The results of thoracoscopic sympathetic trunk transection for palmar hyperhidrosis and sympathetic ganglionectomy for axillary hyperhidrosis. (1/177)

OBJECTIVES: To review our total experience of thoracoscopic sympathetic trunk transection for the treatment of palmar hyperhidrosis and second and third thoracic sympathetic ganglionectomy for axillary hyperhidrosis. DESIGN: Longitudinal cohort study following up consecutive patients for 0.3 to 5.5 years. SUBJECTS: Fifty-four consecutive patients undergoing thoracoscopic sympathectomy for hyperhidrosis. METHODS: Prospective evaluation of immediate technical success, complications, late recurrence of hyperhidrosis and patient acceptability. RESULTS: 100% initial cure for palmar hyperhidrosis, 91% of sympathetic ganglionectomies for axillary hyperhidrosis were technically successful and initially curative. Compensatory sweating 44% patients, most severe after bilateral sympathetic ganglionectomy. Complications occurred in 14% patients, all resolving without further intervention. There were no cases of Horner's syndrome. 13% patients reported a return of some palmar sweating. 5.4% patients developed recurrent palmar hyperhidrosis at 6, 15 and 21 months postoperatively. CONCLUSION: Transection of the sympathetic trunk between the first and second thoracic sympathetic ganglia initially cures 100% of patients treated primarily for palmar hyperhidrosis. Technically successful 2nd and 3rd thoracic sympathetic ganglionectomy initially cures 100% of patients with axillary hyperhidrosis. Compensatory sweating is common after bilateral sympathectomy. Recurrent palmar hyperhidrosis occurs in 5.4% of cases, but can be cured by a second thoracoscopic sympathectomy. Horner's syndrome is an avoidable complication of thoracoscopic sympathectomy.  (+info)

Focal (segmental) dyshidrosis in syringomyelia. (2/177)

The features or mechanisms of dyshidrosis have not been sufficiently clarified. Neither has the difference between hyperhidrosis and hypohidrosis. To clarify the features and mechanisms of dyshidrosis (hyperhidrosis and hypohidrosis) in syringomyelia, the clinical features focusing on hidrosis of 30 patients with syringomyelia and Chiari malformation located from a syringomyelia database were prospectively analysed. The patients were classified into three groups: eight patients (26.7%) had segmental hypohidrosis, 10 (33. 3%) had segmental hyperhidrosis, and 12 (40.0%) had normohidrosis. We found that the Karnofsky functional status for the hyperhydrosis and normohidrosis groups were significantly higher than for the hypohidrosis group (p=0.0012), with no significant differences between the hyperhidrosis and normohidrosis groups. The duration from the onset of syringomyelia to the current dyshidrosis was significantly longer in the hypohidrosis group than in the hyperhidrosis group (p=0.0027). A significant correlation was identified between the duration from the onset of syringomyelia to the time at study and the performance score (r=-0.599, p=0.0003). The results substantiate previous hypotheses that in its early stage syringomyelia causes segmental hyperactivity of the sympathetic preganglionic neurons, and hyperactivity of these gradually subsides as tissue damage progresses. Focal hyperhidrosis may be regarded as a hallmark of a relatively intact spinal cord, as well as normohidrosis.  (+info)

A case of traumatic high thoracic myelopathy presenting dissociated impairment of rostral sympathetic innervations and isolated segmental sweating on otherwise anhidrotic trunk. (3/177)

A 3 year-old boy developed flaccid paraplegia, anesthesia below T3 and impaired vesical control immediately after a car accident. Three months later, the pupils and their pharmacological reactions were normal. Thermal sweating was markedly reduced on the right side of the face, neck, and shoulder and on the bilateral upper limbs, and was absent below T3 except for band like faint sweating on T7 sensory dermatome. The left side of the face, neck and shoulder showed compensatory hyperhidrosis. Facial skin temperature was higher on the sweating left side. Cervico-thoracic MRI suggested almost complete transection of the cord at the levels of T2 and T3 segments. We discussed the pathophysiology of the dissociated impairment of rostral sympathetic innervations and isolated segmental sweating on otherwise anhidrotic trunk.  (+info)

Thoracoscopic sympathetic surgery for hyperhidrosis. (4/177)

Resectional surgery of sympathetic nerves has been known to be the most effective treatment for essential hyperhidrosis and the application of thoracoscopic electrocauterization has provided a minimally-invasive procedure with the least morbidity and a resultant higher satisfaction rate. This paper describes our experience on the 1,167 cases of thoracoscopic sympathetic surgery for the treatment of essential hyperhidrosis. A total of 1,167 patients (674 males (58%) and 493 females (42%), mean age of 26.4 years with palmar (930), craniofacial (190) or axillary (47) hyperhidrosis underwent thoracoscopic sympathetic surgery from July 1992 to March 1999. Since the T2-4 sympathectomy, first performed in July 1992 for a patient of palmar hyperhidrosis, the operative methods have been altered to achieve a higher satisfaction level with the least complication by adopting less invasive procedures. Our current standard procedures being performed are T3 and T2 clipping for palmar and craniofacial hyperhidrosis and T3,4 sympathicotomy for axillary hyperhidrosis, all using a 2 mm needle thoracoscope. As the surgical procedures have been transited to a less invasive method with limited resection using the newest endoscopic devices, the average operation time and complications such as Horner's syndrome and compensatory hyperhidrosis have gradually decreased and thus the long-term satisfaction rate has been raised up to 98% for palmar hyperhidrosis, 92% for craniofacial hyperhidrosis and 89% for axillary hyperhidrosis. The recurrent cases (14/1167) were treated successfully with reoperations of thoracoscopic sympathetic surgery. The optimal goal of therapy could be achieved by complete elimination of the hyperhidrotic symptom, by decreasing the incidence and degree of compensatory hyperhidrosis through a selective and limited resection, and by adopting the least invasive procedures. Sympathicotomy has provided the advantages of a limited extent of denervation and the resultant decrease of compensatory hyperhidrosis compared to sympathectomy. The reversible method of clipping may be an effective, provisionary means for cases of severe, intractable compensatory sweating. For craniofacial hyperhidrosis, T2 sympathicotomy or clipping has been proven to be superior to the T1 sympathectomy due to the decreased occurrence of Horner's syndrome and T3,4 sympathicotomy providing a satisfactory outcome with less compensatory hyperhidrosis for axillary hyperhidrosis.  (+info)

Sympathectomy potentiates the vasoconstrictor response to nitric oxide synthase inhibition in humans. (5/177)

OBJECTIVE: Nitric oxide exerts its cardiovascular actions at least in part by modulation of the sympathetic vasoconstrictor tone. There is increasing evidence that nitric oxide inhibits central neural sympathetic outflow, and preliminary evidence suggests that it may also modulate peripheral sympathetic vasoconstrictor tone. METHODS: To test this latter concept, in six subjects having undergone thoracic sympathectomy for hyperhydrosis, we compared the vascular responses to systemic L-NMMA infusion (1 mg/kg/min over 10 min) in the innervated and the denervated limb. We also studied vascular responses to the infusion of the non-nitric-oxide-dependent vasoconstrictor phenylephrine. RESULTS: L-NMMA infusion evoked a roughly 3-fold larger increase in vascular resistance in the denervated forearm than in the innervated calf. In the denervated forearm, vascular resistance increased by 58 +/- 10 percent (mean +/- SE), whereas in the innervated calf it increased only by 21 +/- 6 percent (P < 0.01, forearm vs. calf). This augmented vasoconstrictor response was specific for L-NMMA, and not related to augmented non-specific vasoconstrictor responsiveness secondary to sympathectomy, because phenylephrine infusion increased vascular resistance similarly in the denervated forearm and the innervated calf (by 24 +/- 7, and 29 +/- 8 percent, respectively). The augmented vasoconstrictor response was related specifically to denervation, because in control subjects, the vasoconstrictor responses to L-NMMA were comparable in the forearm and the calf. CONCLUSIONS: These findings indicate that in the absence of sympathetic innervation, the vasoconstrictor responses to nitric oxide synthase inhibition are augmented.  (+info)

Sympathetic denervation of the upper limb improves forearm exercise performance and skeletal muscle bioenergetics. (6/177)

BACKGROUND: Sympathetic activation may limit exercise performance by restraining muscle blood flow or by negatively affecting skeletal muscle metabolic behavior. To test this hypothesis, we studied the effect of thoracoscopic sympathetic trunkotomy (TST) on forearm exercise duration, blood flow, and muscle bioenergetics in 13 patients with idiopathic palmar hyperhidrosis. METHODS AND RESULTS: Heart rate and beat-by-beat mean arterial pressure were recorded at rest and during right and left rhythmic handgrip before and 4 to 7 weeks after right TST. Forearm blood flow was measured bilaterally at rest and on the right during exercise. Right forearm muscle phosphocreatine content and intracellular pH were assessed by (31)phosphorus magnetic resonance spectroscopy. After right TST, exercise duration increased from 8.9+/-1.4 to 13.4+/-1.8 minutes (P<0.0001) with the right forearm and from 5.7+/-0.4 to 7.6+/-0.9 minutes (P<0.05) with the left (P<0.05 for the interaction between treatment and side). Right forearm blood flow at rest was 66% higher (P<0.01) after right TST, but this difference decreased as the exercise progressed. After right TST, a significant reduction occurred in muscle acidification and phosphocreatine depletion during ipsilateral forearm exercise. This was associated with a significantly reduced mean arterial pressure response to right handgrip, whereas the pressor response to left handgrip did not change. CONCLUSIONS: Sympathetic denervation of the upper limb significantly improves forearm skeletal muscle bioenergetics and exercise performance in patients with idiopathic palmar hyperhidrosis.  (+info)

Effect of thoracic sympathectomy on arm and leg exercise capacity and on lung function. (7/177)

BACKGROUND: Thoracic T(2-4) sympathectomy (TS) relieves palmar hyperhidrosis. These same roots innervate the heart and the lung. Thoracoscopic TS minimizes damage to the chest wall so that the effect of sympathectomy itself on these organs can be studied. We attempted to determine whether attenuated sympathetic output affects arm or leg exercise tolerance and lung function in young adults who underwent this operation. METHODS: Seven subjects, aged 17-30 years, had lung function tests (water spirometer, Godart, Holland), and leg and arm maximal exercise (CPX, MedGraphics, USA), before and 3-6 months after TS. RESULTS: After TS, resting and exercise heart rate and blood pressure were reduced. Baseline leg and arm peak O(2) uptake, 2.08 (0.6) and 1.44 (0.5) liters/min, respectively, were not different from the post-TS values, 2.06 (0.7) and 1.54 (0.5) liters/min (nonsignificant). Post-TS lung functions were not significantly reduced. CONCLUSION: Thoracoscopic T(2-4) sympathectomy does not lead to a clinically important fall in lung function and does not compromise arm or leg exercise capacity. Therefore, TS can be done safely in young subjects with palmar hyperhidrosis.  (+info)

Botulinum toxin A for axillary hyperhidrosis (excessive sweating). (8/177)

BACKGROUND: Treatment of primary focal hyperhidrosis is often unsatisfactory. Botulinum toxin A can stop excessive sweating by blocking the release of acetylcholine, which mediates sympathetic neurotransmission in the sweat glands. METHODS: We conducted a multicenter trial of botulinum toxin A in 145 patients with axillary hyperhidrosis. The patients had rates of sweat production greater than 50 mg per minute and had had primary axillary hyperhidrosis that was unresponsive to topical therapy with aluminum chloride for more than one year. In each patient, botulinum toxin A (200 U) was injected into one axilla, and placebo was injected into the other in a randomized, double-blind manner. (The units of the botulinum toxin A preparation used in this study are not identical to those of other preparations.) Two weeks later, after the treatments were revealed, the axilla that had received placebo was injected with 100 U of botulinum toxin A. Changes in the rates of sweat production were measured by gravimetry. RESULTS: At base line, the mean (+/-SD) rate of sweat production was 192+/-136 mg per minute. Two weeks after the first injections the mean rate of sweat production in the axilla that received botulinum toxin A was 24+/-27 mg per minute, as compared with 144+/-113 mg per minute in the axilla that received placebo (P< 0.001). Injection of 100 U into the axilla that had been treated with placebo reduced the mean rate of sweat production in that axilla to 32+/-39 mg per minute (P<0.001). Twenty-four weeks after the injection of 100 U, the rates of sweat production (in the 136 patients in whom the rates were measured at that time) were still lower than base-line values, at 67+/-66 mg per minute in the axilla that received 200 U and 65+/-64 mg per minute in the axilla that received placebo and 100 U of the toxin. Treatment was well tolerated; 98 percent of the patients said they would recommend this therapy to others. CONCLUSIONS: Intradermal injection of botulinum toxin A is an effective and safe therapy for severe axillary hyperhidrosis.  (+info)