Piriformis ganglion: An uncommon cause of sciatica.

UNLABELLED: Sciatica can occur due to a spinal lesion, intrapelvic tumor, diabetic neuropathy, and rarely piriformis syndrome. The causes of piriformis syndrome vary by a space-occupying lesion. A ganglionic cyst can occur in various lesions in the body but seldom around the hip joint. In addition, sciatica due to a ganglionic cyst around the hip joint has been reported in one patient in Korea who underwent surgical treatment. We experienced two cases of sciatica from a piriformis ganglionic cyst and we report the clinical characterics and progress after non-operative treatment by ultrasonography-guided aspiration. The two cases were diagnosed by magnetic resonance imaging and were treated by ultrasonography-guided aspiration. We followed the patients for more than 6months. The symptoms of piriformis syndrome from the ganglion improved following aspiration and this conservative treatment is a treatment method that can be used without extensive incision or cyst excision. LEVEL OF EVIDENCE: Level IV historical case.

Short-term changes of intraocular pressure after cervical interlaminar epidural injection: a pilot study.

BACKGROUND: Cervical epidural injection (CEI) is widely performed on patients with intervertebral disc herniation. The aim of the present study was to investigate the short-term effects of CEI on non-invasive intraocular pressure (IOP) measurements in subjects with normal eyes. METHODS: This prospective study enrolled 15 patients who were undergoing CEI at the C5/6 level with an interlaminar approach in the left lateral decubitus position. IOP was measured in both eyes by a rebound tonometer (Icare-PRO, Icare Finland Oy, Helsinki, Finland). A total volume of 14 ml (4 ml non-ionic contrast, a mixture of 0.2% lidocaine 1 ml and normal saline 4 ml for irrigation and a mixture of normal saline 4.5 ml with non-particulate betamethasone 2 mg) was injected with 1.0 ml s(-1). IOP was measured 5 min after the lateral decubitus position (T0, baseline), immediately after CEI (T1), and 1 min intervals for 5 min (T2-T6). RESULTS: The values of left and right baseline IOP (T0) were 18.9 (2.0) and 15.6 (2.6) mm Hg, respectively. IOP of left and right eyes at T1 [26.6 (4.2) and 21.2 (2.5) mm Hg, respectively] and T2 [26.2 (4.5) and 21.0 (2.8) mm Hg, respectively] were significantly higher compared with T0. These values immediately decreased at T3 and returned to baseline levels within 5 min after CEI. CONCLUSIONS: CEI resulted in an elevation of IOP of both eyes. However, the effects were transient only lasting a few minutes.

Selective activation of Akt1 by mammalian target of rapamycin complex 2 regulates cancer cell migration, invasion, and metastasis.

Mammalian target of rapamycin complex (mTORC) regulates a variety of cellular responses including proliferation, growth, differentiation and cell migration. In this study, we show that mammalian target of rapamycin complex 2 (mTORC2) regulates invasive cancer cell migration through selective activation of Akt1. Insulin-like growth factor-1 (IGF-1)-induced SKOV-3 cell migration was completely abolished by phosphatidylinositol 3-kinase (PI3K) (LY294002, 10 µM) or Akt inhibitors (SH-5, 50 µM), whereas inhibition of extracellular-regulated kinase by an ERK inhibitor (PD98059, 10 µM) or inhibition of mammalian target of rapamycin complex 1 (mTORC1) by an mTORC1 inhibitor (Rapamycin, 100 nM) did not affect IGF-1-induced SKOV-3 cell migration. Inactivation of mTORC2 by silencing Rapamycin-insensitive companion of mTOR (Rictor), abolished IGF-1-induced SKOV-3 cell migration as well as activation of Akt. However, inactivation of mTORC1 by silencing of Raptor had no effect. Silencing of Akt1 but not Akt2 attenuated IGF-1-induced SKOV-3 cell migration. Rictor was preferentially associated with Akt1 rather than Akt2, and over-expression of Rictor facilitated IGF-1-induced Akt1 activation. Expression of PIP3-dependent Rac exchanger1 (P-Rex1), a Rac guanosine exchange factor and a component of the mTOR complex, strongly stimulated activation of Akt1. Furthermore, knockdown of P-Rex1 attenuated Akt activation as well as IGF-1-induced SKOV-3 cell migration. Silencing of Akt1 or P-Rex1 abolished IGF-1-induced SKOV-3 cell invasion. Finally, silencing of Akt1 blocked in vivo metastasis, whereas silencing of Akt2 did not. Given these results, we suggest that selective activation of Akt1 through mTORC2 and P-Rex1 regulates cancer cell migration, invasion and metastasis.

Efficacy of pre-emptive milrinone in off-pump coronary artery bypass surgery: comparison between patients with a low and normal pre-graft cardiac index.

OBJECTIVE: The effect of pre-emptive milrinone without bolus during off-pump coronary artery bypass surgery (OPCAB) was evaluated in two groups of patients with low and normal pre-graft cardiac index. METHODS: Eighty-two patients were divided into two groups based on their pre-graft cardiac index. Each group was randomly subdivided into two groups to receive either milrinone or normal saline. After the internal mammary artery was harvested, the infusion of milrinone, or normal saline was started and maintained until the end of the anastomosis. The haemodynamic variables were measured: just before the start of milrinone or normal saline after pericardiotomy (baseline value); 10 min after the tissue stabilizer had been applied for the anastomosis of left anterior descending artery, left circumflex artery and right coronary artery; and after the sternal closure. RESULTS: Milrinone reduced the extent of the decrease in cardiac index and stroke volume as well as the extent of the increase in systemic and pulmonary vascular resistance. The extent of the decrease in cardiac index and mixed venous oxygen saturation were greater in normal pre-graft cardiac index group than in low pre-graft cardiac index group regardless of milrinone infusion during anastomoses. The effect of milrinone on haemodynamics showed no significant difference between low and normal pre-graft cardiac index groups. CONCLUSIONS: Pre-emptive milrinone infusion without bolus effectively improved cardiac performance during OPCAB and was especially useful for patients with low pre-graft cardiac index to prevent the decrease in cardiac index and stroke volume index below the critical level.

Implication of adenosine A2A receptors in hypotension-induced vasodilation and cerebral blood flow autoregulation in rat pial arteries.

This study aimed to evaluate the role for adenosine A2A receptors in the autoregulatory vasodilation to hypotension in relation with cerebral blood flow (CBF) autoregulation in rat pial arteries. Changes in pial artery diameters were observed directly through a closed cranial window. Vasodilation induced by adenosine was markedly suppressed by ZM 241385 (1 micromol/l, A2A antagonist) and alloxazine (1 micromol/l, A2B antagonist), but not by 8-cyclopentyltheophylline (CPT, 1 micromol/l, A1 antagonist). CGS-21680-induced vasodilation was more strongly inhibited by ZM 241385 (25.3-fold; P<0.05) than by alloxazine. In contrast, 5'-N-ethylcarboxamido-adenosine (NECA)-induced vasodilation was more prominently suppressed by alloxazine (12.0-fold; P<0.001) than by ZM 241385. The autoregulatory vasodilation in response to acute hypotension of the pial arteries was significantly suppressed by ZM 241385, but not by CPT and alloxazine. Consistent with this finding, the lower limit of CBF autoregulation significantly shifted to a higher blood pressure by 1 micromol/l of ZM 241385 (53.0+/-3.9 mm Hg to 69.2+/-2.9 mm Hg, P<0.01) and 10 micromol/l of glibenclamide (54.7+/-6.5 mm Hg to 77.9+/-4.2 mm Hg, P<0.001), but not by CPT and alloxazine. Thus, it is suggested that adenosine-induced vasodilation of the rat pial artery is mediated via activation of adenosine A2A and A2B receptors, but not by A1 subtype, and activation of adenosine A2A receptor preferentially contributes to the autoregulatory vasodilation via activation of ATP-sensitive K+ channels in response to hypotension and maintenance of CBF autoregulation.

Needle thoracic sympathectomy for essential hyperhidrosis: intermediate-term follow-up.

BACKGROUND: Essential hyperhidrosis is a condition with excessive sweating localized to certain part of the body. A definitive cure can be obtained by upper thoracic sympathectomy. METHOD: Between June and October 1997, 117 patients with essential hyperhidrosis underwent needle thoracoscopic sympathectomy. Of the 94 patients, 42 were men and 52 women. Their ages ranged from 14 to 63 years, with a mean age of 23 years. RESULTS: There were no mortality or life-threatening complications. Symptomatic improvement was found in 95.7%. Compensatory hyperhidrosis was found in 71.2% of the patients, but in these compensatory hyperhidrosis were mostly tolerable. CONCLUSIONS: This therapeutic procedure is minimally invasive and very effective. Further development of the new device and surgical technique are expected to follow.

Role of adenosine A(2B) receptors in vasodilation of rat pial artery and cerebral blood flow autoregulation.

This study was aimed to investigate the underlying mechanism of vasodilation induced by the activation of A(2B) adenosine receptors in relation to cerebral blood flow (CBF) autoregulation. Changes in pial arterial diameters were observed directly through a closed cranial window. N(omega)-nitro-L-arginine methyl ester (L-NAME, nitric oxide synthase inhibitor) significantly suppressed the concentration-dependent vasodilations induced by adenosine and 5'-N-ethylcarboxamido-adenosine (NECA) but not the vasodilation by CGS-21680 (A(2A)-receptor agonist). Moreover, NECA-induced vasodilation was suppressed by alloxazine (1 micromol/l) but not by ZM-241385 (1 micromol/l, A(2A) antagonist), which suggests mediation by A(2B)- receptor activation. Otherwise, the level of nitrite/nitrate was concentration dependently increased in the artificial cerebrospinal fluid (CSF) when adenosine and NECA were suffused over the cortical surface. L-NAME and alloxazine, but not ZM-241385, largely inhibited their releases. The lower limit of CBF autoregulation was little affected following pretreatment with L-NAME or alloxazine. Thus it is suggested that adenosine-induced vasodilation via activation of A(2B)-adenosine receptors of the rat pial artery is coupled to the production of nitric oxide, which contributes little to CBF autoregulation.

Cytotoxic effects of the components in heat-treated mistletoe (Viscum album).

Major cytotoxic components were fractionated from Korean mistletoe and the changes of their cytotoxic effects caused by heat treatment were investigated. The high cytotoxicity of isolated lectin I completely disappeared by heating for 30 min. The fractions of viscotoxins and alkaloids maintained their activities even after heating for 60 and 180 min, respectively. The alkaloid fraction was more cytotoxic to tumor MSV cells than to non-tumor A31 cells and the activity pattern was not changed by heat treatment. The possible contributions of alkaloids and viscotoxins to the activities of heat-treated mistletoe extracts such as tea or decoctions are discussed.

Metabolism of cAMP to adenosine: role in vasodilation of rat pial artery in response to hypotension.

The purpose of this experiment was to examine whether the cAMP-adenosine pathway is implicated in the autoregulatory vasodilation in response to hypotension. Suffusion with cAMP (1-100 micromol/l) or adenosine (0.01-10 micromol/l) caused a sustained vasodilation of the resting pial arteries in a concentration-dependent manner. In contrast, N6,2'-O-dibutyryl-cAMP and 8-bromo-cAMP exerted a weak dilation at high concentration (100 micromol/l). The vasodilation to cAMP (1-100 micromol/l), adenosine (0.01-10 micromol/l), and hypotension was significantly reduced by pretreatment with 3,7-dimethyl-1-propargylxanthine (1 micromol/l), an A2 receptor antagonist, as well as 3-isobutyl-1-methylxanthine (3 micromol/l), an inhibitor of endo- and ectophosphodiesterase, 1, 3-dipropyl-8-p-sulfophenylxanthine (100 micromol/l), an inhibitor of ecto-5'-phosphodiesterase, or alpha,beta-methylene-adenosine 5'-diphosphate (100 micromol/l), an inhibitor of ecto-5'-nucleotidase. However, 8-cyclopentyltheophylline (1 micromol/l), an A1 antagonist, did not elicit a similar response. The increased release of adenosine when the cortical surface was suffused with cAMP (100 micromol/l) was significantly reduced by 3-isobutyl-1-methylxanthine, 1,3-dipropyl-8-p-sulfophenylxanthine, and alpha,beta-methylene-adenosine 5'-diphosphate (each 100 micromol/l). These results indicate that the cAMP-adenosine pathway as a viable metabolic mechanism is implicated in the production of adenosine in the rat pial artery and contributes to the regulation of vasodilation in response to hypotension.

Thoracoscopic sympathetic surgery for hyperhidrosis.

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.

Cytotoxicity of heat-treated Korean mistletoe.

The cytotoxic effects of preparations of Korean mistletoe (Viscum album L. var. coloratum Ohwi) on non-tumorigenic A31 cells and tumorigenic MSV cells were investigated. While the aqueous extract from Korean mistletoe (<8 microg/ml) showed strong cytotoxicity on both cell lines, the heat-treated extract was much less cytotoxic with TD50 values of above 300 microg/ml. The heat-treated extract showed a growth-enhancing effect on non-tumorigenic cells and a cytotoxic effect on tumorigenic cells. The alkaloids fraction, which was isolated from the crude extract, was not cytotoxic to non-tumorigenic A31 cells up to 550 microg/ml, but was cytotoxic to tumorigenic MSV cells at 138 microg/ml. Heat treatment did not change the cytotoxic effects of the alkaloids fraction, indicating that the selective cytotoxicity of the heat-treated mistletoe extract on tumorigenic MSV cells might be due to its alkaloids. In order to study the changes in the cytotoxicity of fermented Korean mistletoe, the crude and heat-treated extracts were inoculated with Lactobacillus plantarum. During 7 days of fermentation, the cytotoxicity of the fermented heat-treated extract was increased while that of the fermented crude extract was not changed significantly.

Middle cerebral artery occlusive disease: the New England Medical Center Stroke Registry.

To analyze the clinical features, vascular lesions, and infarct distribution in Asian and white patients with middle cerebral artery (MCA) territory ischemia, we studied age, sex, race, risk factors, angiographic, and neuroimaging findings among patients in the New England Medical Center Stroke Registry. We included patients with well-defined intrinsic occlusive lesions of the MCAs and patients with embolic MCA territory infarcts. Among 695 patients in the stroke registry, 89 (12.8%) qualified. They had 28 MCA intrinsic stenoses, 17 MCA embolic occlusions (cardiogenic or unknown origin), and 44 carotid artery (CA) stenoses or occlusions. MCA intrinsic disease patients were more often Asians and women, and more often had hypertension. Asians were older than whites. Coronary artery disease (27%), peripheral vascular disease (20.5%), and smoking (39%) were more common in CA disease patients. The most common site of MCA intrinsic stenosis (78%) and embolic occlusion (59%) was the mainstem MCA. Infarcts in patients with MCA intrinsic disease mostly involved the striatocapsular area (61%). Infarcts in patients with MCA embolic occlusion (75%) and CA disease (43%) most often involved the parietal lobe. In our hospital, most patients with MCA intrinsic disease are Asians and women and have hypertension and striatocapsular infarctions. Asian patients are usually older than white patients. The most common site of vascular lesions is the mainstem MCA.

Physiological responses of human adults to foods containing phosphate additives.

An experiment was conducted to assess the physiological effects of a diet rich in foods cotaining phosphate additives. During a 4-week control period, eight adults were fed a balanced diet free of phosphate additives providing approximately 95 g protein 0.7 g Ca and 1.0 g P per day. During a subsequent 4-week period, food items containing phosphate additives were substituted for counterpart items devoid of added phosphates. This diet contained 0.7 g Ca and 2.1 g P per day. The introduction of foods containing phosphate additives was associated with intestinal distress, soft stools or mild diarrhea. These symptoms subsided in six subjects but occurred intermittently throughout the experimental period in the other two subjects. The high-phosphorus diet induced increases in serum phosphorus and urinary phosphorus and decreases in serum calcium and urinary calcium. Hydroxyproline excretion in the urine was increased and cyclic AMP excretion was elevated in six of the eight subjects. These changes are analogous to those seen in experimental animals fed high-phosphorus diets which were shown to be due to enhanced parathyroid activity (secondary hyperparathyroidism). The use of phosphate food additives is discussed with respect to their possible stimulating effect on adult bone resorption.