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PubMedDate not supplied

[Effect of trihexphenidyl on the excitability of alpha motor neurons of the foot plantar flexor in chemically induced parkinsoniam rigidity].

For assessment of the effect of trihexiphenidil on the excitability state of the alpha-motoneurons of the plantar flexor of the foot in patients with drug-induced parkinsonian rigidity curves of the excitability of motoneurons of the soleus muscle were plotted in two variants of experiments: I. with afferent stimulation of the Ia fibres of the soleus muscle as the conditioning and testing stimulus (tibial nerve in the popliteal fossa), II. with afferent stimulation of Ia fibres of the anterior tibial muscle (peroneal nerve behind the fibular capitulum) used as the conditioning stimulus and stimulation of the tibial nerve as the testing stimulus. These investigations were carried out on 12 psychiatric patients who received no drugs at the time of these investigations (control group), 13 similar patients treated with chlorpromazine, 12 treated with phenothiazine compounds with piperazine ring in the side chain. The investigations were repeated 30-50 min. after oral administration of trihexiphenidil 5 mg. In variant I typical excitability curves were obtained and 5 phases could be discerned in them. In patients treated with piperazine-containing phenothiazine derivatives inducting more significant parkinsonian effects phase III - depression - was significantly shortened, and the excitability was raised in phase IV. In variant II phases III and IV were reversed and in phase IV a rise in excitability was observed in place of depression. In variant II in the group of drug-induced parkinsonism as compared with controls the rise in exictability was greater in phase III and depression in phase IV was smaller. The effect of trihexiphenidil in variant I depended on the initial state. In controls and in patients treated with chlorpromazine trihexiphenidil reduced the duration of phase III of depression and decreased its intensity. In atients treated with phenothiazines containing the piperazine ring depression in phase III was weak but increased after trihexiphenidil administration and increased excitability in phase IV was decreased. The curves became similar to those obtained in controls. In variant II in the control group excitability in phase III increased after trihexiphenidil administration.

Administration, Oral↗
PubMed1983

Motor neuron rigidity. An electrophysiological, pharmacological and pathological study.

A 28-year-old male with generalized muscle stiffness and widespread muscle twitching is described. Continuous electrical activity was present at rest and could be abolished only by succinylcholine, curare, and block of the distal part of the peripheral nerve. Muscle biopsy revealed mild myopathic changes. In addition glycogen depletion was found in muscle fibres which were type IIb in one region of the biopsy and type I in another. With carbamazepine treatment marked improvement occurred both clinically and electromyographically. It is concluded that the abnormal electrical activity originated in the terminal branches of the peripheral motor nerve and that this activity was confined to muscle fibres belonging to single motor unit territories.

Adult↗
PubMed1980

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

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 flucuated 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.

Adolescent↗
PubMed1996

[A case of progressive continuous muscular rigidity and painless and rhythmic muscle spasm associated with autoantibody against glutamic acid decarboxylase].

We described a 60-year-old man with 5-year history of insulin dependent diabetes mellitus who developed continuous rigidity of truncal muscle and painless, rhythmic muscular spasm of trunk and proximal lower and upper extremities. The rigidity continued even in sleep. The painless muscle spasm was often precipitated by volitional movement and emotional stimuli. Intravenous administration of diazepam strongly attenuated the muscle spasm as well as truncal rigidity. Surface electromyography showed the continuous contraction of abdominal and paraspinal muscles. The rhythmic, clonic spasm of shoulder, triceps brachii, intercostal, abdominal, paraspinal and quadriceps femoris muscle induced by voluntary neck flexion was not compatible with typical stiff-man syndrome. Antibody against glutamic acid decarboxylase (GAD) was detected in the serum and cerebrospinal fluid of this patient. His condition was getting well with oral intake of sodium valproate. While painless, rhythmic spasm and persistent rigidity during sleep ruled out the patient from typical stiff-man syndrome, he was supposed to have the same pathophysiological mechanism as the anti-GAD autoantibody positive stiff-man syndrome.

Analgesia↗
PubMed1986

The rigid spine syndrome.

Four patients are reported, 3 females and 1 male, with (as a prominent symptom of muscle disease) limitation of flexion of cervical and dorsolumbar spine. The nosological classification of these cases is discussed. In two patients there was evidence of an inclusion body myositis. At necropsy one of these patients had a remarkable distribution of muscle changes.

Adolescent↗
PubMed1979

The effect of decerebrate rigidity on the intracranial pressure: an experimental study.

The mechanical effect of acute decerebrate rigidity upon the ICP and the mechanisms underlying the relationship between them have been investigated with experiments performed on 26 cats. It has been shown that: a) Extreme rigidity of the peripheral musculature with or without partial activation of the trunkal muscles produces no change in ICP, b) the simultaneous elevation of the intra-thoracic and intra-abdominal pressures is the factor primarily operative in raising and maintaining the elevated ICP, c) when cerebrovascular homeostasis is already defective a subsidiary but not unimportant role is played by the elevation of the systemic arterial pressure, d) under conditions of normal brain elastance mild and short-lasting spasms produce no effect on the ICP. In an animal, however, in which the brain elastance had been increased by inflating a small air-filled balloon, similar spasms produced a marked increase in ICP.

Animals↗
PubMed1989

Rigid spine syndrome and rigid spine sign in myopathies.

We studied eight patients with rigid spine syndrome aged 8 to 20 years at the time of first examination. Muscle weakness, rigid spine, and flexion contracture of elbows and ankles were noted in the first 6 years of age. Radiological study of the cervical spine revealed considerable reduction not only of flexion, but also of extension, of the neck. The "alligator sign" was demonstrated. Progression of scoliosis and of contractures reduced the functional capacity in six patients. A restrictive ventilatory syndrome was observed in all, while central apneas with oxygen desaturation were shown in two. Cardiac arrhythmias were observed in four. We suggest that a distinction should be made between myopathic rigid spine and rigid spine syndrome. Myopathic rigid spine is a clinical sign which is rarely sought but is present in several types of well-defined myopathies, meaning the myopathic involvement of the extensor muscles of the spine. Rigid spine syndrome is an axial myopathy with peculiar clinical and radiographic signs and a characteristic natural history.

Adolescent↗
PubMed1998

Rigid spine syndrome. Case report.

We describe a patient who had difficulty in walking since toddling stage and presented proximal upper and lower member weakness which have evolved to a progressive limitation of neck and trunk flexure, compatible with rigid spine syndrome. The serum muscle enzymes were somewhat elevated and the electromyography showed a myopatic change. The muscle biopsy demonstrated an active and chronic myopathy. The DNA analysis through PCR did not display any abnormality for dystrophin gene. The dystrophin by immunofluorescence was present in all fibers, but some interruptions were found in the plasma membrane giving it the appearance of a rosary. The test for merosin was normal.

Child↗
PubMed1999

Abnormalities of elastin and elastic fibers in infantile hypertrophic pyloric stenosis.

Infantile hypertrophic pyloric stenosis (IHPS) is characterized by hypertrophy of the pyloric muscle, causing pyloric-channel narrowing and elongation. The rigidity of the muscle is increased, which is characterized as an "olive." Elastin is an insoluble protein that forms the major structural component of the elastic fibers and maintains the tensile strength of the tissues. To understand the possible histologic and molecular basis of the elasticity of the hypertrophic muscle in IHPS, we determined the distribution of the elastic fibers and elastin expression using Victoria blue van Gieson (VVG) staining and immunohistochemistry. In IHPS, the number of elastic fibers in the connective tissue was significantly increased in the thickened connective-tissue septa (CTS) compared with normal control specimens. In normal pyloric muscle, weak to moderate elastin immunoreactivity was observed in the CTS while no immunoreactivity was observed among the muscle fibers. In IHPS, strong immunoreactivity of elastin was observed in the CTS and moderate immunoreactivity among the hypertrophic smooth-muscle fibers. Our findings suggest that the increase on elastic fibers and elastin expression in the pyloric muscle in IHPS may play an important role in the development of pyloric-muscle rigidity, causing pyloric-canal obstruction.

Elasticity↗