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Late Onset PTST

Late Onset PTST

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Published by Tracy
Information regarding late onset PTSD-symptoms, therapeutic options, etc.
Information regarding late onset PTSD-symptoms, therapeutic options, etc.

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Published by: Tracy on Oct 27, 2009
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Marsha Snyder, PhD, PMHCNS, BC
Late-Onset PosttraumaticStress Disorder
Posttraumatic stress disorder (PTSD) isa complex psychological response to aperceived life-threatening trauma that in-cludes re-experiencing the trauma, avoid-ance, intrusive thoughts, hyperarousal, anddissociation. Exposure to trauma in earlyadulthood increases the potential for fur-ther psychological threats throughout life.In older adult populations, PTSD is an un-derrecognized and undertreated disorderthat can result in psychosocial disability,substance use, and other negative healthoutcomes. This article examines the rangeof symptoms related to PTSD in older adultsand expands on health care provider sensi-tivity to the interrelationship of mental andphysical health when addressing the needsof older adults with this disorder.
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W
ithin the last cen-tury, the average liespan has increasedby 37%, with many people liv-ing well into their 80s and 90s. Itis estimated that by 2030, morethan 15 million older adults willexperience a mental illness. Theaging o the Baby Boomer cohortand greater longevity is responsi-ble or this statistic (U.S. Depart-ment o Health and Human Ser-vices [USDHHS], Ofce o theSurgeon General, 1999). The es-timated prevalence rate or anxi-ety disorders in adults age 55 andolder is approximately 11%. Thispercentage is greater than that o any other disorder associated witholder adults (USDHHS, Ofce o the Surgeon General, 1999). Inparticular, posttraumatic stressdisorder (PTSD) in older adultsis an underrecognized and under-treated disorder that can result inpsychosocial disability, substanceuse, and other negative healthoutcomes. For this reason, thepurpose o this article is to exam-ine this disorder as it relates toolder adults and increase healthcare provider sensitivity to theinterrelationship o mental andphysical health when addressingthe needs o older adults withthis disorder.
DifferentiAl DiAgnosisof PtsD
As Americans live longer,the psychological stressors someindividuals sustained at earlierlie stages can become deterrentsto successul aging (USDHHS,Ofce o the Surgeon General,1999). This is especially trueor individuals who are exposedto trauma related to combat,ravages o war, sexual abuse, orevents a person conceptualizes ascatastrophic, and when availablecoping mechanisms ail (Murray,2005). In the case o older adults,research surrounding trauma andresponses to trauma has been pri-marily inclusive o male veteranpopulations. However, severalstudies do address trauma-relatedissues or civilian older adult e-male populations. An area o re-cent interest is the reoccurrenceo trauma-related stress symp-toms in later lie.
Au s Dd 
The majority o individualsexposed to an acute stress epi-sode will recover in the monthsollowing the traumatic eventand will not require ormal inter-vention. These individuals allwithin the diagnostic categoriesoutlined in the
Diagnostic andStatistical Manual of Mental Dis-orders
, ourth edition, text revi-sion (American Psychiatric As-sociation, 2000) or acute stressdisorder (ASD) (Bryant, 2003).Symptoms related to ASD occurwithin a month o a traumaticevent. Symptoms are categorizedinto six areas:
l
Cluster A—earul re-sponse ater a traumatic event.
l
Cluster B—three dissocia-tive symptoms.
l
Cluster C—re-experienc-ing symptoms.
l
Cluster D—marked avoid-ance.
l
Cluster E—marked anxiety.
l
Cluster F—evidence o sig-nifcant distress or impairment ineveryday task completion.
PtsD
Disturbance in all six areasidentifed or ASD must last aminimum o 2 days and a maxi-mum o 4 weeks beore the diag-nosis o PTSD can be assigned.Three Cluster B symptoms o dis-sociation need to be present or adiagnosis o ASD:
l
Subjective sense o numb-ing or detachment.
l
Reduced awareness o sur-roundings.
l
Derealization, depersonal-ization, or dissociative amnesia.These symptoms block processingo traumatic memories and adap-tation. Interestingly, individualswho develop PTSD do not alwaysreport Cluster B symptoms (Bry-ant, 2003). It is proposed thatboth individuals who experienceall symptoms and those who ex-perience all but Cluster B symp-toms can be at risk or developingPTSD (Bryant, 2003). Symptomscan abate and resurace overmonths or years and can reoccurin ull orce i the person is retrau-matized. While survivor symp-toms can persist as an individualages into older adulthood, howthese symptoms are expressed isvery individual and may dependon genetic and epigenetic ac-tors, premorbid personality traits,early lie experiences, and socialsupport (Weintraub & Ruskin,1999). Consistent fndings reportthat delayed onset o PTSD is rarewhen no prior exposure to traumahas occurred (Andrews, Brewin,Philpott, & Stewart, 2007).
PreDictive fActorsfor PtsD
Age can oer a protectiveshield against the eects o a trau-matic event through the passageo time and successul lie expe-riences. Factors that seem to beassociated with resilience againstthe development o PTSD in-clude marriage, social support,increased socioeconomic sta-tus, and religion (Weintraub &Ruskin, 1999). Across studies, noagreement has been reached onthe symptom combination that ispredictive o PTSD, and or thisreason, increased attention has
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been directed toward biologicalindicators (Bryant, 2003).
bgca idca
The connection between thebasal ganglia, limbic system, andprerontal cortex brain structuresare well supported in the litera-ture. This connection seems toinclude processing o both so-cial and emotional inormation(Flannelly, Koenig, Galek, & El-lison, 2007). The basal ganglia,although primitive, provides anautonomic system or threat as-sessment. The basal ganglia andthe limbic system operate in pre-consciousness or both languageand emotional arousal. For thisreason, in the case o PTSD, as-sessment o threat is excessive andsometimes in error, as the personperceives a threat when there isnone. All three brain components(basal ganglia, limbic system, andprerontal cortex) rely on sensoryinput rom the prerontal cortexand amygdala or their assessmentinormation regarding a threat,as well as past experience andmemories. Judgments regardingthreat potential seem to be routedprimarily through emotional pro-cessing rather than through cog-nitive reasoning and, as a result,are unconscious, rapid, and auto-matic, with the response outcomenot necessarily within a person’sconscious awareness (Flannelly etal., 2007).Another area o biologicalinvestigation is research that ad-dresses the relationship betweenincreased glucocorticoid levelsand PTSD symptoms. On the ba-sis o peripheral and neuroendo-crine studies o individuals withPTSD symptoms, Grossman etal. (2006) reported greater sensi-tivity in the central brain to glu-cocorticoids. This phenomenonwas expressed through height-ened declarative memory sug-gestive o hippocampal involve-ment; impairment in workingmemory suggestive o prerontal,cingulated, temporal, and pari-etal cortexes; and neurotransmit-ter systems associated with dopa-mine and serotonin (Grossmanet al., 2006).Increases in these measuresseem to refect a preexisting vul-nerability trait that heightensthe risk or developing PTSD ol-lowing a traumatic event. Func-tional brain images or patientswho have had PTSD refect sig-nicant activation in the ventralrontoparietal network and lethippocampal area, which areconnected with visual attentionand memory (Bryant, 2003). Asa result, even slight traumaticstimuli can initiate fashbacksin the presence o poor concen-tration and attention. It seemsthis traumatic stimulus becomesassociated with arousal and sub-sequent development o earconditioning that can trigger ur-ther conditioning. Mechanismsor this sensitization are unclear,but it does seem evident that re-petitive activation o traumaticmemories increases sensitivitywithin the limbic system (Bry-ant, 2003).
Pychgca idca
Development and continuedexperience o acute and chronicsymptoms o PTSD are mediatedby cognitive responses to thetraumatic event. These cogni-tive responses are demonstratedthrough persistent negative ap-praisal o the traumatic eventand subsequent events throughdisturbance in memory that ischaracterized by “poor elabo-ration and contextualization,strong associative memory, andstrong perceptual priming” (Bry-ant, 2003, p. 792).As the traumatic event is pro-cessed, understanding and mean-ing are attributed to the eventwithin the contexts o social andcultural environments. Studiesindicate the level o psychologi-cal impact o the trauma experi-ence on the individual dependsheavily on pretrauma unction-ing. Preexisting depression andanxiety and multiple traumaexposures seem to increase anindividual’s vulnerability to thestressors related to trauma, withthe highest rates o PTSD as-sociated with violent or sexualtrauma (Nakell, 2007).
PoPUlAtions At risk
veea su
Veterans who meet criteriaor PTSD also report symptomso major depression, generalizedanxiety disorder, panic disorder,and alcohol abuse. Older vet-erans seen in primary care whoreported depression and symp-toms o PTSD also reported moresuicidal ideation, smoking, andnegative perceptions o theirhealth than did those who didnot report these symptoms. Thesesymptoms contributed to dicul-
Opportunity exists for primary care andpsychiatric nurses to come together and shape asystem of care that is responsive to patient needs.
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