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Repeated ECT and prolactin release in depressed patients
BIOL PSYCHIATRY 1992,31:613-616
613
BRIEF REPORTS
Repeated ECT and Prolactin Release in Depressed Patients Allan I. F. Scott, Sadie M. Gow, William Garden, P. Anne Shering, and Lawrence J. Whalley
Introduction Whereas sham electroconvulsive therapy (ECT) increases the blood concentration of prolactin (PRL) up to two-fold after 15 m~n, real ECT increases PRL concentration several fold (Deakin et al 1983). Sequential study of the effects of electrode placement has established that bilateral ECT releases 25% (Swartz and Abrams 1984)-50% (Papakostos et al 1986) more PRL than does unilateral ECT which may demonstrate a greater hypothalan,ic-stimulating effect of bilateral ECT (Swartz and Abrams 1984). Electroencephalographic (EEG) study of the relationship between the length of cerebral seizure activity and PRL release has been inconclusive (Abrams and Swartz 198~b; Robin et at .~985), as has been the study of the relationship betw~,~:, PRL release and recovery from depression (Deakin et al 1983; Abrams and Swartz 1985a). It has been suggested that the study of pituitary hormone release over a course of ECT may provide important information about alterations in central monoaminergic transmission in depressed patients. (Whalley et al 1982; Aperia et al 1985). The major role of the hypothalamus in the regulation of PRL release is inhibitory through the tuberoinfundibular dopaminergic From the University Department of Psychiatry, Royal Edinburgh Hospital. and UniversityDepartmentof ClinicalChemistry, Royal Infirmary, Edinburgh. Address reprint requests to Dr. Allan I.F. Scott, University Department of Psychiatry, Kennedy Tower, Royal Edinburgh Hospital, Mommgstde Park, Edinburgh. EHIO 5HF, Umted Kingdom. Received February 27, 1991, revised June 17, 1991 © 1992 Soctety of Biological Psych,atry
system. A PRL releasing factor, such as thyrotropin releasing hormor ~ or vasoactive intestinal l~eptide, may be involved in stimulating PRL release and this may involve serotonin (5HT) (Leong et al 1983). After ECT, PRL release has been reported to be significantly reduced later on in a course of treatment for depression as compared to the first treatment (Deakin et al 1983; Abrams and Swartz 1985a; Aperia et al 1985; Cooper et al 1989), suggesting an increase in the responsiveness of post-synapuc dopamine receptors (Abrams and Swartz 1985a; Aperia et al 1985). This finding has not always been confirmed (Whalley et al 1982; Linnoila et al 1984; Haskett et al 1985). The intake of neuroleptic drugs increases both basal and ECl'-induced PRL release (Swartz 1985a; Aperia et a! 1985), but only one report concerned depressed patients free of neuroleptic drugs in the 2 weeks before ECT (Abrams and Swartz 1985a). O~:r aim was to study PRL release over a course of ECT in depressed patients who had not takeL', neuroleptic drugs during their index illness. ECT was monitored by 6-channel EEG because the ~gpatial distribution of epileptic seizures in hum,ms influences PRL release in that generalized se~ :ures release more PRL than focal seizures (Spc.ding et al 1986).
Methods The study protocol was approved by the Psychiatry and Clinical Psychology Ethics of Research Sub-Committee of the Lothian Health Board. The sample consisted of six women and 0006-3223/92/$05.00
614
four men (mean age 56.3 yea~s) who satisfied Research Diagnostic Criteria for Definite Major Depressive Disorder. None of the patients suffered any significant physical illness. No patient had received ECT or neuroleptic drugs in the previous 3 months. At the first ECT, five patients received a tficyclic antidepressant drug, two patients lithium carbonate, one patient chlc,ml hydrate, and one patient rantidine; one patient was drug-free. Drug therapies were unchanged over the course of ECT. The day before the first ECT, the mean score on the Hamilton Rating Scale for Depr;ssion was 22.4 (range 19-26). Anesthesia was induced by thiopentone sodium followed by suxamethonium, the doses being the same for each patient at the first and last treatments. No regular anesthetic premedication was prescribed. The electrical stimulus was provided by a brief-pulse constant current ECT machine (Ectron CCX Series 3) and was standard at the first and last treatments (800 mA, 5 sec, 1.25 msec, 55 Hz = 275 mC). Electrode placement was al.',o standard for each patient (unilateral ECT 3 patients, bilateral ECT 7 patients). Cerebral seizme activity was timed on 6 channels of a portable EEG by an independent rater (Scott et al 1989). Three measures of cerebral seizure activity were made, namely, the time from the end of electrical stimulation to the end of bilateral spike-wave activity, the last spike wave in any channel, and the end of any paroxysmal seizure activity. An intravenous catheter was inserted 60 min before ECT (8:158:45 AM). Blood samples were withdrawn at 15, - 1, + 10, + 15, + 30, and + 6 0 min in relation to electrical stimulation at the first and last ECTs. A course of ECT consisted of 4-10 (mean 6.3) treatments. Prolactin was measured in serum using a twosite immunoradiometnc assay with sucrose separation (Wright and Hunter 1983). The withinassay and between-assay coefficients of variation were less than 4% and 8%, respectivels. All samples from the same patient were analyzed within one assay. The reference range in this laboratory is 60-390 mU/L. All results are mean + SD. All p values are two-tailed. -
Brief Reports
BIOL PSYCHIATRY 1992,31.613-616
Table i . M e a n Serum Prolactin Concentrations
(+_ SD) before and after the First and Last ECTs in Depressed Patients Free of Neuroleptic Drugs (n 10) Serum prolactin concentratio~
(mU/L) Time Before ECT b + 10 min + 15 min + 30 rain + 60 min Peak minus baseline
1st ECT 182 564 640 567 .,60 458
_ --. ± *" ± ±
147 220 336 336 158 336
last EC! ~ 168 644 668 588 427 500
_ ± ± ± ± ±
102 262 276 238 186 340
el'hem were no significant diffemm.~s between the Ist and last
ECT, at any time (paired t-test). bMean of values at - 15 and - ! min.
Results Table I shows that there were no significant differences in serum PRL concentrations at any sampling point between the firstand lastECTs. Peak P R L concentration occurred + 15 min after both the firstand last ECT. ECT-induced PRL release ( + 15 min--basal) did not diminish .-to,., _~- 3 3 6 v e r s u s b e t w e e n " mt~ Ill'bt " " acM t,,,la~t.~tw"r"A¢°,
500 +_ 340 mUlL (t = - 0 . 5 9 , df - 9, p = 0.56). There were no consistent relationships between either the sex of the patient or electrode placement and ECT-induced PRL release over a course of ECT, but the numbers involved were small. In padents free of tricyclic antidepressant drugs (n = 5), ECT-induced PRL release was virtually identical at the first and last ECT (448 -4456 versus 452 _+ 363 mU/L), whereas there was a nonsignificant increase in those takiag a tricyclic antidepressant: 463 +_ !60 versus 349 _+ 121 m U / L ( t = 0.73, df = 4, p = 0.62). The mean lengths of total cerebral seizure activity were 47.9 +_. 32.6 sec at the first ECT and 42.5 +_ 46.5 bec at the last ECT (t = 0.34, p = 0.75). ECT-induced PRL 1eleas~ was unrelated to any measure of seizure length at eider the firs~ or last ECT. For example, the Spearm~'s correlations for total seizure length were rho = - 0 . 1 7 (p = 0.65) at the
Brief Reports
first ECT and rho = 0.12 (p = 0.74) at the last ECT. Discussion We failed to confirm that PRL release is reduced at the last ECT compared to the first ECT in this sample of neuroleptic-free depressed patients. There was a nonsignificant trend for ECTinduced PRL release to increase by the last ECT in patients taking a tricyclic antidepressant drug, whereas PRL release was virtually identical in patients free of such drugs. ECT-induced PRL release was not correlated with generalized spikewave or total cerebral seizure activity, suggesting that ol~ce cerebral seizure activity is generalized, seizure length is not of importance to PRL release. Swartz (1985b) pointed out that studies of the endocrine effects of ECT underestimate the total amount of hormones released from the pituitary, because they ignore the rate of elimination of hormone from the blood. Consequently, we assessed previously the application of a kinetic model of hormone release and elimination to the observed effects of ECT on PRL release, but found that it ,~w,~p~,~i~e to fit a unique curve to the observed data i~ ,.,dy about half of the data-sets (McGuire et al 1989). It remains to be established whether torn| hormone release is more informative than maximum availability (peak co~centration), but positive findings have been achieved simply comparing peak and basal concentrations (Deakin et al 1983; Robin et al 1985; Papakostas et al 1986). There are further methodological problems in the study of the later effects of ECT on PRL release (i.e., as blood concentrations fall to,yards the basal value) because the basal PRL c~..qcentration may be affected by the stressful anticipation of ECT (Rose 1984) ~nd the 24-hr profile of plasma PRL concentration involves a decrease between morning waking and mid-day in health and during depressive illness (Linkowski et al 1989). These confounding effects will be minimized by the study of the earlier effects of ECT when PRL release from the pituitary is presumably the major influence on blood PRL concentration.
BIOL PSYCHIATRY 1992;31:613-616
615
The intake of neuroleptic drugs alters both basal and ECT-induced PRL release. As patients improve during a course of ECT, the need for neuroleptic drug treatment diminishes. If the intake of neuroleptic chugs is reduced at the end of a course of treatment, then this may be an important explanation of changes in PRL release observed in some earlier studies. The reduction of PRL release by the administration of the nonselective 5-HT receptor antagonist methysergide (Papakostas et al 1988), Out not ketanserin, which antagonizes 5-HT2 receptors preferentially (Zis et al 1989), supports a role for 5-HTt receptors in ECT-induced PRL release. These findings may help explain the nonsignificant increase in PRL release at the last ECT in patients who took a ~6cyclic antidepressant, although this requires replication in a larger series of patients. Clomipramine has been sho~vn to enhance the PRL response to L-tryptophan (Anderson and Cowen 1986). This work supported by grants from the Scottish Hospitals Enc~owment Research Trust and the McGhie Fund, University of Edinburgh. PAS supported by Schering Ltd. We thank Katherine Grieve for typing the manuscript.
References Abrams R, Swartz CM (1985a): Electroconvulsive therapy and prolactin release: Relation to treatment response in melancholia. Convulsive Ther I: 38-42. Abrams R, Swartz CM (1985b): Electroconvulsive therapy and prolactin release: Effects of stimulus parameters. Convulsive Ther 1:115-119. Anderson IM, Cowen PJ (1986): Clomipramine enhances prolactin and growth hormone responses to L-tryptophan. Psychopharmacology 89:131133. Aperia B, Thoren M, Wetterberg L (1985): Prolactl~l and thyrotropin in serum during electroconvulsivc therapy in patients with major depressive illness. Acta Psychiatr Scand 72: 302-308. Cooper AJ, Finlayson R, Velamoor VR, Magnus RV, Cemovsky A (1989): Effects of ECT on prolactin, LH, FSH and testosterone in males with major depressive illness. Can J Psychiatry 34:814-817.
616
BIOLPSYCHIATRY 1992;31.6~3-616
Deakin JEW', Fe~ier iN, Crow Tj, Johnstone EC, Lawler P (1983~ 7c~c *,~',/ 12T on pituitary hormone release: ~,~ ~ti,. ,!' .. to seizure, clinical variables and outcome. B,., Psychiatry 143:618624. Haskett RF, Zls AP, Albala AA (1983): Hormone response to repeated electroconvulsive therapy: Effects of naloxone. Biol Psychiatry 20: 623-633. Leong DA, Frawley LS, Neill JD (1983): Neuroendocrine control of prolactin secretion. Ann Rev Physiol 45:109-127. Linkowski P, Cauter EV, L'Hermite-Baleriaux M, et al (1989): The 24-hour profile of plasma prolactin in men with major endogenous depressive illness. Arch Gen Psychiatry 46:813-819. Linnoila M, Litovitz G, Scheinin M, Chang M-D, Curler NR (1984): Effects of electroconvulsive tr¢.atment on monoamine metabolit.zs, growth hormone and p~olactin in plasma. Bici Psychiatry 19: 79-84. McGuire RJ, Scott AIF, Bennie J, S-Watts G (1989): Reliability of the application of a kinetic model of hormone release: Prolactin and oestrogewstimulated neurophysin after electroconvulsive therapy. Convulsive Ther 5: 131-139.
Papakostas Y, Stephanis C, Markianos M, Papadimitriou G (1986): Electrode placement and prolactin response to electroconvulsive therapy. Convulsive Ther 2: 99-107. Papakostas Y, Markianos M, Stephanis C (1988): Methysergide reduces the prolactin response to l~CT. 8iol Psychiatry 24: 465-468. Robin A, Binme CD, Copas JB (1985): Electrophysiological and hormonal responses to three types
Brief Reports
of electroconvulsive therapy. Br J Psychiatry 147: 707-712. Rose RM (1984): Overview of endocrinology o~t :tress. In Brown GM, Coslov S, Reiehlin S (eds), Neuroendocrinology and Psychiatric Disorder. New York: Raven pp 95-122. Scott AIF, Shering PA, Dykes S (1989): Would monitoring by electro-encephalogram improve the practice of electroconvulsive therapy? Br J Psychiatry 145: 853-857. Sperling MR, Pritchard PB, Engel J, Daniel C, Sagel J (1986): Prolactin inpartial epilepsy: an indicator of limbic seizures. Ann Neurol 20:716-722. Swartz CM (1985a): Hormone response to ECT. Biol Psychiai'ry 20: 1334. Swartz CM (1985b): Characterisation of the total amount of prolactin released by ECT. Convulsive Ther: I: 252-257. Swartz C, Abrams R (1984): Prolactin levels after bilateral and unilateral ECT. BrJ Psychiatry 144: 643-645. WhaUey LJ, Dick H, Watts AG, et al (1982): Immediate increases in plasma prolactin and neurophysin but not other hormc aes after electroconvulsive therapy. Lancet ii: 1064-1068. Wright JF, Hunter WM (1983): The sucrose layering separation: A non-centrifugation system. In Hunter WM, Corrie JET (eds), lmmunoassays Jbr Clinical Chemistry. Edinburgh: Churchill Livingstone, pp 170-177. Zis AP, Manji HK, Remick RA, Kelly-Grant BE, Clark CM (1989): Effect of the 5HT2 antagonist ketanscrin on the ECT-induced prolactin release. 8iol Psychiatry 26: 102-106.
613
BRIEF REPORTS
Repeated ECT and Prolactin Release in Depressed Patients Allan I. F. Scott, Sadie M. Gow, William Garden, P. Anne Shering, and Lawrence J. Whalley
Introduction Whereas sham electroconvulsive therapy (ECT) increases the blood concentration of prolactin (PRL) up to two-fold after 15 m~n, real ECT increases PRL concentration several fold (Deakin et al 1983). Sequential study of the effects of electrode placement has established that bilateral ECT releases 25% (Swartz and Abrams 1984)-50% (Papakostos et al 1986) more PRL than does unilateral ECT which may demonstrate a greater hypothalan,ic-stimulating effect of bilateral ECT (Swartz and Abrams 1984). Electroencephalographic (EEG) study of the relationship between the length of cerebral seizure activity and PRL release has been inconclusive (Abrams and Swartz 198~b; Robin et at .~985), as has been the study of the relationship betw~,~:, PRL release and recovery from depression (Deakin et al 1983; Abrams and Swartz 1985a). It has been suggested that the study of pituitary hormone release over a course of ECT may provide important information about alterations in central monoaminergic transmission in depressed patients. (Whalley et al 1982; Aperia et al 1985). The major role of the hypothalamus in the regulation of PRL release is inhibitory through the tuberoinfundibular dopaminergic From the University Department of Psychiatry, Royal Edinburgh Hospital. and UniversityDepartmentof ClinicalChemistry, Royal Infirmary, Edinburgh. Address reprint requests to Dr. Allan I.F. Scott, University Department of Psychiatry, Kennedy Tower, Royal Edinburgh Hospital, Mommgstde Park, Edinburgh. EHIO 5HF, Umted Kingdom. Received February 27, 1991, revised June 17, 1991 © 1992 Soctety of Biological Psych,atry
system. A PRL releasing factor, such as thyrotropin releasing hormor ~ or vasoactive intestinal l~eptide, may be involved in stimulating PRL release and this may involve serotonin (5HT) (Leong et al 1983). After ECT, PRL release has been reported to be significantly reduced later on in a course of treatment for depression as compared to the first treatment (Deakin et al 1983; Abrams and Swartz 1985a; Aperia et al 1985; Cooper et al 1989), suggesting an increase in the responsiveness of post-synapuc dopamine receptors (Abrams and Swartz 1985a; Aperia et al 1985). This finding has not always been confirmed (Whalley et al 1982; Linnoila et al 1984; Haskett et al 1985). The intake of neuroleptic drugs increases both basal and ECl'-induced PRL release (Swartz 1985a; Aperia et a! 1985), but only one report concerned depressed patients free of neuroleptic drugs in the 2 weeks before ECT (Abrams and Swartz 1985a). O~:r aim was to study PRL release over a course of ECT in depressed patients who had not takeL', neuroleptic drugs during their index illness. ECT was monitored by 6-channel EEG because the ~gpatial distribution of epileptic seizures in hum,ms influences PRL release in that generalized se~ :ures release more PRL than focal seizures (Spc.ding et al 1986).
Methods The study protocol was approved by the Psychiatry and Clinical Psychology Ethics of Research Sub-Committee of the Lothian Health Board. The sample consisted of six women and 0006-3223/92/$05.00
614
four men (mean age 56.3 yea~s) who satisfied Research Diagnostic Criteria for Definite Major Depressive Disorder. None of the patients suffered any significant physical illness. No patient had received ECT or neuroleptic drugs in the previous 3 months. At the first ECT, five patients received a tficyclic antidepressant drug, two patients lithium carbonate, one patient chlc,ml hydrate, and one patient rantidine; one patient was drug-free. Drug therapies were unchanged over the course of ECT. The day before the first ECT, the mean score on the Hamilton Rating Scale for Depr;ssion was 22.4 (range 19-26). Anesthesia was induced by thiopentone sodium followed by suxamethonium, the doses being the same for each patient at the first and last treatments. No regular anesthetic premedication was prescribed. The electrical stimulus was provided by a brief-pulse constant current ECT machine (Ectron CCX Series 3) and was standard at the first and last treatments (800 mA, 5 sec, 1.25 msec, 55 Hz = 275 mC). Electrode placement was al.',o standard for each patient (unilateral ECT 3 patients, bilateral ECT 7 patients). Cerebral seizme activity was timed on 6 channels of a portable EEG by an independent rater (Scott et al 1989). Three measures of cerebral seizure activity were made, namely, the time from the end of electrical stimulation to the end of bilateral spike-wave activity, the last spike wave in any channel, and the end of any paroxysmal seizure activity. An intravenous catheter was inserted 60 min before ECT (8:158:45 AM). Blood samples were withdrawn at 15, - 1, + 10, + 15, + 30, and + 6 0 min in relation to electrical stimulation at the first and last ECTs. A course of ECT consisted of 4-10 (mean 6.3) treatments. Prolactin was measured in serum using a twosite immunoradiometnc assay with sucrose separation (Wright and Hunter 1983). The withinassay and between-assay coefficients of variation were less than 4% and 8%, respectivels. All samples from the same patient were analyzed within one assay. The reference range in this laboratory is 60-390 mU/L. All results are mean + SD. All p values are two-tailed. -
Brief Reports
BIOL PSYCHIATRY 1992,31.613-616
Table i . M e a n Serum Prolactin Concentrations
(+_ SD) before and after the First and Last ECTs in Depressed Patients Free of Neuroleptic Drugs (n 10) Serum prolactin concentratio~
(mU/L) Time Before ECT b + 10 min + 15 min + 30 rain + 60 min Peak minus baseline
1st ECT 182 564 640 567 .,60 458
_ --. ± *" ± ±
147 220 336 336 158 336
last EC! ~ 168 644 668 588 427 500
_ ± ± ± ± ±
102 262 276 238 186 340
el'hem were no significant diffemm.~s between the Ist and last
ECT, at any time (paired t-test). bMean of values at - 15 and - ! min.
Results Table I shows that there were no significant differences in serum PRL concentrations at any sampling point between the firstand lastECTs. Peak P R L concentration occurred + 15 min after both the firstand last ECT. ECT-induced PRL release ( + 15 min--basal) did not diminish .-to,., _~- 3 3 6 v e r s u s b e t w e e n " mt~ Ill'bt " " acM t,,,la~t.~tw"r"A¢°,
500 +_ 340 mUlL (t = - 0 . 5 9 , df - 9, p = 0.56). There were no consistent relationships between either the sex of the patient or electrode placement and ECT-induced PRL release over a course of ECT, but the numbers involved were small. In padents free of tricyclic antidepressant drugs (n = 5), ECT-induced PRL release was virtually identical at the first and last ECT (448 -4456 versus 452 _+ 363 mU/L), whereas there was a nonsignificant increase in those takiag a tricyclic antidepressant: 463 +_ !60 versus 349 _+ 121 m U / L ( t = 0.73, df = 4, p = 0.62). The mean lengths of total cerebral seizure activity were 47.9 +_. 32.6 sec at the first ECT and 42.5 +_ 46.5 bec at the last ECT (t = 0.34, p = 0.75). ECT-induced PRL 1eleas~ was unrelated to any measure of seizure length at eider the firs~ or last ECT. For example, the Spearm~'s correlations for total seizure length were rho = - 0 . 1 7 (p = 0.65) at the
Brief Reports
first ECT and rho = 0.12 (p = 0.74) at the last ECT. Discussion We failed to confirm that PRL release is reduced at the last ECT compared to the first ECT in this sample of neuroleptic-free depressed patients. There was a nonsignificant trend for ECTinduced PRL release to increase by the last ECT in patients taking a tricyclic antidepressant drug, whereas PRL release was virtually identical in patients free of such drugs. ECT-induced PRL release was not correlated with generalized spikewave or total cerebral seizure activity, suggesting that ol~ce cerebral seizure activity is generalized, seizure length is not of importance to PRL release. Swartz (1985b) pointed out that studies of the endocrine effects of ECT underestimate the total amount of hormones released from the pituitary, because they ignore the rate of elimination of hormone from the blood. Consequently, we assessed previously the application of a kinetic model of hormone release and elimination to the observed effects of ECT on PRL release, but found that it ,~w,~p~,~i~e to fit a unique curve to the observed data i~ ,.,dy about half of the data-sets (McGuire et al 1989). It remains to be established whether torn| hormone release is more informative than maximum availability (peak co~centration), but positive findings have been achieved simply comparing peak and basal concentrations (Deakin et al 1983; Robin et al 1985; Papakostas et al 1986). There are further methodological problems in the study of the later effects of ECT on PRL release (i.e., as blood concentrations fall to,yards the basal value) because the basal PRL c~..qcentration may be affected by the stressful anticipation of ECT (Rose 1984) ~nd the 24-hr profile of plasma PRL concentration involves a decrease between morning waking and mid-day in health and during depressive illness (Linkowski et al 1989). These confounding effects will be minimized by the study of the earlier effects of ECT when PRL release from the pituitary is presumably the major influence on blood PRL concentration.
BIOL PSYCHIATRY 1992;31:613-616
615
The intake of neuroleptic drugs alters both basal and ECT-induced PRL release. As patients improve during a course of ECT, the need for neuroleptic drug treatment diminishes. If the intake of neuroleptic chugs is reduced at the end of a course of treatment, then this may be an important explanation of changes in PRL release observed in some earlier studies. The reduction of PRL release by the administration of the nonselective 5-HT receptor antagonist methysergide (Papakostas et al 1988), Out not ketanserin, which antagonizes 5-HT2 receptors preferentially (Zis et al 1989), supports a role for 5-HTt receptors in ECT-induced PRL release. These findings may help explain the nonsignificant increase in PRL release at the last ECT in patients who took a ~6cyclic antidepressant, although this requires replication in a larger series of patients. Clomipramine has been sho~vn to enhance the PRL response to L-tryptophan (Anderson and Cowen 1986). This work supported by grants from the Scottish Hospitals Enc~owment Research Trust and the McGhie Fund, University of Edinburgh. PAS supported by Schering Ltd. We thank Katherine Grieve for typing the manuscript.
References Abrams R, Swartz CM (1985a): Electroconvulsive therapy and prolactin release: Relation to treatment response in melancholia. Convulsive Ther I: 38-42. Abrams R, Swartz CM (1985b): Electroconvulsive therapy and prolactin release: Effects of stimulus parameters. Convulsive Ther 1:115-119. Anderson IM, Cowen PJ (1986): Clomipramine enhances prolactin and growth hormone responses to L-tryptophan. Psychopharmacology 89:131133. Aperia B, Thoren M, Wetterberg L (1985): Prolactl~l and thyrotropin in serum during electroconvulsivc therapy in patients with major depressive illness. Acta Psychiatr Scand 72: 302-308. Cooper AJ, Finlayson R, Velamoor VR, Magnus RV, Cemovsky A (1989): Effects of ECT on prolactin, LH, FSH and testosterone in males with major depressive illness. Can J Psychiatry 34:814-817.
616
BIOLPSYCHIATRY 1992;31.6~3-616
Deakin JEW', Fe~ier iN, Crow Tj, Johnstone EC, Lawler P (1983~ 7c~c *,~',/ 12T on pituitary hormone release: ~,~ ~ti,. ,!' .. to seizure, clinical variables and outcome. B,., Psychiatry 143:618624. Haskett RF, Zls AP, Albala AA (1983): Hormone response to repeated electroconvulsive therapy: Effects of naloxone. Biol Psychiatry 20: 623-633. Leong DA, Frawley LS, Neill JD (1983): Neuroendocrine control of prolactin secretion. Ann Rev Physiol 45:109-127. Linkowski P, Cauter EV, L'Hermite-Baleriaux M, et al (1989): The 24-hour profile of plasma prolactin in men with major endogenous depressive illness. Arch Gen Psychiatry 46:813-819. Linnoila M, Litovitz G, Scheinin M, Chang M-D, Curler NR (1984): Effects of electroconvulsive tr¢.atment on monoamine metabolit.zs, growth hormone and p~olactin in plasma. Bici Psychiatry 19: 79-84. McGuire RJ, Scott AIF, Bennie J, S-Watts G (1989): Reliability of the application of a kinetic model of hormone release: Prolactin and oestrogewstimulated neurophysin after electroconvulsive therapy. Convulsive Ther 5: 131-139.
Papakostas Y, Stephanis C, Markianos M, Papadimitriou G (1986): Electrode placement and prolactin response to electroconvulsive therapy. Convulsive Ther 2: 99-107. Papakostas Y, Markianos M, Stephanis C (1988): Methysergide reduces the prolactin response to l~CT. 8iol Psychiatry 24: 465-468. Robin A, Binme CD, Copas JB (1985): Electrophysiological and hormonal responses to three types
Brief Reports
of electroconvulsive therapy. Br J Psychiatry 147: 707-712. Rose RM (1984): Overview of endocrinology o~t :tress. In Brown GM, Coslov S, Reiehlin S (eds), Neuroendocrinology and Psychiatric Disorder. New York: Raven pp 95-122. Scott AIF, Shering PA, Dykes S (1989): Would monitoring by electro-encephalogram improve the practice of electroconvulsive therapy? Br J Psychiatry 145: 853-857. Sperling MR, Pritchard PB, Engel J, Daniel C, Sagel J (1986): Prolactin inpartial epilepsy: an indicator of limbic seizures. Ann Neurol 20:716-722. Swartz CM (1985a): Hormone response to ECT. Biol Psychiai'ry 20: 1334. Swartz CM (1985b): Characterisation of the total amount of prolactin released by ECT. Convulsive Ther: I: 252-257. Swartz C, Abrams R (1984): Prolactin levels after bilateral and unilateral ECT. BrJ Psychiatry 144: 643-645. WhaUey LJ, Dick H, Watts AG, et al (1982): Immediate increases in plasma prolactin and neurophysin but not other hormc aes after electroconvulsive therapy. Lancet ii: 1064-1068. Wright JF, Hunter WM (1983): The sucrose layering separation: A non-centrifugation system. In Hunter WM, Corrie JET (eds), lmmunoassays Jbr Clinical Chemistry. Edinburgh: Churchill Livingstone, pp 170-177. Zis AP, Manji HK, Remick RA, Kelly-Grant BE, Clark CM (1989): Effect of the 5HT2 antagonist ketanscrin on the ECT-induced prolactin release. 8iol Psychiatry 26: 102-106.