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Biomedical subjects

Martin A Katzman

Publications and source records attributed to Martin A Katzman.

8 recordsLinked to original sources
PubMed2005

Pharmacotherapy of post-traumatic stress disorder: a family practitioners guide to management of the disease.

Post-traumatic stress disorder is a difficult to treat, yet common disorder, which is associated with significant morbidity, mortality and societal burden. Comprehensive management of post-traumatic stress disorder must include both psychotherapeutic and pharmacologic components. The current evidence-based pharmacologic management approaches to post-traumatic stress disorder, suggests that first-line treatments for monotherapy are the selective serotonin reuptake inhibitors, sertraline, paroxetine and fluoxetine. Other potential options include other monotherapies including venlafaxine, mirtazapine, tricyclic antidepressants, monoamine oxidase inhibitors, as well as adjunctive usage of atypical antipsychotics, lamotrigine, trazadone and a number of adrenergic agents. A trial of therapy should be at least 8 weeks and continue for at the very least 12 months, but is likely to be much longer. In light of the risks of untreated post-traumatic stress disorder (e.g., suicide and impaired psychosocial functioning), therapy may need to be continued for 2 years or more. Pharmacologic therapy instituted at the time of acute psychologic trauma shows promise for the prevention of post-traumatic stress disorder in the future and warrants further study.

Anticonvulsants↗
PubMed2004

Anxiety sensitivity as a predictor of panic attacks.

Anxiety sensitivity (AS) is the fear of physical symptoms of anxiety and related sensations believed to have harmful consequences. AS may play a central role in the nature and etiology of panic disorder (PD) and the genesis of panic attacks. We collected Anxiety Sensitivity Index (ASI) scores from PD patients and controls to determine if AS accurately predicts panic. ASIs were completed prior to panic induction using the modified Read rebreathing test in both hypoxic and hyperoxic conditions. Total scores first-order factors, and individual item ASI scores were correlated with panic presence (Spearman correlation) for each of the hypoxic and hyperoxic rebreathing tests for both study populations. Control subjects' data correlated significantly for items 4, 8, and 11 of the ASI for the hyperoxic (n=9; r(S)=0.63, 0.70, and 0.63, respectively) and items 4 and 8 for the hypoxic rebreathing tests (n = 9; r(S) = 0.63 and 0.70, respectively). Panic patients' data correlated significantly for item 1 of the ASI for hyperoxic tests (n=8; r(S)=0.76) and item 5 for the hypoxic tests (n = 8; r(S) = 0.95). Total ASI scores or first-order factors (physical, social concerns, and mental incapacitation) scores of either study group did not correlate significantly with panic presence. AS may not be a reliable predictor of panicogenic responses to CO2-induced panic in either PD or normal control populations. AS may not be an ultimate causal element in eliciting panic attacks.

Adult↗
PubMed2004

Effects of CCK-tetrapeptide in patients with social phobia and obsessive-compulsive disorder.

Panicogenic sensitivity to CCK-tetrapeptide (CCK-4) is enhanced in panic disorder patients relative to normal controls (NC). We sought to determine whether CCK-4 sensitivity is augmented in patients with social phobia (SP) (n = 12) and obsessive-compulsive disorder (OCD) (n = 8) versus NC (n = 12). We also determined whether CCK-4 could elicit syndrome-specific symptoms in SP and OCD patients. The study employed a single-blind, placebo-controlled, within-subject design. Behavioral, cardiovascular and hormonal responses to a submaximal dose (20 microg) of CCK-4 were evaluated. Panic frequency after the placebo and CCK-4 challenge varied as a function of diagnosis. Differences in panic frequency between groups and between challenge agents within each group did not, however, reach statistical significance. Further, the number and intensity of panic symptoms, intensity of subjective anxiety, autonomic reactivity and hormonal release after CCK-4 administration did not distinguish the groups. Core symptoms of SP and OCD were unaffected by CCK-4. These data failed to detect significant differences between groups on behavioral, cardiovascular and hormonal response to CCK-4. The lack of effect of CCK-4 on SP and OCD symptoms suggests that this peptide does not play a salient role in the pathophysiology of these disorders.

Adrenocorticotropic Hormone↗
PubMed2004

Acupuncture increases nocturnal melatonin secretion and reduces insomnia and anxiety: a preliminary report.

The response to acupuncture of 18 anxious adult subjects who complained of insomnia was assessed in an open prepost clinical trial study. Five weeks of acupuncture treatment was associated with a significant (p = 0.002) nocturnal increase in endogenous melatonin secretion (as measured in urine) and significant improvements in polysomnographic measures of sleep onset latency (p = 0.003), arousal index (p = 0.001), total sleep time (p = 0.001), and sleep efficiency (p = 0.002). Significant reductions in state (p = 0.049) and trait (p = 0.004) anxiety scores were also found. These objective findings are consistent with clinical reports of acupuncture's relaxant effects. Acupuncture treatment may be of value for some categories of anxious patients with insomnia.

Acupuncture↗
PubMed2004

Treatments for generalized anxiety disorder.

Generalized anxiety disorder is characterized by excessive chronic anxiety in association with many somatic symptoms. The disorder has pervasive effects on quality of life, including work, social and educational aspects and requires long-term therapy. Available studies in patients are the Diagnostic and Statistical Manual of Mental Disorders, third edition-revised and fourth edition, which have defined generalized anxiety disorder and demonstrate the efficacy of benzodiazepines, azapirones, some antidepressants and psychotherapy. Benzodiazepines are effective anxiolytics for short-term use but are accompanied by many adverse events. The antidepressants, paroxetine and venlafaxine (Efexor), have demonstrated efficacy in patients with generalized anxiety disorder with mild side-effect profiles. They have the additional benefit of efficacy in depression, which frequently occurs comorbidly in these patients. Long-term efficacy has been shown with venlafaxine in the treatment of this chronic condition, confirming that as in depression, the goal must not just be remission beyond simple symptom resolution but also on to improved functioning and quality of life. Psychotherapy with applied relaxation, cognitive therapy and cognitive behavioral therapy show the most promise in resolving and maintaining treatment gains in the long-term. These approaches may be useful alone or in combination with adjunctive pharmacotherapy to achieve remission. Based on current evidence, the recommended approach to achieving long-term benefits for patients with generalized anxiety disorder is antidepressant therapy with paroxetine or venlafaxine in combination with cognitive behavioral therapy.

Anti-Anxiety Agents↗
PubMed2002

Central and peripheral chemoreflexes in panic disorder.

Klein (Arch Gen Psychiatry, 50, 1993, 306-317) has suggested that panic disorder patients have a false suffocation alarm that may be associated with a lowered threshold for carbon dioxide detection. We compared the thresholds and sensitivities of the central and peripheral chemoreflexes between panic disorder patients and age- and sex-matched healthy volunteers to test this aspect of the hypothesis. We used a modified version of Read's rebreathing technique in 11 panic disorder patients and 10 healthy volunteers to examine the peripheral and central chemoreflex characteristics in these two populations. Subjects were examined during three rebreathing tests: training, hyperoxic (central chemoreflex alone) and hypoxic (combined central and peripheral chemoreflex). Panic symptoms were retrospectively assessed between groups using a DSM-IV derived Panic Symptom Scale. Comparisons of panic disorder patients with agoraphobia and healthy volunteers showed no significant differences in sensitivities or thresholds. Klein's hypothesis is not supported by these data. If a false suffocation alarm exists, its triggering may not be implemented within the respiratory chemoreflexes.

Adult↗
PubMed2002

Effects of tryptophan depletion on central and peripheral chemoreflexes in man.

Klein (Arch. Gen. Psychiatry 50, 306-317, 1993) suggests that panic attacks are the result of a defective 'suffocation alarm' threshold that presents with carbon dioxide (CO(2)) hypersensitivity, exaggerated ventilatory response and panic in panic disorder (PD) patients. Serotonergic deficiencies enhance this ventilatory response in PD patients, as per 'suffocation alarm' theory predictions, suggesting that serotonin (5-HT) normalizes the ventilatory response. Other research supports a serotonin system-mediated stimulation of ventilation. Knowledge of 5-HT's role on ventilatory output and its neurophysiological sources impacts on the 'suffocation alarm' theory validity and predictive value. We used tryptophan depletion (TRP-) in concert with a modified Read rebreathing test to determine the effect of deficient serotonergic modulation on the central and peripheral chemoreflex threshold and sensitivity of response to CO(2) in 11 healthy men. TRP- did not affect central or peripheral chemoreflex threshold or sensitivity of response to CO(2). However, basal ventilation was significantly elevated during TRP-. In contrast to 'suffocation alarm' theory predictions, decreased 5-HT neurotransmission does not significantly affect the respiratory chemoreflex response to CO(2), impacting on non-chemoreflex drives to breathe. Panic associated respiratory abnormalities may be related to defective 5-HT modulation of non-chemoreflex drives to breathe, unrelated to any respiratory chemoreflex abnormality.

Adult↗