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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parkinson's disease (PD) is a chronic progressive neurological disorder characterized by tremor, muscle rigidity, slowness of movement (bradykinesia), and gait instability. In early disease, PD is well managed in an office setting, however, as the disease progresses, a variety of syndromes may result in emergency department visits. The scenarios most likely to require an emergent evaluation are severe motor "off" periods with immobility, involuntary movements (dyskinesia), psychosis, acute confusion, panic disorder, and pain. Other less frequent presentations are also discussed. This article uses illustrative cases to provide a framework to discuss emergency department diagnosis and management issues in caring for these patients.
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PMID:Emergency department presentations of patients with Parkinson's disease. 1075 Sep 35

Parkinson's disease is a neurodegenerative disorder that manifests clinically with variable degrees of tremor, muscle rigidity, bradykinesia and postural instability. Tremor-predominant Parkinson's disease is characterised by prominent tremor of one or more limbs with a relative lack of significant rigidity and bradykinesia. Despite the lack of other disabling motor symptoms, the tremor of tremor-predominant Parkinson's disease can be very disabling, especially if a postural and kinetic component exists. A wide variety of treatments for Parkinson's disease tremor are currently available and include use of oral medications, injections with botulinum toxin and neurosurgical procedures. Some of the first line medications (levodopa, dopamine agonists, anticholinergics) are very effective in controlling tremor. However, some patients with Parkinson's disease tremors are unresponsive to first line drugs and treatment with second line medications (clozapine, amantadine, clonazepam, propranolol, neurontin) should be attempted. In the small number of patients with disabling tremor that is refractory to all medications, neurosurgical intervention should be considered. Both thermocoagulation and deep brain stimulation at several different neuroanatomical sites (thalamus, globus pallidus, subthalamic nucleus) offer good to excellent tremor control with relatively low risk to the patient.
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PMID:Tremor-predominant Parkinson's disease. Approaches to treatment. 1087 22

We describe an autopsy case of parkinsonism with bradykinesia, muscle rigidity, and dementia as major symptoms. The patient had developed bradykinesia at the age of 62, and then muscle rigidity, a parkinsonian posture, bradylalia, and dementia gradually appeared. Neurological examination revealed rigidity in the neck and limbs, with motion and speech being generally slow. He lacked involuntary movements including alien hand, tremor, chorea, and dystonia. Vertical gaze palsy, both upward and downward was noted, but other cranial nerves were intact. He was diagnosed as suffering from PSP clinically based on vertical gaze palsy, bradykinesia, instability on standing and gait, and dementia. Levodopa was only transiently effective. Within three years he became bed-ridden and in a state of akinetic mutism. At age 65 he died from pneumonia. Neuropathology revealed severe neuronal degeneration and gliosis in the substantia nigra. Because atrophy of the tegmentum of brainstem, dentate nuclei, inferior olivary nuclei was very mild and Alzheimer neurofibrillary tangles in the brainstem were relatively few, PSP was ruled out. Cortical neuronal degeneration was not apparent, but in the deep layer of cingulate gyrus, frontal lobe, and insula, there were several ballooned neurons. Gallyas-Braak silver staining showed no tuft-shaped astrocytes, specific for PSP, but it disclosed astrocytic plaques in the basal ganglia and the cerebral cortex. At present, astrocytic plaques are recognized as a hallmark of corticobasal degeneration (CBD), along with ballooned neurons in the cerebral cortex. The present case thus illustrates that CBD has a wide spectrum and may include cases in which degeneration of cerebral cortex is very mild.
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PMID:[An autopsy case of corticobasal degeneration without prominent cortical pathology--an imitator of progressive supranuclear palsy]. 1096 56

This open-label clinical study was conducted for patients with schizophrenia in order to investigate the efficacy, safety and optimal dose of olanzapine. One hundred and fifty-six of the 159 enrolled patients were included in the analysis set. For the primary efficacy measure, the Final Global Improvement Rating (FGIR) score, 15.4% of patients had remarkable improvement, 58.3% of patients had moderate improvement or more, 79.5% of patients had slight improvement or more, and 10.3% of patients had increase in disease symptomatology (worsening). Results from the Brief Psychiatric Rating Scale (BPRS) in all individual items were improved from baseline. Olanzapine was effective not only against positive psychotic symptoms but also against negative symptoms. This was consistent with results from the Positive and Negative Syndrome Scale (PANSS). For the majority of patients, a dose range of 7.5-10.0mg/day, as a lower bound on the minimally effective dose, was suggested by the results of the dose to first response based on improvement in Global Improvement Rating (GIR) analyses. The ratio of olanzapine dose to equivalent haloperidol dose was estimated at 1.2 :1. The most commonly reported treatment-emergent signs and symptoms (TESS) occurring at a frequency of 10% or more were insomnia, weight increase, excitement, sleepiness, anxiety, malaise and dull headaches. There was a low incidence of extrapyramidal treatment-emergent signs and symptoms; the most commonly reported were akathisia (6.4%), tremor (5.8%) and muscle rigidity (2.6%).
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PMID:Olanzapine optimal dose: results of an open-label multicenter study in schizophrenic patients. Olanzapine Late-Phase II Study Group. 1099 65

Pathophysiological mechanisms of major symptoms of Parkinson's disease are discussed from experiences of stereotaxic surgery. Tremor completely disappears by a lesion in the ventral intermediate nucleus(Vim) which receives proprioceptive sense from the periphery. Rigidity is alleviated by a lesion in the globus pallidus(GP) and the ventral lateral nucleus(VL) equally. Since GP projects to the prefrontal motor cortex via VL, surgery to either of those structures causes the same result. Akinesia is classified into three types: secondary akinesia, primary akinesia, and akinesia due to psychomotor dysfunction. Gradual spread of neuronal degeneration within the substantia nigra pars compacta may explain the progression of akinesia. Psychological or psychiatric disorder becomes major symptom in the late stage. Posteroventral pallidotomy may change emotional state in some cases by influencing the limbic motor circuit.
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PMID:[Clinical pathophysiology of parkinsonian symptoms: from experiences of stereotaxic surgery]. 1106 35

Pallidotomy has recently regained acceptance as an effective treatment for Parkinson's disease. From our 50 cases of unilateral pallidotomy and 10 cases of staged bilateral pallidotomy, details and indications of the procedure is described. The unilateral pallidotomy is quite effective for L-dopa induced dyskinesia, which usually completely disappears soon after the operation. The effect is long-lasting. When on-off phenomenon exists, unilateral pallidotomy improves off-stage rigidity or akinesia. Symptoms during on-stage are not changed. Indications of pallidotomy is that(1) L-dopa induced dyskinesia, and(2) on-off phenomenon. Bilateral pallidotomy, even by staged one, causes severe drooling, or speech disturbance(the volume of the voice decreases and the articulation worsens), and is not recommended. Vim thalamotomy is, on the other hand, the established treatment for tremor of Parkinson's disease or of essential tremor. The effect is long-lasting. Rigidity or akinesia is not expected to be improved so much.
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PMID:[Details and indications of pallidotomy and thalamotomy for Parkinson's disease]. 1106 49

Tremor is the most common initial symptom and one of the cardinal features of Parkinson's disease. Mild tremor causes only minimal disability, but severe tremor causes more significant disability and distress for the patient than rigidity and/or bradykinesia. Anticholinergic agents, levodopa/DCI and dopamine agonists are most common and beneficial in parkinsonian tremor, but efficacies of these medications are variable among patients. Rigidity and bradykinesia are more responsive to levodopa/DCI therapy than tremor. Clozapine is an atypical neuroleptic agent, not on the market in Japan, and has been reported to decrease or ameliorate parkinsonian tremor through the studies of open label and double blind crossover as a new drug for parkinsonian tremor.
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PMID:[Pharmacological treatment of parkinsonian tremor]. 1106 52

GAIT ARRESTS: They affect the evolution of the disease. This freezing phenomenon which induces falls sometimes constitutes an initial sign. Like the gait initiation failure, freezing can be controlled by sensory stimulation, notably visual inputs, but also by more sustained attention. FALLS ARE MAINLY CONNECTED WITH BOTH POSTURAL INSTABILITY AND RIGIDITY: They are poorly influenced by dopaminergic therapies. The progressive decrease of step width represents a main factor in their occurrence. PRECOCITY OF GAIT DISORDERS IS UNUSUAL IN PARKINSON'S DISEASE: Other parkinsonian syndromes such as progressive supranuclear palsy, multiple system atrophy and vascular parkinsonian syndrome must then be evoked. Their association with a cognitive impairment and abnormal sphincter behaviour infers a diagnosis of normal pressure hydrocephalus. GAIT IMPROVES WITH L-DOPA THERAPY: Speed, step length and duration of the swing phase are increased without change of cadence. Progressive loss of L-dopa efficiency on gait and postural stability contrasts with the persistent effect on tremor, rigidity and bradykinesia; a functional abnormality of nondopaminergic systems can explain these symptoms. In the following stages, gait troubles increased by motor fluctuations and abnormal involuntary movements are less controlled by L-dopa therapy. PHYSICAL THERAPY PLAYS A MAJOR ROLE IN THERAPEUTIC MANAGEMENT: An individual or collective rehabilitation project must be established according to the stage of evolution; the exercises aim to protect postural control and coordination. Visual or sound rhythmic inputs can be employed in the case of gait initiation failure. THE EFFECTS OF FUNCTIONAL NEUROSURGERY ARE IN THE COURSE OF EVALUATION: Thermolesion and chronic electrical stimulation of deep brain structures have opposite effects on gait troubles. Bilateral thalamotomy or pallidotomy are sometimes a source of disequilibrium. Chronic thalamic stimulation does not induce either benefits or adverse effects. On the other hand, stimulation of the internal pallidum improves gait kinematic parameters; improved postural adjustments have also been reported. The effect of subthalamic nucleus stimulation is comparable to that of L-dopa, however the long-term effect remains to be evaluated.
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PMID:[Gait disorders in Parkinson disease. Gait freezing and falls: therapeutic management]. 1128 86

We report a 56-year-old woman with progressive gait disturbance. Her mother had Parkinson's disease with onset at age 70. She died at age 74 and the post-mortem examination confirmed the diagnosis of Lewy body positive Parkinson's disease. The patient was well until the age of 50(1995) when she noted an onset of resting tremor and difficulty of gait. She also developed delusional ideation and was admitted to a psychiatric service of another hospital, where a major tranquilizer was given. The delusion disappeared but she developed marked rigidity. The major tranquilizer was discontinued and an anticholinergic and amantadine HCl were given. She showed marked improvement to Hoehn and Yahr stage II and was discharged. In 1995, when she was 52 years of the age, she developed delusion again and a major tranquilizer was given. She developed marked parkinsonism again and became Hoehn and Yahr stage V. The major tranquilizer was discontinued and she was treated with levodopa/carbidopa, trihexyphenidyl, bromocriptine, and dops. She improved remarkably to stage II. She was admitted to our service on October 8, 1996 for drug adjustment. She was alert and not demented. She was anxious but delusion or hallucination was noted. Higher cerebral functions were intact. Cranial nerve functions were also intact except for masked face and small voice. Her posture was stooped and steps were small. She showed retropulsion and moderate bradykinesia. Resting tremor was noted in her left hand. Rigidity was noted in both legs. No cerebellar ataxia or weakness was noted. Deep tendon reflexes were within normal range and sensation was intact. Her cranial MRI revealed some atrophic changes in the putamen, in which a T 2-high signal linear lesion was seen along the lateral border of the putamen bilaterally. In addition, posterior part of the putamen showed T 2-low signal intensity change. She was treated with 1.6 mg of talipexole, 6 mg of trihexyphenidyl, and 100 mg of L-dops. She was in stage III of Hoehn and Yahr. She developed neurogenic bladder with a large amount of residual urine for which she required catheterization. She was transferred to another hospital. Despite drug adjustment, she lost response to levodopa and her parkinsonism deteriorated gradually. She also developed syncope orthostatic hypotension. In April of 1998, she developed intracerebral hemorrhage and was admitted again on April 19, 1998. She was unable to stand and showed marked akinesia and rigidity. She was in stage V of Hoehn and Yahr. Her cranial CT scan revealed bilateral high-density lesions in the posterior parietal lobes. She developed dysphagia for which she required gastrostomy. She was transferred to another hospital but her clinical condition deteriorated further. On December 22, 1999, she developed fever and dyspnea and was admitted to our service again. She developed cardial arrest at the emergency room from hypoxia. She was resuscitated; however, she was comatose with loss of brain stem reflexes. Later on she developed generalized myoclonus. She developed cardiac arrest and pronounced dead on December 28, 1999. The patient was discussed in a neurological CPC. The chief discussant arrived at the conclusion that the patient had striatonigral degeneration because of poor response to levodopa in the later course, autonomic failures, and MRI changes. Some other participants thought that the patient had a form of familial Parkinson's disease. Opinions were divided into these two possibilities. Post-mortem examination revealed that the substantia nigra showed intense neuronal loss and gliosis, however, no Lewy bodies were seen. In addition, intracytoplasmic inclusions were seen in oligodendrocytes. The putamen was markedly atrophic in its posterior part with marked gliosis and neuronal loss. The ventromedial part of the pontine nucleus also showed neuronal loss and intracytoplasmic glial inclusions. Pathologic diagnosis was multiple system atrophy. In the parietal lobe, an arteriovenous malformation with bleeding was noted. This is very unique case. Although her mother had Lewy body-positive Parkinson's disease, the patient had Lewy body-negative multiple system atrophy with a-synuclein-positive glial inclusions. Whether this is just a coincidental occurrence or the presence of a genetic load for Parkinson's disease might triggered her multiple system atrophy is an interesting question to be answered in future.
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PMID:[A-56-year-old woman with parkinsonism, whose mother had Parkinson's disease]. 1142 77

This first clinical study of olanzapine in Japanese patients with schizophrenia was conducted to investigate the efficacy and safety of olanzapine. Eighty-one patients were included in the analysis set. Mean modal dose for those patients were 9.4 +/- 3.6 mg/day. For the primary efficacy measure (Final Global Improvement Rating score), 14.8% of patients had remarkable improvement, 59.3% of patients had moderate improvement or better, and 86.4% of patients had slight improvement or better. Results from the Brief Psychiatric Rating Scale showed improvement from baseline in all clusters including positive psychotic symptoms (thought disturbance) but also against negative symptoms (anergia). The most commonly reported treatment-emergent signs and symptoms with > or =10% incidence, were insomnia, weight increase, excitement, sleepiness, and anxiety. There was a low incidence of extrapyramidal treatment-emergent signs and symptoms, and events reported were tremor (6.2%), muscle rigidity (3.7%), and akathisia (2.5%). The most commonly reported treatment-emergent laboratory changes, with > or = 20% of incidence, were prolactin elevations (24.3%) followed by increases in triglycerides (20.4%). However, mean prolactin values tended to be normalized during the study. This study result suggests that olanzapine is an "atypical" antipsychotic.
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PMID:Efficacy and safety of olanzapine, an atypical antipsychotic, in patients with schizophrenia: results of an open-label multicenter study in Japan. 1144 86


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