PTSD in Combat Veterans With Cognitive Decline

Discussion

Posttraumatic stress symptoms were present during the immediate aftermath of the initial trauma exposure for this patient. He managed to lead a relatively successful and productive life, sustained a marriage, and raised a family. The onset of cognitive decline precipitated a recrudescence of PTSD symptomology. In fact, the effects of combat trauma seem more malignant and extreme at the time of the memory disorders evaluation than at any prior time in his life.

A number of case reports have been published in recent years that describe comorbid presentations of cognitive disorder and PTSD symptomatology.^3-6 A clinicalconsensus that cognitive decline can exacerbate previously well-managed symptoms of earlier psychological trauma seems to be emerging. Several published casestudies have noted that comorbid presentation of dementia and PTSD is often marked by violence, psychotic symptoms, and increased risk of hospitalization.^7-9

PTSD Research

Unfortunately, systematic investigation into the relationship between PTSD and cognitive decline is in its infancy. Previous authors have posited various mechanisms to explain the exacerbation of dormant PTSD symptoms after cognitive decline.^10,11 Some have attributed the phenomenon to an age-related failure of either repression or avoidance or to a compromised ability to actively focus their attention elsewhere.^2,12 A finding of preservative errors on neuropsychological tests has been associated with an inability to organize and inhibit intrusive thought.¹³ In one case, the effects of combat trauma were purported to be denied, repressed, and largely forgotten for 30 years until rekindled by the patient’s deteriorating health and loss of employment.¹⁴ Several case examples have been presented in which physical illness, interpersonal loss, retirement, or losses of social support were other factors.^15-18 Two major studies of veterans with PTSD, found that subjects were twice as likely to develop dementia.^3,4 There is a strong association between chronic psychological stress and later development
of dementia. In a study by Wilson and colleagues, subjects with higher baseline stress had twice the chance of developing Alzheimer disease.19 Similar findings of
accelerated or higher cognitive decline were found by other studies, too.^17,20

Hippocampal damage associated with prolonged, intense psychological stress has been cited as a possible contributor to PTSD symptom recrudescence in older adults.²¹ It is well known that emotional arousal leads to better-encoded memories. In the context of a cognitive disorder marked by gradual memory loss, traumatic memories might be the last to go.²² Another proposed biologic mechanism is a reduction in hippocampal volume and decreased inhibition of the amgydala, which results in preferential recall of the nondeclarative, amygdaloidal traumatic memories.⁸

Research on selective area damage in the hippocampus opens a new era of understanding of consequences of stress. The dentate gyrus (DG) is the main area of hippocampus that helps in neurogenesis and cornus ammonis 3 (CA3) for dendritic branching.^23-25 In recent studies by Wang and colleagues, PTSD has been found to be associated with selective volume loss of the CA3/DG subfields, consistent with animal studies.^24-28 Abundance of glucocorticoid receptors in the hippocampus, especially at CA3^,29,30 may make it more vulnerable to the neurotoxic effect of glucocorticoids, causing suppression of neurogenesis,²⁹ diminished dendritic branching,30 loss of synapses,^26,31 and eventually diminished neuroplasticity,32 because CA3/DG is the main target of neurotoxicity by glucocorticoid and inflammatory damage.

The results of neuroimaging studies suggest that decreased integration of the prefrontal cortex and the hippocampus results in impaired short-term memory and perhaps increasing the prominence of long-term distressing memories.³³ Clinical observation confirms that patients with PTSD experience vivid, intense, detailed, and realistic recollections of remote memories at a time when their ability to recall nontraumatic autobiographical detail is severely compromised.