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.
Both prospective and retrospective studies have shown that PTSD symptoms can evolve, even after a 20-year long symptom-free period, and reemergence of PTSD
symptoms is not uncommon. 34,35 A longer delay usually presents with less severe symptoms. 36 The unavailability of complete information regarding a patient’s past adjustment to psychological trauma has encouraged some experts to label exacerbation of PTSD symptoms precipitated by cognitive disorder as delayed onset PTSD. In most cases, it seems that this is more accurately described as a recrudescence of symptoms that were better managed previously. The picture is clouded by the often bizarre and extreme manifestation of PTSD symptoms in patients with memory disorders. The course of PTSD often does involve a delay between the time of exposure to trauma and symptom manifestation. In addition, symptom intensity can fluctuate significantly over the course of this often chronic illness.
The suffering associated with PTSD is often personal and concealed. Family and other collateral sources may be able to report only on social and occupational functioning. The authors recommend increased attention to proper assessment of (1) remote trauma history in patients being evaluated for memory disorders; and (2) cognitive decline in patients with history of PTSD. The problem of underreported cognitive decline is well known, although its extent is not. Early detection may help to mitigate the combined effects of these conditions. Aggressive early treatment of symptoms during the onset of cognitive dysfunction may prolong patients’ ability to remain at home.
Mr. B’s case was marked by significant tension in the home. Education and support of caregivers is essential to maintaining care in the least restrictive setting, such as the patient’s home. Families might be utterly bewildered by a patient’s apparently sudden preoccupation with traumatic memories. For many, this might be the first time they have ever heard the patient speak at length about the traumatic events. Simple strategies to limit exposure to distressing stimuli, improve grounding, and understand the effects of trauma can be taught. Psychopharmacologic intervention to improve sleep, slow cognitive decline, and decrease behavioral disturbances may be indicated.
Behavioral disturbance is frequently encountered when treating patients with cognitive impairment. In the limited literature on the subject, patients with both PTSD and cognitive impairment do not seem to be more prone to behavioral disturbance than patients with cognitive impairment alone. 9 However, the case reports cited here demonstrate a high incidence of violence or potential violence in these comorbid patients. Routine assessment of potential harm from firearms or other weapons should be conducted assiduously.
It is possible that Vietnam War veterans may be more likely than previous veterans to exhibit behavioral disturbances in the context of cognitive decline and PTSD. A higher incidence of aggression, violence, and resistance to authority has been documented in this group. 37 Substance abuse and dependence also occurs with higher frequency in this cohort and may complicate treatment of cognitive impairment and PTSD. 38,39 A large number of these veterans may initially present to non-VA health care providers and these clinicians may be unaware of a patient’s prior combat exposure and thus fail to accurately assess PTSD.
Although the relation of PTSD and vulnerability to dementia has been well established, it is unknown how the presence of PTSD symptomatology impacts dementia symptoms or how the presence of dementia impacts PTSD symptoms. Posttraumatic stress disorder and dementia share similar risks like traumatic brain injury, low IQ, poor education, substance abuse, precipitated by