Ari A. Gershon

Teva Pharmaceuticals (Israel)

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Mark Weiser

Sheba Medical Center

Leon Grunhaus

Hebrew University of Jerusalem

Shimon Burshtein

Sheba Medical Center

John M. Davis

University of Illinois Chicago

Revital Amiaz

Sheba Medical Center

Iosif Gaboș Grecu

Universitatea de Medicină, Farmacie, Științe și Tehnologie „George Emil Palade” din Târgu Mureș

Pinhas N. Dannon

Tel Aviv University

Gabriela Marian

Academy of Romanian Scientists

Camelia Petcu

Spitalul Clinic de Psihiatrie Alexandru Obregia

Nicolae Vlad

Spitalul Clinic de Psihiatrie Alexandru Obregia

Cooperative Institutions

Tel Aviv University

Sheba Medical Center

Columbia University

Bar-Ilan University

Jerusalem Mental Health Center

Teva Pharmaceuticals (Spain)

New York State Psychiatric Institute

Teva Pharmaceuticals (United States)

Ben-Gurion University of the Negev

Spitalul Clinic de Psihiatrie Alexandru Obregia

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Applying Transcranial Magnetic Stimulation (TMS) Over the Dorsal Visual Pathway Induces Schizophrenia-like Disruption of Perceptual Closure

Brain Topography (2016)

Revital Amiaz Dana Vainiger Ari A. Gershon Mark Weiser Michal Lavidor

10.1007/s10548-016-0487-1

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Citations (8)

Transcranial Magnetic Stimulation in the Treatment of Depression

American Journal of Psychiatry (2003)

Ari A. Gershon Pinhas N. Dannon Leon Grunhaus

OBJECTIVE: Transcranial magnetic stimulation (TMS) is a noninvasive and easily tolerated method of altering cortical physiology. The authors evaluate evidence from the last decade supporting a possible role for TMS in the treatment of depression and explore clinical and technical considerations that might bear on treatment success. METHOD: The authors review English-language controlled studies of nonconvulsive TMS therapy for depression that appeared in the MEDLINE database through early 2002, as well as one study that was in press in 2002 and was published in 2003. In addition, the authors discuss studies that have examined technical, methodological, and clinical treatment parameters of TMS. RESULTS: Most data support an antidepressant effect of high-frequency repetitive TMS administered to the left prefrontal cortex. The absence of psychosis, younger age, and certain brain physiologic markers might predict treatment success. Technical parameters possibly affecting treatment success include intensity and duration of treatment, but these suggestions require systematic testing. CONCLUSIONS: TMS shows promise as a novel antidepressant treatment. Systematic and large-scale studies are needed to identify patient populations most likely to benefit and treatment parameters most likely to produce success. In addition to its potential clinical role, TMS promises to provide insights into the pathophysiology of depression through research designs in which the ability of TMS to alter brain activity is coupled with functional neuroimaging.

Depression

10.1176/appi.ajp.160.5.835

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Citations (521)

Ropinirole Augmentation for Depression

Journal of Clinical Psychopharmacology (2018)

Ari A. Gershon Revital Amiaz Haim Shem-David Leon Grunhaus

Evidence both from animal and human studies suggests a role for dopaminergic pathways in the treatment of depression. Ropinirole, a selective agonist of dopamine D2/D3, is in use for the treatment of parkinsonism. Preliminary evidence suggests that such agonists might be useful as antidepressants. We tested whether an add-on ropinirole is an effective in depressed patients.We conducted a double-blind, randomized, placebo-controlled trial of add-on ropinirole in depressed patients unresponsive to at least one antidepressant. We recruited 32 unipolar and bipolar patients who remained depressed (modified 21-item Hamilton Depression Rating Scale) despite at least 4 weeks of treatment with an adequate dose of antidepressant medication. Patients received either 2 mg of oral ropinirole or placebo twice daily added on to their current medication and were evaluated weekly for 7 weeks using the Hamilton Depression Rating Scale and Montgomery-Asberg Depression Rating Scale.No difference in primary or secondary outcome measures was detected between the treatment and control groups.These results differ from previous studies and are unexpected in light of theoretical considerations. This may indicate that there are differences in pharmacological activity between ropinirole and other dopaminergic agents such as pramipexole.

Ropinirole

Pramipexole

Depression

10.1097/jcp.0000000000000984

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Citations (9)

Naltrexone augmentation in OCD: A double-blind placebo-controlled cross-over study

European Neuropsychopharmacology (2008)

Revital Amiaz Leah Fostick Ari A. Gershon Joseph Zohar

Clomipramine

Fluvoxamine

10.1016/j.euroneuro.2008.01.006

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A randomized controlled trial of allopurinol vs. placebo added on to antipsychotics in patients with schizophrenia or schizoaffective disorder

Schizophrenia Research (2012)

Mark Weiser Ari A. Gershon Katya Rubinstein Camelia Petcu Maria Ladea

Allopurinol

10.1016/j.schres.2012.02.014

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Citations (33)

Dopamine D2-Like Receptors and the Antidepressant Response

Biological Psychiatry (2006)

Ari A. Gershon Tali Vishne Leon Grunhaus

Cyclic adenosine monophosphate

10.1016/j.biopsych.2006.05.031

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Citations (151)

P.2.d.025 Allopurinol for mania. A randomized trial of allopurinol versus placebo as add-on treatment in manic bipolar patients

European Neuropsychopharmacology (2013)

Shimon Burshtein Mark Weiser Ari A. Gershon Gabriela Marian Nicolae Vlad

Clinical Global Impression

Regimen

Bipolar I disorder

10.1016/s0924-977x(13)70596-0

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Allopurinol for mania: a randomized trial of allopurinol versus placebo as add‐on treatment to mood stabilizers and/or antipsychotic agents in manic patients with bipolar disorder

Bipolar Disorders (2014)

Mark Weiser Shimon Burshtein Ari A. Gershon Gabriela Marian Nicolae Vlad

Objective An emerging body of evidence supports a role for dysfunctional purinergic neurotransmission in mood disorders. Adenosine agonists have been shown to have properties similar to those of dopamine antagonists; there is a well‐characterized interaction between adenosine and dopamine receptors in the ventral striatum, and increasing adenosinergic transmission has been demonstrated to reduce the affinity of dopamine agonists for dopamine receptors. Allopurinol increases adenosine levels in the brain, and hence is hypothesized to reduce the symptoms of mania. Two randomized, placebo‐controlled trials administering add‐on allopurinol to manic patients showed significantly greater improvements in Young Mania Rating Scale ( YMRS ) scores for drug compared to placebo, while a more recent, relatively small, add‐on study showed negative results. Based on these data, our objective was to examine the efficacy of allopurinol as add‐on treatment to mood stabilizers and/or antipsychotic agents in manic patients with bipolar disorder. Methods We performed a large, well‐powered, multicenter, six‐week, randomized, placebo‐controlled trial of allopurinol added to mood stabilizers and/or antipsychotic agents in 180 patients with bipolar disorder in an acute manic episode. Results Both groups showed improvement on the YMRS (effect size of 1.5 for placebo and 1.6 for allopurinol), with no difference observed between groups on YMRS scores ( t = 0.28, p = 0.78). There was no difference in the proportion of patients who responded to treatment (defined as showing at least 50% improvement in YMRS score) between the two groups (p = 0.92), or in dropout rates (p = 0.84). Limitations None of our patients received lithium. However, the side effects of lithium and its narrow therapeutic index made the use of lithium less common and, therefore, our study results reflect common current clinical practice. In the present study, we used a variety of antipsychotic and/or mood stabilizing treatments, to which we added allopurinol; one might hypothesize that add‐on allopurinol has a different effect in combination with different antipsychotic agents or mood stabilizers. Conclusions The findings of this large, well‐powered study do not support add‐on allopurinol as a treatment for acute mania. This study did not test the efficacy of allopurinol as monotherapy.

Mood stabilizer

Bipolar I disorder

10.1111/bdi.12202

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Citations (31)

Central nervous system effects of the histamine‐3 receptor antagonist CEP‐26401, in comparison with modafinil and donepezil, after a single dose in a cross‐over study in healthy volunteers

British Journal of Clinical Pharmacology (2019)

Anne Catrien Baakman Rob Zuiker Joop van Gerven Nicholas J. Gross Ronghua Yang

Aims In previous studies, the histamine‐3 receptor antagonist CEP‐26401 had a subtle effect on spatial working memory, with the best effect seen at the lowest dose tested (20 μg), and a dose‐dependent disruption of sleep. In the current study, 3 low‐dose levels of CEP‐26401 were compared with modafinil and donepezil. Methods In this double‐blind, placebo‐ and positive‐controlled, randomized, partial 6‐way cross‐over study, 40 healthy subjects received single doses of placebo, CEP‐26401 (5, 25 or 125 μg) or modafinil 200 mg or donepezil 10 mg. Pharmacokinetic and pharmacodynamic measurements were performed predose and at designated time points postdose. Results The main endpoint between‐errors of the spatial working memory‐10‐boxes task only improved for the 125 μg dose of CEP‐26401 with a difference of 2.92 (confidence interval [CI] –1.21 to 7.05), 3.24 (CI –1.57 to 8.04) and 7.45 (CI 2.72 to 12.19) for respectively the 5, 25 and 125 μg dose of CEP‐26401, −1.65 (CI –0.572 to 1.96) for modafinil and − 3.55 (CI –7.13 to 0.03) for donepezil. CEP‐26401 induced an improvement of adaptive tracking, saccadic peak velocity and reaction time during N‐back, but a dose‐related inhibition of sleep and slight worsening of several cognitive parameters at the highest dose. CEP‐26401 significantly changed several subjective visual analogue scales, which was strongest at 25 μg, causing the same energizing and happy feeling as modafinil, but with a more relaxed undertone. Discussion Of the doses tested, the 25 μg dose of CEP‐26401 had the most optimal balance between favourable subjective effects and sleep inhibition. Whether CEP‐26401 can have beneficial effects in clinical practice remains to be studied.

Pharmacodynamics

10.1111/bcp.13885

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Citations (11)

Transcranial magnetic stimulation: a new tool in the fight against depression

Dialogues in Clinical Neuroscience (2002)

Leon Grunhaus Pinhas N. Dannon Ari A. Gershon

Since its introduction to the clinical realm in 1985, transcranial magnetic stimulation (TMS) has rapidly developed into a tool for exploring central nervous system function in both health and disease. The antidepressant effects of TMS were initially observed in 1993. Since then, a solid body of evidence has accumulated suggesting antidepressant effects for both slow TMS (sTMS) and repetitive TMS (rTMS). This review is divided into four parts. First, it addresses the basic concepts governing TMS, and then, second, it discusses the technical parameters involved in administering TMS. Knowledge of these parameters is necessary for understanding how TMS is administered, and how manipulation of the technique impacts on the results obtained. Third, we review the most relevant studies on the antidepressant effects of sTMS and rTMS published to date. Finally, we discuss cortical excitability and how the understanding of this basic neurophysiological function of cortical neurons can be used for monitoring the effects of TMS. In our discussion, we conclude that the time has arrived for TMS to be offered to depressed patients as a treatment.

Depression

Brain stimulation

Neuromodulation

10.31887/dcns.2002.4.1/lgrunhaus

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Citations (4)