Quantification of the electromyogram in neurospastic disorders

Levine, Irving; Jossmann, Paul B.; DeAngelis, Vincent; Kane, Madeleine

doi:10.1002/cpt196456part2893

Clin Pharma and Therapeutics

1964

DOI: 10.1002/cpt196456part2893

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Quantification of the electromyogram in neurospastic disorders

Irving Levine

Paul B. Jossmann

Vincent DeAngelis

et al.

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1967

1980

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Cited by 5 publications

(3 citation statements)

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“…Several methods have been described for assessing spasticity objectively. They have been based on measurement of the integrated electromyogram (EMG) during passive movement or induced spasm (Levine, Jossmann, De Angelis, and Kane, 1964;Leavitt and Beasley, 1964;Levine, Jossmann, Friend, De Angelis, and Kane, 1969) and measurement of the resistance to passive movement of the spastic limb (Leavitt and Beasley, 1964;Timberlake, 1964;Webster, 1964).…”

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confidence: 99%

A new agent for the control of spasticity

Jones

Burke

Marosszeky

et al. 1970

Journal of Neurology, Neurosurgery & Psychiatry

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SUMMARY In a preliminary controlled trial, CIBA 34,647-Ba, a gamma aminobutyric acid derivative, was found to be more effective than placebo in reducing spasticity due to spinal injuries. In an uncontrolled trial, 34,647-Ba also appeared more effective than diazepam. The intensity of spasticity was measured electromyographically by the amplitude of the stretch reflex at various velocities, and the results were correlated with those obtained by clinical assessment. 34,647-Ba was effective in both complete and incomplete spinal cord lesions and it is suggested that it has an action at the spinal level. No significant side-effects were encountered.There is no pharmacological agent in current use which will reliably suppress spasticity while preserving residual muscle power. Diazepam is probably the most useful but it is not always effective, and higher dosage may be precluded by the development of Preclinical studies in CIBA Laboratories have shown that this drug depresses monosynaptic and polysynaptic reflex transmission in both spinal and decerebrate preparations. Intravenous administration in the decerebrate animal decreases the firing rate of tonically active fusimotor fibres but has no effect on the discharge rate of de-efferented muscle spindles or on the neuromuscular junction.

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confidence: 99%

A new agent for the control of spasticity

Jones

Burke

Marosszeky

et al. 1970

Journal of Neurology, Neurosurgery & Psychiatry

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“…There are two traditional techniques for the measurement of muscle tone: (1) the monitoring of electromyographic activity (EMG), based on the principle that increased muscle contraction is associated with increased electrical activity under physiological conditions (Hoefer and Putnam, 1940;Levine et al, 1964), and (2) the measurement of the resistance of a passively moved limb, with or without EMG recording (Brumlic and Boshes, 1961;Webster, 1964;Nashold, 1966).…”

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confidence: 99%

Two methods of measuring muscle tone applied in patients with decerebrate rigidity.

Tsementzis¹,

Gillingham²,

Gordon³

et al. 1980

Journal of Neurology, Neurosurgery & Psychiatry

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SUM MARY Two methods were used to measure muscle tone in patients with decerebrate rigidity. In the first method forces of square waveform were applied and the calculated compliance of the joint was used as an index of rigidity. Oscillatory transients were seen at the same frequency as the physiological tremor. The range of normal variation in compliance was large and the values measured in the patients fluctuated markedly which limited the value of this index. In the second method, where forces of sinusoidal waveform were employed, the resonant frequency of the joint was measured and used as an index of rigidity. This index proved reliable and reproducible.

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“…Patients were divided into two groups-one group of 5 was brought directly into the Outpatient Clinic Polygraph Laboratory for testing, while the remaining 10 were tested at home by means of telephone telemetry (telemedography ). [4][5][6][7] Selection was based essentially on severity of illness, those with more advanced disease remaining at home.…”

mentioning

confidence: 99%

Effect of 5‐imino‐2,2,4,4‐tetrakis (trifluoromethyn imidazolidine (EXP 338) on spasticity: A quantitative evaluation

Levine

Jossmann

Friend

et al. 1968

Clin Pharma and Therapeutics

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In preclinical studies, 5-imino-2,2,4,4-tetrakis (trifluoromethyl) Departments of Neurological Research, Neuropsychiatric Examining Service, and Therapeutics, Veterans Adminiotration Outpatient ClinicThe structure of 5-imino-2,2.,4,4-tetrakis (triRuoromethyl) imidazolidine (EXP 338)" is shown in Fig. l,1 Preclinical studies revealed that this preparation is capable of reducing abnormal neural activity by its effect on polysynaptic reRex arcs and to a lesser degree upon monosynaptic circuits in experimental animals. No evidence of peripheral interference with neuromuscular transmission was found.8 Toxicology studies revealed no toxicity which would preclude clinical trial. Subsequently it was given to about 20 patients with neurologic diseases for 1 to 60 days without any apparent alterations in urine or blood. 2 Studies in mice with 14C-Iabeled drug indicated a half-life of 8 hours and that the drug was rapidly absorbed and uniformly distributed. 9 Adverse effects of drowsiness, disorientation, ataxia, and convulsions had followed single doses of 50 to 100 mg. of the test drug given orally.2Received for publication Dec. 19, 1967. Accepted for publication April 9, 1968. ·IND, DuPont, Wilmington. Del. 448A quantitative, non blind evaluation of oral EXP 338 was carried out on 15 pa-

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Quantification of the electromyogram in neurospastic disorders

Cited by 5 publications

References 0 publications

A new agent for the control of spasticity

A new agent for the control of spasticity

Two methods of measuring muscle tone applied in patients with decerebrate rigidity.

Effect of 5‐imino‐2,2,4,4‐tetrakis (trifluoromethyn imidazolidine (EXP 338) on spasticity: A quantitative evaluation

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