Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hyperhidrosis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,603 records · Page 89Linked to original sources

[Treatment of facial blushing with endoscopic thoracal sympathicotomy. 85 per cent of patients are satisfied, but there are adverse effects].

Endoscopic transthoracic sympathicotomy, otherwise an established treatment for palmar hyperhidrosis, was used to treat patients troubled by facial blushing, one of the commonest symptoms of social phobia. The results were evaluated by means of a questionnaire answered by 90 per cent (219/244) of the patients, who rated their symptoms on a visual analogue scale (0-10) after a mean follow-up of eight months. According to the ratings, blushing was significantly reduced from a mean (+/- SEM) of 8.7 +/- 0.1 to 2.2 +/- 0.2 (p < 0.0001). Of the series as a whole, 85 per cent declared themselves satisfied with the outcome.

Adolescent↗

Hyperhydrosis in paraplegia.

A 20-year-old man suffered head, chest, and abdominal trauma in an auto accident resulting in a traumatic dissecting aneurysm of the thoracic aorta. Hypotension developed. The aneurysm was resected and replaced with a prosthetic graft. Postoperatively, the patient was found to be paraplegic below T-9, areflexic and anesthetic to pain and temperature, with preservation of vibration and position senses. In the ensuing nine months, the patient regained considerable sensory function in his lower extremities and had severe constant hyperhydrosis below the T-9 dermatome. The exaggerated sweating was unaffected by temperature change and anxiety. It was diminished by methantheline bromide treatment but never abolished. The spinal cord lesion is postulated to be anterior horn cell loss, with preservation of interneurons and intermediolateral gray columns. Disinhibition of sympthetic circuits or sprouting of axons are proposed mechanisms.

Adult↗

Peripheral motor neuropathy associated with autonomic dysfunction in two sisters: new hereditary syndrome?

We describe two sisters with distal, slowly progressive muscular weakness and hypotrophy since childhood, autonomic dysfunction characterized by profuse sweating, distal cyanosis related to cold weather, orthostatic hypotension, and esophageal achalasia. Nerve conduction velocity of several motor nerves was slow, and although no sensory abnormalities were present, sural nerve biopsy revealed severe nonspecific demyelination. No similar patients could be found in the literature and we therefore suggest the possibility that these individuals have a newly recognized hereditary syndrome.

Adult↗

Nonmotor complications in Parkinson's disease.

Parkinson's disease (PD) is most often considered a disorder of movement. Whereas bradykinesia, rigidity, tremor, and postural instability result in disability, nonmotor complications in PD may be of equal or greater significance in some patients. This review will discuss many of the nonmotor complications in PD, including cognitive, autonomic, sleep, and sensory difficulties that may occur.

Antidepressive Agents↗

Pathogenesis of apparent life-threatening events in infants with esophageal atresia.

Many infants with a repaired esophageal atresia (EA) undergo fundoplication, aortopexy, or glossopexy because the mechanisms most responsible for airway obstruction and/or apparent life-threatening event (AO/ALTE) syndrome are considered to be gastroesophageal reflux (GER), tracheal compression (TC), or obstructive apnea, respectively. In the present study, we investigated whether these mechanisms are independent or interrelated. We developed a database of 120 consecutive patients with EA treated by the senior author between 1967-2002. We studied the clinical manifestations of patients with a cervical esophagostomy and/or blind lower esophageal stump, which ruled out TC and/or proximal esophageal GER as a mechanism for AO/ALTE. Of 25 neonates who underwent section/ligation of lower tracheo-esophageal fistula and/or feeding gastrostomy, 10 critically ill neonates died. Of 15 survivors, 9 infants had a feeding gastrostomy without an esophagostomy. Of these, 6 infants presented one or more episodes of AO, and 8 presented ALTE with or without AO. Subsequently, 5 of the 9 infants underwent an esophagostomy. Eventually, 11 infants had a feeding gastrostomy with an esophagostomy. Of the latter, 5 infants presented one or more episodes of AO, and 6 presented ALTE without AO. In conclusion, oral feeding, proximal esophageal GER, and TC are not essential for AO/ALTE syndrome to occur. They are probably factors which offer evidence of an underlying problem with control of upper airway patency.

Bradycardia↗