Panic Disorder
- Panic Attack
- Panic Disorder
- Recurrent Panic Attacks
- Anticipatory Anxiety
- Agoraphobia
- Hypochondriasis
- Demoralisation
- Epidemiology
- Age of Onset
- Situation of Onset
- Stressful Life Events
- Early Life Events
- Maternal Over-Protection
- Separation Anxiety
- Short and Long-term Outcomes
- Comorbidity
- Panic Disorder: Pathogenesis
- Biological Findings
- Provocative Agents
- Neurotransmitter Systems
- Neuroanatomical Models
- Brain Imaging
- Psychological Models
- Psychodynamic Models
- Behavioural Models
- Cognitive Models
- Areas of Controversy and Debate
- The Evolutionary Perspective
- Panic Disorder: Treatment
- Pharmacotherapy
- Benzodiazepines
- Tricyclic Antidepressants
- Monoamine Oxidase Inhibitors
- Selective Serotonin Re-uptake Inhibitors
- Other Drugs
- Psychotherapy
Brain Imaging Treatment Depression Anxiety Add
Reiman et al., using positron emission tomography (PET), noted an exaggeration of the asymmetrical (right greater than left) parahippocampal gyrus cerebral blood flow in association with hypocapnia in lactate-sensitive PD subjects. Nordahl et al. replicated the finding of exaggerated parahippocampal asymmetry (right greater than left) in PD patients using deoxyglucose PET. Using single positron emission tomography (SPECT), bilateral hippocampal hypoperfusion and exaggerated asymmetry (right greater than left) of inferior frontal cortical perfusion blood flow in lactate-sensitive PD subjects were noted. SPECT studies using the BDZ antagonist-iomazenil also showed an increased asymmetry (right greater than left) of ligand binding in the inferior and middle prefrontal cortex in PD patients.
In a PET study measuring regional cerebral blood flow (r-CBF) during an unexpected panic attack, panic was associated with decreased r-CBF in the right orbitofrontal, prelimbic, anterior cingulate and anterior temporal cortices. Bisaga et al. found a significant increase in glucose metabolism in the left hippocampus and parahippocampal area in PD patients at rest in comparison with that found in normal subjects. In addition, a significant decrease was found in metabolism in the right inferior parietal and right superior temporal brain regions of the PD subjects when compared with that of the normal subjects. Nordahl et al. found the same abnormally low left/right hippocampal and posterior inferior prefrontal regional cerebral glucose metabolic rates (r-CMRglc) ratios in treated PD patients and untreated PD patients. The general pattern of an exaggeration of the normally observed right to left asymmetry in panic-sensitive subjects is of interest and seems to be consistent, though it requires further investigation.
A second feature of neuroimaging in PD is the cerebral hypervasoconstriction observed during hyperventilation and panic attacks. SPECT studies of lactate infusion demonstrated generally increased cerebral blood flow (CBF), except in panic patients experiencing an attack during infusion, in which case there was a blunting or decrease in CBF. SPECT studies with yohimbine-induced anxiety also revealed vasoconstriction. Other groups have noted that even in healthy subjects high levels of anxiety are accompanied by decreases in CBF and brain metabolism. Regionally ‘‘perceived’’ anoxia in key areas of the brain that are activated by inadvertent hyperventilation and ensuing hypocapnea may mediate escape responses from situations that are phylogenetically selected for their occasional potential for fatal consequence. More recent PET data by Reiman has posited abnormal function of internally cued alarm ‘‘systems’’, particularly in the anterior insular cortex and anterior temporal regions in patients with PD.