Skip to main content

Neurobiology of Panic Disorder

Image
By

Neurobiology of Panic Disorder

"There is most evidence for changes in Gamma-aminobutyric acid, with lowered cortical Gamma-aminobutyric acid type levels measured by magnetic resonance spectroscopy, and diminished benzodiazepine-receptor binding in the parietotemporal regions in unmedicated patients with panic disorder (Hasler et al., 2008)."

This happens in panic disorder. Gamma-aminobutyric acid is the major inhibitory neurotransmitter in the brain. Benzodiazepine also binds to Gamma-aminobutyric acid type A receptors and increases its firing rate, thus resulting in hyperpolarisation of the cell because of increased chloride influx. So, specific regions in the brain are hyperexcitable in patients with panic disorder.

Summary of Hasler et al. 

Context

Studies have implicated the benzodiazepine receptor system in the pathophysiologic mechanism of panic disorder  by indirect evidence from pharmacological challenge studies and by direct evidence from single-photon emission computed tomography and positron emission tomography neuroimaging studies
  1. The benzodiazepine receptor binding potential was decreased in multiple areas of the frontal, temporal, and parietal cortices and was increased in the hippocampus/ parahippocampal region in subjects with panic disorder vs controls
  2. The most significant decrease was in the dorsal anterolateral prefrontal cortex; the most significant increase in the hippocampus/parahippocampal gyrus
  3. In subjects with panic disorder, the severity of panic and anxiety symptoms correlated positively with benzodiazepine receptor binding in the dorsal anterolateral prefrontal cortex but negatively with binding in the hippocampus/parahippocampal gyrus
  4. These data provide evidence of abnormal benzodiazepine–Gamma-aminobutyric acid type A receptor binding in panic disorder, suggesting that basal and/or compensatory changes in inhibitory neurotransmission play roles in the pathophysiologic mechanism of panic disorder. 

Hasler G, Nugent AC, Carlson PJ, Carson RE, Geraci M, Drevets WC. Altered cerebral gamma-aminobutyric acid type A-benzodiazepine receptor binding in panic disorder determined by [11C]flumazenil positron emission tomography. Arch Gen Psychiatry. 2008;65(10):1166-1175. doi:10.1001/archpsyc.65.10.1166
Labels:

Comments

  1. Justpsychiatry12 January 2021 at 20:25

    Hasler G, Nugent AC, Carlson PJ, Carson RE, Geraci M, Drevets WC. Altered cerebral gamma-aminobutyric acid type A-benzodiazepine receptor binding in panic disorder determined by [11C]flumazenil positron emission tomography. Arch Gen Psychiatry. 2008;65(10):1166-1175. doi:10.1001/archpsyc.65.10.1166

    ReplyDelete

Post a Comment

Your Thoughts?

Popular posts from this blog

ADVOKATE: A Mnemonic Tool for the Assessment of Eyewitness Evidence

By
ADVOKATE: A Mnemonic Tool for Assessment of Eyewitness Evidence A tool for assessing eyewitness  ADVOKATE is a tool designed to assess eyewitness evidence and how much it is reliable. It requires the user to respond to several statements/questions. Forensic psychologists, police or investigative officer can do it. The mnemonic ADVOKATE stands for: A = amount of time under observation (event and act) D = distance from suspect V = visibility (night-day, lighting) O = obstruction to the view of the witness K = known or seen before when and where (suspect) A = any special reason for remembering the subject T = time-lapse (how long has it been since witness saw suspect) E = error or material discrepancy between the description given first or any subsequent accounts by a witness.  Working with suspects (college.police.uk)
Post a Comment
Read more

ICD-11 Criteria for Attention Deficit Hyperactivity Disorder (ADHD) 6A05

By
ICD-11 Criteria for Attention Deficit Hyperactivity Disorder (ADHD) 6A05 Attention deficit hyperactivity disorder is characterised by a persistent pattern (at least 6 months) of inattention and/or hyperactivity-impulsivity that has a direct negative impact on academic, occupational, or social functioning. There is evidence of significant inattention and/or hyperactivity-impulsivity symptoms prior to age 12, typically by early to mid-childhood, though some individuals may first come to clinical attention later. The degree of inattention and hyperactivity-impulsivity is outside the limits of normal variation expected for age and level of intellectual functioning. Inattention refers to significant difficulty in sustaining attention to tasks that do not provide a high level of stimulation or frequent rewards, distractibility and problems with organisation. Hyperactivity refers to excessive motor activity and difficulties with remaining still, most evident in structured situations that re...
Post a Comment
Read more

ICD-11 Criteria for Anorexia Nervosa (6B80)

By
ICD-11 Criteria for Anorexia Nervosa (6B80) Anorexia Nervosa is characterised by significantly low body weight for the individual’s height, age and developmental stage that is not due to another health condition or to the unavailability of food. A commonly used threshold is body mass index (BMI) less than 18.5 kg/m2 in adults and BMI-for-age under 5th percentile in children and adolescents. Rapid weight loss (e.g. more than 20% of total body weight within 6 months) may replace the low body weight guideline as long as other diagnostic requirements are met. Children and adolescents may exhibit failure to gain weight as expected based on the individual developmental trajectory rather than weight loss. Low body weight is accompanied by a persistent pattern of behaviours to prevent restoration of normal weight, which may include behaviours aimed at reducing energy intake (restricted eating), purging behaviours (e.g. self-induced vomiting, misuse of laxatives), and behaviours aimed at incr...
Post a Comment
Read more