Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old man was admitted to the hospital with a 1,5-year history of progressive dementia, supranuclear ophthalmoplegia, pseudobulbar palsy, rigidity and dystonia in the neck and the upper trunk. Magnetic resonance imagings showed severe atrophy of the frontal lobe and the brainstem. He was diagnosed as having progressive supranuclear palsy (PSP). Rigidity, nuchal dystonia, frequent micturition, and profuse sweating ameliorated after trazodone administration. Furthermore, additional administration of L-dopa and droxidopa improved his pseudobulbar palsy, akinesia, and lack of initiative. Single photon emission tomography using IMP after medication showed increased IMP-uptake in the frontal areas and the basal ganglia compared with that before medication. This patient illustrates a substantial role of impairments in the serotonin system in the production of some PSP symptoms.
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PMID:[A case of progressive supranuclear palsy showing improvement of rigidity, nuchal dystonia and autonomic failure with trazodone]. 783 44

1. The effects of reversible and irreversible pharmacological manipulations of the neuronal activity in the subthalamic nucleus (STN) on parkinsonian motor signs and neuronal activity in the internal segment of the globus pallidus (GPi) were studied in African green monkeys rendered parkinsonian by treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. 2. Muscimol injections (< or = 1 microliter, 1 microgram/microliter) into STN reduced neuronal activity recorded at the injection site within minutes. This was immediately followed by reduced akinesia, tremor, and rigidity, as well as the emergence of dyskinesias in contralateral limbs. The motor effects were accompanied by generalized behavioral activation, lasted between 10 and 60 min, and were strongly dependent on the site of injection, with injections into the lateral "arm area" of STN first affecting contralateral arm movements and injections into the "leg" area affecting leg movements first. 3. Bicuculline injections (< or = 1 microliter, 1 microgram/microliter) into STN marginally increased the neuronal activity and induced neuronal discharge in bursts. Rigidity, akinesia, and tremor in the contralateral limbs were not changed. 4. Injections of ibotenic acid in two animals (2 and 7 microliters, 10 micrograms/microliters) resulted in 70 and 51% destruction of STN, respectively. Similarly to the muscimol injections, this resulted in a reduction of the neuronal activity, a reversal of parkinsonian motor signs, and the development of dyskinesias in the contralateral limbs. 5. Although tremor was significantly reduced after STN lesions, periodic oscillatory neuronal activity in GPi persisted. The strength of modulation of the neuronal oscillation was not significantly changed after STN lesion. 6. The percentage of cells in GPi exhibiting increases in discharge in response to torque application was significantly reduced after STN lesion. The magnitude and duration of the responses with increase in firing rate were reduced after STN lesioning. 7. These results support the hypothesis that abnormally increased tonic and phasic activity in STN leads to abnormal GPi activity and is a major factor in the development of parkinsonian motor signs. Furthermore they imply that cells in the basal ganglia have the intrinsic property of discharging in periodic bursts, which is unmasked under parkinsonian conditions.
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PMID:The primate subthalamic nucleus. III. Changes in motor behavior and neuronal activity in the internal pallidum induced by subthalamic inactivation in the MPTP model of parkinsonism. 798 16

Stereotactic thalamotomy of the VIM (ventral intermediate) nucleus is considered as the best neurosurgical treatment for Parkinsonian and essential tremors. However, this surgery, especially when bilateral, still presents a risk of recurrence and neurological complications. We observed that acute VIM stimulation at frequencies higher than 60 Hz during the mapping phase of the target suppressed the tremor of Parkinson's disease (PD) and essential tremor (ET). This effect was immediately reversible at the end of the stimulation. This was initially proposed as an additional treatment for patients already thalamotomized on the contralateral side, and then extended as a regular procedure for extra-pyramidal dyskinesias. Since January 1987, we implanted 126 thalami in 87 patients (61 PD, 13 ET, 13 dyskinesias of various origins). Deep brain stimulation electrodes were stereotactically implanted under local anaesthesia, using stimulation and micro-recording to delineate the best site of stimulation. Electrodes were subsequently connected to implantable programmable stimulators. The optimal frequency was around 130 to 185 Hz. The results (evaluated by a neurologist from 0 = no effect to 4 = perfect relief) are related to the type of tremor. Altogether, 71% of the 80 patients benefited from the procedure with grade 3 and 4 results. In 88% of the PD cases, the results were good (grade 3) or excellent (grade 4) and stable with time. Rigidity was moderately for a long improved but akinesia was not. The same level of improvement was observed in 68% of the ET patients and only in 18% of the other types of dyskinesias.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic VIM thalamic stimulation in Parkinson's disease, essential tremor and extra-pyramidal dyskinesias. 810 99

We report a 75-year-old man with parkinsonism who died suddenly. The patient was well until 64 years of the age when he had an onset of tremor in his left hand. He was treated with a medicine in another hospital, and his tremor subsided. Five years after the onset, he started to note difficulty in fine finger movements and gait disturbance. He tended to lean backward with frequent falls. He was treated with bromocriptine, trihexyphenydil, and L-dops without apparent improvement. He visited our out patient clinic on November 11, 1993 when he was 75 years of the age. Neurologic examination at that time revealed an alert and well oriented man in no acute distress. Higher cerebral functions were intact. In the cranial nerves, he showed restriction in the upward as well as down ward gaze (40% of normal). He showed masking of the face and spoke in small voice. He walked in a stooped posture with small steps; retropulsion was present. Muscle rigidity was moderately positive in the neck, however, no rigidity was noted in the limbs. No abnormal involuntary movements were seen. He showed moderate bradykinesia and difficulty in finger tapping. Muscle stretch reflexes were normally elicited and the plantar response was flexor bilaterally. Sensation was intact. The autonomic nervous system appeared intact. He was treated with 300 mg/day of Sinemet with marginal improvement in his balance. In February 4, 1994, he had a common cold. On the next day, his parkinsonism worsened and he became unable to walk by himself. He was found unconscious in the bathroom on the same day. He was brought to our hospital by an ambulance. Upon arrival, he was unresponsive and was not breathing. Blood pressure could not be measured. Pupils were dilated without reaction to light. Cardiac resuscitation was attempted, however, ventricular fibrillation appeared on an EEG monitor, and he was pronounced dead at eleven o'clock in the morning. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had progressive supranuclear palsy because of vertical gaze palsy, axial rigidity, and poor response to levodopa. Regarding the cause of his sudden death, the chief discussant thought that he developed pulmonary embolism. Postmortem examination revealed non-bacterial thrombotic endocarditis in the heart, but this did not appeared to be related to his sudden death. Multiple disseminated small emboli were found occluding small arteries of the left lung; this was consistent with acute pulmonary embolism, and this was thought to be the cause of his sudden death. In the central nervous system, marked atrophy of the globus pallidus was noted; both internal as well as external segments showed marked atrophy; no myelinated fibers were seen in the globus pallidus. Neuronal cell loss was marked in the globus pallidus, the subthalamic nucleus, and the substantia nigra. No Lewy bodies or tangles were seen. The histologic diagnosis was consistent with pallido-nigro-luysian atrophy. Brownish pigments such as seen in Hallervorden-Spatz disease were seen in the globus pallidus. In addition, formy spheroids were seen in the substantia nigra. However, iron deposits were not so strong as to suggest Hallervorden-Spatz disease. Pallido-nigro-luysian atrophy is a rare neurodegenerative disorder. It is interesting to note that this condition may mimic progressive supranuclear palsy or pure akinesia clinically.
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PMID:[A 75-year-old man with parkinsonism and sudden death]. 853 59

The neural mechanism of parkinsonian motor symptoms, i.e., rigidity, tremor and akinesia, which are the result of nigrostriatal dopamine deficiency, is interpreted from long-term observations on the effect of surgical and pharmacological treatment of the disease in relation to the neuropathological findings within the substantia nigra zona compacta (SNc). Rigidity, tremor and secondary akinesia start first with degeneration of the ventral tier of the SNc followed by spread of the pathology to the dorsal tier, which may produce primary akinesia. Later, locus ceruleus pathology will be added. Spread of pathology is extremely slow in the juvenile or early onset parkinsonism (JP) compared with that in Parkinson's disease (PD). This spreading of pathology from one functional system to another might be one of the key factors responsible for the progressive worsening of the disease, which is different in speed between JP and PD.
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PMID:The neural mechanisms and progressive nature of symptoms of Parkinson's disease--based on clinical, neurophysiological and morphological studies. 861 10

Recent neuropathological findings define that 10-20% of the Parkinson patients belong to the atypical Parkinson's syndrome due to multi-system disease marked by typical Parkinsonian symptoms such as rigor, tremor and akinesia and early onset of severe autonomic, cerebellar or pyramidal disorders. Symptoms like postural hypotension, dysphagia, hypersalivation, urinary bladder dysfunction, thermodysregulation, abnormalities in eye movement, early falls or dementia etc. are frequently seen in these patients. In these patients dopamin depletion in the nigrostriatal pathway is combined with degeneration of other cerebral structures like olivopontocerebellar and intermediolateral columns. Patients need high dosages of L-dopa and other antiparkinsonian drugs with poor prognosis in general. First, we report on an atypical Parkinson patient who developed acute dyspnoea and muscle rigidity after general anaesthesia; second, on another patient who took a long time to recover from general anaesthesia. Both responded to antiparkinsonian drugs, the first to orally applied L-dopa, the second to intravenous amantadine. Most probably the interruption of the treatment with high dosages of L-dopa (in these patients given in 2-4 hours intervals) had caused these complications. The special nature of the anaesthesiological management of atypical Parkinson patients is reviewed.
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PMID:[Perioperative management of the patient with atypical Parkinson disease]. 886 35

Parkinson's disease, a chronic incurable disorder, has a significant impact on quality of life. Parkinson's disease results from chronic degeneration of cells in the basal ganglia that produce dopamine. It typically affects elderly individuals producing muscle rigidity and akinesia. Traditionally, Parkinson's disease has been controlled by medications. However, for some patients, medications may no longer be effective, or may produce drug-related complications. For this group of patients, pallidotomy is gaining support as an intervention to control the debilitating symptoms of Parkinson's disease, thus enabling a person to perform everyday tasks. Although the procedure was developed in the 1950s, contemporary technology has allowed a resurgence of the intervention. With the focus on relief of two of the major symptoms of Parkinson's disease, the pallidotomy procedure is gaining support as a surgical intervention for this disease. Therefore, it is important for the health care team to have an understanding of the disease process, surgical intervention and postoperative care to enhance quality outcomes for this patient population.
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PMID:Pallidotomy: a surgical intervention for control of Parkinson's disease. 888 May 95

Rigidity, tremor, akinesia and disorder of postural reflex are the main clinical features of Parkinson's disease. We presented the mechanism underlying rigidity and assessed central motor conduction time (CMCT) using magnetic, with or without vibratory, stimulations. Basal ganglia, especially, the internal pallidum, and the thalamus play major roles in the mechanism of rigidity in Parkinson's disease. Hyperexcitability of the spinal motor nucleus due to low threshold has been recognized. Magnetic stimulation is painless and is simpler than electric stimulation. Therefore, this method is used clinically for evaluating conduction disturbance of the upper motor neurons in multiple sclerosis, cerebrovascular disease and so on. CMCT measured by magnetic and/or electric stimulation may be abbreviated or normal in Parkinson's disease, according to the literature, though controversy persists in this regard. In our study, CMCT was normal in Parkinson patients. However, CMCT was reduced in patients with rigidity and tremor. Furthermore, in a portion of the patients, CMCT was further abbreviated by also applying vibratory stimulation. These observations support the hypothesis that cells in the thalamus, cortex and spinal cord and/or pathways in these portions of the central nervous system are excitable or activated in Parkinson patients with rigidity and tremor. However, elucidation of the mechanisms underlying rigidity and tremor awaits further investigation.
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PMID:[Central motor conduction time using magnetic and vibratory stimulation in Parkinson's disease, especially in patients with rigidity]. 901 45

An autopsy case of pure akinesia (PA) is reported. The patient manifested L-dopa-unresponsive akinesia without accompanying rigidity, tremor, eye movement disorder or dementia from the age of 58 years. Brain magnetic resonance T2-weighted imaging at the age of 63 showed high intensity areas in the subthalamic regions, but brain atrophy was not observed. She received amantadine-HCl and L-threo-3,4-dihydroxyphenylserine (L-DOPS) for 5 years. At the age of 66, she died of the severe illness accompanied by consciousness disturbances, hyperthermia, muscle rigidity, abnormal blood pressure and elevated serum enzymes which were derived from the muscle. We considered her condition to be neuroleptic malignant syndrome (NMS). Pathologically the brain revealed degeneration in the subthalamic nucleus, globus pallidus and substantia nigra. Neurofibrillary tangles were detected in the temporal cortex, hippocampus, amygdaloid body and spinal cord, as well as in the basal ganglia, thalamus and brain stem. These findings were consistent with that of progressive supranuclear palsy (PSP); the change in the ventral pons was insignificant, suggesting that PA may have minimum involvement in the ventral pons. The skeletal muscle showed scattered necrosis that was compatible with NMS. As far as we know, this is the first report of NMS accompanied with PA.
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PMID:Pure akinesia manifested neuroleptic malignant syndrome: a clinical variant of progressive supranuclear palsy. 908 64

Posteroventral pallidotomy (PVP) has been shown to alleviate motor symptoms in Parkinson's disease (PD), e.g., rigidity, secondary akinesia due to existence of muscle rigidity and slight tremor, but not the marked tremor. For the latter, additional lesion of the ventral intermediate nucleus of the thalamus is necessary. Akinesia was divided into three subtypes, and the influence of PVP on each type is described. Primary akinesia is not changed by either PVP or thalamotomy but responds well to L-dopa. Psychological symptoms, i.e., depressive mood, loss of initiation or abulia, and lowered emotional activity, which are generally termed as bradyphrenia, benefit well from PVP but less from thalamotomy. This effect is interpreted as due to the lesion extending into the ventral pallidum, where a small posterior part of the limbic-motor projections may possibly be involved. Such experience suggests that the third type of akinesia in PD, named the 'psychomotor or limbic-motor type' by the author, can be improved by the surgical procedure on the ventral globus pallidus. These observations offer an important chance to understand the psychological symptoms in PD as a result of dopamine deficiency of ventral tegmental area neurons projecting to the ventral striatum, which further influences the ventral pallidum.
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PMID:Pallidotomy revisited. Analysis of posteroventral pallidotomy. 971 34


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