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Comorbidity for Panic Disorder

PD is often associated with other anxiety disorders and with depression. Based on lifetime rates, the odds ratios for comorbidity of PD with agoraphobia range from 7.5 in the ECA to 21.4 in Puerto Rico, and those of PD with major depression range from 3.8 in Savigny to 20.1 in Edmonton . In the NCS the odds ratio is 10.6 for agoraphobia and 5.7 for major depression. The presence of agoraphobia with PD represents more severe disturbance and involves a higher likelihood of one or more comorbid diagnoses.

Goisman et al. found lifetime panic with and without agoraphobia to co-exist with at least one other anxiety disorder 37% of the time. Klerman et al. found 33% of 254 subjects with PD to have comorbid agoraphobia and 72% of these 254 to have comorbid agoraphobia, major depression, alcohol abuse, or drug abuse. Johnson et al. found more than two-thirds of ECA subjects with lifetime PD to meet criteria for more than one of 10 other axis I diagnoses. Cassano et al. found 70% of 302 patients with current DSM-III-R panic disorder to also have at least one of seven additional current syndromes of which the most common is GAD. Uncomplicated panic is most likely to exist independently, but even this disorder is found alone in less than 50% of the time: GAD and social phobia were the most frequent comorbid diagnosis. Panic with agoraphobia is seen as a sole diagnosis on 40% lifetime. The comorbid diagnoses at similar rates (about 20%) are simple and social phobia and GAD. Joyce et al. found lifetime DSM-III GAD to be more frequent in subjects with a history of panic attacks with‘‘moderate phobic avoidance’’ than in those with a history of panic attacks alone. Subjects with agoraphobia without a history of PD have at least two additional diagnoses at almost twice the frequency of subjects with uncomplicated PD and GAD was the disorder most frequently comorbid, followed by social phobia and simple phobia; 32% of subjects had agoraphobia without a history of PD as the sole diagnosis

A possible explanation of high comorbidity between anxiety disorders is that these disorders may share some common aetiologic pathways. Barlow notes that the experience of some symptoms of anxiety may lead to an anticipation of more anxiety: this anticipation, in fact, is itself anxiety-provoking, leading to ever-increasing expectation, pattern recognition, and further expectation. If this is the case, then it is likely that having one anxiety diagnosis should decrease the threshold for having a second. The studies indicate that this second diagnosis is often GAD: this argument could lead to a call to abolish GAD as a separate entity and regard it only as a somewhat inevitable non-specific by-product of having any of a number of chronic anxiety disorders. In addition, PD appears to be more likely to be preceded by another psychiatric disorder than to be a chronologically primary condition. Apart from the affective disorders, there are relatively few other psychiatric conditions appearing after the onset of PD. This finding implies that some primary disorders (e.g., simple phobia, social phobia, substance abuse) may represent a specific predisposition for the development of PD.

There are reports that 35% to 91% of patients with panic disorder also suffer from a major depressive episode during their life. Data from family and twin studies have suggested that anxiety and depression are present in pure forms in the relatives of probands, but that some degree of overlap in the transmission of these disorders occurs as well: these data are inconclusive as to whether one condition predisposes another or whether there is common aetiology. Leckman et al. found that first-degree relatives of patients dually diagnosed with major depression and PD have markedly increased morbidity risk for depression, panic, phobias and alcoholism. In many cases, both disorders occur at the same time. In others PD occurs before the onset of depressive disorder as well as before the onset of substance abuse.

Breier et al. found that patients with PD and/or agoraphobia who had a current or past major depressive episode had more severe symptoms of both anxiety and depression than those who had never been depressed. In a naturalistic study, Van Valkenburg et al. reported that patients with secondary depression had an earlier age at onset of their PD but did not differ from non-depressed patients with PD in their treatment response or psychosocial outcome. While it might be reasonable to expect that patients with depression would have suffered from PD longer than those without depression, patients with and without histories of depression have had PD for similar lengths of time . Also, while it is conceivable that patients with more severe agoraphobic avoidance would be more likely to experience depression than patients with less severe avoidance, this is not supported by empirical evidence. Thus, there is little support for the hypothesis that the depression, which frequently complicates PD, is aetiologically secondary to the long-term demoralising effects of chronic agoraphobic avoidance.

The co-existence of social phobia and PD is far from rare. The patients comorbid with social phobia and PD have an earlier PD age of onset; have more obsessive compulsive disorders and more severity in the social phobia scale from the Fear Questionnaire of Marks and Mathews. While neither duration of PD nor agoraphobic severity was related to a history of major depression, the concomitant diagnosis of social phobia was associated with significantly greater lifetime risk for depression. The data, however, should not be used to support a casual relationship. It is possible that in making concomitant diagnoses of social phobia, we are identifying a subgroup of PD patients with a constellation of personality traits that includes low self-esteem, extreme self-consciousness, and a endency towards negative self-appraisal. Such a subgroup could be at considerable risk from depression based on psychological, particularly cognitive, factors. Additionally, the social isolation experienced because of social avoidance could contribute to a propensity for becoming depressed. Alternatively, concomitant social phobia may merely be a marker for a more severe illness.

Since the co-occurrence of significant obsessive-compulsive symptoms has also been noted to increase the lifetime risk for depression in patients with PD, it is possible that PG complicated by the presence of any other disorder, rather than social phobia specifically, may increase the risk for depression.

Another risk factor in PD is the development of alcohol abuse, which some view as ‘‘self-medication’’. Unquestionably, intake of alcohol initially decreases anticipatory anxiety in patients with PD, but alcoholism later becomes a complication ). Several studies suggest that PD has a higher than expected prevalence among alcoholics compared with the prevalence in the general population. The question concerning primary and causal relationship between the two disorders, i.e. whether alcoholism leads to the development of anxiety disorders or vice versa, is less clear. George et al. suggest that a possible mechanism for the link between alcoholism and anxiety is a kindling process: the hyper-responsive CNS state that results from repeated alcohol withdrawal may, in susceptible individuals, give rise to a heightened state of anxiety and panic attacks even during sobriety. The model of kindling process has been proposed by Ballanger and Post. They demonstrated that the alcohol withdrawal syndrome becomes progressively more severe with increasing years of heavy daily alcohol abuse, irrespective of age. They propose that repeated episodes of withdrawal in chronic alcoholics serve as stimuli for kindling of subcortical structures, primarily limbic, hypothalamic, and thalamic nuclei. They hypothesise that the spectrum of withdrawal symptoms from mild withdrawal with tremor and autonomic symptoms to the more severe withdrawal symptoms of hallucinations, psychic symptoms, epileptic seizures, and delirium tremens are secondary to cumulative physiological changes which accompany a kindling-like process in a double-blind controlled study, found that carbamazepine, because of its ability both to retard the development of kindling and suppress established kindled foci, is as effective and safe as benzodiazepine treatment for alcohol withdrawal.

Marazziti et al. found that current anxiety disorders, especially panic and related conditions, are the most common psychiatric disorders associated with headache. These findings were particularly true of the subgroup of migraine with aura; in the relatively few patients withmooddisorders, depressionwas nearly always comorbid PD and past history of depression was mainly a characteristic of the tension headache group. These data are compatible with the hypothesis that migraine, especially that with aura, PD and some forms of depressive illness are part of the same spectrum. Irritable bowel syndrome (IBS) is fairly common in patients seeking treatment for PD: in Kaplan’s study 46.3% patients with PD met the criteria for IBS. Patients with PD and IBS were more likely to report symptoms of back pain as well as personal history of bowel disease compared with patients with panic disorder but without IBS.

Otoneurological abnormalities have been reported in PD; vestibular abnormalities are most prevalent in the patients with PD with moderate to severe agoraphobia. Vestibular dysfunction was associated with space and motion discomfort and with frequency of vestibular symptoms between, but not during, panic attacks. The constellation of vestibular test most specific for agoraphobia was one indicating compensated peripheral vestibular dysfunction. Therefore a subclinical vestibular dysfunction may contribute to the phenomenology of PD, particularly in the development of agoraphobia in panic disorder. PD and subsyndromal panic are relatively common and may be unrecognised and inadequately treated in patients who present respiratory symptoms. There were no significant differences between patients with and without panic in the severity of pulmonary function abnormalities or in the response to bronchodilators. However, patients with panic attacks were significantly more likely to report dyspnea at rest and irritable bowel symptoms and tended to report difficulty swallowing. Bouwer and Stein found a specific association between PD and a history of traumatic suffocation which is significantly more frequent among the PD patients than among the comparison subjects. Within the PD group, patients with a history of traumatic suffocation were significantly more likely to exhibit predominantly respiratory symptoms and nocturnal panic attacks, while patients without such a history were significantly more likely to have predominantly cardiovascular symptoms, oculovestibular symptoms and agoraphobia.

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