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Results for “Muscle Rigidity”

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PubMed1979

Pathophysiological mechanisms in cerebral palsy.

To investigate some of the pathophysiological mechanisms in cerebral palsy, surface electromyograms (EMG) were recorded from pairs of flexor/extensor muscles during both voluntary and passive flexion/extension of upper and lower limbs of 20 patients. Elbow, knee, or ankle joint angles were measured simultaneously, as well as the force required to flex/extend the limbs passively at frequencies of 0.1--1.0 Hz. In addition, single motor units were recorded from the first dorsal interosseous muscles of six of the patients. Almost all patients showed resistance to passive movements (hypertonia). This hypertonia did not necessarily impair voluntary flexion/extension movements if alternating EMG activity was maintained in at least one of the pairs of flexor/extensor muscles involved in the movement. In six severly involved patients, there was a complete breakdown in the reciprocal relationship between reciprocally acting pairs of flexor/extensor motoneurones, which resulted in synchronous activation (co-contractions) of flexor/extensor muscles during both voluntary and passive movements. In these patients the hyperactive segmental reflex added to the disabling effects of co-contractions during voluntary movements. Single motor units recorded from patients with dystonic movements were recruited with variable delays (2--10 s) and usually discharged intermittently at high frequencies (60--120/s). This abnormla motor unit discharge pattern may relate to pathology of the basal ganglia.

Adolescent↗
PubMed1983

Syndromes of abnormal muscular activity: overlap between continuous muscle fibre activity and the stiff man syndrome.

Four patients with muscular pain, fasciculations, contractures or cramps are presented. Evidence of peripheral nerve involvement was revealed by electromyography and nerve conduction studies. Muscle biopsy showed mild signs of denervation and reinnervation and, at electron microscopy, dilatations of terminal cisternae were found. All patients showed a remarkable improvement after therapy with diphenylhydantoin or carbamazepine. These clinical, neurophysiological and morphological data underline the role of peripheral nerve pathology in various syndromes of abnormal continuous muscular activity.

Adult↗
PubMed1990

Observations on the reflex effects seen in Parkinson's disease on terminating a period of tendon vibration.

Vibration was applied to the tendon of flexor carpi radialis while recording the EMG of the wrist flexors in 29 Parkinsonian patients. Cessation of the vibration led to a small short-latency (approximately 25 ms) reduction in the level of activity which did not differ in magnitude from the normal. Moreover, there was no sign of any subsequent long-latency reduction of activity. Thus the maintained tonic activity of Parkinsonian muscles seems unlikely to be due to an enhancement of the tonic reflex actions of the Ia afferents, especially via the short-latency pathway. In addition, the findings argue against reduction of either Ia or Ib firing being responsible for the delayed excitatory "Westphal" (or "shortening") response that may occur in parkinsonism on allowing a muscle to shorten; this was never found on terminating vibration, even when present on muscle release.

Afferent Pathways↗
PubMed1991

The effect of posture on the normal and pathological auditory startle reflex.

The effect of posture on the EMG pattern of the normal auditory startle reflex was investigated. The startle response to an unexpected auditory tone was studied in eleven normal subjects when standing, and in six normal subjects when sitting relaxed or tonically plantar flexing both feet. Reflex EMG activity was recorded in the tibialis anterior and soleus about twice as frequently when standing, than when sitting relaxed. In addition, the median latencies to onset of reflex EMG activity in the tibialis anterior and soleus were about 40 and 60 ms shorter during standing, than when sitting relaxed. No short latency EMG activity was recorded in the calf muscles during tonic plantar flexion of the feet, while sitting. The effect of posture on the EMG pattern of the pathological auditory startle reflex was studied in five patients with hyperekplexia. In three patients the latency to onset of reflex EMG activity in the tibialis anterior was shorter when standing, than when sitting relaxed. The EMG pattern of the reflex response to sound was studied in detail in two of these patients and consisted of up to three successive components. The expression of each EMG component depended on the postural set of the limbs. In particular, a distinct short latency component was found in posturally important muscles following auditory stimulation. This short latency component was not recorded when sitting relaxed. It is concluded that the EMG pattern of the physiological and pathological auditory startle response is not fixed, but may change with the postural stance of the body. This finding supports the theory that the normal startle reflex and the abnormal startle reflex in hyperekplexia have a common brainstem origin.

Adolescent↗
PubMed1993

Stiff muscles.

Explore the source record for details and available documents.

Humans↗
PubMed1998

Continuous muscle fibre activity: a case treated with acetazolamide.

A case is reported of the continuous muscle fibre activity syndrome, which includes a group of disorders characterised by sustained motor unit activity due to hyperactivity of peripheral nerve motor axons. In this patient the muscle stiffness and myokymic movements were successfully treated with acetazolamide, which acts as a membrane stabiliser either by blockade of chloride and bicarbonate membrane transport or by producing kaliuresis and raising the transmembrane potential by decreasing extracellular potassium.

Acetazolamide↗
PubMed2000

Contribution of thixotropy, spasticity, and contracture to ankle stiffness after stroke.

OBJECTIVES: Increased resistance to stretch of muscles after stroke may be the result of centrally mediated neural factors such as spasticity or local, peripheral factors such as muscle contracture or thixotropy. The aim was to investigate evidence for an abnormal thixotropic response and compare this with two other factors-contracture and spasticity-which could potentially contribute to muscle stiffness after stroke. METHODS: Thirty patients with stroke whose calf muscles were assessed clinically as stiff and 10 neurologically normal subjects were recruited. To measure thixotropy, their calf muscles were stretched through two cycles after two prestretch conditions: one in which the muscles were maintained in a shortened position and one in which they were maintained in a lengthened position. Spasticity was defined as the presence of tonic stretch reflexes in relaxed muscles. Contracture was defined as being present when maximum passive ankle dorsiflexion fell at least 2 SD below the mean value of the control subjects. RESULTS: Both controls and patients with stroke exhibited a thixotropic response but this was no greater in the patients than the controls. About one third of the patients displayed muscle contracture and most exhibited spasticity. Contracture made a significant contribution (p=0.006) to the clinical measure of calf muscle stiffness while spasticity made a significant contribution (p=0.004) to the laboratory measure of calf muscle stiffness. CONCLUSIONS: Measuring thixotropy at the level of joint movement was sufficiently sensitive to determine the thixotropic response in both neurologically normal subjects and patients impaired after stroke. The thixotropic response was not higher than normal after stroke, suggesting that whereas thixotropy may produce enough immediate resistance to impede movement in those who are very weak, it is not a substantial contributor to long term muscle stiffness. Contracture did significantly contribute to muscle stiffness, supporting the importance of prevention of contracture after stroke. Spasticity contributed to muscle stiffness only when the limb was moved quickly.

Aged↗
PubMed1981

Evaluation of the anaesthetic properties of ketamine and a ketamine/xylazine/atropine combination in sheep.

The anaesthetic properties of ketamine in sheep were evaluated and compared with the results of a combination of ketamine/xylazine and ketamine/xylazine/atropine. Premedication of xylazine/atropine followed by intravenous injection of ketamine hydrochloride appeared to result in satisfactory immobilisation and anaesthesia for surgical operations of short duration. This combination effectively reduced some of the undesirable effects of ketamine, such as muscle rigidity, insufficient suppression of reflexes and tachycardia. The action on haematological factors was studied and significant increases in blood glucose content were detected during anaesthesia.

Anesthesia↗
PubMed2001

Parkinson's disease: clinical signs and symptoms, neural mechanisms, positron emission tomography, and therapeutic interventions.

Parkinson's disease is one of the most frequent neurodegenerative brain diseases. Its time course is slow and is characterized by progressive loss of dopaminergic and other brainstem neurons resulting in malfunctioning of the cerebral neuronal systems responsible for motor functions. The clinical signs are slowness of movement, muscle rigidity and rest-tremor amongst other features. The cause of the disease is unknown, but recently involvement of genetic factors is being researched. Positron emission tomography (PET) allows in vivo determination of striatal dopaminergic activity. This has increased our insight in the pathophysiology of the disease and permits direct study of disease progression at a biochemical level and equally to monitor whether potential neuroprotective interventions are indeed effective. Thus far no drug has emerged but promising substances are currently being studied.

Brain↗
PubMed1995

CT analysis of postoperative changes after thalamotomy for Parkinson's disease.

Stereotactic operations have long been used to relieve agitation and muscle rigidity in Parkinson disease. Because of its high-density resolution, CT is quite effective to portray the location, size, shape and density of the thermocoagulative focus. The foci were classified into different types according to their changes in different time periods. Correlation with pathological changes was discussed.

Adult↗
PubMed1997

Transplantation of autologous sympathetic ganglion into the brain with Parkinson's disease. Long-term follow-up of 35 cases.

Transplantation of autologous sympathetic ganglion was performed in 35 patients with Parkinson's disease. Approximately half the patients showed improvement of parkinsonian symptoms over the 3 years following transplantation. The patients showed amelioration of bradykinesia and gait disturbance, but tremor and muscle rigidity were not improved by transplantation. The other half of the patients did not show amelioration after transplantation. No serious complications were encountered, though mild ptosis was observed in all patients. The mechanism of improvement of symptoms might be the release of dopamine from the grafted sympathetic ganglion. Transplantation of autologous sympathetic ganglion can be a therapeutic modality for Parkinson's disease.

Adult↗
PubMedDate not supplied

Striatonigral degeneration combined with olivopontocerebellar atrophy with subcortical dementia and hallucinatory state.

We present an autopsied case of striatonigral degeneration (SND) combined with olivopontocerebellar atrophy (OPCA) with subcortical dementia and hallucinatory state. A Japanese woman without a remarkable family history showed hand tremor at the age of 35 years, followed by bradykinesia, muscle rigidity, orthostatic hypotension, neurogenic bladder and pyramidal signs. No obvious cerebellar symptoms were found. Various antiparkinsonian drugs were administered, but were not markedly effective for the parkinsonism. She developed a mild dementia characterized by mild memory disturbance with preservation of orientation, slowing of thought processes, emotional lability toward sadness, impaired ability to manipulate acquired knowledge and poor calculating, and by the absence of aphasia, apraxia and agnosia. The features in this patient were consistent with those seen in subcortical dementia. She also had auditory hallucinations. MRI revealed hypointense T2 signals in the putamina and substantia nigra. T1-weighted MRI demonstrated atrophy of both the pons and cerebellum in addition to atrophy of the putamina and substantia nigra. EEG showed slowing of background activity. She died of cardiac failure at the age of 47. Autopsy disclosed brain stem tegmental atrophy, SND, OPCA and many glial cytoplasmic inclusions in the central nervous system, but well-preserved cerebrum. We discuss the relationship between the psychiatric symptoms and pathologic findings of brain stem tegmentum.

Autopsy↗
PubMed1989

Clinical differentiation between lethal catatonia and neuroleptic malignant syndrome.

Lethal catatonia, a syndrome described several decades before the advent of neuroleptic drugs, has been regarded by many investigators as clinically similar to, and perhaps indistinguishable from, neuroleptic malignant syndrome. However, published case reports of the two syndromes indicate differences in mode of onset, signs and symptoms, and outcome. Lethal catatonia often begins with extreme psychotic excitement, which, if persistent, can lead to fever, exhaustion, and death. Neuroleptic malignant syndrome begins with severe extrapyramidally induced muscle rigidity. Because lethal catatonia often requires neuroleptic treatment and neuroleptic malignant syndrome necessitates immediate cessation of neuroleptics, their early clinical differentiation is important.

Acute Disease↗