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Electroencephalographic effects of nicotine gum in humans
$172
W.B. Pickworth and R.I. Herning
P29.04 QUANTITATIVE EEG PROFILES OF DIAZEPAM A N D T W O PARTIAL B E N Z O D I A Z E P I N E R E C E P T O R AGON1STS (RO 16-6028 AND R O 17-1812) IN VOLUNTEERS.
(Baltimore, MD, USA)
R. Scherschlicht
EEG effects of gum delivered nicotine (2 and 4 mg) and placebo gum were compared in nicotine-deprived, (12 hr) heavy smokers in a double blind experiment. EEGs from FT, 1=8, C~, and T 6 were frequency analysed by means of a dedicated computer during two 3 min sessions (eyes closed; eyes openmath task) before and after the gum. Preliminary analysis suggests that during the resting EEG session, the 4 mg dose increased alpha frequency, decreased theta power, but had little effect on alpha power; the 2 mg dose appeared ineffective. The EEG changes attending the eyes open-math task session were generally unaffected by either dose of nicotine. It appears that gum-delivered nicotine has effects similar to those of smoked nicotine. These results are consistent with the observation that nicotine relieves the behavioural lethargy and EEG changes associated with its deprivation in the heavy smoker. Further, the EEG pattern recorded during eyes open-math task are resistant to drug-induced changes.
(Basle, Switzerland)
P29.02 ELECTROENCEPHALOGRAPHIC EFFECTS OF N I C O T I N E G U M IN H U M A N S .
P29.03 I N S U L I N I N D U C E D CHANGES IN DIABETICS.
HYPOGLYCAEMIA:
EEG
In a double blind study, the effects of 0.05 and 0.1 mg Ro 16-6028 and Ro 17-1812 p.o. on absolute power density per frequency band of a symmetric central (C3-C4) waking EEG recorded with closed eyes were compared with those of 10 mg diazepam p.o. and placebo in 6 male healthy volunteers. EEG records of 5 min duration were made before and up to 6 h after drug intake. Diazepam increased power in the beta 1 ( < 18 Hz) and beta 2 ( > 18 Hz) range, very strongly reduced power in the alpha range and moderately to slightly reduced power in the delta and theta ranges. In contrast, Ro 17-1812 predominantly reduced power in the delta and theta ranges and tended to reduce power in both beta ranges. Alpha power was not changed by the low, but reduced by the high dose. Again in contrast, Ro 16-6028 increased delta power, did not affect power in the theta, alpha and beta 2 ranges and only slightly increased power in the beta 1 range. In spite of the c o m m o n property of being ligands to the benzodiazepine receptor, the 3 compounds, thus, affected the EEG differently. Accordingly, different clinical profiles are to be expected.
B. Stigsby, S. Pramming and B. Thorsteinsson
(Hellerup, Denmark) The EEGs of 13 fasting, recumbent, alert insulin-dependent diabetic patients, mean age: 28 (20-40) and mean duration of diabetes 12 (3-28) years, were evaluated by period analysis during gradua ! lowering of B-glucose (BG) to hypoglycaemic levels (median 1.7 m m o l / l ) by i.v. insulin infusion. A glycaemic threshold for EEG changes of 2.2 _+0.11 m m o l / l (mean _+SEM) was established, as no EEG changes were observed above this BG level. At BG = 1.9 m m o l / l theta activity increased concomitantly with decreased alpha activity (p < 0.025). This was accentuated at BG =1.7 m m o l / l where delta activity also appeared (p < 0.025). After termination of insulin as BG increased spontaneously to 2.7 m m o l / l the changes remitted and almost disappeared after intravenous glucose. Bisynchronous bursts of 2 - 4 Hz activity were seen fronto-temporally in half the patients at BG < 2 mmol/1. No inter-hemispheric differences were observed. All patients revealed signs of hypoglycaemia at BG < 2 m m o l / l independent of a rapid fall in BG. Thus, EEG slowing during hypoglycaemia occurs abruptly at concentrations of approximately 2 mmol/1, accentuates during additional BG reduction, and shows delayed recovery after restoration of normo-glycaemia.
P29.05 VEP LATENCY DELAY BY A SINGLE D O S E O F HALOPERIDOL. H. van Duijn, M.K.F. Beckmann and J.C. Stoof
(Amsterdam, The Netherlands) Dopamine (DA) is supposed to play a role as a neurotransmitter in the neuronal circuits necessary for the production of visual evoked potentials (VEPs). In Parkinsonian patients a delay in the VEP latency has been reported which could be partially normalized after 1-dopa treatment. A VEP latency delay has been described after long-term treatment of schizophrenic patients with DA-receptor blocking drugs (BodisWollner et al., Ann. Neurol. 1982, 11; 478). We have studied the effect of a single dose (2.5 mg i.m.) of haloperidol on VEPs in 5 male volunteers. VEPs were evoked by flash and pattern reversal (checkerboard) stimuli and latencies of maximal occipital peaks were measured. After dark adaptation VEPs were recorded with 20 min intervals; the drug was injected after the second series. As a parameter for drug action plasma prolactin was estimated; haloperidol induced an approximately 8-fold increase 60 min after administration. VEP control sessions were held following the same protocol apart from drug administration. VEP latencies were stable or slightly decreasing during the course of a control session, whereas haloperidol induced an
W.B. Pickworth and R.I. Herning
P29.04 QUANTITATIVE EEG PROFILES OF DIAZEPAM A N D T W O PARTIAL B E N Z O D I A Z E P I N E R E C E P T O R AGON1STS (RO 16-6028 AND R O 17-1812) IN VOLUNTEERS.
(Baltimore, MD, USA)
R. Scherschlicht
EEG effects of gum delivered nicotine (2 and 4 mg) and placebo gum were compared in nicotine-deprived, (12 hr) heavy smokers in a double blind experiment. EEGs from FT, 1=8, C~, and T 6 were frequency analysed by means of a dedicated computer during two 3 min sessions (eyes closed; eyes openmath task) before and after the gum. Preliminary analysis suggests that during the resting EEG session, the 4 mg dose increased alpha frequency, decreased theta power, but had little effect on alpha power; the 2 mg dose appeared ineffective. The EEG changes attending the eyes open-math task session were generally unaffected by either dose of nicotine. It appears that gum-delivered nicotine has effects similar to those of smoked nicotine. These results are consistent with the observation that nicotine relieves the behavioural lethargy and EEG changes associated with its deprivation in the heavy smoker. Further, the EEG pattern recorded during eyes open-math task are resistant to drug-induced changes.
(Basle, Switzerland)
P29.02 ELECTROENCEPHALOGRAPHIC EFFECTS OF N I C O T I N E G U M IN H U M A N S .
P29.03 I N S U L I N I N D U C E D CHANGES IN DIABETICS.
HYPOGLYCAEMIA:
EEG
In a double blind study, the effects of 0.05 and 0.1 mg Ro 16-6028 and Ro 17-1812 p.o. on absolute power density per frequency band of a symmetric central (C3-C4) waking EEG recorded with closed eyes were compared with those of 10 mg diazepam p.o. and placebo in 6 male healthy volunteers. EEG records of 5 min duration were made before and up to 6 h after drug intake. Diazepam increased power in the beta 1 ( < 18 Hz) and beta 2 ( > 18 Hz) range, very strongly reduced power in the alpha range and moderately to slightly reduced power in the delta and theta ranges. In contrast, Ro 17-1812 predominantly reduced power in the delta and theta ranges and tended to reduce power in both beta ranges. Alpha power was not changed by the low, but reduced by the high dose. Again in contrast, Ro 16-6028 increased delta power, did not affect power in the theta, alpha and beta 2 ranges and only slightly increased power in the beta 1 range. In spite of the c o m m o n property of being ligands to the benzodiazepine receptor, the 3 compounds, thus, affected the EEG differently. Accordingly, different clinical profiles are to be expected.
B. Stigsby, S. Pramming and B. Thorsteinsson
(Hellerup, Denmark) The EEGs of 13 fasting, recumbent, alert insulin-dependent diabetic patients, mean age: 28 (20-40) and mean duration of diabetes 12 (3-28) years, were evaluated by period analysis during gradua ! lowering of B-glucose (BG) to hypoglycaemic levels (median 1.7 m m o l / l ) by i.v. insulin infusion. A glycaemic threshold for EEG changes of 2.2 _+0.11 m m o l / l (mean _+SEM) was established, as no EEG changes were observed above this BG level. At BG = 1.9 m m o l / l theta activity increased concomitantly with decreased alpha activity (p < 0.025). This was accentuated at BG =1.7 m m o l / l where delta activity also appeared (p < 0.025). After termination of insulin as BG increased spontaneously to 2.7 m m o l / l the changes remitted and almost disappeared after intravenous glucose. Bisynchronous bursts of 2 - 4 Hz activity were seen fronto-temporally in half the patients at BG < 2 mmol/1. No inter-hemispheric differences were observed. All patients revealed signs of hypoglycaemia at BG < 2 m m o l / l independent of a rapid fall in BG. Thus, EEG slowing during hypoglycaemia occurs abruptly at concentrations of approximately 2 mmol/1, accentuates during additional BG reduction, and shows delayed recovery after restoration of normo-glycaemia.
P29.05 VEP LATENCY DELAY BY A SINGLE D O S E O F HALOPERIDOL. H. van Duijn, M.K.F. Beckmann and J.C. Stoof
(Amsterdam, The Netherlands) Dopamine (DA) is supposed to play a role as a neurotransmitter in the neuronal circuits necessary for the production of visual evoked potentials (VEPs). In Parkinsonian patients a delay in the VEP latency has been reported which could be partially normalized after 1-dopa treatment. A VEP latency delay has been described after long-term treatment of schizophrenic patients with DA-receptor blocking drugs (BodisWollner et al., Ann. Neurol. 1982, 11; 478). We have studied the effect of a single dose (2.5 mg i.m.) of haloperidol on VEPs in 5 male volunteers. VEPs were evoked by flash and pattern reversal (checkerboard) stimuli and latencies of maximal occipital peaks were measured. After dark adaptation VEPs were recorded with 20 min intervals; the drug was injected after the second series. As a parameter for drug action plasma prolactin was estimated; haloperidol induced an approximately 8-fold increase 60 min after administration. VEP control sessions were held following the same protocol apart from drug administration. VEP latencies were stable or slightly decreasing during the course of a control session, whereas haloperidol induced an