/pdf/interoception-and-mental-health-a-roadmap-3xwkdxcaor.pdf

Interoception and Mental Health: A Roadmap

Background: To determine the efficacy of adding haloperidol to the treatment of patients with obsessive-compulsive disorder (OCD), with or without a comorbid chronic tic disorder, who were refractory to adequate treatment with the serotonin-uptake inhibitor fluvoxamine alone. It was hypothesized that OCD patients with a concurrent chronic tic disorder would preferentially respond to this treatment. Methods: Sixty-two patients with a primary DSM-III-R diagnosis of OCD received placebo fluvoxamine for 1 week, followed by 8 weeks of active fluvoxamine. Thirty-four of these patients were refractory to fluvoxamine and were randomized in a double-blind fashion to 4 weeks of treatment with either haloperidol (n=17) or placebo (n=17) added to ongoing fluvoxamine treatment. The placebo-treated group included five women and 12 men, six inpatients and 11 outpatients, and eight patients with a comorbid chronic tic disorder. The haloperidol-treated group consisted of two women and 15 men, three inpatients and 14 outpatients, and seven patients with a comorbid chronic tic disorder. All 34 patients completed the entire study. The Yale-Brown Obsessive Compulsive Scale (Y-BOCS) and the Clinical Global Impression scale were the principal measures of treatment outcome. Results: Haloperidol addition was significantly better than placebo in reducing the severity of obsessive-complusive symptoms as measured by the Y-BOCS. Eleven of 17 patients responded to the haloperidol, compared with none of 17 patients given placebo. Eight of eight patients with comorbid chronic tic disorders, such as Tourette's disorder, responded to double-blind haloperidol addition to ongoing fluvoxamine treatment. Haloperidol addition was of little benefit in treating OCD patients without tics. Fluvoxamine blood levels were not related to treatment response. Conclusions: The results of this study suggest that OCD patients with a comorbid chronic tic disorder constitute a clinically meaningful subtype of OCD that might require conjoint serotonin-uptake inhibitor/neuroleptic therapy for effective symptom reduction.

Haloperidol Addition in Fluvoxamine-Refractory Obsessive-Compulsive Disorder: A Double-blind, Placebo-Controlled Study in Patients With and Without Tics

Anxiety disorders, the most common psychiatric conditions in the United States, have generated a great deal of research and scientific debate Panic disorder, the best-studied anxiety disorder, is often believed to be either a biological disease or a psychological disease The authors present a neuroanatomical model of panic disorder that attempts to reconcile these views The model locates the three components of the disease--the acute panic attack, anticipatory anxiety, and phobic avoidance--in three specific sites of the CNS: the brainstem, limbic system, and prefrontal cortex, respectively The authors suggest experiments to test their model

A neuroanatomical hypothesis for panic disorder.

Tryptophan depletion during continuous CSF sampling in healthy human subjects.

OBJECTIVE: Respiratory abnormalities may play a central role in the pathophysiology of panic disorder. The current study was undertaken to examine the respiratory response in the largest series of subjects to date during three respiratory challenges that used improved methodology. METHOD: Fifty-nine patients with DSM-III-R panic disorder and 39 normal volunteers were challenged with 5% and 7% CO2 inhalation and room air hyperventilation separated by room air breathing with continuous spirometry. RESULTS: Patients with panic disorder were more sensitive to the anxiogenic effects of CO2 than were normal subjects, and CO2 was a more potent stimulus to panic than hyperventilation. Patients increased their respiratory rate more quickly during CO2 inhalation than did comparison subjects, and this increase preceded the panic attacks. Patients who panicked in response to 5% CO2 demonstrated continued rise in end-tidal CO2, while the end-tidal CO2 of the comparison groups stabilized. Low end-tidal CO2 and high var...

https://ajp.psychiatryonline.org/doi/pdfplus/10.1176/ajp.154.11.1557

Respiratory Psychophysiology of Panic Disorder: Three Respiratory Challenges in 98 Subjects

• One hypothesis that could account for the anxiogenic response to breathing air supplemented with carbon dioxide seen in panic anxiety patients is that panic patients might have abnormally high central medullary chemoreceptor sensitivity. Chemoreceptor sensitivity was assessed by using a rebreathing technique to measure the ventilatory response to CO 2 in 14 medication-free patients with agoraphobia and panic attacks and 23 healthy subjects. Ventilatory response to CO 2 was similar in patients and controls (mean±SEM, 1.58 ± 0.16 vs 1.58±0.14 L/min/mm Hg), suggesting that abnormal chemoreceptor sensitivity does not explain the behavioral sensitivity of panic patients to CO 2 . Anxiety ratings Increased markedly during rebreathing both in patients and controls; anxiety increases were significantly greater in patients than In healthy subjects matched for age, sex, and rebreathing duration. Alprazolam treatment in eight patients markedly attenuated anxiety increases during rebreathing. Differences in anxiogenic sensitivity to CO 2 between patients and controls may be due to differences in the regulation of noradrenergic or other neuronal systems.

Carbon dioxide sensitivity in panic anxiety. Ventilatory and anxiogenic response to carbon dioxide in healthy subjects and patients with panic anxiety before and after alprazolam treatment.

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Carbon dioxide sensitivity in panic anxiety. Ventilatory and anxiogenic response to carbon dioxide in healthy subjects and patients with panic anxiety before and after alprazolam treatment.