Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026827 (hypotonia)
 5,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty infants with cerebral palsy including monoplegia, diplegia, quadriplegia, hemiplegia, choreoathetosis, hypotonia with mental retardation and cerebellar ataxia, underwent Computed Cranial Tomography (CCT). Specific morphological anomalies such as ventricular dilatation with or without diverticulum, cortical atrophy, low density areas and calcifications, occur with varying frequency in each clinical groups. There exists a good correlation between the pathogenesis of the lesions, clinical data and CCT pictures.
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PMID:Cranial computerized tomography in cerebral palsy. An attempt at anatomo-clinical and radiological correlations. 720 4

Cerebral palsy is an established symptom complex that results from heterogeneous etiologies. Our understanding of the relative contribution of underlying etiologies to the occurrence of cerebral palsy is largely derived from studies lacking systematic neurologic evaluation or the application of contemporary imaging modalities. Throughout a 10-year inclusive period, the case records of all consecutive patients diagnosed with cerebral palsy in a single pediatric neurology practice were reviewed with reference to clinical features and diagnostic yield. A total of 217 cases of cerebral palsy were identified (129 male, 88 female): 77 (35.5%) spastic quadriplegic, 68 (31.3%) spastic hemiplegic, 39 (18%) spastic diplegic, five (2.7%) spastic monoplegic, 12 (5.5%) mixed, 12 (5.5%) ataxic-hypotonic, two (0.9%) dyskinetic, two (0.9%) Worster-Drought syndrome. Overall etiologic yield was 82.0%, varying according to type of cerebral palsy: 50% dyskinetic, 59% diplegia, 80% monoplegia, 80.9% hemiplegia, 90.9% quadriplegia, 91.7% ataxic hypotonia, and 100% mixed/Woster-Drought. The top five etiologic entities identified were periventricular leukomalacia, 24.9%; intrapartum asphyxia, 21.7%; cerebral dysgenesis, 17.1%; intracranial hemorrhage, 12.9%; and vascular, 9.7%. Although a single etiology was apparent in 144 (66.4%) of the cases, multiple etiologies were believed to be contributory in 34 (15.6%) of the cases. The etiologic profile varied according to such features as the type of cerebral palsy, gestational age, and the source (high-risk neonatal population or not) of the patients. Features of the child's cerebral palsy, such as microcephaly, neonatal difficulties, prior or coexisting epilepsy, and high-risk source, were found to be predictive of eventual etiologic yield. This contemporary evaluation of cerebral palsy etiologic yield suggests that it is much higher than previously reported and varies, depending on key clinical features.
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PMID:Etiologic yield of cerebral palsy: a contemporary case series. 1287 96

Modifications of phonation occurring after total thyroidectomy (TT) are usually attributed to surgical malpractice, but other causes of voice impairment even in nonoperated subjects should also be taken into account. This study analyzes 208 patients who underwent TT from January 1, 1999 through December 31, 2001. Follow-up ended on December 31, 2003. Only cases in which the surgeon ruled out the possibility of operative damage to the laryngeal nerves were included. All patients underwent pre- and postoperative clinical and instrumental nose and throat examination (NTE). Preoperatively, 86 patients (41%) showed hoarseness or dysphagia: 4 (2%) monoplegia and 12 (6%) hypomobility of the vocal cords due to impaired function of the recurrent laryngeal nerve (RLN); 6 (3%) cord hypotonia due to impairment of the superior laryngeal nerve (SLN); 34 (16%) dysphagia: and 30 (14%) hoarseness due to other causes. At follow-up 1 month after surgery, 71 patients (34%) had an onset of previously absent signs and symptoms: 8 (4%) had palsy of one vocal cord (2% permanent); 6 (3%) had cord hypomobility (all temporary); 12 (6%) had cord hypotonia due to disease of the SLN, 4 of which (2%) were permanent; 44 patients (21%) had symptoms due to scarring and adhesions between the laryngotracheal axis and the prethyroid muscles and between these and the skin. One patient (0.5%) had a nodular cord lesion that occurred after 3 months. Overall, more than one-third of the patients had preoperative voice modifications or swallowing impairment, around one-third had these problems after TT, and less than one-third were free of pre- and postoperative complications. The surgeon's care to avoid damage to the anatomica integrity of the of laryngeal nerves does not exclude functional problems of the nerves and of laryngeal dynamics. In fact, such problems could be referred to outcomes linked to the operation itself (hematoma, edema, scarring adhesion) or to events that only temporarily follow surgery but must be considered as an unavoidable sequel (e.g., neuritis, viral neuritis, myopathy). The patient should undergo a careful clinical and instrumental NTE to detect conditions prior to surgery, and the information provided by the surgeons should be thorough to allow the patient to be aware of all possible sequels and consequences.
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PMID:Recurrent laryngeal nerve damage and phonetic modifications after total thyroidectomy: surgical malpractice only or predictable sequence? 1589 96