Endovascular ablation of a temporal lobe epileptogenic focus - a complication of Wada testing.

The authors report on a patient with a long history of medically refractory temporal lobe epilepsy. During pre-operative evaluation for anterior temporal lobectomy he underwent a Wada test for speech and memory lateralization. During the procedure, he suffered a focal cerebral infarct, within the right medial temporal lobe, at the site of the epileptic focus. This resulted in the resolution of his seizure disorder. The possibility of endovascular management of seizure disorders of the temporal lobe should be investigated further as a potentially minimal invasive therapeutic option for medically intractable epilepsy.

New insights into the mechanism of neurally mediated syncope.

OBJECTIVE: To determine the role of the cerebral cortex in neurally mediated syncope, the electroencephalograms (EEG) of patients recorded during head up tilt table test were analysed. DESIGN: Retrospective study. SETTING: University hospital. PATIENTS: 18 patients with syncope or near syncope underwent head up tilt table test with simultaneous ECG and EEG monitoring. METHODS: Standard 70 degrees tilt table test was done with simultaneous ECG and EEG monitoring. EEG waveforms were analysed by both visual inspection and spectral analysis. RESULTS: 6 of 18 patients (33%) had a positive tilt table test. Before syncope slow waves increased in patients with a positive test. In addition, five of six tilt positive patients (83%) had slow wave activity that lateralised to the left side of the brain (mean (SD) 822 (724) v 172 (215) micro V(2), p < 0.05), while none of the tilt negative patients exhibited lateralisation (24 (15) v 26 (19) micro V(2), NS). Spectral analysis showed that the lateralisation occurred in the delta frequency. The lateralisation preceded the event by 5-56 seconds (18 (21) seconds). CONCLUSIONS: EEG activity lateralises to the left hemisphere of the brain before syncope. The lateralisation precedes syncope and is associated with the onset of bradycardia, hypotension, and clinical symptoms. These findings suggest that the central nervous system may have a role in neurally mediated syncope.

Long-term compliance with nasal continuous positive airway pressure therapy of obstructive sleep apnea.

In an attempt to identify predictors of long-term compliance with nasal continuous positive airway pressure (CPAP), we reviewed the records of 125 patients with obstructive sleep apnea (OSA) referred to our center for nasal CPAP trials. Severity of sleep apnea, sleep staging, daytime hypersomnolence, effectiveness of nasal CPAP, previous palatal surgery, and adverse reactions were compared in compliant and noncompliant patients. Nineteen patients did not tolerate a nasal CPAP trial in the laboratory or refused home nasal CPAP therapy. Ten patients were unavailable for follow-up. Of the remaining 96 patients, 23 (24 percent) had discontinued therapy, while 73 (76 percent) were still using nasal CPAP at 14.5 +/- 10.7 months (mean +/- SD). There were no statistically significant differences between the compliant and noncompliant patients in baseline apnea plus hypopnea index (AHI), baseline sleep staging, AHI while receiving nasal CPAP, sleep staging while receiving nasal CPAP, or frequency of adverse reactions during therapy. Severe daytime sleepiness was present in 65 of the 73 compliant patients and in 12 of the 23 noncompliant patients (p less than 0.05). Ten of 43 in the compliant group had previous palatal surgery compared with ten of 23 noncompliant patients (p less than 0.05). Our data confirm earlier observations in smaller samples that compliant and noncompliant patients have equally severe sleep apnea and good initial responses to nasal CPAP. Long-term compliance with nasal CPAP may be associated with the severity of daytime hypersomnolence on presentation. Previous palatal surgery was more frequent in patients who did not tolerate long-term nasal CPAP therapy.

Feedback control of human alpha rhythm from the central area.

Twenty subjects, aged 17 to 25, were given from 5 to 10 sessions of training in controlling alpha. They were divided into three groups, respectively reinforced for increasing alpha from the central area, reinforced for decreasing alpha from the central area, and given noncontingent reinforcement. Compared with the initial baseline, the alpha of the noncontingent subjects did not change, while those reinforced for increases were reliably higher and those reinforced for decreases reliably lower than the noncontingent group. A slight trend toward improvement during successive sessions was not reliable. Since the experiment was conducted in the Soviet Union, the subjects had no expectations of an "alpha experience." Although tests showed a slight elevation in mood at the end of the sessions, there were no differences among the groups. There was an increase in reports of fatigue after the training sessions. There were no reports of using visual or somatomotor maneuvers as a means of controlling alpha. Furthermore, alpha rhythm control was not found to be consistently correlated with changes in heart rate, respiration, or mood, as determined by cross-correlation analysis.

Effect of central venous pressure on brain tissue pressure and brain volume.

In cats, brain tissue pressure (BTP) was measured by the wick-catheter method. The BTP was positive, but lower than cerebrospinal fluid pressure. Elevation on central venous pressure led only to a transient proportional increase of BTP. When the calvaria and dura of one hemisphere were removed, the rise of BTP was even less. Water content of the brain was normal in either case, even after prolonged venous hypertension. Venous hypertension led in all cases to a marked increase of the brain volume which was caused by vessel dilatation. In brain edema, produced by rinsing the brain surface with ouabain and concentrated saline, BTP was increased permanently by venous hypertension. The water content of the brain was much greater than normal. From these results it was concluded that congestive edema does not occur in the brain unless the tissue is damaged. However, venous hypertension does cause brain swelling.

Increase in cerebral perfusion pressure by arterial hypertension in brain swelling. A mathematical model of the volume-pressure relationship.

Brain swelling was produced in monkeys and cats by the inflation af an epidural balloon against the parietal lobe. Resulting changes in intracranial pressure (ICP) were correlated to variation in systemic arterial pressure (SAP). Intracranial perfusion pressure (ICPP) defined as the difference between SAP and ICP, was found to vary with the degree of arterial hyper-and hypotension. The relationship between SAP and ICP can be explained by an existing equilibrium between extramural pressure and vessel wall circumferential tension. A positive perfusion pressure can exist in brain swelling as long as vessel wall tension is preserved and the degree of expanding brain tissue volume is held below certain limits.

Evidence for higher functions of the cerebellum: eating and grooming elicited by cerebellar stimulation in cats.

Well-organized eating and grooming behaviors were elicited in cats by stimulation of a zone in the cerebellum that extended from the fastigial nucleus to the superior cerebellar peduncle. Behaviors appeared to result from the facilitation of specific sensorimotor mechanisms, rather than the induction of generalized "drive" states. The results emphasize the need for a broad view of cerebellar function.