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Can hypoglycaemia cause obsessions and
ruminations?
Rippere V
Med Hypotheses (England) Sep 1984, 15 (1) p3-13
Two cases of obsessional ruminations apparently secondary
to functional hypoglycaemia are described. Both patients are
young Caucasian males with obsessional histories at the start
of dietary treatment of 18 and 6 years, respectively. In both
cases, reactive hypoglycaemia was confirmed by glucose
tolerance test. The first case made a complete recovery on
dietary treatment which has lasted over two years; previous
treatment with drugs, behaviour therapy, and counselling were
unsuccessful The response of the second case has been less
outstanding due to poor compliance, but improvement and
worsening have been systematically related to the extent of
his adherence to the suggested dietary regimen. These cases
raise questions for further research on this neglected
subgroup of obsessional patients.
Dietary treatment of chronic obsessional
ruminations.
Rippere V
Br J Clin Psychol (England) Nov 1983, 22 (Pt 4)
p314-6
Chronic obsessional ruminations may prove resistant to
psychological treatment because they are not psychological in
nature but epiphenomena of brain dysfunction secondary to
nutritional factors. The case is described of a chronic,
treatment-resistant ruminator who made a dramatic and lasting
recovery when a high protein breakfast was added to his
elimination diet regimen, undertaken when years of
psychological and pharmacological treatment had failed.
Biochemical and clinical evidence supports the hypothesis that
hypoglycaemia secondary to inappropriate diet was the cause of
his disorder. Dietary contributions to obsessional ruminations
should probably be sought early on in the assessment of such
patients.
Sequential administration of augmentation
strategies in treatment-resistant obsessive-compulsive
disorder: preliminary findings.
Blier P; Bergeron R
Neurobiological Psychiatry Unit, McGill University, Montreal,
Quebec, Canada.
Int Clin Psychopharmacol (England) Mar 1996, 11 (1)
p37-44
Given that an important proportion of patients with
obsessive-compulsive disorder (OCD) fail to respond adequately
to serotonin (5-HT) reuptake inhibitors (SRI), augmentation
strategies aimed at enhancing further 5-HT transmission by
different mechanisms were attempted sequentially in 13
SRI-resistant patients. Addition of the 5-HT1A l
beta-adrenergic antagonist pindolol did not alter OCD
symptomatology but produced a rapid improvement of depressive
symptoms. The 5-HT1A agonist buspirone as well as
5-hydroxytryptophan, the immediate precursor of 5-HT, added to
the SRI-pindolol regimen, were not effective in attenuating
the intensity of OCD. Tryptophan, added to the SRI-pindolol
regimen, produced a significant improvement after 4 weeks,
with further amelioration after 6 weeks (36% decrease of the
Yale-Brown Obsessive Compulsive Score), which was maintained
with treatment prolongation.
Plasma melatonin and cortisol circadian patterns in
patients with obsessive- compulsive disorder before and after
fluoxetine treatment.
Monteleone P; Catapano F; Tortorella A; Di Martino S; Maj
M
Institute of Psychiatry, Second University of Naples,
Italy.
Psychoneuroendocrinology (England) 1995, 20 (7)
p763-70
The circadian rhythms of melatonin and cortisol were
evaluated in seven outpatients with obsessive-compulsive
disorder (OCD) before and after 8 weeks of fluoxetine
treatment (20 mg/day in the first 2 weeks, and 40 mg/day
afterwards), and in seven healthy subjects matched to patients
on age, sex and season of testing. The results confirm our
previous findings of a decreased 24-h production of melatonin
(p < .05; two-way ANOVA with repeated measures) and of an
increased circadian secretion of cortisol (p < .01) in OCD
patients with respect to matched controls, and show, for the
first time, that these hormonal alterations do not
significantly change after 2 months of fluoxetine
administration, in spite of a good clinical improvement. These
data suggest that the normalization of the biochemical changes
underlying the altered endocrine parameters in
obsessive-compulsive patients is not necessary for effective
therapy or clinical remission.
Neuroendocrine responses to intravenous
L-tryptophan in obsessive compulsive disorder.
Fineberg NA; Cowen PJ; Kirk JW; Montgomery SA
Academic Department of Psychiatry, St Mary's Hospital,
London, UK.
J Affect Disord (Netherlands) Oct 1994, 32 (2)
p97-104
We studied the neuroendocrine responses produced by
intravenous L-tryptophan (TRP) in 16 untreated patients with
obsessive compulsive disorder (OCD) and 16 matched healthy
controls. The increase in plasma growth hormone seen following
TRP was significantly greater in the OCD patients, while
TRP-induced prolactin release did not differ from controls.
Taken in conjunction with findings from other neuroendocrine
studies the data suggest that some aspects of 5-HT1A
neurotransmission may be increased in OCD. This increase may
represent a compensatory change which promotes adaptation to
stress in non-depressed OCD patients.
Tryptophan depletion in patients with obsessive-
compulsive disorder who respond to serotonin reuptake
inhibitors.
Barr LC; Goodman WK; McDougle CJ; Delgado PL; Heninger GR;
Charney DS; Price LH
Clinical Neuroscience Research Unit, Abraham Ribicoff
Research Facilities, Connecticut Mental Health Center, New
Haven.
Arch Gen Psychiatry (United States) Apr 1994, 51 (4)
p309-17
METHODS: The effects of short-term tryptophan depletion
were examined in 15 patients with DSM-III-R
obsessive-compulsive disorder who had demonstrated symptom
reduction following treatment with serotonin reuptake
inhibitors. Patients received a 24-hour, low-tryptophan
(160-mg/d) diet followed the next morning by a drink of 15
amino acids. A double-blind, placebo-controlled cross-over
design was used.
RESULTS: The diet and the amino acid drink reduced free
plasma tryptophan levels by a mean of 84% 5 hours later.
Short-term tryptophan depletion did not significantly change
mean ratings of obsessions and compulsions. In contrast, mean
depression ratings were significantly increased with
tryptophan depletion compared with the control
(tryptophan-supplemented) testing.
CONCLUSION: Maintenance of serotonin reuptake
inhibitor-induced improvement of obsessive and compulsive
symptoms, unlike remission of depressive symptoms, may not
depend on ongoing short-term availability of serotonin.
Circadian rhythms of melatonin, cortisol and
prolactin in patients with obsessive- compulsive
disorder.
Monteleone P; Catapano F; Del Buono G; Maj M
Institute of Psychiatry, First Medical School, University of
Naples, Italy.
Acta Psychiatr Scand (Denmark) Jun 1994, 89 (6)
p411-5
Plasma melatonin, cortisol and prolactin (PRL) levels were
measured over a 24-h period in 13 drug-free patients with
obsessive-compulsive disorder and in matched healthy subjects.
The circadian profiles of melatonin and PRL were altered in
patients; the circadian rhythm of cortisol was preserved,
although at a higher level compared with normal controls.
These changes were significantly related to the severity of
the obsessive-compulsive symptoms. Further studies need to
clarify the state- or trait-dependent character of these
abnormalities.
Biological approaches to treatment-resistant
obsessive compulsive disorder.
Goodman WK; McDougle CJ; Barr LC; Aronson SC; Price LH
Yale University School of Medicine, Department of Psychiatry,
New Haven, CT 06519.
J Clin Psychiatry (United States) Jun 1993, 54 Suppl
p16-26
Biological approaches to the patient with
treatment-resistant obsessive compulsive disorder are briefly
reviewed. The most commonly employed strategy involves
combining a potent serotonin reuptake inhibitor (SRI) (e.g.,
clomipramine or fluvoxamine) with another medication that may
exert effects on the brain serotonin system. Open-label
reports regarding the addition of tryptophan, fenfluramine,
lithium, or buspirone to ongoing SRI therapy of obsessive
compulsive disorder are encouraging. However, the
anti-obsessive compulsive efficacy of SRI-lithium and
SRI-buspirone combination therapy has not been confirmed in
recent controlled trials. Preliminary evidence suggests that
addition of neuroleptic may benefit SRI-refractory obsessive
compulsive disorder patients who have a comorbid chronic tic
disorder. Other biological approaches (e.g., electroconvulsive
therapy and psychosurgery) are considered in terms of their
narrowly defined roles in the treatment of patients with
SRI-resistant obsessive compulsive disorder. Finally, an
algorithm is proposed for those patients with obsessive
compulsive disorder who fail to respond to an adequate trial
with a potent SRI. (115 Refs.)
Pharmacotherapy of obsessive compulsive
disorder.
Goodman WK; McDougle CJ; Price LH
Clinical Neuroscience Research Unit, Yale University School
of Medicine, New Haven, CT 06519.
J Clin Psychiatry (United States) Apr 1992, 53 Suppl
p29-37
The authors briefly review studies of the efficacy of
potent serotonin reuptake inhibitors (SRIs) (e.g.,
clomipramine, fluvoxamine) in obsessive compulsive disorder
(OCD) and compare the use of antidepressants in the treatment
of depression and OCD. They propose an algorithm for those
patients with OCD who fail to respond to an adequate trial
with a potent SRI and discuss the promise and limitations of
adding tryptophan, fenfluramine, lithium, buspirone, or a
neuroleptic to ongoing SRI therapy. Other biological
approaches (e.g., ECT, psychosurgery) are considered in terms
of their narrowly defined roles in the treatment of patients
with SRI-resistant OCD. (68 Refs.)
Plasma tryptophan levels and plasma
tryptophan/neutral amino acids ratio in patients with mood
disorder, patients with obsessive- compulsive disorder, and
normal subjects.
Lucca A; Lucini V; Piatti E; Ronchi P; Smeraldi E
Istituto di Ricovero e Cura a carattere scientifico H. San
Raffaele, Department of Neuropsychiatric Sciences, University
of Milan, School of Medicine, Italy.
Psychiatry Res (Ireland) Nov 1992, 44 (2) p85-91
Fasting plasma tryptophan (TRP) levels and ratios of total
plasma tryptophan to the sum of five large neutral amino acids
(LNAAs)--tyrosine, phenylalanine, leucine, isoleucine, and
valine--that compete with tryptophan for passage across the
blood-brain barrier were found to be significantly lower in a
group of 28 patients with major depression compared with 29
normal subjects and 21 patients with obsessive-compulsive
disorder (OCD). The OCD group was divided in two subgroups:
patients with OCD alone and patients with a co-diagnosis of
major depression. Since it has been considered that these
biological parameters reflect brain tryptophan and serotonin
levels, our results suggest their importance in relation to
the presence or absence of depressive symptoms. The values of
the other LNAAs and their sum did not differ significantly
among the groups.
Melatonin and cortisol secretion in patients with
primary obsessive-compulsive disorder.
Catapano F; Monteleone P; Fuschino A; Maj M; Kemali D
Institute of Psychiatry, First Medical School, University of
Naples, Italy.
Psychiatry Res (Ireland) Dec 1992, 44 (3)
p217-25
Plasma levels of melatonin and cortisol were measured over
a 24-hour period in seven patients with primary
obsessive-compulsive disorder (OCD) and seven matched healthy
control subjects. In OCD patients, the 24-hour secretion of
melatonin was reduced as compared with that in healthy control
subjects, whereas its circadian rhythm was preserved. In
addition, in OCD patients, the overall secretion of cortisol
was higher than that in control subjects, but there was no
change in the circadian pattern of cortisol secretion. No
correlation was found between clinical parameters and hormone
levels.
Role of serotonin in obsessive- compulsive
disorder.
Baumgarten HG; Grozdanovic Z
Institute of Anatomy, University Clinic Benjamin Franklin,
Free University of Berlin, Germany.
Br J Psychiatry Suppl (England) 1998, (35)
p13-20
BACKGROUND: Serotonin may play a role in the
pathophysiology of obsessive-compulsive disorder (OCD) because
of the anti-obsessional effect of selective serotonin reuptake
inhibitors (SSRIs).
METHOD: The literature is reviewed on knowledge of the role
of serotonergic neurons in brain function, studies on
monoamine metabolites in cerebrospinal fluid (CSF), various
stress neuropeptides, neuroendocrine and behavioural challenge
after administration of direct and indirect serotomimetic
compounds, and neuroanatomical data on brain circuits
organising behaviour.
RESULTS: In most of the OCD cases analysed, CSF
5-hydroxyindoleacetic acid and homovanillic acid
concentrations do not significantly differ from age-corrected
controls. However, a relationship appears to exist between
pre-treatment levels of these metabolites and clinical
response to drugs acting on the serotonin transporter.
Abnormalities in CSF arginine vasopressin,
corticotropin-releasing hormone, oxytocin and somatostatin
levels have been reported in OCD. Long-term treatment with
high-doses of clomipramine, fluvoxamine, and fluoxetine tend
to correct these neuropeptide abnormalities.
CONCLUSIONS: We hypothesise that continuous treatment with
SSRIs alters serotonin turnover and neuropeptide expression
patterns in OCD-entertaining functional forebrain/midbrain
circuits.
Psychiatric manifestations of homocystinuria due to
cystathionine beta-synthase deficiency: prevalence, natural
history, and relationship to neurologic impairment and vitamin
B6-responsiveness.
Abbott MH; Folstein SE; Abbey H; Pyeritz RE
Am J Med Genet (United States) Apr 1987, 26 (4)
p959-69
Homocystinuria commonly affects the central nervous system
(CNS), primarily as mental retardation, seizures, and stroke.
Case reports have long suggested a predisposition to
schizophrenia, but no careful study of predisposition to
psychiatric illness has been performed. Accordingly, we
evaluated 63 persons with homocystinuria due to cystathionine
beta-synthase deficiency for psychiatric disturbance,
intelligence, evidence of other CNS problems, and
responsiveness to vitamin B6. The overall rate of clinically
significant psychiatric disorders was 51%, predominated by
four diagnostic categories: episodic depression (10%), chronic
disorders of behavior (17%), chronic obsessive - compulsive
disorder (5%), and personality disorders (19%). The average IQ
was 80 +/- 27 (1 SD); and an IQ of less than or equal to 79
was two-thirds more common among vitamin B6-nonresponsive
patients compared to vitamin B6-responsive patients.
Aggressive behavior and other disorders of conduct were
particularly common among patients with mental retardation and
among vitamin B6-nonresponsive patients.
Alphainf 2-adrenoreceptor status in obsessive-
compulsive disorder
Lee M.A.; Cameron O.G.; Gurguis G.N.M.; Glitz D.; Smith C.B.;
Hariharan M.; Abelson J.L.; Curtis G.C.
Cleveland VA Med Ctr, Psychiatry Service, 10000 Brecksville
Road,Brecksville, OH 44141 US
Biological Psychiatry (United States) 1990, 27/10
(1083-1093)
Ten patients with obsessive -compulsive disorder (OCD) and
13 normal control subjects received intravenous infusions of 2
x 10sup -sup 6 g/kg of clonidine and normal saline on separate
days. Responses to the drug relating to plasma growth hormone
(GH), 3-methoxy-4-hydroxyphenylglycol (MHPG), heart rate,
blood pressure, and several symptoms were determined.
Additionally, platelet alphainf 2-adrenoreceptor binding was
measured in most of the subjects. GH, MHPG, blood pressure,
and heart rate responses to clonidine did not differ between
groups. As expected, patients reported more symptoms than
normal subjects, and clonidine was sedating for both groups.
Patients did not differ from normal subjects in the symptom
response to clonidine. The maximum number of binding sites
(B(max)) for tritiated clonidine was significantly greater in
OCD patients than in normals. This pattern of alphainf
2-adrenoreceptor status is different than the patterns in
major depression and panic anxiety.
Vitamin Binf 1inf 2 and folic acid serum levels in
obsessive compulsive disorder
Hermesh H.; Weizman A.; Shahar A.; Munitz H.
Geha Psychiatric Hospital, Beilinson Medical Center, 49 100
Petah Tiqva Israel
Acta Psychiatrica Scandinavica (Denmark) 1988, 78/1
(8-10)
Vitamin Binf 1inf 2 and folate serum levels were studied in
30 patients with obsessive compulsive disorder (OCD), and in
two control groups comprised of 30 chronic schizophrenics and
30 normal healthy subjects. Six patients (20%) of the OCD
group had abnormal low levels of vitamin Binf 1inf 2. This
prevalence was significantly higher than that of the control
groups. No clinical neurological or haematological
abnormalities accompanied the reduced vitamin Binf 1inf 2
levels. Possible implication of this finding for the
pathophysiology of OCD in a subgroup of patients and the
possibility that the Binf 1inf 2 deficiency could be the
consequence rather than the cause of OCD are suggested.
Controlled trials of inositol in psychiatry.
Levine J
Ministry of Health Mental Health Center, Faculty of Health
Sciences, Ben Gurion University of the Negev, Beersheva,
Israel.
Eur Neuropsychopharmacol (Netherlands) May 1997, 7 (2)
p147-55
Inositol is a simple polyol precursor in a second messenger
system important in the brain. Cerebrospinal fluid inositol
has been reported as decreased in depression. A double-blind
controlled trial of 12 g daily of inositol in 28 depressed
patients for four weeks was performed. Significant overall
benefit for inositol compared to placebo was found at week 4
on the Hamilton Depression Scale. No changes were noted in
hematology, kidney or liver function. Since many
antidepressants are effective in panic disorder, twenty-one
patients with panic disorder with or without agoraphobia
completed a double-blind, placebo-controlled, four week,
random-assignment crossover treatment trial of inositol 12 g
per day. Frequency and severity of panic attacks and severity
of agoraphobia declined significantly with inositol compared
to placebo. Side-effects were minimal. Since serotonin
re-uptake inhibitors benefit obsessive compulsive disorder
(OCD) and inositol is reported to reverse desensitization of
serotonin receptors, thirteen patients with OCD completed a
double-blind controlled crossover trial of 18 g inositol or
placebo for six weeks each. Inositol significantly reduced
scores of OCD symptoms compared with placebo. A controlled
double-blind crossover trial of 12 g daily of inositol for a
month in twelve anergic schizophrenic patients, did not show
any beneficial effects. A double-blind controlled crossover
trial of 6 g of inositol daily vs. glucose for one month each
was carried out in eleven Alzheimer patients, with on clearly
significant therapeutic effects. Antidepressant drugs have
been reported to improve attention deficit disorder (ADDH)
with hyperactivity symptomatology. We studied oral inositol in
children with ADDH in a double-blind, crossover,
placebo-controlled manner. Eleven children, mean age 8.9 +/-
3.6 years were enrolled in an eight week trial of inositol or
placebo at a dose of 200 mg/kg body weight. Results show a
trend for aggravation of the syndrome with myo- inositol as
compared to placebo. Recent studies suggest that serotonin
re-uptake inhibitors are helpful in at least some symptoms of
autism. However a controlled double-blind crossover trial of
inositol 200 mg/kg per day showed no benefit in nine children
with autism. Cholinergic agonists have been reported to
ameliorate electroconvulsive therapy (ECT)-induced memory
impairment. Inositol metabolism is involved in the second
messenger system for several muscarinic cholinergic receptors.
Inositol 6 g daily was given in a crossover-double-blind
manner for five days before the fifth or sixth ECT to a series
of twelve patients, without effect. These results suggest that
inositol has therapeutic effects in the spectrum of illness
responsive to serotonin selective re-uptake inhibitors,
including depression, panic and OCD, and is not beneficial in
schizophrenia, Alzheimer's ADDH, autism or ECT-induced
cognitive impairment.
Inositol treatment of obsessive- compulsive
disorder.
Fux M; Levine J; Aviv A; Belmaker RH
Ministry of Health Mental Health Center, Faculty of Health
Sciences, Ben Gurion University of the Negev, Beersheva,
Israel.
Am J Psychiatry (United States) Sep 1996, 153 (9)
p1219-21
OBJECTIVE: Earlier studies reported that inositol, a simple
polyol second messenger precursor, was effective in controlled
trials for patients with depression and panic. In this study
its effectiveness in obsessive - compulsive disorder was
investigated.
METHOD: Thirteen patients with obsessive - compulsive
disorder completed a double-blind, controlled crossover trial
of 18 g/day of inositol or placebo for 6 weeks each.
RESULTS: The subjects had significantly lower scores on the
Yale-Brown Obsessive Compulsive Scale when taking inositol
than when taking placebo.
ONCLUSIONS: The authors conclude that inositol is effective
in depression, panic, and obsessive -compulsive disorder, a
spectrum of disorders responsive to selective serotonin
reuptake inhibitors.
Role of inositol in the treatment of psychiatric
disorders. Basic and clinical aspects
Vadnal R.; Parthasarathy L.; Parthasarathy R.
Dr. R. Vadnal, Mental Hlth./Behavioural Scis. Serv., VA
Medical Center, 800 Zorn Avenue, Louisville, KY 40206 United
States
CNS Drugs (New Zealand) 1997, 7/1 (6-16)
Myo-inositol is a ubiquitous carbohydrate that is present
in large amounts in brain tissue and is involved in neuronal
signalling and osmoregulation. This sugar is an essential
component of the inositol signalling system, which is a
postreceptor second messenger signalling system found in many
cells. Myo-inositol is the precursor of membrane inositol
phospholipids, which are critically linked to a number of CNS
receptor signalling systems, including muscarinic,
serotonergic, adrenergic, metabotropic and histaminergic
systems, and those linked to cholecystokinin, tachykinins,
neurotensin, platelet activating factor and other
transmitters. Upon stimulation of these receptors, a signal is
transmitted through a guanosine triphosphate (GTP)-binding
protein (G(q)), which then activates the enzyme phospholipase
C. This results in the release of a second messenger, inositol
1,4,5-trisphosphate (InsPinf 3), from membrane inositol
phospholipids. InsPinf 3 then causes the release of free
intracellular calcium into the cytosol, activating a number of
enzymes or receptors. Myo-inositol in the brain is derived
from 3 sources: (i) receptor stimulation (a salvage pathway);
(ii) de novo synthesis from glucose; and (iii) uptake of
dietary myo-inositol through plasma membrane myo-inositol
transporters. Most myoinositol is probably derived from the
first 2 sources, which are controlled through the
lithium-sensitive enzyme myo-inositol monophosphatase
(IMPase). This enzyme acts upon myo-inositol monophosphates,
hydrolysing them to release free myo-inositol . Recent
biochemical, molecular and crystallographic studies have
demonstrated that the overall metabolism of brain inositol is
closely modulated by this enzyme. Lithium salts, which are
commonly used in various psychiatric conditions, inhibit this
enzyme, and this action has been implicated as a therapeutic
mechanism of action of lithium. A change in the availability
of CNS inositol may lead to altered brain cell signalling
pathways and, eventually, to the development of a
neuropsychiatric disorder. Recent evidence indicates that
myo-inositol has psychoactive effects, with initial studies
demonstrating effectiveness in the treatment of depression,
panic disorder and obsessive - compulsive disorder. At
present, the exact mechanism of these clinical effects is
uncertain. The development of various inositol system-based
drugs may lead to future psychoactive drugs designed to
modulate a second messenger cascade of events rather than a
receptor system, and will lead to further understanding of CNS
disease from a post-receptor second messenger perspective.
Lithium and tryptophan augmentation in
clomipramine-resistant obsessive- compulsive disorder.
Rasmussen SA
Am J Psychiatry (United States) Oct 1984, 141 (10)
p1283-5
Obsessive -compulsive patients with symptoms resistant to
clomipramine were treated by lithium or L -tryptophan
augmentation. The improvement noted supports the hypothesis
that increasing serotonergic neurotransmission ameliorates
obsessive symptoms.
Vitamin B12 and folic acid serum levels in
obsessive compulsive disorder.
Hermesh H; Weizman A; Shahar A; Munitz H
Geha Psychiatric Hosp, Beilinson Medical Ctr, Sackler School
of Medicine, Tel Aviv Univ, Israel.
Acta Psychiatr Scand (Denmark) Jul 1988, 78 (1)
p8-10
Vitamin B12 and folate serum levels were studied in 30
patients with obsessive compulsive disorder (OCD), and in two
control groups comprised of 30 chronic schizophrenics and 30
normal healthy subjects. Six patients (20%) of the OCD group
had abnormal low levels of vitamin B12. This prevalence was
significantly higher than that of the control groups. No
clinical neurological or haematological abnormalities
accompanied the reduced vitamin B12 levels. Possible
implication of this finding for the pathophysiology of OCD in
a subgroup of patients and the possibility that the B12
deficiency could be the consequence rather than the cause of
OCD are suggested.
Obsessive compulsive disorder arising in a
75-year-old woman
Bajulaiye R.; Addonizio G.
New York Hospital-Cornell Medical Center, Westchester
Division, 21Bloomingdale Road, White Plains, NY 10605 United
States
International Journal of Geriatric Psychiatry (United
Kingdom) 1992, 7/2 (139-142)
Presented is the case of a 75-year-old woman with obsessive
compulsive disorder with an unusual age of onset at age 72
years. The patient was resistant to various treatments, but
responded to lithium augmentation of fluoxetine.
Lithium augments fluoxetine treatment of obsessive
compulsive disorder
Ruegg R.G.; Evans D.L.; Comer W.S.; Golden R.N.
Psychiatry Dept, University of North Carolina School of
Medicine, Chapel Hill, NC 27599-7160 US
Lithium (United Kingdom) 1992, 3/1 (69-71)
Fluoxetine is a potent serotonin uptake inhibitor effective
in the treatment of obsessive compulsive disorder (OCD).
However, clinical response is often partial. Lithium carbonate
(Li) has been used to potentiate clomipramine and doxepine
treatment of OCD. We report our experience using Li to augment
fluoxetine in four OCD patients
WS 1490 (kava extract) in the treatment of anxiety
neurosis
Hahn G.
Engelstrasse 18,W-8520 Erlangen Germany
Fortschritte der Medizin (Germany) 1992, 110/9
(86)
No abstract.
Inhibition of platelet MAO-B by kava
pyrone-enriched extract from Piper methysticum Forster
(kava-kava).
Uebelhack R, Franke L, Schewe HJ
Department of Psychiatry, Humboldt-Universitat zu Berlin
(Charite), Germany.
Pharmacopsychiatry 1998 Sep;31(5):187-92
Kava-kava, a psychoactive beverage, induces relaxation,
improves social interaction, promotes sleep and plays an
important role in the sociocultural life in the islands of the
South Pacific. On the other hand, standardized extracts of
kava-kava roots are used for the therapy of anxiety, tension
and restlessness. Kava pyrones, the major constituents of kava
kava, are generally considered to be responsible for the
pharmacological activity in humans and animals. To obtain more
information on the mechanisms by which kava-kava exerts
psychotropic properties we investigated the in vitro effects
of kava-kava extract and pure synthetic kava pyrones on human
platelet MAO-B, in comparison to amitriptyline, imipramine and
brofaromine. Kava-kava extract was found to be a reversible
inhibitor of MAO-B in intact platelets (IC50 24 microM) and
disrupted platelet homogenates (IC50 1.2 microM). Structural
differences of kava pyrones resulted in a different potency of
MAO-B inhibition. The order of potency was desmethoxyyangonin
> (+/-)-methysticin > yangonin >
(+/-)-dihydromethysticin > (+/-)- dihydrokavain >
(+/-)-kavain. The two most potent kava pyrones,
desmethoxyyangonin and (+/-)-methysticin displayed a
competetive inhibition pattern with mean Ki 0.28 microM and
1.14 microM respectively. The inhibition of MAO-B by kava
pyrone-enriched extracts might be an important mechanism for
their psychotropic activity.
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