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Implicit and explicit learning and memory processes in acute hippocampal impairment: The role of stress

Conditions
G45.4
Transient global amnesia
Registration Number
DRKS00007874
Lead Sponsor
niversitätsMedizin Mannheim
Brief Summary

Transient global amnesia (TGA) is a disorder characterized by a sudden attack of severe anterograde memory disturbance that is frequently preceded by emotional or physical stress and resolves within 24 h. By using MRI following the acute episode in TGA patients, small lesions in the hippocampus have been observed. Hence, it has been hypothesized that the disorder is caused by a stress-related transient inhibition of memory formation in the hippocampus. To study the factors that may link stress and TGA, we measured the cortisol day-profile, the dexamethasone feedback inhibition and the effect of experimental exposure to stress on cortisol levels (using the socially evaluated cold pressor test and a control procedure) in 20 patients with a recent history of TGA and in 20 healthy controls. We used self-report scales of depression, anxiety and stress, and a detailed neuropsychological assessment to characterize our collective. We did not observe differences in mean cortisol levels in the cortisol day-profile between the two groups. After administration of low-dose dexamethasone, TGA patients showed significantly stronger cortisol suppression in the daytime profile compared to the control group (p = 0.027). The mean salivary cortisol level was significantly higher in the TGA group prior to and after the experimental stress exposure (p = 0.008 and 0.010 respectively), as well as prior to and after the control condition (p = 0.022 and 0.024, respectively). The TGA group had higher scores of depressive symptomatology (p = 0.021) and anxiety (p = 0.007), but the groups did not differ in the neuropsychological assessment. Our findings of a stronger pharmacological suppression and higher cortisol levels in anticipation of experimental stress in participants with a previous TGA indicate a hypersensitivity of the HPA axis. This suggests that an individual stress sensitivity might play a role in the pathophysiology of TGA.

Detailed Description

Not available

Recruitment & Eligibility

Status
Complete
Sex
All
Target Recruitment
40
Inclusion Criteria

Arm 1:
- transient global amnesia
- patient is still in the Episode

Arm 2:
- healthy control subject, no acute disease

Both groups:
- right-handed person
- written consent to participate in the study

Exclusion Criteria

Arm 1:
- episode of anterograde amnesia has already ended

Both groups:
- contraindication against MRI
- taking cortisol preparations

Study & Design

Study Type
observational
Study Design
Not specified
Primary Outcome Measures
NameTimeMethod
Changes in brain networks measured with resting-state fMRI (T0, T1, T2), between the two groups and within the TGA Group (arm 1) over time
Secondary Outcome Measures
NameTimeMethod
Group comparison between arm 1 and arm 2 concerning: <br>- acute cortisol values and cortisol dynamic<br>- cortisol day profile and dexamethasone suppression test<br>- stress reactivity (SECPT and control procedure)<br>- neuropsychological Parameters<br>- stress scales<br>- fear conditioning fMRI<br>- DTI<br>- hippocampus volumetry<br>- further clinical, laboratory and MRI Parameters<br><br>Descriptive statistics of the TGA group (arm 1):<br>- Dynamics of the cortisol values in the acute Phase<br>- neuropsychological characterization in the acute phase<br>- number and localization of DWI changes
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