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PubMed2001

An animal model of extrapyramidal side effects induced by antipsychotic drugs: relationship with D2 dopamine receptor occupancy.

1. Muscle rigidity was assessed quantitatively and objectively as increases in electromyographic (EMG) activity (muscle rigidity) in the hindlimb muscles of the rat following subcutaneous administration of haloperidol, fluphenazine and thioridazine. 2. Behavioural changes were assessed as increases in the catalepsy score, defined as the time taken for an animal to move off an inclined grid. 3. Increased tonic EMG activity, or the presence of catalepsy was related to the level of occupancy of dopamine D2 receptors in the striatum and substantia nigra of the brain, measured using ex vivo quantitative autoradiography. 4. Increases in tonic EMG activity and the induction of catalepsy were associated with >80% occupancy of striatal and nigral D2 receptors by fluphenazine, while haloperidol increased tonic EMG activity at D2 occupancies of >57%. 5. Thioridazine at doses ranging from 1-15 mg/kg failed to increase EMG activity and occupied <61% of striatal D2 receptors. 6. Overall the findings support the hypothesis that muscle rigidity is observed when a threshold level of D2 receptors in the striatum and substantia nigra are occupied by antipsychotic drugs. 7. This conclusion is consistent with the results of positron emission tomography (PET) studies in humans, and those from our past studies in rats using raclopride, chlorpromazine and clozapine, in which a threshold of approximately 70% striatal and nigral D2 receptor occupancy has been demonstrated.

Animals↗
PubMed1998

The role of striatal glutamate receptors in models of Parkinson's disease.

The aim of the study was to examine the effect of antagonists of the NMDA receptor on the parkinsonian-like muscle rigidity in rats. Reserpine and haloperidol increased the muscle resistance of the hind foot to passive movements, as well as the reflex electromyographic (EMG) activity in the gastroenemius and tibialis anterior muscles. MK-801 (0.32-1.28 mg/kg s.c.), an uncompetitive antagonist of the NMDA receptor, and L-701,324 (5-40 mg/kg i.p.), an antagonist of the glycine site, reduced the muscle tone and the reflex EMG activity enhanced by reserpine or haloperidol. AP-5 (2 and 5 micrograms/0.5 microliter), a competitive antagonist of the NMDA receptor, and 5,7-dichlorokynurenic acid (1.0-4.5 micrograms/0.5 microliter), the glycine site antagonist injected bilaterally into the rostral striatum, inhibited the muscle rigidity induced by haloperidol. In contrast, AP-5, injected alone bilaterally into the intermediate-caudal striatum induced muscle rigidity. The present results suggest that: (1) the inhibitory effect of the NMDA receptor antagonists on the parkinsonian-like muscle rigidity depends, at least partly, on their action on the rostral striatum; (2) the blockade of NMDA receptors in the intermediate-caudal striatum may reduce the beneficial impact of these compounds.

Animals↗
PubMed2000

Fentanyl-induced chest wall rigidity and laryngospasm in preterm and term infants.

OBJECTIVE: To assess the occurrence of muscle rigidity after fentanyl administration in premature and term neonates. DESIGN: Prospective case series, observational study. SETTING: A university hospital neonatal intensive care unit. PATIENTS: 8/89 preterm and term infants (25-40 wks gestational age) who received fentanyl for perioperative analgesia and sedation or intensive care procedures. INTERVENTIONS: Mechanical or bag mask ventilation and antagonization with naloxone. MEASUREMENTS AND MAIN RESULTS: We observed chest wall rigidity in 8 patients after low dosage of fentanyl (3-5 microg/kg body weight). All patients presented with respiratory distress, hypercapnia, and hypoxemia leading to bradycardia. In two patients, laryngospasm was noted and associated with muscle rigidity, thus making intubation impossible. Naloxone (20-40 microg/kg body weight) reversed the laryngospasm and muscle rigidity immediately, allowing restitution within 1 min. In our patient population, we found fentanyl-induced chest wall rigidity in 4% of neonates after fentanyl administration. CONCLUSION: Even low doses of fentanyl can lead to thoracic rigidity in neonates. Additionally, we observed laryngospasm in two patients and speculate that it might be a variant of muscle rigidity.

Fentanyl↗
PubMed2005

Ziprasidone- and lithium-induced neuroleptic malignant syndrome.

OBJECTIVE: To report a case of ziprasidone- and lithium-induced neuroleptic malignant syndrome (NMS). CASE SUMMARY: A 47-year-old white male with a history of schizoaffective disorder was admitted to the hospital due to an exacerbation of severe mania. He had been taking lithium 450 mg twice daily and divalproex sodium 750 mg/day. On hospital day 2, ziprasidone 80 mg twice daily was added, and as-needed doses of intramuscular ziprasidone 20 mg and lorazepam 2 mg were used for agitation. On day 6, the patient developed hyperthermia (39.4 degrees C), elevated creatine kinase 26,000 units/L and white blood cell (WBC) count (20.7 x 10(3)/microL), myoglobinuria, hypotension (68/40 mm Hg), altered mental status, and tachypnea (28 breaths/min). This case is notable for the absence of muscle rigidity, which presents in greater than 90% of patients with NMS taking traditional antipsychotics. DISCUSSION: This case of ziprasidone- and lithium-induced NMS is of probable cause, as determined by the Naranjo probability scale. The patient presented with symptoms consistent with NMS 4 days after initiation of ziprasidone and lithium. The majority of NMS cases present with the core features of hyperthermia, muscle rigidity, and elevated CK levels. Other frequently seen symptoms include altered mental status, tachypnea, tachycardia, elevated WBC count, hypotension, diaphoresis, and myoglobinuria. Our patient presented with 2 of the core symptoms, but did not develop muscle rigidity at any time. NMS criteria include muscle rigidity as one of the major presenting symptoms. Recent literature suggests that perhaps NMS due to novel antipsychotics presents with less muscle rigidity than is seen with traditional agents due to their lower affinity for the dopamine D2 receptor. CONCLUSIONS: This case illustrates that NMS due to the novel antipsychotic ziprasidone may present with many of the core symptoms of the syndrome, but possibly less muscle rigidity than is seen with traditional agents.

Antipsychotic Agents↗
PubMed1994

Antiparkinsonian action of MK-801 on the reserpine-induced rigidity: a mechanomyographic analysis.

MK-801, a non-competitive antagonist of NMDA receptors, is known to exhibit a beneficial action in many animal models of Parkinson's disease. The aim of this study was to examine the influence of MK-801 on the reserpine-induced muscle rigidity. The rigidity was estimated by a direct mechanomyographic method. This method consists in successive bending and straightening of a rat's hind foot in the ankle joint and measuring the resistance of the foot to passive movements. Reserpine in doses of 5-10 mg/kg ip, given alone or in combination with alpha-methyl-p-tyrosine (alpha MT, 250 mg/kg ip), induced rigidity. The strongest muscle rigidity was induced by 10 mg/kg of reserpine 1 hour after administration. MK-801 (0.32-1.28 mg/kg sc) injected 70 min after reserpine (10 mg/kg ip) decreased the rigidity induced by the latter compound. Similarly, MK-801 (1.28 mg/kg sc), administered 27 h 40' after joint treatment with reserpine (10 mg/kg ip) and alpha MT (250 mg/kg ip), strongly inhibited the reserpine-induced muscle rigidity. The obtained results show that the glutamatergic hyperactivity plays a significant role in the reserpine-induced rigidity. As the reserpine-induced motor disturbances are commonly accepted to be an animal model of parkinsonian symptoms, it may be assumed that the NMDA receptor blocking component may contribute substantially to the therapeutic action of antiparkinsonian drugs.

Animals↗
PubMed2005

MTEP, a new selective antagonist of the metabotropic glutamate receptor subtype 5 (mGluR5), produces antiparkinsonian-like effects in rats.

The aim of the present study was to examine a potential antiparkinsonian-like action of 3-[(2-methyl-1,3-thiazol-4-yl)ethynyl]pyridine (MTEP), a new non-competitive antagonist of mGluR5, in the rat models. This compound has affinity for mGluR5 in a nanomolar concentration range and seems to be superior to the earlier known antagonists in terms of its specificity and bioavailability. Catalepsy and muscle rigidity induced by haloperidol administered at doses of 0.5 and 1 mg/kg were regarded as models of parkinsonian akinesia and muscle rigidity, respectively. MTEP at doses between 0.5 and 3 mg/kg i.p. decreased the haloperidol-induced muscle rigidity measured as an increased muscle resistance of the rat's hind leg in response to passive extension and flexion at the ankle joint. The strongest and the longest effect was observed after the dose of 1 mg/kg. MTEP (0.5-3 mg/kg i.p.) also reduced the haloperidol-induced increase in electromyographic (EMG) activity recorded in the gastrocnemius and tibialis anterior muscles. MTEP (3 and 5 mg/kg i.p.) inhibited the catalepsy induced by haloperidol. The present study confirms earlier suggestions that the antagonists of mGluR5 may possess antiparkinsonian properties. However, selective mGluR5 antagonists may be more effective in inhibiting parkinsonian muscle rigidity than parkinsonian akinesia.

Animals↗
PubMed2001

Blockade of the metabotropic glutamate receptor subtype 5 (mGluR5) produces antiparkinsonian-like effects in rats.

The aim of the present study was to examine a potential beneficial effect of the blockade of metabotropic glutamate receptor subtype 5 (mGluR5) by the selective non-competitive antagonist, 2-methyl-6-(phenylethynyl)pyridine (MPEP), in models of parkinsonian symptoms in rats. Haloperidol, 0.25, 0.5 and 1mg/kg ip, was used to induce hypolocomotion, catalepsy and muscle rigidity, respectively. The locomotor activity was estimated by an open-field test, the catalepsy -- by a 9-cm cork test. The muscle rigidity was measured as an increased resistance of a hind leg to passive extension and flexion at the ankle joint. Additionally, increases in the electromyographic activity were recorded in the gastrocnemius and tibialis anterior muscles. MPEP (1.0-10mg/kg ip) inhibited the muscle rigidity, electromyographic activity, hypolocomotion and catalepsy induced by haloperidol. MPEP administered alone (5mg/kg ip) did not induce catalepsy, nor did it influence the muscle tone or locomotor activity in rats. The present results suggest that blockade of mGluR5 receptors may be important to amelioration of both parkinsonian akinesia and muscle rigidity.

Animals↗
PubMed2006

A rare saccade velocity profile in Stiff-Person Syndrome with cerebellar degeneration.

Stiff-Person Syndrome (SPS) is an immune-mediated disorder of the central nervous system characterized by muscle rigidity, episodic muscle spasms, and high titers of antibodies against glutamic acid decarboxylase (GAD). The presence of cerebellar ataxia in SPS is extremely rare, but occurs. Clinical observations of ocular motor abnormalities have been noted in a few SPS patients. The purpose of this study is to provide a detailed quantitative documentation of ocular motor abnormalities in a patient with SPS and progressive cerebellar signs. Detailed clinical assessment of a woman with SPS and precise eye movement recordings using the magnetic search coil technique was performed. In addition to other ocular motor abnormalities that included longer latencies for saccades, downbeat nystagmus, and loss of downward smooth pursuit, a rare saccade velocity profile consisting of multi-component saccades was observed. We postulate that these ocular motor findings are related to impairment of GABAergic neurotransmission because antibodies to glutamic acid decarboxylase (GAD-Abs) have been implicated in the pathogenesis of both SPS and some cases of cerebellar ataxia. In addition, this unusual saccadic velocity profile may have important implications for modeling the saccadic system and furthering a complete understanding of saccade generation.

Cerebellum↗
PubMed2001

High-dose intravenous immune globulin for stiff-person syndrome.

BACKGROUND: Stiff-person syndrome is a disabling central nervous system disorder with no satisfactory treatment that is characterized by muscle rigidity, episodic muscle spasms, high titers of antibodies against glutamic acid decarboxylase (GAD65), and a frequent association with autoimmune disorders. Because stiff-person syndrome is most likely immune-mediated, we evaluated the efficacy of intravenous immune globulin. METHODS: We assigned 16 patients who had stiff-person syndrome and anti-GAD65 antibodies, in random order, to receive intravenous immune globulin or placebo for three months, followed by a one-month washout period and then by three months of therapy with the alternative agent. Efficacy was judged by improvements in scores on the distribution-of-stiffness index and heightened-sensitivity scale from base line (month 1) to the second and third month of each treatment phase. Direct and carryover effects of treatment were compared in the two groups. RESULTS: Among patients who received immune globulin first, stiffness scores decreased significantly (P=0.02) and heightened-sensitivity scores decreased substantially during immune globulin therapy but rebounded during placebo administration. In contrast, the scores in the group that received placebo first remained constant during placebo administration but dropped significantly during immune globulin therapy (P=0.01). When the data were analyzed for a direct and a first-order carryover effect, there was a significant difference in stiffness scores (P=0.01 and P<0.001, respectively) between the immune globulin and placebo groups, and immune globulin therapy had a significant direct treatment effect on sensitivity scores (P=0.03). Eleven patients who received immune globulin became able to walk more easily or without assistance, their frequency of falls decreased, and they were able to perform work-related or household tasks. The duration of the beneficial effects of immune globulin varied from six weeks to one year. Anti-GAD65 antibody titers declined after immune globulin therapy but not after placebo administration. CONCLUSIONS: Intravenous immune globulin is a well-tolerated and effective, albeit costly, therapy for patients with stiff-person syndrome and anti-GAD65 antibodies.

Adult↗
PubMed1950

Therapy of Parkinson's disease.

The most disabling form of Parkinsonism is that occurring after encephalitis. It may occur in persons of any age. The results of surgical treatment, which has been used for the most part only for seriously handicapped patients, have been discouraging in general, although in a few isolated circumstances operation has been of dramatic benefit.The solanaceous alkaloids-atropine, stramonium and hyoscine-either in pure forms or in mixed extracts or tinctures - are the best established drugs at present for the treatment of the postencephalitic forms of Parkinsonism. They have not proven too helpful for patients in the older age group with paralysis agitans. The antihistaminic compounds, particularly Benadryl,(R) have been a very valuable addition. They are of greatest value for patients in the older age group. The newer synthetic compounds, Artane(R) and Panparnit,(R) are also valuable additions. Amphetamine and the related and subsequently produced agents in this group are very helpful for patients showing undue fatigue and lethargy. Tolserol(R) is proving helpful, particularly for patients with painful spasms of rigid muscles.

Diphenhydramine↗
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↗
PubMed1992

Elucidation of dose-effect relationships for different opiate effects using alfentanil in the spontaneously ventilating rat.

In addition to producing antinociception and mild sedation, opiates diminish spontaneous movement and produce muscle rigidity. Examination of the relationship between different opiate effects may lead to a better understanding of the mechanism and sites of action of opiate anesthesia. Previous studies have compared the dose-effect relationships for morphine and fentanyl between antinociception and loss of righting reflex. However, neither muscle rigidity nor lack of spontaneous movement (as measured by catalepsy) has been fully examined or directly compared with either antinociception or loss of righting reflex. This study, therefore, compared five clinically relevant opiate endpoints (antinociception, muscle rigidity, catalepsy, loss of righting reflex, and respiratory depression) using the mu-selective agonist alfentanil in the spontaneously ventilating rat. Rats were randomized to receive alfentanil (0-500 micrograms/kg) subcutaneously. For muscle rigidity, 59 rats had electromyographic activity measured with percutaneous hindlimb electrodes. After alfentanil injection, electromyographic data were recorded for 60 min. For antinociception and catalepsy, 49 rats were studied for 120 min after alfentanil. Catalepsy was measured from the time the rat's forelimbs were placed on a 10-cm-high bar until either limb was removed. Antinociception was studied by measuring tail-flick response to hot (55 degrees C) water. For righting reflex, 40 rats were studied for 120 min. Alfentanil-induced respiratory depression was assessed in 40 rats with indwelling tail arterial catheters. Alfentanil was administered after baseline arterial blood gas measurements, and then additional samples were obtained for 45 min. For each effect, data were converted into quantal responses and were then transformed to probit-log dose-response curves for analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Alfentanil↗
PubMed1998

[A case report of steroid-responsive progressive encephalomyelitis with rigidity showing muscle stiffness limited to the upper body].

A 37-year-old female presented with progressive encephalomyelitis with rigidity for a period of about three months. Spasms began with several minutes of paroxysmal painful muscle stiffness in the left upper limb, followed by pain and muscle spasms in the upper limbs, shoulders, neck and back. The paroxysmal painful spasms were easily evoked by light touches and startling. The patient had contracture in the upper limbs and difficulty in relaxing the muscles. She also developed brain stem signs such as left sixth nerve palsy. The serum antinuclear antibody was positive (1 : 160). The cerebrospinal fluid examination revealed mild pleocytosis and protein elevation. Brainstem MRI, cervical MRI, and electroencephalography were normal. Surface electromyography in the arm and neck muscles showed continuous motor unit discharge elicited by passive movement of the right arm. Diazepam and baclofen were minimally beneficial. After treatment with intravenous injection of high-dose methylprednisolone and sequential oral prednisolone administration, the patient showed substantial improvement. This disorder may be part of a clinical spectrum that has an underlying autoimmune basis.

Administration, Oral↗
PubMed1991

Management of otolaryngic patients susceptible to malignant hyperthermia without dantrolene.

Malignant hyperthermia (MH) is an adverse reaction most frequently associated with the administration of halogenated inhalational anesthetic agents and the depolarizing muscle relaxant succinylcholine. Characteristic findings are a hypermetabolic state accompanied by extreme hyperpyrexia, acidosis, rhabdomyolysis, and generalized muscle rigidity, often involving the masseter muscles. Dantrolene sodium, which was approved in 1979 by the FDA for use in the prevention of MH in high-risk patients, has neurologic and gastrointestinal side effects. At the Children's National Medical Center (CNMC), 24 children identified as being at risk for the development of a MH reaction were anesthetized for otolaryngic procedures by using "non-triggering" anesthetics and without use of dantrolene sodium. These patients represent 56% of all patients at risk for MH or masseter muscle rigidity (MMR) reactions during an 8-year period at the CNMC. There were no complications. Concomitant muscle biopsies were performed, and caffeine/halothane contracture studies were completed in 18 of these patients, demonstrating 11 susceptible or equivocal responses. The data suggest that children undergoing common otolaryngic procedures who are at risk for development of MH may be safely anesthetized without the use of prophylactic dantrolene sodium.

Anesthesia↗
PubMedDate not supplied

NMDA receptors in the rostral and intermediate-caudal striatum play an opposite role in regulation of the muscle tone in rats.

The aim of the study was to assess the contribution of the NMDA receptors in the caudate-putamen to the regulation of the muscle tone. The experiment was carried out on male Wistar rats. The hind foot of a rat was flexed or extended at the ankle joint by 25 degrees and the resistance of the foot to passive movements was measured. Haloperidol (1 mg/kg ip) induced the muscle rigidity. The competitive antagonist of NMDA receptors, (+/-)-2-amino-5-phosphonopentanoic acid (AP-5), injected in doses of 2 and 5 micrograms/0.5 microliter bilaterally into rostral regions of the caudate-putamen, inhibited the muscle rigidity induced by haloperidol. In contrast, AP-5 injected bilaterally in the same doses into the intermediate-caudal region of the caudate-putamen in rats not pretreated with haloperidol, induced muscle rigidity. The present results seem to suggest that NMDA receptors localized in the rostral and intermediate-caudal regions of the caudate-putamen play an opposite role in regulation of the muscle tone in rats.

2-Amino-5-phosphonovalerate↗
PubMed1995

Botulinum toxin A for spasticity, muscle spasms, and rigidity.

We studied the effects of botulinum toxin A in 12 patients with spasticity and in eight patients with rigidity. The study design was a double-blind, placebo-controlled crossover trial with botulinum toxin A versus saline. Using the Ashworth Scale for spasticity and the Unified Parkinson's Disease Rating Scale for rigidity, we gave the patients a tone grade before and 2 weeks after treatment. Improvement in tone by two grades or more was considered clinically significant. In the spasticity group, botulinum toxin A reduced the tone of all patients significantly, improved functionality and nursing care in eight of 12 patients, and alleviated painful spasms in five of five patients. In the rigidity group, muscle tone was decreased in seven of eight patients, functionality improved in four of seven, and joint and muscle pain decreased in four of five. We conclude that botulinum toxin A is effective against the disabling effects of spasticity and rigidity. The treatment was well tolerated.

Adolescent↗
PubMed1986

Physical injuries, contractures and rigidity of skeletal muscle.

The authors condensed their knowledge of physical injuries of skeletal muscle, particularly injuries caused by mechanical energy, atmospheric pressure, radiation, extremes of temperature and electricity. The possible perils, outcomes and consequences are discussed. Special attention is given to the military medical projections.

Anterior Compartment Syndrome↗