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Treatment resistant OCD subjects, defined as those patients who undergo an adequate trial of SRI (clomipramine or SSRI) and do not respond or show unsatisfactory results, account for 40-50% of all patients. Once the appropriateness of the trial has been assessed, several options exist for the clinicians. If clomipramine or citalopram have been used, an appropriate strategy consists in giving the same drug intravenously. Double-blind studies exist on the efficacy of clomipramine IV, while data are missing for citalopram. Another option that should be considered first, although data are scarce, is the addition of a cognitive behavioral therapy, when available, in the forms of exposure and response prevention. When such options are not suitable or available, augmentation of the ongoing SRI with another compound represents the preferable strategy. Double-blind, placebo-controlled studies have shown the efficacy of adding pindolol (7.5 mg/d), risperidone (2 mg/d) and olanzapine (5-10 mg/d). Other agents have been proposed, but data emerging from double-blind studies were negative or contradictory. Another option available is switching from CMI to SSRI, or vice versa, or from SSRI to SSRI. Data regarding such treatment strategy, however, are highly preliminary, based on a couple of open label reports and on studies performed in treatment resistant depression. An unresolved question is whether augmentation should be preferred to switching. No data exist in OCD; a practical approach would suggest augmentation first, considering that response should be obtained faster than by switching compound. When all the available and effective strategies prove uneffective, clinicians should consider switching the patient to other compounds in monotherapy, such as venlafaxine, sumatriptan, inositol, although research is strongly needed before conclusions on the efficacy of such compounds can be drawn.

Our purpose in this study was to compare the prevalence and pattern of Axis I and II comorbidities between patients with and without nocturnal panic (NP) attacks. One hundred and sixteen subjects with panic disorder (PD; according to DSM-IV criteria) were included: We assessed Axis I and II comorbidities using the Structured Clinical Interview for DSM-IV Axis I and II disorders, respectively. Of the sample, 27.6% of subjects had recurrent nocturnal panic attacks (NP group). Subjects with NP did not differ from those without in any sociodemographic or clinical characteristics. In the sample (94 subjects), 81% had at least one lifetime comorbid Axis I disorder, without significant differences between subjects with and without nocturnal panic even when considering comorbidity rates for single disorders; a trend toward significance was found for anorexia nervosa and somatization disorder, which both were more frequent among subjects with NP. Concerning Axis II disorders, 49.1% of the sample (57 subjects) met the criteria for at least one personality disorder, without significant differences between patients with and without NP. No significant differences were detected in comorbidity rates for any single Axis II personality disorder. Personality might play a relevant role in influencing treatment approaches to PD, but it does not appear to be a differential focus of concern in patients with compared to those without NP.

Recent research has hypothesized an association between traumatic events and nocturnal panic (NP). The purpose of this study was to investigate whether the onset of nocturnal panic attacks is associated with a higher frequency of and/or greater severity of stressful or traumatic life events than that of patients with panic disorders (PDs) who experience daytime panic attacks (DPs) while awake. A secondary aim was to investigate whether NP is associated with specific life events at the onset of the disorder. Our sample comprised 129 subjects with PD (DSM-IV). We investigated the number and types of stressful life events that occurred in the year prior to PD onset using a semistructured interview. Of the sample, 28.7% had recurrent nocturnal panic attacks (NP group). Subjects with and without recurrent NP did not differ on any sociodemographic or clinical characteristic. Neither the number nor type of life event distinguished those with or without NP. The subgroup of patients with PD with recurrent NP appears to represent a variant of PD with a possible increased vulnerability to conditions of diminished arousal as a trigger of panic attacks. However, the hypothesis that this vulnerability might be determined by life events that occur in the period preceding PD onset was not supported by the findings of this study.