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)

Emotional facial paresis (EFP) refers to hemifacial paresis of emotionally evoked or spontaneous smiling or weeping with preserved volitional movements of the face. The anatomical location for this phenomenon has been controversial. We report a 15-year-old boy with EFP. Follow-up MRI demonstrated infarction limited to the head of the caudate, putamen and anterior limb of the internal capsule on the contralateral side. This case lends support for selective damage at a striatal or capsular site in the production of EFP.
J Neurol Sci 1990 Sep
PMID:Emotional facial paresis with striatocapsular infarction. 224 29

The effects of cyproheptadine, a serotonergic antagonist, were studied in seven patients with spastic paresis of spinal origin. Six patients were included in a double blind crossover trial (maximal dose 24 mg/day). The patients were evaluated on both their spasticity and locomotor function. Four of the patients also participated in an open trial in which cyproheptadine was administered for a minimum of six months at optimal dose. Patients walked on a treadmill at full weight bearing when possible, or with 40% of their body weight externally supported, as required, by an overhead harness system. Cyproheptadine considerably decreased the sustained ankle clonus and episodes of spontaneous spasms observed in all the patients who previously presented these manifestations of spasticity. Two patients who required body weight support (BWS) during locomotion could walk at full weight bearing during cyproheptadine therapy. A more normal timing of EMG patterns in these patients during cyproheptadine therapy was associated with temporal distance changes and marked improvement of joint angular displacement. In contrast, the other patients showed marginal changes in the EMG and the kinematic pattern but eventually managed to walk at a higher speed. These preliminary results suggest that cyproheptadine can reduce spasticity and enhance locomotor function in spinal cord injured patients.
J Neurol Neurosurg Psychiatry 1990 Sep
PMID:The effects of cyproheptadine on locomotion and on spasticity in patients with spinal cord injuries. 224 57

Logistic regression was used to investigate the effects of host characteristics, production, and 23 veterinary diagnoses on the risks of two reticuloruminal disorders, ruminal acidosis and traumatic reticuloperitonitis among 61,124 Finnish Ayrshire cows. Lactational incidence risks were .3% for ruminal acidosis and .6% for traumatic reticuloperitonitis. The relative risk of ruminal acidosis was not related to parity, whereas the risk of traumatic reticuloperitonitis decreased with increasing parity. The risk of traumatic reticuloperitonitis was not related to milk yield of individual affected cows in their current or previous lactation (305-d, 4% FCM), whereas the risk of ruminal acidosis increased with current milk yield. Ketosis, early metritis, nonparturient paresis, and acute and chronic mastitis were risk factors for both reticuloruminal disorders. Parturient paresis was a risk factor for ruminal acidosis. Foot and leg problems were risk factors for traumatic reticuloperitonitis. Herd milk yield in the current or previous lactations was not a risk factor for either disorder nor were the two disorders risk factors for each other. Ruminal acidosis, but not traumatic reticuloperitonitis, had significant seasonal variation with the risk being least in summer. The low risk of ruminal acidosis in summer was not due to seasonality of calving.
J Dairy Sci 1990 Sep
PMID:Effect of diseases, production, and season on traumatic reticuloperitonitis and ruminal acidosis in dairy cattle. 225 85

Presented are the causes and clinical picture of the compensatory positioning of the head arising in the consequence of ocular changes and changes in the muscles of the neck. The material was divided into 3 groups: 1) with paresis of the ocular muscles (20 cases), 2) caused by nystagmus (20 cases) and 3) torticollis of muscular origin (20 cases). The basis of the differential diagnosis of compensatory positioning of the head of ocular origin and of torticollis of muscular origin as well as the criterion of a cooperation between the ophthalmologist and the orthopaedic surgeon are delineated.
Klin Oczna 1990 Sep
PMID:[Compensatory head positioning as a result of ocular changes or torticollis of muscular origin in children]. 226 51

We report three patients who lapsed into coma and subsequently manifested hypersomnolence, amnesia and vertical gaze paresis. Computed tomography revealed bilateral paramedian thalamic infarcts. This clinical symptomatology comprises the paramedian diencephalic syndrome.
J Assoc Physicians India 1990 Sep
PMID:Paramedian diencephalic syndrome. Report of 3 cases. 226 88

Auriculotherapy (ear-point acupuncture) was used in dogs (n = 30) suffering from thoracolumbar disc disease, Types I-IV, with a duration of 1 to (47 means = 8) d. During auriculotherapy treatment, no analgaesics or antiinflammatory medications were used. Pressure-sensitive and electrically detectable points on the concave aspect of the external auricle were stimulated by insertion of stainless steel acupuncture needles for 20 min. One to 6 needles were used on each occasion in a maximum of 3 treatments. Fifty per cent of dogs recovered completely and 23% improved. Dogs with backpain only (Type I) and dogs with paresis (Type II) responded best with mean recovery times of 1.7 and 3.2 d respectively. The analgaesic effects were especially impressive. Auriculotherapy failed in 3 (50%) paralysed dogs (Types III and IV) in which post-mortem examinations confirmed focal myelitis and myelomalacia. Four of 12 dogs (33%) recorded relapsed in 1.4 to 26 weeks after successful treatment.
J S Afr Vet Assoc 1990 Sep
PMID:A clinical study of auriculotherapy in canine thoracolumbar disc disease. 904 18

The congenital osseous abnormalities associated with achondroplasia include stenosis of the foramen magnum and the upper cervical spinal canal. In the pediatric achondroplastic patient, such stenosis may lead to cervicomedullary compression with serious sequelae, including paresis, hypertonia, delayed motor mile-stones, and respiratory compromise. Using a standardized protocol the authors have treated 15 young achondroplastic patients with documented cervicomedullary compression by craniocervical decompression and duroplasty. Following this procedure, significant improvement in presenting neurological or respiratory complaints was noted in all patients. The mortality rate in this series was zero. The major cause of morbidity associated with this procedure was perioperative cerebrospinal fluid (CSF) leakage from the surgical wound, presumably related to coexisting abnormalities of CSF dynamics. This problem was successfully managed by temporary or, when necessary, permanent CSF diversion procedures. It is concluded that craniocervical decompression is an effective and safe treatment for young achondroplastic patients with cervicomedullary compression.
J Neurosurg 1990 Sep
PMID:Craniocervical decompression for cervicomedullary compression in pediatric patients with achondroplasia. 238 75

Hemidiaphragmatic paralysis occurs in some patients following CAB surgery, possibly related to an intraoperative stretch or cold-induced phrenic injury. To determine the time and extent of recovery of phrenic nerve function, we studied five patients with left phrenic paresis or paralysis after CAB. The FVC, FEV1, Pmax and PEmax pressures, latency of conduction and amplitude of CDAP with phrenic nerve stimulation, and diaphragmatic excursion during fluoroscopy were measured for 12 months after CAB. Left phrenic paralysis was substantiated in four of five patients, and paresis was present in the other patient. Recovery of the left phrenic nerve occurred in all patients, complete in one and partial in four, but was delayed and continued for up to 12 months. We conclude that phrenic nerve recovery is delayed after CAB-associated injury and may be incomplete up to 14 months later, in keeping with rates of regeneration of other peripheral nerves.
Chest 1990 Sep
PMID:Recovery after unilateral phrenic injury associated with coronary artery revascularization. 239 43

The nasogastric tube can produce sudden, life-threatening bilateral vocal cord paralysis and is often an unrecognized cause of this clinical entity. The pathophysiologic mechanism is thought to be paresis of the posterior cricoarytenoid muscles secondary to ulceration and infection over the posterior lamina of the cricoid. Since our initial report of this entity in 1981, several cases have been photo-documented. Study of whole organ sections of an involved larynx have demonstrated the histopathology. Diabetic renal transplant patients appear to be particularly susceptible to the condition, due to prolonged gastroparesis and requirement for nasogastric tube drainage. Esophagoscopy should be performed promptly in these patients when pharyngodynia, hoarseness, or evolving stridor present in the postoperative period.
Laryngoscope 1990 Sep
PMID:The nasogastric tube syndrome. 189 58

We have used automatic decomposition electromyography (ADEMG) to study 41 muscles in 29 patients with well-defined peripheral and central motor disorders. In motor neuron diseases motor unit action potentials (MUAPs) showed increased amplitudes, firing rates and firing variability. Relatively large MUAPs sometimes were not identified by the computer program if they lacked sufficient high-frequency signal content, or were too variable in shape. In myopathies the MUAPs showed reduced amplitudes, durations and turns, and sometimes dramatic increases in firing rates. Also, the mean number of MUAPs per recording site was often increased, indicating excessive recruitment. In polymyositis (the best studied myopathy) the nature and magnitude of the MUAP shape and firing abnormalities were usually similar at different levels of contractile force, suggesting that motor units are affected without regard to recruitment order. In upper motor neuron paresis (multiple sclerosis), the shape properties of the MUAPs were normal, but mean firing rates were reduced, and firing variability increased. These findings confirm many of the traditional criteria for distinguishing neurogenic from myopathic disease electrophysiologically at the level of the individual MUAP. In addition, they demonstrate the potential diagnostic sensitivity of MUAP firing rate measurements for detecting neuromuscular dysfunction, and for differentiating between some cases of central and peripheral paresis, but not for distinguishing peripheral neurogenic from myopathic weakness, since firing rates tend to increase in both. Increased firing rate variability may be a marker of central or peripheral neurogenic weakness.
Electroencephalogr Clin Neurophysiol 1989 Sep
PMID:Motor unit firing rates and firing rate variability in the detection of neuromuscular disorders. 247 26


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