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Query: UMLS:C0030552 (
paresis
)
5,831
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The authors experienced a case of histiocytosis X with a large intracranial mass resulting in a convulsive seizure. The patient showed left exophthalmos and a skin rash one year and two months after birth. Histiocytosis X was diagnosed from a skin biopsy, and predonine, endoxan and vincristine were administered. The rash disappeared, but the exophthalmos remained. At the age of two years and nine months, punched-out lesions appeared in the skull and 4,000 rads of radiation was applied. Thereafter, the exopthalmos persisted but there was no particular problem in the course. However, a convulsive seizure with fever suddenly appeared at nine years and ten months of age and the patient was hospitalized. At the time of admission, the general condition was good and there were no abnormalities in neurological tests. In neuroradiological examinations, a calcified and poorly vascularized mass 8 cm in maximum diameter was found to occupy the left middle cranial fossa. Chondrosarcoma was strongly suspected from these findings, but there was also symmetrical thickening of bone cortex in the peripheries of the long bones of the extremeties which appeared to be the recovery process from bone destruction caused by histiocytosis X. Therefore, the formation of an intracranial mass by histiocytosis X was diagnosed and surgery was performed. When left osteoplastic fronto-temporal craniotomy was performed, the mass was found to be raising the temporal lobe and it could be easily separated from the surrounding tissue. However, these was firm adherence to dura mater of the middle cranial fossa (especially that of the superior orbital fissure). Histologically, there were many cells with small nuclei, no polymorphism, abundant and clear cytoplasm which were darkly stained and slightly atypic. These findings matched those for histiocytosis X. Cases of histiocytosis X rarely show symptoms of the central nervous system or infiltration of the central nervous system. Only 31 such cases were seen in the literature investigated by the authors. Neurological symptoms include pyramidal symptoms such as
hemiparesis
and impairment of the cranial nerves, particularly
paresis
of the optic, trigeminal, facial and acoustic nerves. Convulsive seizures were seen in only five cases including the one reported here. It is also rare for intracranial masses to be formed in cases of histiocytosis X and only six cases, including the authors', have been found with masses of a maximum diameter of more than 5 cm.
...
PMID:[Case of histiocytosis X with a large intracranial mass]. 660 36
Calcification of ligamenta flava in the cervical spine is rarely seen. Only few cases in the literature have been available. Recently we have had experience with two cases on that lesion who had progressive radiculomyelopathy. The purpose of this report is not only case presentation but also an analysis of 11 cases from the literature in clinical, radiological and histological aspects. Case 1 was a 60-year-old woman who had numbness in both hands, mild weakness of the right foot on walking and clumsiness of the right hand. Ten years before she had suffered tbc. meningitis, but no history of neck injury. Neurological examination revealed spastic
paresis
in right extremities, muscle atrophy in both forearms, hypesthesia and hypalgesia in both hands and feet. Vibration sense was disturbed below the knee joint and both feet. Sphincter function was normal. Radiological examination of cervical spine revealed oval calcified nodules in the posterior spinal canal at the level of C34, C45, C56 and C67. These were all situated in the paramedian portion and symmetrically situated at C56. Air myelogram demonstrated that the spinal cord was displaced forward and choked by the posterior situated calcification. Cervical laminectomy was carried out from C2 through Th1 and calcified nodules in the hypertrophied ligamenta flava were successfully removed. Case 2 was also 66-year-old woman who had been suffering from cerebral thrombosis with left
hemiparesis
. In addition with left
hemiparesis
she started to complain with paresthesia in right hand, deteriorated numbness in left extremities and gait disturbance developed a year later.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Radiculomyelopathy due to calcification of the cervical ligamenta flava--report of 2 cases and a review of literature]. 665 77
Naloxone has recently been reported to be of benefit in the treatment of central nervous system ischemia. To study the effect of naloxone in an experimental stroke model, we subjected 40 awake monkeys to middle cerebral artery (MCA) occlusion 2 weeks after the placement of a MCA ligature by a transorbital technique. Cerebral blood flow (CBF) was monitored with stereotactically placed H2 electrodes, and the neurological course was serially recorded. Infarct size was determined 2 weeks after MCA occlusion. Twenty animals served as control and received no naloxone; 10 of these underwent permanent occlusion, and 10 underwent 4-hour MCA occlusion. In 25 treatment animals, naloxone was administered in three different intravenous dosages: (a) naloxone, 2-mg/kg bolus 20 minutes postocclusion and 2 mg/kg/hour X 4 hours, in 10 animals with permanent MCA occlusion; (b) naloxone, 10-mg/kg bolus 20 minutes postocclusion and 10 mg/kg/hour X 4 hours, in 10 animals with 4-hour MCA occlusion; and (c) naloxone, 20-mg/kg bolus, in 5 animals with various neurological deficits. MCA occlusion typically produced a moderate deficit:
hemiparesis
, hemianopsia, and facial
paresis
. In most instances, naloxone in the 2- and 10-mg/kg dose regimens produced little or no change in the neurological function. CBF decreased after MCA occlusion and was unaffected by naloxone in most cases. Infarct size was not significantly different between the control and treated groups. However, the 20-mg/kg dose consistently produced a nonfunctional, transient increase in total body motor tone in normal and hemiparetic animals. Naloxone did not significantly improve useful neurological function, CBF, or infarct size in an experimental primate stroke model.
...
PMID:Effect of naloxone on experimental stroke in awake monkeys. 670 56
This case study involves a 44-year-old man with flaccid dysarthria, right
hemiparesis
, left facial
paresis
, left vocal fold paralysis, and aphagia following multiple gunshot wounds. He was treated surgically with a tracheostomy, feeding gastrostomy, left temporalis muscle sling, left cricopharyngeal myotomy, hypoglossal nerve anastomosis, and left true vocal fold Teflon injection. After seven years, the patient was referred for speech therapy. The areas of glottic closure, velopharyngeal closure, and tongue strength and mobility were stressed initially in speech therapy. Since these mechanisms were related to his aphagia, it was hypothesized that the oral motor activities used for speech would also aid in swallowing. After nine weeks of intensive practice, gains were noted in strength and movement for the tongue, velum and larynx. Shortly thereafter, he swallowed blender-texture food.
...
PMID:Dysarthria and aphagia: a case study of neuromuscular treatment. 674 1
Thrombosis of the basilar artery occurred in a 27-year-old woman after physical exercise (bowling). She became deeply unconscious without change so that four days after onset urokinase was administered. The neurological status than markedly improved, with partial regression of the
paresis
and the cranial nerve deficits, and she became responsive again. Angiography after four-day urokinase administration demonstrated complete recanalisation of the basilar artery. Subsequent rehabilitative measures led to almost complete disappearance of all symptoms. Later neurological tests revealed merely very discrete left
hemiparesis
, mainly of the arm.
...
PMID:[Fibrinolytic treatment of severe thrombosis of the basilar artery (author's transl)]. 701 63
Unilateral recurrent laryngeal nerve paralysis with atrophic vocal cord and persisting glottic insufficiency as well as
hemiparesis
of the larynx caused by lesions of the upper parts of the vagal nerve have to be managed surgically. Instead of the nowadays often applied Teflon-injection the authors prefer the following techniques of surgical medialization. 1. Medial shifting of the paralyzed vocal cord by subperiostal implantations of autogenous cartilage through a window in the thyroid ala. 2. "Wing door thyroplasty" with medialization of a door like part of the thyroid cartilage which is locked by a cartilage chip in the desired position. The results of the surgical treatment of 19 patients (13
paresis
of the recurrent laryngeal nerve, 6 lesions of the upper part of the vagal nerve) showed an obvious improvement with regard to voice and aspiration. There have been no postoperative complications. These methods can be an alternative to Teflon-injections.
...
PMID:[Medialization of the paralyzed vocal cord by cartilage chips and "wing door thyroplasty"]. 711 95
The diagnosis of pontine hemorrhage was made by computerized axial tomography in a 12 year old boy, who presented with acute central
hemiparesis
and contralateral abducens
paresis
.
...
PMID:[Pontine hemorrhage in a 12 year old boy. Demonstration by cranial computer tomography (author's transl)]. 719 42
Eleven cases presenting a syndrome of the medulla oblongata are discussed with reference to the findings of clinical and angiographic investigation. The diagnosis of Wallenberg's syndrome is justified when the classic symptoms are apparent (Horner's syndrome, nystagmus, dysphonia and dysphagia, ataxia, ipsilateral sensory impairment of the face and contralateral elsewhere, and accompanying vegetative disturbances). If additional symptoms such as a facial or extra-ocular muscle
paresis
, especially
hemiparesis
, exist, another, more lateral or medial, syndrome of the oblongata should be considered. Angiographic findings vary considerably, ranging from a normal vertebral artery or posterior inferior cerebellar artery (PICA) to an occlusion of these arteries (in three and two of the 11 cases respectively). Modification are often seen in the anterior inferior cerebellar artery (AICA). A kind of complementary supply in the PICA-AICA region must occasionally exist. Localised processes affecting these vessels rather than diffuse multifocal vascular processes would lead to Wallenberg's syndrome. It is difficult to conclude from the clinical picture where a possible responsible vascular narrowing or obliteration may lie, even if pareses of the limb were present.
...
PMID:[Clinical and angiographic findings in vascular medullary syndromes (author's transl)]. 731 26
In a prospective investigation of 55 consecutively selected patients with right-sided apoplectic lesions, denial and neglect of
hemiparesis
was registered in a standardized way using fixed criteria. The patients were all fully conscious and could cooperate in a detailed investigation. About half of the patients had denial and neglect of
hemiparesis
(1/4 denial, 1/5 neglect). The syndrome(s) of denial/neglect was not related to sensory defects or defects in the sense of position. Denial of
hemiparesis
was related to extent of lesion, neglect of
hemiparesis
was not. Both syndromes were related to age of patients. The resemblance between denial and neglect of
hemiparesis
is pointed out. It is argued, that the two phenomena could be seen as one syndrome released by right-sided brain lesions, the difference being a matter of degree. The cognitive factors in denial/neglect are thought upon as factors, than can be seen in right-sided lesions together with
paresis
, visual defects, but apparently not necessarily associated with the named defects.
...
PMID:Denial and neglect of hemiparesis in right-sided apoplectic lesions. 734 92
Clinical evidence is presented to support the contention that the sternocleidomastoid muscle is innervated primarily by undecussated fibers from the ipsilateral hemisphere. Stroke patients often show contralateral
hemiparesis
accompanied by weakness in head turning to the side of the
paresis
.
...
PMID:Undecussated innervation to the sternocleidomastoid muscle: a reinstatement. 736 10
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