Oral Health-related quality of life after coronectomy for impacted mandibular third molar in the first postoperative week.

BACKGROUND: Coronectomy of a mandibular impacted third molar is a surgical treatment to minimize the risk for inferior alveolar nerve damage. We aimed to determine whether this procedure affected the oral health-related quality of life (OHRQoL) within the first postoperative week. MATERIAL AND METHODS: This prospective study included 50 patients that underwent a coronectomy for an impacted mandibular third molar. The patients completed the Oral Health Impact Profile-14 (OHIP-14) questionnaire and questions about pain and analgesic intake on every day during the first postoperative week. RESULTS: Mean OHIP-14 scores were highest during the first three postoperative days; the highest mean score (26.40, SD: 8.67) was observed on the first postoperative day. Mean OHIP scores gradually declined during the first postoperative week, and the mean OHIP-14 score was 9.82 (SD: 9.15) on the seventh day. Physical pain was the highest contributor to the overall OHIP-14 score. Pain gradually declined with time; the lowest mean pain score (3.38, SD: 2.2) was observed on the seventh day. OHIP-14 and pain scores were not significantly different between sexes or between different grades of impaction. OHIP-14 scores were positively correlated with pain scores. CONCLUSIONS: A mandibular third molar coronectomy had a strong effect on patient OHRQoL, particularly during the first three postoperative days.

Assessment of tumor blood flow distribution by dynamic contrast-enhanced CT.

A distinct feature of the tumor vasculature is its tortuosity and irregular branching of vessels, which can translate to a wider dispersion and higher variability of blood flow in the tumor. To enable tumor blood flow variability to be assessed in vivo by imaging, a tracer kinetic model that accounts for flow dispersion is developed for use with dynamic contrast-enhanced (DCE) CT. The proposed model adopts a multiple-pathway approach and allows for the quantification of relative dispersion in the blood flow distribution, which reflects flow variability in the tumor vasculature. Monte Carlo simulation experiments were performed to study the possibility of reducing the number of model parameters based on the Akaike information criterion approach and to explore possible noise and tissue conditions in which the model might be applicable. The model was used for region-of-interest analysis and to generate perfusion parameter maps for three patient DCE CT cases with cerebral tumors, to illustrate clinical applicability.

The value of serial plasma nuclear and mitochondrial DNA levels in acute spontaneous intra-cerebral haemorrhage.

BACKGROUND: Increased plasma nuclear and mitochondrial DNA levels may be connected to disease severity following spontaneous intra-cerebral haemorrhage (ICH). This study tested the hypothesis that plasma nuclear and mitochondrial DNA levels are substantially increased in acute ICH and can predict treatment outcomes. METHODS: Serial plasma nuclear and mitochondrial DNA levels were examined in 60 consecutive patients admitted within 24 h after onset of spontaneous ICH and in 60 volunteer control subjects. Additional samples were obtained on days 4, 7, 10, and 14 after onset of ICH regardless of clinical deterioration. RESULTS: Only plasma nuclear DNA, not plasma mitochondrial DNA, levels in patients with spontaneous ICH significantly correlated with Glasgow Coma Scale (GCS) (r = -0.467, P = 0.001) and ICH volume (r = 0.515, P ≤ 0.001) on presentation. Plasma nuclear DNA levels increased significantly from day 1 to day 7 in patients with poor outcome. Higher plasma nuclear DNA levels (cut-off value >18.7 ng/ml) on presentation were associated with poor outcomes in spontaneous ICH patients. CONCLUSION: Plasma nuclear DNA levels reflect the severity of cerebral damage such that higher levels are associated with poorer outcome. Plasma nuclear DNA level can be considered a neuropathologic marker of acute spontaneous ICH.

CBG Santiago: a novel CBG mutation.

CONTEXT: Corticosteroid-binding globulin (CBG; SERPIN A6) gene mutations are rare; only four mutations have been described, often in association with fatigue and chronic pain, albeit with incomplete penetrance. PATIENT: We report a kindred with a novel SERPINA6 mutation. The proband, a 9-yr-old male, had excessive postexertional fatigue, weakness, and migraine. MAIN OUTCOME MEASURES AND RESULTS: Investigations revealed low morning and ACTH-stimulated peak cortisol levels. SERPIN A6 sequencing detected a novel exon 2 single base deletion (c.13delC) leading to a frameshift generating a stop codon within the signal peptide coding region (p.Leu5CysfsX26) and 50% reduced CBG levels in heterozygotes. The patient's father and two sisters share the mutation. Symptom expression within the family may have been modified by a polymorphic CBG allele (c.735G>T). Exogenous hydrocortisone had no effect on the fatigue. CONCLUSION: This report documents the fifth CBG gene mutation in humans and the second causing major effects on CBG levels. Individuals with low CBG levels may be misdiagnosed as having secondary hypocortisolism. The association with fatigue and idiopathic pain is again noted and may relate to altered stress system function. Variability of the phenotype may relate to other genetic variations of the CBG gene or environmental factors.

Perioperative management of the hypothalamic-pituitary-adrenal axis in patients with pituitary adenomas: an Australasian survey.

BACKGROUND: There is limited consensus regarding optimal glucocorticoid administration for pituitary surgery to prevent a potential adrenal crisis. AIM: To assess the investigation and management of the hypothalamic-pituitary-adrenal (HPA) axis in patients undergoing trans-sphenoidal hypophysectomy in Australasia. METHODS: A questionnaire was sent to one endocrinologist at each of 18 centres performing pituitary surgery in Australasia. Using hypothetical case vignettes, respondents were asked to describe their investigation and management of the HPA axis for a patient with a: non-functioning macroadenoma and intact HPA axis, non-functioning macroadenoma and HPA deficiency and growth hormone secreting microadenoma undergoing trans-sphenoidal hypophysectomy. RESULTS: Responses were received from all 18 centres. Seventeen centres assess the HPA axis preoperatively by measuring early morning cortisol or a short synacthen test. Preoperative evaluation of the HPA status influenced glucocorticoid prescription by 10 centres, including 2/18 who would not prescribe perioperative glucocorticoids for a patient with a macroadenoma and an intact HPA axis. Tumour size influenced glucocorticoid prescribing patterns at 7/18 centres who prescribe a lower dose or no glucocorticoids for a patient with a microadenoma. Choice of investigations for definitive postoperative assessment of the HPA axis varied with eight centres requesting an insulin tolerance test, four centres a 250 µg short synacthen test and six centres requesting other tests. CONCLUSIONS: There is wide variability in the investigation and management of perioperative glucocorticoid requirements for patients undergoing pituitary surgery in Australasia. This may reflect limited evidence to define optimal management and that further well-designed studies are needed.

Characteristics of plasma NOx levels in severe sepsis: high interindividual variability and correlation with illness severity, but lack of correlation with cortisol levels.

Objectives Nitric oxide (NO) concentrations are elevated in sepsis and their vasodilatory action may contribute to the development of hyperdynamic circulatory failure. Hydrocortisone infusion has been reported to reduce nitric oxide metabolite (NOx) concentrations and facilitate vasopressor withdrawal in septic shock. Our aim was to determine whether NOx concentrations relate to (i) protocol-driven vasopressor initiation and withdrawal and (ii) plasma cortisol concentrations, from endogenous and exogenous sources. Demonstration of a relation between NOx, cortisol and vasopressor requirement may provide an impetus towards the study of hydrocortisone-mediated NOx suppression as a tool in sepsis management. Design A prospective study of 62 patients with severe sepsis admitted to the intensive care unit. Measurements Plasma NOx, total and free cortisol, and corticosteroid-binding globulin (CBG) concentrations were measured and related to protocol-driven vasopressor use for 7 days following admission. Results Patients who developed septic shock (n = 35) had higher plasma NOx, total and free cortisol, and lower CBG concentrations than the nonseptic shock group (n = 27). Cortisol, CBG and NOx concentrations correlated with illness severity. Free cortisol, and to a lesser extent total cortisol, but not NOx concentrations, predicted septic shock. NOx concentrations were higher in nonsurvivors, and the concentrations were characteristically stable within individuals but marked interindividual differences were only partly accounted for by illness severity or renal dysfunction. NOx concentrations did not correlate with cortisol, did not relate to vasopressor requirement and did not fall after standard dose hydrocortisone, given for clinical indications. Conclusions Nitric oxide production increased with sepsis severity but did not correlate with plasma cortisol or vasopressor requirement. NOx levels were not suppressed reproducibly by hydrocortisone. High interindividual variability of NOx levels suggests that absolute NOx levels may not be a suitable target for individualized hydrocortisone therapy.

Suppressive effects of intrathecal granulocyte colony-stimulating factor on excessive release of excitatory amino acids in the spinal cerebrospinal fluid of rats with cord ischemia: role of glutamate transporters.

Recently, the hematopoietic factor, granulocyte colony-stimulating factor (G-CSF), has been shown to exhibit neuroprotective effects in CNS injuries. Our previous study demonstrated that intrathecal (i.t.) G-CSF significantly improved neurological defects in spinal cord ischemic rats. Considerable evidence indicates that the release of excessive amounts of excitatory amino acids (EAAs) plays a critical role in neuron injury induced by ischemic insult. In the present study, we used a spinal cord ischemia-microdialysis model to examine whether i.t. G-CSF exerted antiexcitotoxicity effects in a rat model of spinal cord ischemia. I.t. catheters and a microdialysis probe were implanted in male Wistar rats. The results revealed that spinal cord ischemia-induced neurological defects were accompanied by a significant increase in the concentration of EAAs (aspartate and glutamate) in the spinal dialysates from 30 min to 2 days after reperfusion. I.t administration of G-CSF immediately after the performance of surgery designed to induce ischemia led to a significant reduction in ischemia-induced increases in the levels of spinal EAAs. Moreover, i.t. G-CSF also brought about a significant reduction in the elevation of spinal EAA concentrations induced by exogenous i.t. administration of glutamate (10 microl of 500 mM). I.t. G-CSF attenuated spinal cord ischemia-induced downregulation of expression of three glutamate transporters (GTs), glial transporter Glu-Asp transporter (GLAST), Glu transporter-1 (GLT-1), and excitatory amino acid carrier 1 (EAAC1) protein 48 h after spinal cord ischemic surgery. Immunohistofluorescent staining showed that i.t. G-CSF significantly upregulated expression of the three GTs in the gray matter of the lumbar spinal cord from 3 to 24 h after injection. We propose that i.t. G-CSF possesses an ability to reduce the extent of spinal cord ischemia-induced excitotoxicity by inducing the expression of glutamate transporters.

Intrathecally injected granulocyte colony-stimulating factor produced neuroprotective effects in spinal cord ischemia via the mitogen-activated protein kinase and Akt pathways.

Granulocyte colony-stimulating factor (G-CSF) is a potent hematopoietic factor. Recently, this factor has been shown to exhibit neuroprotective effects on many CNS injuries. Spinal cord ischemic injury that frequently results in paraplegia is a major cause of morbidity after thoracic aorta operations. In the present study, we examined the neuroprotective role of G-CSF on spinal cord ischemia-induced neurological dysfunctions and changes in the mitogen-activated protein kinase (MAPK) and Akt signaling pathways in the spinal cord. Spinal cord ischemia was induced in male Wistar rats by occluding the descending aorta with a 2F Fogarty catheter for 12 min 30 s. Immediately after ischemia surgery, the rats were administered G-CSF (10 mug) or saline by intrathecal (i.t.) injection. The rats were divided into four groups: control, ischemia plus saline, ischemia plus G-CSF and G-CSF alone. The neurological dysfunctions were assessed by calculating the motor deficit index after ischemia surgery. The expressions of MAPK and Akt were studied using Western blotting and double immunohistochemistry. First, we observed that ischemia plus i.t. G-CSF can significantly reduce the motor function defects and downregulate phospho-p38 and phospho-c-Jun N-terminal kinase protein expressions-this can be compared with the ischemia plus saline group. In addition, G-CSF inhibited the ischemia-induced activation of p38 in the astrocytes. Furthermore, we concluded that i.t. G-CSF produced a significant increase in phospho-Akt and phospho-ERK in the motor neurons and exhibited beneficial effects on the spinal cord ischemia-induced neurological defects.

Risk factors and outcome of seizures after spontaneous aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Seizures are important neurologic complications of spontaneous aneurysmal subarachnoid hemorrhage (SAH). A better understanding of the risk factors of seizures following aneurysmal SAH is needed to predict those who will require treatment. METHODS: A total of 137 adult patients were enrolled in this two-year retrospective study. Baseline prognostic variables were analyzed based on Cox's proportional hazards model after a minimum of one-year follow-up. RESULTS: Seizures occurred in 21 patients who had SAH, including acute symptomatic seizures in 11.7% (16/137) and unprovoked seizures in 3.6% (5/137). None progressed to status epilepticus during hospitalization. After a minimum of one-year follow-up, the mean Glasgow Outcome Score was 3.5 +/- 1.4 for patients with seizures and 3.1 +/- 1.1 for those without. CONCLUSIONS: Higher mean World Federation of Neurological Societies grade on presentation was predictive of seizure, but seizure itself was not a significant prognostic predictor after a minimum of one-year follow-up. Regarding potential side effects of anti-epileptic drugs, anti-epileptic therapy should be carefully administered to patients with seizures after aneurysmal SAH.

Moderate weight loss reduces renin and aldosterone but does not influence basal or stimulated pituitary-adrenal axis function.

Body fat mass and nutrition influence secretion of the adrenocortical hormones--aldosterone and cortisol--via several mechanisms. However, there are no data on adrenocortical function following widely prescribed mild diet-induced weight loss (10%) in obese subjects. In the present study, 25 healthy obese volunteers (BMI 32.9+/-4.3 kg/m (2)) followed a 30% calorie restricted diet over 12 weeks. Hypothalamic-pituitary-adrenal (HPA) axis function was assessed by 24-hour urine free cortisol/cortisone and a 1 mcg ACTH stimulation test with measurement of total and free cortisol and corticosteroid-binding globulin (CBG). The renin-angiotensin-aldosterone system (RAAS) was assessed by measurement of plasma aldosterone and renin under salt depleted (30 mmol/d) and loading (250 mmol/d) conditions. Volunteers' weight fell by 8.5+/-0.8 kg (8.9+/-0.7%) and seated systolic blood pressure fell by 8.7+/-2.7 mmHg and diastolic blood pressure by 7.0+/-1.4 mmHg (p<0.01). Plasma aldosterone and renin levels fell significantly with weight loss (aldosterone: 853+/-156-635+/-73 pmol/l; renin: 35.4+/-7-24+/-3 mU/l, both p<0.05). The volunteers were relatively salt insensitive (mean arterial pressure change with salt intake: 4 mmHg) and this was not affected by weight loss. Moderate weight loss had no effect on 24-hour urine free cortisol/cortisone, or on basal, or ACTH-stimulated free and total cortisol, or CBG. Hence this conventional weight loss program reduces blood pressure and activity of the RAAS via an effect on renin release. Despite various described influences of fat mass and energy restriction on HPA axis function, there were no changes in basal and stimulated HPA axis function with moderate weight loss. There may be a threshold effect of weight loss/energy restriction required to alter HPA axis function, or moderate weight loss may lead to a counterbalanced effect of stimulatory and inhibitory influences on HPA axis function.

Corticosteroid-binding globulin gene polymorphisms: clinical implications and links to idiopathic chronic fatigue disorders.

Corticosteroid-binding globulin (CBG) binds cortisol with high affinity, facilitating transport of cortisol in blood, although tissue-specific CBG-cortisol interactions have long been postulated. There are three heritable, human CBG gene mutations that can reduce CBG-cortisol binding affinity and/or reduce circulating CBG levels. In some families, fatigue and low blood pressure have been associated with affinity altering or CBG level reducing mutations. The limited numbers of reports raise the possibility of ascertainment bias as many cases presented with features suggesting cortisol deficiency. The recent description of a genetically CBG-deficient mouse listed fatigue, manifest as reduced activity levels, as part of the phenotype, which also included immune aberrations. Severe CBG mutations may produce fatigue, but one study suggests that these are a rare cause of idiopathic fatigue. A mechanism for the effect of CBG mutations on fatigue is not readily apparent because free cortisol levels are normal, although we speculate that CBG may have an effect on cortisol-brain transport.

Value of free cortisol measurement in systemic infection.

Systemic infection induces an increase in plasma cortisol which accords approximately with illness severity. However, both basal and synthetic ACTH stimulated cortisol levels are not strong predictors of mortality. Moreover, plasma cortisol levels do not readily define those patients who have been clinically observed to respond, with respect to blood pressure elevation, to exogenous hydrocortisone. It is likely that free cortisol, accounting for 6-20% of circulating total (bound plus free) cortisol has most of the life-saving effects on circulation and metabolism in severe sepsis, as corticosteroid-binding globulin bound and albumin-bound cortisol have reduced access to tissues. In addition, sepsis reduces CBG and albumin levels, hence blunting the effect of increasing illness severity on total cortisol. Our recent studies suggest that free cortisol correlates more closely to sepsis severity than total cortisol and that free cortisol levels can be estimated using the plasma CBG and total cortisol, obviating the need for direct free cortisol measurement. Studies directed at determining if free cortisol is a better guide than total cortisol to the need for hydrocortisone supplementation may be of value.

Abnormal puberty in paediatric Cushing's disease: relationship with adrenal androgen, sex hormone binding globulin and gonadotrophin concentrations.

OBJECTIVE: Paediatric Cushing's disease is frequently associated with abnormal puberty. We addressed the hypothesis that prepubertal patients show excessive virilization and pubertal patients show suppression of LH and FSH secretion. DESIGN AND MEASUREMENTS: Serum androstenedione (A4), dehydroepiandrosterone sulphate (DHEAS), testosterone (T), and sex hormone binding globulin (SHBG) were determined at diagnosis and converted to standard deviation scores. LH, FSH concentrations were also determined. Severity of CD was assessed from the sleeping midnight cortisol concentration. Puberty was staged and excessive virilization defined as advance in pubic hair stage for breast stage or testicular volume (TV). PATIENTS: Twenty-seven CD patients (17 male, 10 female), median age 13.4 years (range 5.9-17.8) were studied. RESULTS: In the CD group as a whole, A4, DHEAS, T standard deviation scores (SDS) values were normal. SHBG SDS values (n = 19) were low (median -1.93, -4.32-0.86) correlating with BMI (r = -0.49). A4, DHEAS, T, SHBG, LH and FSH did not correlate with midnight cortisol, but A4 and T SDS correlated with ACTH at 09.00 h (both r = 0.51). Thirteen patients (11 male, 2 female) had excessive virilization with increased A4 (P = 0.033), DHEAS (P = 0.008), testosterone (P = 0.033) and decreased SHBG (P = 0.004) compared with subjects without excessive virilization. Pubertal boys (TV > or = 4 ml) (n = 7) and girls (breasts > or = stage 2) (n = 8) had low median LH and FSH. Boys had an LH concentration of 1.2 mU/l (0.3-3.5), FSH, 0.9 mU/l (0.2-6.4) and median T SDS, -1.95 (-3.8-4.65), while girls had an LH concentration of 1 mU/l (0.3-7.4). CONCLUSIONS: Many patients had abnormal puberty and excessive virilization associated with increased adrenal androgens and decreased SHBG. Pubertal patients had low LH and FSH suggesting impaired pituitary-gonadal axis function.

Postneurosurgical nosocomial bacterial brain abscess in adults.

BACKGROUND: Bacterial brain abscess after a neurosurgical procedure has become an important occurrence in the hospital setting. However, no information about the frequency, clinical relevance, and the outcome has been reported. PATIENTS AND METHODS: Over a period of 19 years (1986- 2004), a total of 31 patients were retrospectively identified as having brain abscesses after neurosurgical procedures and were enrolled in this study. RESULTS: Those included in this study accounted for 0.17% (31/18600) of all neurosurgical procedures in the same period. There was an increased percentage of adult postneurological nosocomial brain abscess compared to all adult bacterial brain abscesses in recent years. The majority of cases were due to Gram-negative bacilli and polymicrobial infections, including both Gram-negative bacilli and Staphylococcus species. Furthermore, the appearance of multi-antibiotic resistant strains was also noted during the study period. The overall fatality rate was 16%. CONCLUSION: Post-neurosurgical states have become important predisposing factor for bacterial brain abscess. In patients that undergo neurosurgical procedures and develop smoldering fever, progressively disturbed consciousness, headache, and new onset focal neurologic signs, immediate neuro-imaging studies should be undertaken to determine whether bacterial brain abscess is present. Although mortality may be related to the primary brain pathology, early diagnosis and timely use of appropriate antibiotics based on antimicrobial susceptibility testing are also essential for survival.

Factors predictive of fatality in massive middle cerebral artery territory infarction and clinical experience of decompressive hemicraniectomy.

To determine the factors predictive of fatality in massive middle cerebral artery (MCA) territory infarction and outcome of decompressive hemicraniectomy, 62 patients who were retrospectively verified with first event massive MCA infarctions were enrolled in this study. Amongst them, 21 received decompressive hemicraniectomy during hospitalization. Clinical data between early and late hemicraniectomy groups were also compared. Significant deterioration occurred in 40 cases, 21 of whom received decompressive hemicraniectomy. The other 19 received conservative treatment. The mortality rate of these 40 cases between decompressive hemicraniectomy and conservative treatment was 29% (six of 21) and 42% (eight of 19), respectively. Factors that predicted fatalities in our massive MCA infarction patients with or without decompressive hemicraniectomy were total scores of baseline GCS at the time of admission, associated with coronary artery diseases, and significant deterioration during hospitalization. This study confirms the lifesaving procedure of hemicraniectomy that prevents death in patients deteriorating because of cerebral edema after infarction, although it may produce severe disability with an unacceptably poor quality of life in survival. Despite high mortality and morbidity, decompressive hemicraniectomy to prevent cerebral herniation when significant deterioration is demonstrated are essential for maximizing the potential for survival.

Septic shock and sepsis: a comparison of total and free plasma cortisol levels.

CONTEXT: Severe systemic infection leads to hypercortisolism. Reduced cortisol binding proteins may accentuate the free cortisol elevations seen in systemic infection. Recently, low total cortisol increments after tetracosactrin have been associated with increased mortality and hemodynamic responsiveness to exogenous hydrocortisone in septic shock (SS), a phenomenon termed by some investigators as relative adrenal insufficiency (RAI). HYPOTHESIS: Free plasma cortisol may correspond more closely to illness severity than total cortisol, comparing SS and sepsis (S). DESIGN: This was a prospective study. SETTING: This study took place in a tertiary teaching hospital. PATIENTS: Patients had SS (n = 45) or S (n = 19) or were healthy controls (HCs; n = 10). AIM: The aim of the study was to compare total with free cortisol, measured directly and estimated by Coolens' method, corticosteroid-binding globulin (CBG), and albumin in patients with SS (with and without RAI) and S during acute illness, recovery, and convalescence. RESULTS: Comparing SS, S, and HC subjects, free cortisol levels reflected illness severity more closely than total cortisol (basal free cortisol, SS, 186 vs. S, 29 vs. HC, 13 nmol/liter, P < 0.001 compared with basal total cortisol, SS, 880 vs. S, 417 vs. HC, 352 nmol/liter, P < 0.001). Stimulated free cortisol increments varied greatly with illness category (SS, 192 vs. S, 115 vs. HC, 59 nmol/liter, P = 0.004), whereas total cortisol increments did not (SS, 474 vs. S, 576 vs. HC, 524 nmol/liter, P = 0.013). The lack of increase in total cortisol with illness severity is due to lower CBG and albumin. One third of patients with SS (15 of 45) but no S patients met a recently described criterion for RAI (total cortisol increment after tetracosactrin < or = 248 nmol/liter). RAI patients had higher basal total cortisol (1157 vs. 756 nmol/liter; P = 0.028) and basal free cortisol (287 vs. 140 nmol/liter; P = 0.017) than non-RAI patients. Mean cortisol increments in RAI were lower (total, 99 vs. 648 nmol/liter, P < 0.001; free, 59 vs. 252 nmol/liter, P < 0.001). These differences were not due to altered CBG or albumin levels. Free cortisol levels normalized more promptly than total cortisol in convalescence. Calculated free cortisol by Coolens' method compared closely with measured free cortisol. CONCLUSIONS: Free cortisol is likely to be a better guide to cortisolemia in systemic infection because it corresponds more closely to illness severity. The attenuated cortisol increment after tetracosactrin in RAI is not due to low cortisol-binding proteins. Free cortisol levels can be determined reliably using total cortisol and CBG levels.

Treatment outcomes and prognostic factors in patients with supratentorial low-grade gliomas.

Low-grade gliomas account for 10-15% of all adult primary intracranial tumours. Currently, there is no consensus on the treatment strategy for low-grade gliomas. This study was designed to evaluate the treatment outcomes, prognostic factors and radiation-related late complications, as well as to assess whether or not post-operative radiotherapy has benefit on local control and overall survival in this population. We retrospectively reviewed 93 consecutive adult patients with supratentorial low-grade gliomas diagnosed at our institution from July 1985 to December 1997. All patients underwent surgical intervention and 60 of them received post-operative radiotherapy. With a median follow-up of 110 months for surviving patients, the 5-year overall and progression-free survival rates were 57% and 47%, respectively. 46 patients experienced local progression of disease during the follow-up period. In multivariate analysis, age at diagnosis, extent of surgery and post-operative Karnofsky performance status showed independent prognostic significance for progression-free and overall survival rates. Post-operative radiotherapy had independent prognostic value for progression-free survival. This analysis has changed our practice and we suggest that aggressive surgical resection and post-operative radiotherapy might be considered for patients with low-grade gliomas. Further efforts should be made to optimize radiotherapy techniques and to integrate new therapeutic modalities.

Neuromuscular hamartoma arising in the brachial plexus.

We report a case brachial plexus neuromuscular hamartoma (choristoma) in a 28-year-old man who complained of numbness of the left hand and forearm for several years. MRI revealed a circumscribed, rounded mass in the left brachial plexus. The patient is well 2 years after surgery, with no neurological deficit.