International Society for Traumatic Stress Studies

Frontotemporal Dementia-Like Syndrome Following Recall of Childhood Sexual Abuse

Posted 24 June 2015 in StressPoints by David Brody, MD & Lisa J. Cohen, PhD

Can posttraumatic stress disorder present as dementia? 

In their recently published article in the Journal of Traumatic Stress, Drs. Lisa Cohen and David Brody reported the case of a 50-year-old woman who developed severe cognitive impairment following retrieval of previously repressed memories of childhood sexual abuse.  Two years prior to the onset of dementia-like symptoms, the patient presented for psychiatric treatment having experienced a brief psychotic episode.  She responded well to antidepressant and antipsychotic medication plus supportive psychotherapy.  After six months, her medication was tapered to discontinuation.  Her psychosis recurred almost immediately in the context of family stressors related to coping with her father’s incarceration for sexually abusing her nephew. Medication treatment was again highly effective.  Her case was now conceptualized as a type of psychotic posttraumatic stress disorder and her psychotherapy began to address her memories of possible abuse by her father. 

Six months prior to the onset of cognitive decline, the patient began to recover memories of being sexually abused by her father.  The patient relayed what seemed like memory fragments, discontinuous sensory-emotional experiences of pain, bodily discharge, surprise and confusion.  About a month after she reported her first nightmare of the abuse, her husband reported acute and dramatic cognitive decline.  The patient quickly became disabled, took medical leave from her job, and required 24-hour supervision.  She was unable to fold laundry, use the stove safely, or even dress herself appropriately. She evidenced gross loss of motor coordination, with difficulty chewing and walking and lost 7% of her normal body weight, despite denial of loss of appetite. She was spatially disoriented and wandered away when not supervised. She was verbally and motorically perseverative as well as somewhat disinhibited, displaying overly familiar behavior with her therapist.
 
A full neurological work up was negative, excepting strongly elevated CRP and high normal B12 levels, which were quickly normalized without clinical improvement.  Based on the clinical presentation, the patient was diagnosed with fronto-temporal dementia (versus cortico-basal degeneration) by a neurologist and neuropsychologist. 

Nine months after the onset of the apparent dementia, memantine was started and the patient began to improve; by month five of memantine treatment, her husband judged her to be 85% improved and her neurologist and neuropsychologist withdrew the dementia diagnosis.  Thirty months from the onset of illness and 21 months after initial improvement, she returned to work.  

In their discussion of the case, Drs. Cohen and Brody cite pre-clinical research establishing a link between brain inflammation and posttraumatic behavior (Wilson, McLaughlin, Nair, Ebenezer, Dange  & Francis, 2013). The patient’s response to memantine is particularly notable, raising the question of whether there is a glutamatergic role in dissociation and/or PTSD. The authors cite research suggesting that glutamate, as the major excitatory neurotransmitter in the brain, plays an important role in extinguishing traumatic memories and that memantine may indeed be effective in treating PTSD (Battista, Hierholzen, Khouzam, 2007; Myers, Carlezon, & Davis, 2011).  The authors also consider the possibility that an encephalopathic process may have played a role in the context of the emergence of previously repressed traumatic memories.  Although this case remains a diagnostic conundrum, reports of additional cases with similar presentations would support the notion that persistent, severe, and reversible cognitive impairment may constitute a previously unrecognized and atypical posttraumatic response.
 

Discussion questions:

  1. Could marked but transient cognitive impairment be an atypical symptom of posttraumatic stress?
  2. Could PTSD be conceptualized as a neuroinflammatory disorder?  What markers of neuroinflammation are elevated in response to stress?
  3. What are the risks of exploring possible childhood trauma in symptomatic patients who report no memories of abuse despite indications that such a history might be likely?


Author Bios:


David Brody, MD is an attending psychiatrist at Mt. Sinai Beth Israel Medical Center in NYC and assistant clinical professor of psychiatry at The Icahn School of Medicine at Mt. Sinai. 
 
Lisa J. Cohen, PhD is a professor of psychiatry at the Icahn School of Medicine at Mt. Sinai and a supervising psychologist at Mount Sinai Beth Israel.  Dr. Cohen divides her time between clinical work, teaching and research.
 

References:

 
Battista, M.A., Hierholzen, R., Khouzam, H. (2007). Pilot trial of memantine in the
treatment of posttraumatic stress disorder. Psychiatry: Interpersonal and Biological Processes. 70, 167-174.

Myers, K.M., Carlezon, W.A. Jr, Davis M. (2011). Glutamate receptors in extinction
and extinction-based therapies for psychiatric illness. Neuropsychopharmacology, 36, 274–293.

Wilson, C.B., McLaughlin, L.D., Nair, A., Ebenezer, P.J., Dange, R., & Francis, J. (2013). Inflammation and oxidative stress are elevated in the brain, blood, and adrenal glands during the progression of post-traumatic stress disorder in a predator exposure animal model. PLoS ONE, 8(10). doi:10.1371/journal.pone.0076146