Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 62-year-old woman developed neurologic deficits 7 months after pulmonary lobectomy for alveolar cell carcinoma of the lung. CT scan of the head demonstrated two metastases with marked peritumoral edema. Administration of Decadron, chemotherapy and 3,000 rad cranial radiation resulted in dramatic improvement of dysphasia and right hand paresis. Almost 2 months later, rhythmic, involuntary movements of the left hand developed. There was progression to multifocal seizures, grand mal seizures, postictal depression, status epilepticus, and coma, with death 9 days after onset of the movement disorder. Bronchoalveolar carcinoma was widely disseminated in lungs and bones, and as three metastases in brain. Bland "ischemic" necrosis in a pseudolaminar pattern was present in the neocortex. Innumerable Cowdry type A intranuclear inclusion bodies were seen in neurons, astrocytes, and oligodenodroglia. Immunofluorescence demonstrated Herpes simplex virus type 2 antigen and electron microscopy revealed virions with the morphology of the Herpes group. The case is significant for (1) the concurrence of intracranial metastases and Herpes simplex encephalitis, and (2) the causal agent, Herpes simplex virus type 2. The implication for the clinical neurocientist is the potential in a patient with systemic cancer, for the causation of neurologic complications by more than one factor or mechanism.
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PMID:Herpes simplex type 2 encephalitis concurrent with known cerebral metastases. 22 22

Lesions of the upper motor neurons cause a spastic syndrome and a central paresis. The consequence of these "plus" and "minus" symptoms on locomotor function is a spastic movement disorder. Strategies of physical therapy for the spastic movement disorders are discussed in relation to research findings in neurophysiology and muscle physiology. The main therapeutic technics are physiotherapy, functional electrical stimulation (FES) and biofeedback training (BFB). Various methodological problems which arise in carrying out and evaluating therapeutic studies are described. Valid prognostic criteria are essential in order to achieve an optimal use of the different therapeutic procedures. This review underlines the need for further research, since some important questions remain open.
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PMID:[Spastic movement disorders: non-medicamentous therapies based on neurophysiologic principles]. 179 50

Ocular bobbing is a distinctive movement disorder occurring in a variety of related forms herein classified as `typical', `monocular', and `atypical'. `Typical' ocular bobbing occurs in patients with paralysis of horizontal conjugate eye movements and consists of abrupt, spontaneous downward jerks of the eyes with a slow return to the mid position. The `monocular' type reflects co-existing unilateral third nerve paresis in addition to the bobbing. The `atypical' type includes either a variation unexplained by associated oculomotor palsy, or bobbing with intact spontaneous or reflex horizontal eye movements. The clinical spectrum of ocular bobbing, its varied causes, and its prognostic significance are exemplified in a report of nine cases.
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PMID:Clinical spectrum of ocular bobbing. 553 97

Stretch-evoked electromyographic (EMG) activity and torque signals have been studied in elbow joint muscles of both sides of patients with spastic hemiparesis and healthy subjects. In order to reveal differences in the generation of muscle tone between clinical assessment and functional movement, stretches of different velocities and amplitudes were applied during passive and quasi-functional active motor tasks. In spastic patients the strength and duration of the EMG responses following stretching of flexor and extensor muscles during both passive and active tasks were dependent on the stretch velocity and duration, respectively. This effect was seen on both the spastic and unaffected side. Under passive conditions EMG activity after stretching was negligible in the limb muscles of healthy subjects, of small amplitude in unaffected limbs of the patients, but was strong in affected muscles. Under active conditions, the amplitude of the early (M1) component of the EMG signal was larger, while the later components (M2 and M3) were smaller. These differences were due more to a change in reflex gain than to a change in reflex threshold when the stretch velocity signal was the basis for calculation. It is suggested that in spastic paresis, modulation of stretch-induced EMG activity in the spastic limb becomes restricted to a smaller range with a poor ability to switch off under passive conditions. Furthermore, the reflex EMG activity suffers a reduced facilitation under active conditions. In comparison with unaffected limbs the stretch-evoked torque on the affected side was increased under passive conditions (due to the extra EMG activity) and decreased under active conditions (due to a reduced EMG activity). An increased torque to EMG ratio was found in spastic flexor and extensor muscles during active tasks. This is thought to be due to changes in mechanical muscle fibre properties suffered as a consequence of defective muscle activation following cerebral lesions. The consequences for clinical assessment of muscle tone and therapy of spastic movement disorder are discussed.
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PMID:Stretch-induced electromyographic activity and torque in spastic elbow muscles. Differential modulation of reflex activity in passive and active motor tasks. 835 19

Movement disorders following midbrain haemorrhage are infrequently encountered in rehabilitation, and are uncommonly corrected by pharmacologic means. This report describes a 20 year-old male with a prior history of cocaine abuse who presented with a 4 day history of dysarthria and blurred vision following methamphetamine abuse. Physical examination demonstrated hypertension, left facial hemispasm, bilateral upward gaze paresis and ataxic gait. Magnetic resonance imaging/magnetic resonance angiography (MRI/MRA) showed multifocal parenchymal haematomas in the mesencephalic tegmentum, subcortical left front region and right anterior thalamus consistent with cavernous angiomas. The patient was transferred to rehabilitation on hospital day 5. The following day, he developed choreoathetoid movements, dystonia, and aphasia, secondary to an extension of the midbrain haemorrhage. Cogentin was initiated with slight improvement in choreoathetoid movements. The patient began intensive multidisciplinary rehabilitation therapy but after 18 days of therapy, the patient remained totally dependent in activities of daily living (ADLs), transfers, mobility and was unable to communicate in any manner. A trial of Sinemet was initiated, with resultant steady improvement in functional ability over the next month. By discharge, the patient was independent in ADLs and ambulation. By 9 months post discharge follow-up, the patient was fully independent with normal cognition, and had self tapered all medications without ill effect. Dopamine agonist trials of appropriate duration appear indicated in cases of movement disorder (paucity or excess) following midbrain lesions.
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PMID:Pharmacologic management of movement disorder after midbrain haemorrhage. 965 26

Since the first paraplegic centre was established in 1945, life expectancy and life quality of paraplegics have considerably improved. However, endeavours to enhance the mobility of these patients have been less successful. The most promising approach, functional electric stimulation of paralysed muscles, is poorly accepted by patients at present because of technical problems. This study describes current approaches which may help to improve patients' mobility. A central motor lesion is perceived by the patient as a movement disorder of the legs, e.g. a gait disorder. Neurological investigation indicates, on the basis of exaggerated tendon reflexes and increased resistance of the non-activated leg muscles to stretching, that spastic paresis underlies the movement disorder. This combination of symptoms and clinical (physical) signs suggests that the exaggerated tendon tap reflexes are responsible for muscle hypertonia and the latter causes the movement disorder. However, electromyography during movement shows that the exaggerated short latency reflexes are associated with loss or attenuation of the functionally essential polysynaptic spinal reflexes. In the event of impaired supraspinal control there is loss of monosynaptic stretch reflex inhibition combined with reduced facilitation of polysynaptic spinal reflexes. Development of tension in tonically active calf muscles in patients with spastic paresis during gait occurs independently of spinal reflex activity. From electrophysiological and histological observations it can be assumed that transformation of motor units resulting in simple and less well adapted regulation of muscle tone allows movements such as gait. The reduction of muscle tone obtained with antispastic drugs is usually associated with paresis and may therefore hamper locomotion. Locomotor training represents a new attempt to improve the mobility of patients with incomplete paraplegia. It includes activation of neuronal circuits within the spinal cord below the level of the lesion. In incomplete paraplegics a coordinated leg muscle activation pattern and corresponding leg movements can be triggered and trained in patients standing on a treadmill with partial weight support. Improvement of training of the spinal cord locomotor centre can be expected from triggering of spinal cord reflexes and regeneration of spinal tract fibres, which is expected to be possible in the near future.
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PMID:[Focus on current research: improving the mobility of paraplegic patients]. 1089 54

An acute central nervous system lesion is followed by a phase of "shock" with flaccid muscle tone. After some weeks the syndrome of spastic paresis develops which is characterized by increased muscle tone and exaggerated tendon tap reflexes. During the last years it could be shown that the characteristic spastic movement disorder is mainly due to secondary changes of muscle properties which require a specific treatment. Exaggerated reflexes do only little contribute to the movement disorder.
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PMID:[Basic principles and therapy of spasticity]. 1114 82

In a prospective series of 34 incident patients with primary cervical dystonia (CD), 6 showed clinical or radiological signs of cervical radiculopathy (RP) or myelopathy (MP) during the course of their movement disorder. Age at onset in these patients was in the range reported for pure spondylotic cervical RP without an accompanying movement disorder. Radiologically, spondylosis was mild in 1 case and absent in 2 cases. The intervals between onset of CD and RP were shorter than in literature reports of RP/MP in dystonic-athetotic patients of cerebral paresis. Clinically, RP/MP in patients with CD mostly appears at mid-cervical levels, whereas cases with cerebral paresis are more frequently affected at higher cervical segments. We propose that RP/MP does not occur more frequently in CD than in pure spondylotic cervical RP.
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PMID:Radiculopathy and myelopathy in patients with primary cervical dystonia. 1138 61

Vocal fold paresis may be present in patients with voice complaints. Identification of paresis is important so that appropriate neurolaryngologic evaluation can be ordered and the appropriate treatment can be offered. Repetitive phonatory tasks (RPTs) fatigue patients vocally and may elicit signs of subtle paresis. In this study, four laryngologists independently reviewed the RPT portions of routine fiberoptic voice examinations of 100 patients in a blinded fashion. All patients had presented with voice complaints, were suspected of having a movement disorder of the larynx, and had been referred for laryngeal electromyography (LEMG). Predictions were compared with LEMG results and with predictions made at the time of each initial evaluation. Although RPTs are useful to laryngologists, predictions based on the entire examination are more accurate. LEMG can confirm clinical suspicions or identify paresis missed on fiberoptic laryngeal examination.
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PMID:Repetitive phonatory tasks for identifying vocal fold paresis. 1630 Nov 10

Antispastic medications that are directed to reduce clinical signs of spasticity, such as exaggerated reflexes and muscle tone, do not improve the movement disorder. Medication can even increase weakness which might interfere with functional movements, such as walking. In this chapter we address how spasticity affects mobility and how this should be taken into account in the treatment of spasticity. In clinical practice, signs of exaggerated tendon tap reflexes associated with muscle hypertonia are the consequence of spinal cord injury (SCI). They are generally thought to be responsible for spastic movement disorders. Most antispastic treatments are, therefore, directed at the reduction of reflex activity. In recent years, a discrepancy between spasticity as measured in the clinic and functional spastic movement disorder was noticed, which is primarily due to the different roles of reflexes in passive and active states, respectively. We now know that central motor lesions are associated with loss of supraspinal drive and defective use of afferent input with impaired behavior of short-latency and long-latency reflexes. These changes lead to paresis and maladaptation of the movement pattern. Secondary changes in mechanical muscle fiber, collagen tissue, and tendon properties (e.g., loss of sarcomeres, subclinical contractures) result in spastic muscle tone, which in part compensates for paresis and allows functional movements on a simpler level of organization. Antispastic drugs should primarily be applied in complete SCI. In mobile patients they can accentuate paresis and therefore should be applied with caution.
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PMID:Spasticity. 2309 14


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