Disease relevance of Panic Disorder

• Among the patients with panic disorder, 58% panicked with sodium lactate, 39% with 5% CO2, and 23% with room air hyperventilation [1].
• Heart rate and plasma norepinephrine responsivity to a physiologic challenge, ie, orthostasis, were measured in 20 patients with panic disorder (PD) and 20 age- and sex-matched normal control subjects [2].
• Overcoming hypersensitivity to fluoxetine in a patient with panic disorder [3].
• Both mitral valve prolapse (MVP) and panic attacks have been reported to be associated with autonomic dysfunction, but previous studies have been limited by the lack of clear separation between patients with MVP and those with panic attacks and the use of noncomparable control subjects [4].
• This increase in brain lactate may result from decreased cerebral blood flow due to hypocapnia, and individuals with panic disorder may have greater sensitivity to this regulatory mechanism [5].

Psychiatry related information on Panic Disorder

• In contrast, comparison of these findings with a prior study showed that patients with panic disorder and agoraphobia who received yohimbine manifested significantly greater increases in MHPG levels and ratings of anxiety, nervousness, and depression than depressed patients [6].
• The effects on measures of anxiety from two doses of oral caffeine (250 and 500 mg) and placebo were compared in 12 patients with generalized anxiety disorder (GAD), 12 patients with panic disorder, and 12 normal subjects [7].
• Significantly more patients treated with alprazolam than with imipramine hydrochloride or placebo remained in therapy and experienced panic attack and phobia relief during the acute treatment phase [8].
• A subgroup of patients with PTSD were observed to experience yohimbine-induced panic attacks (70% [14/20]) and flashbacks (40% [8/20]), and they had larger yohimbine-induced increases in plasma 3-methoxy-4-hydroxyphenylglycol levels, sitting systolic blood pressure, and heart rate than those in healthy subjects [9].
• At that point, 43% (10/23) of the fluvoxamine recipients vs 25% (5/20) of cognitive therapy and 4% (1/23) of placebo recipients were free of panic attacks [10].

High impact information on Panic Disorder

• The brain cholecystokinin-B/gastrin receptor (CCK-B/gastrin) has been implicated in mediating anxiety, panic attacks, satiety, and the perception of pain [11].
• This asymmetry was present in seven patients with panic disorder and a positive response to lactate infusion but was absent in six normal controls and in three patients with panic disorder associated with a negative response to lactate [12].
• Panic attacks and idiopathic cardiomyopathy [13].
• Patients with panic disorders show a deficit of GABAA receptors in the hippocampus, parahippocampus and orbitofrontal cortex [14].
• Benzodiazepine receptor sensitivity in panic disorder [15].

Chemical compound and disease context of Panic Disorder

• Urinary excretion of noradrenaline metabolite decreased in panic disorder [16].
• Buspirone metabolite and panic attacks [17].
• Panic attacks and excessive aspartame ingestion [18].
• BACKGROUND: There is debate about combining benzodiazepines with selective serotonin reuptake inhibitors in the acute treatment of panic disorder [19].
• Early coadministration of clonazepam with sertraline for panic disorder [19].

Biological context of Panic Disorder

• These findings indicate that the regulation of noradrenergic activity is aberrant in some patients with panic disorder, since a previous study demonstrated that patients with panic disorder exhibit increased plasma MHPG levels, blood pressure, and behavioral responses to the alpha 2-adrenergic receptor antagonist yohimbine [20].
• The number of binding sites in patients with panic attacks, as measured with tritiated clonidine, was lower than in depressed persons and was the same as in normal subjects [21].
• We evaluated the functional sensitivity of the gamma-aminobutyric acid-benzodiazepine supramolecular complex in 9 patients with panic disorder and 10 psychiatrically healthy control subjects by comparing the effects of four logarithmically increasing doses of intravenous diazepam on saccadic eye movement velocity, memory, and self-rated sedation [22].
• Positron emission tomographic measurements of regional blood flow were used to assess local neuronal activity in patients with panic disorder and in normal control subjects before and during the infusion of sodium lactate [23].
• In an open trial, five of eight panic disorder patients and none of five control subjects panicked after inhalation of two breaths of 35% CO2 and 65% O2; none panicked after placebo [24].

Anatomical context of Panic Disorder

• Electroencephalographic recordings with nasopharyngeal electrodes on the day following sleep deprivation were normal, further suggesting that patients with panic disorder do not have seizure activity characteristic of temporal lobe epilepsy [25].
• The locus ceruleus and cortico-releasing factor are implicated in the biological circuit associated with panic attacks, while psychological research indicates that catastrophic thinking, phobic responses to somatic sensations, and repressed anger, grief, and traumatic events play a part in triggering attacks [26].
• Lymphocyte cholecystokinin concentrations in panic disorder [27].
• Cerebrospinal fluid gamma-aminobutyric acid in patients with panic disorder [28].
• BACKGROUND: Abnormal left/right (L/R) hemispheric ratios of regional cerebral glucose metabolic rates (rCMRglc) (hippocampus and inferior prefrontal cortex) have been noted in unmedicated panic disorder patients [29].

Gene context of Panic Disorder

• Antipanic medications suppress the ability of cholecystokinin to induce panic attacks, and may alter the expression of the cholecystokinin gene [30].
• Our genetic dissection of the CCK system thus far suggests that the CCK-B receptor gene variation may contribute to the neurobiology of panic disorder [31].
• CONCLUSIONS: The findings support the hypothesis that comorbid panic disorder identifies a genetic subtype of bipolar disorder and suggest a role for COMT and 5-HTT in vulnerability to these disorders [32].
• Investigation of the DAOA/G30 locus in panic disorder [33].
• CRH may be involved in experimentally-occurring and perhaps in naturally-occurring panic attacks as well [34].

Analytical, diagnostic and therapeutic context of Panic Disorder

• The effects of oral administration of caffeine (10 mg/kg) on behavioral ratings, somatic symptoms, blood pressure and plasma levels of 3-methoxy-4-hydroxyphenethyleneglycol (MHPG) and cortisol were determined in 17 healthy subjects and 21 patients meeting DSM-III criteria for agoraphobia with panic attacks or panic disorder [35].
• The authors studied the response of 10 macaque monkeys to administration of sodium lactate, a panicogenic agent used in human panic disorder research, after treatment with the tricyclic antidepressant imipramine, the triazolobenzodiazepine alprazolam, or placebo [36].
• The authors determined its prevalence in a group of neurology patients and assessed its diagnostic validity as a panic disorder subtype by evaluating the response of the patients with nonfearful panic disorder to sodium lactate and antipanic pharmacotherapy [37].
• CONCLUSIONS: These results suggest that the L/L genotype of the COMT gene may be related to the development and treatment outcome of panic disorder in some patients [38].
• The authors conducted a 16-week double-blind, crossover study in 11 patients with panic disorder to study the effects of verapamil, a calcium channel blocker commonly used in the treatment of cardiovascular disorders, on the treatment of panic disorder [39].

References