Biomedical subjects

Yehuda Sasson

Publications and source records attributed to Yehuda Sasson.

7 recordsLinked to original sources

PubMed2006

Natural course of posttraumatic stress disorder: a 20-month prospective study of Turkish earthquake survivors.

OBJECTIVE: A 20-month prospective follow-up of survivors of the severe earthquake in Turkey in 1999 examined the natural course of posttraumatic stress disorder (PTSD) and the contribution of different symptom clusters to the emergence of PTSD. METHOD: Subjects were randomly sampled in a suburb of Istanbul that was severely affected by the earthquake. A total of 464 adults were assessed with a self-report instrument for PTSD symptoms on 3 consecutive surveys that were administered 1 to 3, 6 to 10, and 18 to 20 months following the earthquake. RESULTS: The prevalence of PTSD was 30.2% on the first survey and decreased to 26.9% and 10.6% on the second and third surveys, respectively. Female subjects showed initially higher (34.8%) PTSD rates compared with male subjects (19.1%). However, gender differences disappeared by the time of the third survey due to high spontaneous remission rates in female subjects. Low levels of chronic and delayed-onset PTSD were observed. A major contribution of the avoidance symptoms to PTSD diagnosis was identified by statistical analysis. CONCLUSIONS: Initial PTSD following an earthquake may be as prevalent as in other natural disasters, but high rates of spontaneous remission lead to low prevalence 1.5 years following the earthquake. Initial avoidance characteristics play a major role in the emergence of PTSD.

Adult↗

PubMed2005

Posttraumatic obsessive-compulsive disorder: a case series.

This report documents emerging posttraumatic obsessive-compulsive disorder in 13 Israeli military veterans diagnosed with both obsessive-compulsive disorder (OCD) and posttraumatic stress disorder (PTSD), for whom the onset of OCD was clearly associated with the trauma. Data presented include four detailed case reports that delineate relations between symptomatology in the two disorders. Clinical and theoretical implications of these data are discussed.

Adult↗

PubMed2005

Anxiogenic effects of Sumatriptan in panic disorder: a double-blind, placebo-controlled study.

BACKGROUND: Several lines of evidence point to serotonergic abnormalities in patients with panic disorder (PD). Our goal was to further examine central serotonergic function in panic patients using autonomic and subjective responses to the postsynaptic serotonin 5-HT1D receptor agonist Sumatriptan. METHOD: Using a double-blind, randomized, placebo-controlled design, we assessed autonomic and subjective responses to oral Sumatriptan (100 mg) and placebo in 15 patients with PD, free of medication. Subjective responses were measured using the Hamilton Anxiety Rating Scale (HAM-A), National Institute of Mental Health Anxiety Scale (NIMHA), a modified version of the Panic Symptom Inventory (PI), Hamilton Depression Rating Scale (HAM-D), and Montgomery-Asberg Depression Rating Scale (MADRS). RESULTS: PD patients exhibited significantly enhanced autonomic and subjective responses following challenge with Sumatriptan. We observed an increased pulse rate and augmentation of various parameters measured on different anxiety scales. A constant inclination of aggravation of the measured parameters was detected during the hour post challenge. CONCLUSION: Oral administration of Sumatriptan, a 5-HT1D agonist, has been associated with an anxiogenic effect in PD patients.

Adolescent↗

PubMed2004

Serotonergic dissection of obsessive compulsive symptoms: a challenge study with m-chlorophenylpiperazine and sumatriptan.

We have conducted a pharmacological challenge experiment in 10 medication-free obsessive compulsive (OC) disorder (OCD) patients. We used a placebo-controlled paradigm for m-chlorophenylpiperazine (mCPP) and sumatriptan challenges. Endocrine, physiological and behavioral variables were assessed at baseline and over a 3-hour period after the challenge. Both cortisol and prolactin were significantly elevated in OCD patients following mCPP administration. Both mCPP and sumatriptan caused significant OC symptom exacerbation with the response to sumatriptan being more robust. We conclude that the 5-HT(1Dbeta) receptor may play a role in the pathophysiology of OCD.

Adult↗

PubMed2003

Brain reactivity to specific symptom provocation indicates prospective therapeutic outcome in OCD.

A pertinent question in biological psychiatry is what differentiates responders and non-responders to pharmacological treatment. One possibility is that individual differences in the symptomatic spectrum as well as in the underlying biology of the disorder lead to the known 40% failure in pharmacological treatment. Our study aimed to maximize individual brain markers of obsessive-compulsive disorder (OCD) by applying single photon emission computed tomography (SPECT) during a provoked symptomatic state prior to and following treatment. Four brain SPECT scans were obtained from 26 OCD patients prior to and at 6 months of sertraline treatment. At each time point, two SPECT scans were performed in a counterbalanced order of two specific states; one a symptom-provoking condition and the other a relaxed condition. At 6 months of treatment, patients were divided into responders and non-responders according to a predetermined clinical criterion. Prospective responders showed significantly lower brain perfusion in the dorsal-caudal anterior cingulum and higher brain perfusion in the right caudate, when compared to non-responders, only during symptom provocation. When pre- and post-treatment scans during symptom provocation were compared, only responders showed significant change in brain response: increased perfusion in the left anterior temporal cortex and prefrontal cortex at 6 months' treatment. These findings suggest that obtaining functional brain imaging during specific symptom provocation emphasizes individual differences in brain reactivity. Thus can indicate prospective responders to symptom-related treatment in OCD and mark the relevant brain regions for effective response to treatment.

Adult↗

PubMed2003

Bipolar comorbidity: from diagnostic dilemmas to therapeutic challenge.

Comorbidity in bipolar disorder is the rule rather than the exception more than 60% of bipolar patients have a comorbid diagnosis and is associated with a mixed affective or dysphoric state; high rates of suicidality; less favourable response to lithium and poorer overall outcome. There is convincing evidence that rates of substance use and anxiety disorders are higher among patients with bipolar disorder compared to their rates in the general population. The interaction between anxiety disorders and substance use goes both ways: patients with bipolar disorder have a higher rate of substance use and anxiety disorder, and vice versa. Bipolar disorder is also associated with borderline personality disorder and ADHD, and to a lesser extent with weight gain. As more than 40% of bipolar patients have anxiety disorder, it is indicated that while diagnosing bipolar patients, systematic enquiry about different anxiety disorders is called for. This also presents a therapeutic challenge, since agents that effectively treat anxiety disorders are associated with the risk of induced mania. Therefore, the treating psychiatrist needs to carefully evaluate the potential benefit of treating the anxiety against the potential cost of inducing a manic episode. A possible solution would be to use, when possible, a non-pharmacological intervention, such as a cognitivebehavioural approach. Alternately, it is suggested that the clinician attempts to ensure that the patient receives adequate treatment with mood stabilizers before slowly and carefully attempting the addition of anti-anxiety compounds with a relatively lower risk of mania induction (e.g. SSRIs compared to TCAs).

Anxiety↗

PubMed2002

Refractory obsessive-compulsive disorder: state-of-the-art treatment.

Nonresponse to treatment in obsessive-compulsive disorder is common, associated with substantial impairment, and understudied. Little practical advice is available to clinicians on next-step treatment strategies for patients who have not responded well to 2 trials of selective serotonin reuptake inhibitors (SSRIs). Available options include continuation of SSRI treatment, switching to another SSRI or selective serotonin-norepinephrine reuptake inhibitor, augmenting with atypical neuroleptics or cognitive-behavioral therapy, or utilizing novel treatment approaches. The authors synthesize state-of-the-art treatment and give practical advice for clinicians.

Antipsychotic Agents↗