The results of this study did not show an initial difference in hippocampal volume between trauma survivors who developed PTSD and those who did not. Smaller hippocampal volume, therefore, was not a necessary risk factor for developing PTSD in this group of subjects. In addition, individuals who developed PTSD did not show a progressive reduction of the hippocampus between 1 week and 6 months.
These results are in apparent contrast to those of the aforementioned MRI studies of PTSD (1
). This discrepancy can be explained in several ways. First, structural damage to the hippocampus may result from exposure to prolonged traumatization, such as in child abuse or a 1-year war experience in Vietnam. Second, it is possible that more than 6 months of expressing PTSD are required to produce discernible reduction of the hippocampus. Third, the previous results could have been due to substance abuse or alcohol consumption, not properly accounted for by retrospective questionnaires. Finally, a smaller hippocampus may confer a specific vulnerability to highly chronic PTSD. Prolonged PTSD in Vietnam veterans has, in fact, been associated with other related findings, such as lower education level and lower premilitary IQ (see, for instance, reference 17). The current study's groups did not differ significantly in level of education.
Another explanation may be linked to the age at which the traumatic event occurred. Subcortical gray matter and limbic structures (septal area, hippocampus, and amygdala) show an increase in volume until the third decade of life (18
). In two of the four previous MRI studies (3
) the subjects were traumatized as children. The two others (1
) concerned Vietnam veterans, most of whom would have served in Vietnam between the ages of 18 and 21. All four studies, therefore, examined adults whose traumatic events occurred during a period of normal development of subcortical structures. The subjects in the current study, in contrast, were older, and none was younger than 20 at the time of the traumatic event. The negative results in the study of children with PTSD by De Bellis et al. (7
) might also be explained by the fact that the MRI scans of those subjects were taken when the subjects were very young, that is, in the midst of hippocampal maturation. This could have masked the full effect of the psychological insult, which may not manifest itself before adulthood.
The size of the current study group, the severity of PTSD at 6 months, and the fact that the first MRI images were acquired 1 week after the traumatic event call for a discussion of potential methodological confounds. First, a type II error might have occurred such that the current results do not exclude a true reduction of hippocampal volume in PTSD. The smallest significant reduction previously reported was 5% (4
). Given the current study's finding of larger hippocampi in PTSD (3% at 1 week), the probability of having missed a hypothetical reduction of 5% in hippocampal volume between 1 week and 6 months is, for the left hippocampus, less than 4% (one-tailed t=1.77, df=35) and, for the right hippocampus, less than 3% (one-tailed t=2.01, df=35).
Second, the current study group may not have had a severe form of PTSD at 6 months. Indeed, scores of patients with chronic PTSD on the Clinician-Administered PTSD Scale are usually higher. However, the mean total score of the current PTSD group (57.90) resembles scores reported for 218 trauma survivors 4 months after the traumatic events (total score=54.6) (19
) and for PTSD patients 6 months after road traffic accidents (total score=60.1) (20
). Moreover, a similar mean score (58.0) was associated with a smaller hippocampus in the previously mentioned study of survivors of child abuse (4
). The mean score on the Mississippi Scale for Combat-Related PTSD of the current PTSD group (110.80) is similar to the scores obtained in most studies of PTSD.
Third, a reduction of hippocampal volume could have occurred between the traumatic event and the 1-week assessment, such that the initial MRI scan may not represent pretrauma anatomy. Acute stress has, in fact, a rapid (21
) and reversible (23
) effect on hippocampal cells. The data supporting this effect, however, are mainly histological and come from studies of nonprimates. However, Fuchs and Flugge (25
) have shown that measurable reduction in hippocampal volume does not occur before 21 days of continuous exposure to stress. Furthermore, in this study, a hypothetical acute stress-induced reduction in hippocampal volume should have equally affected the PTSD and non-PTSD subjects (as both groups reported substantial and similar distress at 1 week). Hence, the likelihood of having missed an acute and early reduction of the hippocampus among PTSD patients in this study is minimal.
Finally, the results of this study are in line with those from published neuropsychological studies (e.g., references 26, 27), in which hippocampal functions
were not impaired in PTSD following recent traumatic events, whereas frontal lobe tasks, such as attention and set shifting, were impaired. Accordingly, the hippocampus may not be the primary dysfunctional area of the brain in PTSD following recent trauma. Moreover, reduced hippocampal volume has also been found in other prolonged mental disorders, such as depression (26
), alcohol abuse (8
), and schizophrenia (e.g., reference 29), and hippocampal reduction in primates has been observed after prolonged social stress (6
). Hippocampal atrophy, therefore, may be a common outcome of several pathogenic processes that share the element of protracted distress.