by a unilateral injection of 100 ng/0.5 microliter of picrotoxin. Bilateral injections of 250 ng/l microliter of picrotoxin into the intermediate-ventral parts of the caudato-putamen (CP) abolished the catalepsy but had no effect on the muscle rigidity induced by an intranigral injection of the drug. Bilateral injections of 250 ng/l microliter of picrotoxin into the globus pallidus (GP) did not influence the catalepsy and rigidity induced by the intranigral injection of the drug. The results indicate that the impulses, connected with the catalepsy evoked from the SNR seem to be transmitted back to the CP and blocked therein by inhibition of GABAergic synapses in its intermediate-ventral part. The impulses, connected with the muscle rigidity evoked from the SNR, presumably do not return to the striatum.

Animals↗
PubMedDate not supplied

Fentanyl-induced muscle rigidity as affected by pretreatment with amantadine hydrochloride.

STUDY OBJECTIVE: To determine whether the degree of muscle rigidity in humans caused by the administration of high-dose fentanyl is affected by pretreatment with amantadine hydrochloride, a drug that stimulates the release of dopamine in the basal ganglia. DESIGN: Randomized, observer-blinded comparison of regimes. SETTING: Inpatient surgery at a university-affiliated teaching hospital. PATIENTS: Sixteen patients scheduled for elective surgery in whom the administration of high-dose fentanyl was felt to be appropriate. INTERVENTIONS: Eight patients in the control group were given diazepam 5 mg orally 1 hour prior to induction of anesthesia. Eight patients in an experimental group were given the same dose of diazepam and also were treated with amantadine 1 g orally in divided doses over a period of 25 hours prior to their scheduled surgery. At the time of surgery, all patients were given fentanyl 50 micrograms/kg intravenously at a rate of 1 mg/min and were clinically evaluated for the degree of muscle rigidity of the chest wall, abdomen, and extremities. MEASUREMENTS AND MAIN RESULTS: A single observer, blinded to the technique, evaluated and recorded the degree of muscle rigidity present in the chest wall, abdomen, and upper extremities immediately after administration of the fentanyl and 3 minutes later. The observer was the same individual in all instances. In no case did the muscle rigidity compromise our ability to adequately oxygenate the patient. CONCLUSIONS: Muscle rigidity associated with the administration of high-dose fentanyl is not attenuated by prior administration of amantadine in the dose range studied.

Abdominal Muscles↗
PubMed1992

An in vivo alpha-2 assay reversal of opioid-induced muscular rigidity and neuroleptic-induced ptosis.

A method is described to detect selective alpha-2 adrenergic agonists in vivo. Palpebral ptosis is induced in rats by the neuroleptic agent haloperidol (Hal), or by tetrabenazine (TBZ) methanesulfonate. Twenty minutes later, test compounds are injected, and ptosis is scored. In a separate test, muscular rigidity is induced by the opioid, fentanyl, and subsequently, test compounds are assessed for their ability to reverse muscular rigidity. Results indicate that only alpha-2 agonists reliably reverse neuroleptic-induced and TBZ-induced ptosis, as well as opioid-induced rigidity. An alpha-1 antagonist reversed only rigidity, whereas, alpha-2 antagonists and beta-agonists were generally ineffective in all tests. Therefore, the ability to reverse neuroleptic and TBZ-induced ptosis along with the ability to reverse opioid-induced muscular rigidity is a characteristic unique to alpha-2 agonists.

Adrenergic alpha-Agonists↗
PubMed1997

Opioid-induced rigidity after intravenous fentanyl.

BACKGROUND: Large doses of intravenous opioids may cause severe rigidity and prevent spontaneous or controlled ventilation. The mechanism of this effect appears to be neuraxis dopamine antagonism. Rigidity after analgesic doses of fentanyl has not been reported previously. CASE: A pregnant woman receiving haloperidol for multiple psychiatric conditions presented for evaluation of vaginal bleeding. Intravenous fentanyl was administered to facilitate vaginal examination. Severe rigidity of the extremities and truncal region occurred, which prevented spontaneous or assisted ventilation. CONCLUSION: Opioid administration may result in rigidity and respiratory embarrassment. Decreased analgesic requirements in pregnancy and concomitant butyrophenone administration may predispose to opioid-induced rigidity.

Adult↗
PubMed1997

Involvement of spinal adenosine A1 and A2 receptors in fentanyl-induced muscular rigidity in the rat.

In the present study, using hydrophilic adenosine antagonists either selective to A1 or A2 receptors, we investigated the central and spinal adenosinergic participation in fentanyl-induced muscular rigidity. Adult Sprague-Dawley rats were anesthetized with ketamine and were under mechanical ventilation. Fentanyl (100 micrograms/kg, i.v.) consistently elicited electromyographic (EMG) activation in the sacrococcygeal dorsalis lateralis muscle. This implied muscular rigidity was not blocked by i.c.v. administration of the adenosine A1 antagonist, 1-allyl-3,7-dimethyl-8-p-sulfophenyl-xanthine (ADSPX; 20 or 40 nmol/2.5 microliters), except at higher dose (80 nmol). Equimolar doses of the adenosine A2 antagonist, 3,7-dimethyl-1-propargylxanthane (DMPX), did not exert any inhibitory effect on fentanyl-induced rigidity. Intrathecal (i.t.) administration of the same doses of ADSPX (20, 40 or 80 nmol/10 microliters) appreciably suppressed the EMG activation. However, the rigidity was only inhibited by 40 or 80 nmol (i.t.) of DMPX, but not by the lowest dose. High-dose (80 nmol, i.t.) adenosine A1 or A2 antagonist per se did not induce motor impairment or hindlimb paralysis in conscious animals. These results suggest that adenosine A1 and A2 receptors in the spinal cord may play a more crucial role than those in the central nervous system (CNS) in fentanyl-induced muscular rigidity in rats.

Animals↗
PubMed2002

Progressive encephalomyelitis with rigidity presenting as a stiff-person syndrome.

Diagnosis criteria of stiff-person syndrome (SPS) include progressive, fluctuating muscular rigidity and spasms with normal neurological examination. The presence of unusual features such as prominent limb rigidity with segmental signs and contracture, evidence of brainstem dysfunction, profound autonomic disturbances, CSF pleiocytosis or MRI abnormalities in patients with SPS presentation allows to classify these patients as progressive encephalomyelitis with rigidity (PER). We report a 50 year-old woman suffering from severe painful spasms of abdominal wall and limb muscles. Neurological examination showed pyramidal signs. EMG disclosed continuous muscle activity with superimposed discharges. Treatment with high doses of diazepam and baclofen led to moderate improvement of generalised stiffness. However, the right arm became more rigid with oedema and vasomotor changes. Subsequently, bilateral nystagmus and internuclear opthalmplegia appeared. There was mild CSF pleiocytosis. Associated auto-immune thyroiditis was found with positive anti-microsome antibodies and decreased thyroid hormones. Search for profound neoplasm was negative. The patient had three subacute bouts then she improved with methylprednisolone. The initial clinical presentation mimicking a SPS with subsequent diffuse involvement of the central nervous system and a striking localisation of a severe rigidity to one arm allowed to suspect the diagnosis of PER. The relationship between SPS and PER remains unclear because of the rarity of these disorders. The observation reported in this paper gives evidence that both the disorders are probably two clinical presentations of the same pathogenic process.

Anti-Inflammatory Agents↗
PubMed1999

Masseter muscle rigidity after vecuronium.

Masseter muscle rigidity after suxamethonium, usually occurring in children induced with halothane, is associated with malignant hyperthermia. A case is reported in which masseter muscle rigidity occurred in an adult following vecuronium. From the limited data available, this and two similar reported cases, it appears that non-depolarizing muscle relaxants can, very rarely, cause masseter muscle rigidity in adults. This masseter muscle rigidity may complicate airway management, but is unlikely to progress to generalized rigidity and malignant hyperthermia.

Adult↗
PubMed2005

Measurement of peripheral muscle resistance in rats with chronic ischemia-induced paraplegia or morphine-induced rigidity using a semi-automated computer-controlled muscle resistance meter.

In experimental and clinical studies, an objective assessment of peripheral muscle resistance represents one of the key elements in determining the efficacy of therapeutic manipulations (e.g. pharmacological, surgical) aimed to ameliorate clinical signs of spasticity and/or rigidity. In the present study, we characterize a newly developed limb flexion resistance meter which permits a semi-automated, computer-controlled measurement of peripheral muscle resistance (PMR) in the lower extremities during a forced flexion of the ankle in the awake rat. Ischemic paraplegia was induced in Sprague-Dawley rats by transient aortic occlusion (10 min) in combination with systemic hypotension (40 mm Hg). After ischemia the presence of spasticity component was determined by the presence of an exaggerated EMG activity recorded from gastrocnemius muscle after nociceptive or proprioceptive afferent activation and by velocity-dependent increase in muscle resistance. Rigidity was induced by high dose (30 mg/kg, i.p.) of morphine. Animals with defined ischemic spasticity or morphine-induced rigidity were then placed into a plastic restrainer and a hind paw attached by a tape to a metal plate driven by a computer-controlled stepping motor equipped with a resistance transducer. The resistance of the ankle to rotation was measured under several testing paradigms: (i) variable degree of ankle flexion (40 degrees, 50 degrees, and 60 degrees), (ii) variable speed/rate of ankle flexion (2, 3, and 4 sec), (iii) the effect of inhalation anesthesia, (iv) the effect of intrathecal baclofen, (v) the effect of dorsal L2-L5 rhizotomy, or (vi) systemic naloxone treatment. In animals with ischemic paraplegia an increased EMG response after peripheral nociceptive or proprioceptive activation was measured. In control animals average muscle resistance was 78 mN and was significantly increased in animals with ischemic spasticity (981-7900 mN). In ischemic-spastic animals a significant increase in measured muscle resistance was seen after increased velocity (4 > 3 > 2 sec) and the angle (40 degrees > 50 degrees > 60 degrees) of the ankle rotation. In spastic animals, deep halothane anesthesia, intrathecal baclofen or dorsal rhizotomy decreased muscle resistance to 39-80% of pretreatment values. Systemic treatment with morphine induced muscle rigidity and corresponding increase in muscle resistance. Morphine-induced increase in muscle resistance was independent on the velocity of the ankle rotation and was reversed by naloxone. These data show that by using this system it is possible to objectively measure the degree of peripheral muscle resistance. The use of this system may represent a simple and effective experimental tool in screening new pharmacological compounds and/or surgical manipulations targeted to modulate spasticity and/or rigidity after a variety of neurological disorders such as spinal cord traumatic or ischemic injury, multiple sclerosis, cerebral palsy, or Parkinson's disease.

Anesthetics, Inhalation↗
PubMed1988

Intracranial pressure increases during alfentanil-induced rigidity.

Intracranial pressure (ICP) was measured during alfentanil-induced rigidity in rats. Ten rats had arterial, central venous (CVP), and subdural cannulae inserted under halothane anesthesia. The animals were mechanically ventilated to achieve normocarbia (PCO2 = 42 +/- 1 mmHg, mean +/- SE). Following instrumentation, halothane was discontinued and alfentanil (125 mu/kg) administered iv during emergence from halothane anesthesia. In the five rats that developed somatic rigidity, ICP and CVP increased significantly above baseline (delta ICP 7.5 +/- 1.0 mmHg, delta CVP 5.9 +/- 1.3 mmHg). These variables returned to baseline when rigidity was abolished with metocurine. In five rats that did not become rigid, ICP and CVP did not change following alfentanil. These observations suggest that rigidity should be prevented when alfentanil, and, presumably, other opiates, are used in the anesthetic management of patients with ICP problems.

Alfentanil↗
PubMed1997

Involvement of cerulospinal glutamatergic neurotransmission in fentanyl-induced muscular rigidity in the rat.

BACKGROUND: Investigators in the authors' laboratory previously established the critical participation of the cerulospinal noradrenergic pathway in muscular rigidity elicited by fentanyl. The identification of colocalization of glutamate with tyrosine hydroxylase in most locus ceruleus neurons suggests a role for cerulospinal glutamatergic neurotransmission in fentanyl-induced muscular rigidity. This suggestion and the subtype(s) of glutamate receptors involved were investigated here. METHODS: Electromyographic signals activated by bilateral microinjection of 2.5 microg fentanyl into the locus ceruleus were recorded differentially from the left sacrococcygeus dorsi lateralis muscle of adult male Sprague-Dawley rats. The effect of intrathecal administration at the lower lumbar spinal cord of various N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists or agonists on this index of muscular rigidity was studied. Rats were under mechanical ventilation, and intravenous infusion of ketamine (30 mg x kg(-1) x h(-1)) was maintained until 10 min before fentanyl was administered. RESULTS: Microinjection of fentanyl bilaterally into the locus ceruleus increased the root mean square and decreased the mean power frequency values of electromyographic signals. The efficacy of fentanyl to elicit muscular rigidity in this manner was significantly reduced by previous intrathecal administration of either 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801), D-(-)-2-amino-5-phosphonovaleric acid (AP5), or (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP). Intrathecal administration of kainic acid or NMDA also resulted in significant electromyographic activation. CONCLUSIONS: In addition to the cerulospinal noradrenergic mechanism, the cerulospinal glutamatergic pathway and both NMDA and non-NMDA receptors in the spinal cord may mediate fentanyl-induced muscular rigidity in the rat.

Analgesics, Opioid↗
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↗