Neuropsychiatric Symptoms in Dementia Patients With and Without a History of Traumatic Brain Injury

Abstract

The authors aim to determine if a history of traumatic brain injury (TBI) assessed before dementia onset is associated with a higher risk of neuropsychiatric symptoms after dementia onset. A population-based incident series of people with dementia were assessed for TBI prior to onset of dementia and for neuropsychiatric symptoms after the onset, using the Neuropsychiatric Inventory. Participants with predementia TBI were more likely to exhibit disinhibition (12.7%Address correspondence to Vani Rao, M.D., Division of Geriatric Psychiatry and Neuropsychiatry, Department of Psychiatry, Johns Hopkins University, 5300 Alpha Commons Dr., 4th Floor, #444, Baltimore, MD 21224; vrao@jhmi.edu. These results were presented as a poster by DP at Northeastern Ohio Universities College of Medicine's Summer Research Fellowship Program on 9/3/08 in Rootstown, Ohio, and as an oral presentation at Summa Health System on 1/8/09 in Akron, Ohio. DP is a Medical Student Training in Aging Research (MSTAR) scholar and presented these results at the 2009 American Geriatric Society Annual Scientific Meeting. While patients affected by dementia and TBI independently are at increased risk for neuropsychiatric symptoms, no published data have examined the question of whether people with dementia who have sustained a TBI in the past are at increased risk for developing neuropsychiatric symptoms. Given that dementia and TBI are both associated with damage to the frontal cortex and associated frontal-subcortical circuits, and damage to these circuits from a variety of insults predisposes patients to psychopathology, 9 we hypothesized that, in persons with dementia, TBI prior to the onset of dementia would be a risk factor for increased neuropsychiatric symptoms associated with frontal lobe damage such as disinhibition, irritability, depression, apathy, and aggression. We examined this question in a population-based study of persons with dementia whose history of TBI was assessed prior to the onset of dementia and in whom dementia-onset was assessed prospectively (incident cohort). NIH Public Access METHODSThis is a prospective study involving persons with incident dementia who took part in the Cache County Study on Memory, Health, and Aging (CCSMHA). The CCSMHA is an ongoing population-based study of the epidemiology and progression of dementia. The study has been approved by Institutional Review Boards at Duke University Medical Center, Johns Hopkins University, and Utah State University. Informed consent was obtained from either the study participants or appropriate next of kin. This study has been described previously. 10,11 Briefly, a total of 5,092 respondents (5,677 were invited) ages 65 years and older participated in the study. All participants underwent a multistage screening and assessment for prevalent dementia (Wave 1). Those with dementia in Wave 1 and those that did not develop dementia or dropped out between Waves 1 and 3 were excluded from these analyses (n=4,265). TBI AssessmentHead injury was assessed prior to the onse...

Traumatic brain injury (TBI) in older adults: aging with a TBI versus incident TBI in the aged

“…Data from the National Alzheimer's Coordinating Center (NACC) suggest that TBI may be a risk factor for early-onset Alzheimer's disease (AD; onset <65 years) (Mendez et al , 2015) and that disinhibition is more likely to occur in those with AD who have a history of TBI. This association between pre-dementia TBI and disinhibition has been shown previously (Rao et al , 2010). However, in a recent meta-analysis, no statistically significant association was found between TBI and mild cognitive impairment or AD (Crane et al , 2016).…”

Prevalence of Traumatic Brain Injury in Early Versus Late-Onset Alzheimer’s Disease

“…In CTE, NFTs initially deposit perivascularly and in superficial cortical layers, especially in the frontal lobes [46, 48], and CTE may manifest with early clinical “frontal” symptoms such as disinhibition, irritability, and mood disturbances, and even suicidal behavior [48, 49]. These neurobehavioral changes are similar to the disinhibition and other behavioral changes present in our EOAD participants and other demented individuals who have a history of TBI [50, 51]. …”

Executive (dys)function after traumatic brain injury: special considerations for behavioral pharmacology

“…While many people recover with minimal complications, a significant portion goes on to develop chronic behavioral and cognitive deficits, resulting in an estimated 1–2% of people with TBI-related disabilities ( Thurman et al , 1999 ; Zgaljardic et al , 2015 ), and accounting for a staggering $76.5 billion USD economic burden as of 2010, with 10-year costs averaging $270 000 per patient ( Corso et al , 2006 ; Coronado et al , 2012 ; Ponsford et al , 2013 ). Brain injury is considered to be a major risk factor in the development of neurodegenerative disorders, including Parkinson’s and Alzheimer’s diseases ( Semchuk et al , 1993 ; Plassman et al , 2000 ), and is associated with increased rates of depression, anxiety, attention-deficit disorders, suicidality, and substance abuse following such central nervous system damage ( Moor et al , 2006 ; Vaishnavi et al , 2009 ; Rao et al , 2010 ; Konrad et al , 2011 ; Reeves and Panguluri, 2011 ; Zgaljardic et al , 2015 ). Notably, these disorders impair a wide variety of behaviors commonly considered under the umbrella of ‘executive function,’ including memory, behavioral flexibility, impulsivity, and decision-making ( Alves et al , 2014 ; Bredemeier and Miller, 2015 ; Day et al , 2015 ; Sharp et al , 2015 ; Kingdon et al , 2016 ).…”