Abstract Aromatic hydrocarbon solvents, used widely in industry, cause central nervous system symptoms in exposed workers. Acute effects of m-xylene were studied in nine voluntary subjects exposed experimentally to stable or varying concentrations of m-xylene at rest or while exercising. Each subject participated in four exposure and two control sessions in a single-blind fashion. The time-weighted average (TWA) m-xylene concentration was always 200 parts per million (ppm) (8.2 μmol/l) during the 4-h exposure period, complying to a TWA of 4.1 μmol/l ·- 8 h, which is equivalent to the hygienic limit allowed in work situations. The short-term peak concentrations were 400 ppm or less. Electroencephalography was recorded at the beginning of exposure, during exposure, and after exposure was stopped. Eighteen 60-s EEG samples for each subject on each experimental day were analyzed automatically. Exercise increased theta percentage and delta power and percentage; these changes were more prominent in the control session without exposure. Exposure increased the dominant alpha frequency and alpha percentage during the early phase of exposure and also counteracted the effects of exercise. The effects of short-term m-xylene exposure on EEG were minor, and no deleterious effects were noted. Perhaps alpha activation is indicative of stimulating and excitatory effects induced by m-xylene exposure, which has been noted heretofore in the absorption phase of alcohol intake.
Objective: To evaluate electroencephalogram-derived quantitative variables after out-of-hospital cardiac arrest. Design: Prospective study. Setting: University hospital intensive care unit. Patients: Thirty comatose adult patients resuscitated from a witnessed out-of-hospital ventricular fibrillation cardiac arrest and treated with induced hypothermia (33°C) for 24 hrs. Interventions: None. Measurements and Main Results: Electroencephalography was registered from the arrival at the intensive care unit until the patient was extubated or transferred to the ward, or 5 days had elapsed from cardiac arrest. Burst-suppression ratio, response entropy, state entropy, and wavelet subband entropy were derived. Serum neuron-specific enolase and protein 100B were measured. The Pulsatility Index of Transcranial Doppler Ultrasonography was used to estimate cerebral blood flow velocity. The Glasgow-Pittsburgh Cerebral Performance Categories was used to assess the neurologic outcome during 6 mos after cardiac arrest. Twenty patients had Cerebral Performance Categories of 1 to 2, one patient had a Cerebral Performance Categories of 3, and nine patients had died (Cerebral Performance Categories of 5). Burst-suppression ratio, response entropy, and state entropy already differed between good (Cerebral Performance Categories 1–2) and poor (Cerebral Performance Categories 3–5) outcome groups (p = .011, p = .011, p = .008) during the first 24 hrs after cardiac arrest. Wavelet subband entropy was higher in the good outcome group between 24 and 48 hrs after cardiac arrest (p = .050). All patients with status epilepticus died, and their wavelet subband entropy values were lower (p = .022). Protein 100B was lower in the good outcome group on arrival at ICU (p = .010). After hypothermia treatment, neuron-specific enolase and protein 100B values were lower (p = .002 for both) in the good outcome group. The Pulsatility Index was also lower in the good outcome group (p = .004). Conclusions: Quantitative electroencephalographic variables may be used to differentiate patients with good neurologic outcomes from those with poor outcomes after out-of-hospital cardiac arrest. The predictive values need to be determined in a larger, separate group of patients.
Brain perfusion was studied interictally with 99mTc-HM-PAO SPECT in 47 adult patients with partial epilepsy and normal brain CT. Epilepsy was classified as secondarily generalized in 24 patients, as complex partial in 17 patients and as simple partial in 6 patients. In 24 patients good seizure control was not achieved as these patients had a median number of 78 seizures during the preceeding month, while in the rest of the patients seizure controll was relatively good (less than 6 seizures during preceeding month). Local brain hypoperfusion was observed in 41 or 87% of the patients. Hypoperfusion was located close to the EEG foci in 76% and equally often with temporal and frontal foci. Hypoperfusion and the EEG focus were located on the same side in 83%. Hypoperfusion was more frequent in secondarily generalized epilepsy and simple partial epilepsy than in complex partial epilepsy. Left-sided hypoperfusion was especially associated with complex partial epilepsy. It is likely that the significant epileptogenic brain area was revealed in patients with SPECT focus and EEG focus in the same brain area. In one of our patients MRI showed a small temporal lesion which on successful removal was identified as a low-grade oligodendroglioma. Abnormalities of regional brain uptake of HM-PAO demonstrated by SPECT in patients with partial epilepsy and normal brain CT give further information about pathophysiology in partial epilepsy; this may be of use both for selecting appropriate therapy and in presurgical localization of foci.
We studied nocturnal and early morning variations in the concentration of plasma atrial natriuretic peptide (ANP) in 17 men who habitually snored. The subjects had a mean age of 51.0 +/- 5.8 years, range 41-62 y with a mean body mass index (BMI) of 32.9 +/- 7.3 kg/m2. The concentration of plasma ANP was measured by radioimmunoassay of venous samples at 10 p.m., midnight, 6 p.m. and 8 p.m. All night sleep recordings were conducted with the static charge sensitive bed to monitor body and breathing movements and a BIOX III Pulse Oximeter for the blood oxygen saturation level. Nine patients were defined as having the obstructive sleep apnea syndrome (OSAS). No significant diurnal variation for ANP concentrations was detected. At 8 a.m. five OSAS patients and two others had ANP concentrations above normal (70 pg/ml). Neither mean oxygen saturation during the night nor arterial hypertension discriminated between the high and low ANP groups at 8 a.m. The best discriminators for a high concentration of ANP at 8 p.m. were marked obesity (BMI greater than or equal to 30 kg/m2), over 400 movements lasting less than five seconds, and over 30% of active sleep per night. In a multivariate regression analysis age, percentage of active sleep during the night, BMI and the median oxygen saturation level during the night explained 76.4% of the total variance of ANP at 8 a.m. In a similar analysis the median oxygen saturation level during the night and BMI both explained the variance of ANP significantly. The whole model explained 53.7% of the variance of the ANP concentrations at 6 a.m.(ABSTRACT TRUNCATED AT 250 WORDS)
Summary: A double‐blind crossover trial with 2 g L‐tryptophan ‐and placebo was carried out with five familial and two sporadic patients with progressive myoclonus epilepsy (PME) without Lafora bodies. L‐Tryptophan improved the clinical condition in six out of seven patients. Clinical improvement in ambulation, myoclonic jerks, and general condition was most evident. The change was statistically significant. In visual assessment of EEGs, the amount of paroxysmal activity and dysrhythmia of the background activity decreased in six out of seven patients on L‐tryptophan. The quantitative EEG revealed a decrease in the power bands of theta, alpha, and beta activity in five of six patients on the second day of L‐tryptophan treatment. In familial PME cases, the responses were consistently beneficial. With long‐term L‐tryptophan therapy, the effect disappeared or was even reversed in three of seven patients after 3 to 4 weeks. These findings indicate that therapy with serotonin precursors is worthy of further trial in PME and that deficient tryptophan metabolism may play a part in the etiology of PME without Lafora bodies. RÉSUMÉ Une étude en double‐aveugle avec le L‐tryptophane et un placebo a été effectuée chez 7 sujets atteints ďépilepsie myoclonique progressive (EMP) sans corps de Lafora: 5 cas familiaux et 2 sporadiques. Le L‐tryptophane a significativement amélioréľétat clinique de 6 des 7 patients, agissant principalement sur la démarche, les myoclonies et ľétat général. De même ľEEG a été amélioré six fois sur sept: atténuation de la dysrythmie et diminution des paroxysmes. ľétude quantitative de ľEEG a révélé de plus une diminution de ľénergie dans la bande des activités théta, alpha et béta cinq fois sur six patients dans le deuxieme jour du traitement. Dans les cas familiaux la réponse au traitement a été uniformément bénéfique. Mais dans les traitements de longue durée les effets du L‐tryptophane ont disparu ou se sont même inversés chez trois de sept sujets après trois ou quatre semaines. Pareilles constatations indiquent que les essais de traitement des EMP par les précurseurs de la sérotonine méritent ďêtre poursuivis et qu'un déficit de métabolisme du tryptophane peut jouer un rôle dans ľétiologie des EMP sans corps de Lafora. RESUMEN Se ha llevado a cabo un estudio doble ciego en cinco casos de epilepsía mioclónica progresiva sin cuerpos de Lafora (PME) y dos enfermos con mioclonías esporádicas tratados con 2 g L‐triptófano y placebo. Cinco de siete enfermos mejoraron con la administración de L‐triptófano, siendo la seguridad en la marcha, las mioclonías y el estado general los factores más beneficiados. Los cambios fueron estadisticamente significativos. El análisis visual de los EEG reveló una reducción de la cantidad de la actividad paroxística y de la disrítmía de la actividad de fondo en seis de siete pacientes que tomaban L‐triptófano. El EEG cuantitativo mostró una disminución de las bandas theta, alfa y beta en cinco de seis enfermos al segundo día de tratamiento con L‐triptófano. En los cases de PME familiar los resultados fueron consistentemente beneficiosos. En tres de siete casos de tratamiento prolongado los efectos desaparecieron ó, incluso, fueron opuestos a la tercera ó cuarta semana. Estos hallazgos indican que el tratamiento del sídrome de PME con precursores de la serotonina merece intentos adicionales y que una deficiencia en el metabolismo del triptófano puede contribuir a la etiología de la PME sin cuerpos de Lafora. ZUSAMMENFASSUNG Eine Doppelblindcross‐over‐Studie mit 2 g L‐Tryptophan und Placebo wurde mit 5 familiären und zwei sporadischen Fällen von progressiver Myoklonus‐Epilepsie (PME) ohne Laforakörperchen unternommen. L‐Tryptophan verbesserte den klinischen Zustand bei 6 von 7 Patienten. Die Gangsicherheit, myoklonische Zuckungen und der Allgemeinzustand waren am deutlichsten betroffen. Die Veränderung war statistisch signifikant. Bei der visuellen Auswertung der EEG hatten die paroxysmale Aktivität und die Dysrhythmie der Hintergrundstätigkeit bei 6 von 7 Patienten unter L‐Tryptophan abgenommen. Die quantitative EEG‐Auswertung zeigte eine Abnahme der Leistung im Theta‐ Alpha‐ und Beta,‐Band bei 5 von 6 Patienten am 2. Tag der L‐Tryptophan‐Behandlung. Bei familiären PME‐Fällen waren die Wirkungen durchaus günstig. Unter der Langzeittherapie mit L‐Tryptophan verschwand die Wirkung bei 3 von 7 Patienten nach 3 bis 4 Wochen oder sie verkehrte sich ins Gegenteil. Diese Beobachtungen zeigen an, daß es sich lohnt, die Therapie mit Serotonin‐Vorstufen beim PME‐Syndrom weiter zu erproben; ein unzureichender Tryptophan‐Metabolismus mag eine Rolle in der Ätiologie der PME ohne Laforakorperchen spielen.
