Table 1 Summary of neurochemical studies.

From: Neurochemical and genetic factors in panic disorder: a systematic review

Study

Sample

Measurement

Intervention

Findings

P value

Comment

Maddock et al. [25]

N = 34 participants

n = 22 patients (13 remitted, 8 symptomatic)

n = 12 HC

MRI, 1H-MRS

Vigilance task

Sig. increase in visual cortex lactate/NAA during visual stimulation compared with baseline across groups

<0.0001

Matched for gender, age, and education.

Remitted PD patients were free of panic attacks and other significant PD symptoms for at least 4 months.

Subjects were evaluated by a psychiatrist with the Structured Clinical Interview for DSM-IV.

  

PD > HC, sig. main effect of group for percentage change from baseline lactate/NAA during visual stimulation and subsequent recovery periods.

0.0018

    

Sig. main effect of time for mean lactate double peaks before and during visual stimulation.

 

Zwanzger et al. [26]

N = 18 HC right-handed male subjects (26.9 years ± 4.5 years)

H-MRS

CCK-4 challenge

Sig. increase in panic symptoms as indicated by increased between the API scores

<0.0001

All subjects had to be free of any medication. Any drug intake was ruled out by urine toxicology screening.”

   

Sig. increase in panic symptoms as indicated by increased between the PSS scores

<0.0001

   

Sig. increase in HR in experimentally induced panic

<0.0001

   

Glutamatergic baseline concentration seems to mainly determine the extent of percentage of Glx/Cr increase

<0.0001

   

Sig. increase in CCK-4-related HPA axis stimulation mirrored by a significant effect on plasma cortisol levels 10–15 min after CCK-4 administration

0.0002

    

Sig. positive correlation between maximum Glx/Cr concentrations and API max

0.0090

No effects were found for the correlation between maximum Glx/Cr concentrations and API max

    

Sig. positive correlation between baseline Glx/Cr concentrations and HR max

0.0270

 

Mueller et al. [29]

N = 66

n = 22 PD

n = 21 MD

n = 23 HC

EEG

Gambling task

N300H latencies did not differ between groups

>0.05

 
  

PD > HC, N300H magnitudes significantly higher

<0.02

 
  

PD without MD comorbidity > HC, N300H magnitudes remained significantly higher

0.0100

 
  

PD > MD, temporal N300H spread significantly different

<0.05

 
  

PD > HC, temporal N300H spread significantly different

<0.005

 
  

PD/MD treated with SRIs > PD/MD not treated with SRI at the time of the study, showed significantly larger N300H spread

<0.014

 
  

PD > HC, P300 significantly increased

<0.01

 
    

Group x peak cardiac acceleration, no main effect or interaction

>0.2

 
    

PD > HC, significantly greater N300H when controlling for P300 amplitude

<0.03

 

Jakuszkowiak-Wojten et al. [30]

N = 28

n = 14 psychotropic drug=native outpatients with PD without agoraphobia

n = 14 HC

Saliva samples

None

No. sig difference in salivary cortisol between PD and HC at awakening

0.7700

 
  

No. sig difference in salivary cortisol between PD and HC at awakening + 15 min

0.4260

 
  

No. sig difference in salivary cortisol between PD and HC at awakening + 30 min

0.5140

 
  

No sig. difference between PD and HC with changes in time and CAR parameters

  
   

No sig. difference in AUCg (nmol/L*min) between PD and HC

0.5610

 
   

No sig. difference in AUCi (nmol/L*min) between PD and HC

0.1380

 

Wichmann et al. [31]

n = 30 PD/AG

n = 4 PD without AG

n = 34 HC

CBT

DEX-CRH test

CBT for patient group

Between groups, no sig. difference in DEX-CRH suppression rate

1.0000

 
  

At cortisol levels baseline, PD < HC, sig. difference of cortisol levels measured 75 min prior to CRH-injection

0.0160

 
  

At cortisol levels baseline, PD < HC, sig. difference of cortisol levels measured 1 min prior to CRH-injection

0.0400

 
  

At ACTH baseline, no sig group differences in 75 min prior to the CRH-injection

  
  

At ACTH baseline, no sig group differences in 1 min prior to the CRH-injection

  
   

At baseline, sig. main effect of time for cortisol levels and the BDI sum score.

≤0.001

 
    

No sig. time x group interaction effect

0.4320

 
    

No sig. main effect of group

0.7670

 
    

At ACTH concentration baseline and the BDI sum score, sig. main effect of time is observed

≤0.001

 
    

At ACTH concentration baseline and the BDI sum score, no time x group interaction effect

0.5970

 
    

At ACTH concentration baseline and the BDI sum score, no main effect of group

0.8090

 
    

With psychotherapy, sig. correlation between mean cortisol concentrations and ACQ loss of control outcome score

0.0050

 
    

With psychotherapy, no sig. correlation between mean cortisol concentrations and PAS, ACQ physical concerns and total score, BSQ and MI outcome scores

≥0.028

 

Kim et al. [32]

  

IL6

MDD, PD > HC at baseline levels were higher

0.022

 
    

MDD, PD > HC at 3rd visit has levels were higher

0.003

 
    

PD > MDD, HC at the 4th visit, IL-6 levels were significantly higher

0.016

 
    

In PD, significantly negative association with treatment response

0.022

 
   

Leptin

MDD, PD > HC showed significantly higher levels in 3rd visit

0.032

 
    

MDD, PD > HC showed significantly higher levels in 4th visit

0.003

 
  1. API Acute Panic Inventory, PSS Panic Symptom Scale, Glx/Cre glutamate + glutamine/creatine, EEG electroencephalogram, N300H centromedial brain activity 300 ms after presentation of motivationally meaningful stimuli, CAR cortisol awakening response, AUCg area under curve with respect to the ground, AUCi area under curve with respect to the increase, CCK4 cholecystokinin-tetrapeptide, SRI serotonin reuptake inhibitors, BDI Beck’s Depression Inventory, ACQ Agoraphobic Cognitions Questionnaire, PAS Panic and Agoraphobia Scale, BSQ Body Sensation Questionnaire, MI Mobility Inventory, ACTH adrenocorticotropic hormone.