The gradual emergence of symptoms following exposure to traumatic events has presented a major conceptual challenge to psychiatry. The mechanism that causes the progressive escalation of symptoms ...with the passage of time leading to delayed onset post-traumatic stress disorder (PTSD) involves the process of sensitization and kindling. The development of traumatic memories at the time of stress exposure represents a major vulnerability through repeated environmental triggering of the increasing dysregulation of an individual's neurobiology. An increasing body of evidence demonstrates how the increased allostatic load associated with PTSD is associated with a significant body of physical morbidity in the form of chronic musculoskeletal pain, hypertension, hyperlipidaemia, obesity and cardiovascular disease. This increasing body of literature suggests that the effects of traumatic stress need to be considered as a major environmental challenge that places individual's physical and psychological health equally at risk. This broader perspective has important implications for developing treatments that address the underlying dysregulation of cortical arousal and neurohormonal abnormalities following exposure to traumatic stress.
Objectives
Several medical and psychiatric disorders have stage‐based treatment decision‐making methods. However, international treatment guidelines for posttraumatic stress disorder (PTSD) fail to ...give specific treatment recommendations based on chronicity or stage of the disorder. There is convincing evidence of a finite range of PTSD symptom trajectories, implying that different phenotypes of the disorder can be distinguished, which are highly relevant for a staging typology of PTSD.
Methods
State‐of‐the‐art review building on prior work on staging models in other disorders as a mapping tool to identify and synthesize toward PTSD.
Results
We propose a four‐stage model of PTSD ranging from stage 0: trauma‐exposed asymptomatic but at risk to stage 4: severe unremitting illness of increasing chronicity. We favor a symptom description in various chronological characteristics based on neurobiological markers, information processing systems, stress reactivity, and consciousness dimensions. We also advocate for a separate phenomenology of treatment resistance since this can yield treatment recommendations.
Conclusion
A staging perspective in the field of PTSD is highly needed. This can facilitate the selection of interventions that are proportionate to patients' current needs and risk of illness progression and can also contribute to an efficient framework to organize biomarker data and guide service delivery. Therefore, we propose that a neurobiologically driven trajectory‐based typology of PTSD can help deduct several treatment recommendations leading to a more personalized and refined grid to strategize, plan and evaluate treatment interventions.
The psychiatric sequelae of traumatic injury Bryant, Richard A; O'Donnell, Meaghan L; Creamer, Mark ...
The American journal of psychiatry,
03/2010, Letnik:
167, Številka:
3
Journal Article
Recenzirano
Traumatic injury affects millions of people each year. There is little understanding of the extent of psychiatric illness that develops after traumatic injury or of the impact of mild traumatic brain ...injury (TBI) on psychiatric illness. The authors sought to determine the range of new psychiatric disorders occurring after traumatic injury and the influence of mild TBI on psychiatric status.
In this prospective cohort study, patients were drawn from recent admissions to four major trauma hospitals across Australia. A total of 1,084 traumatically injured patients were initially assessed during hospital admission and followed up 3 months (N=932, 86%) and 12 months (N=817, 75%) after injury. Lifetime psychiatric diagnoses were assessed in hospital. The prevalence of psychiatric disorders, levels of quality of life, and mental health service use were assessed at the follow-ups. The main outcome measures were 3- and 12-month prevalence of axis I psychiatric disorders, levels of quality of life, and mental health service use and lifetime axis I psychiatric disorders.
Twelve months after injury, 31% of patients reported a psychiatric disorder, and 22% developed a psychiatric disorder that they had never experienced before. The most common new psychiatric disorders were depression (9%), generalized anxiety disorder (9%), posttraumatic stress disorder (6%), and agoraphobia (6%). Patients were more likely to develop posttraumatic stress disorder (odds ratio=1.92, 95% CI=1.08-3.40), panic disorder (odds ratio=2.01, 95% CI=1.03-4.14), social phobia (odds ratio=2.07, 95% CI=1.03-4.16), and agoraphobia (odds ratio=1.94, 95% CI=1.11-3.39) if they had sustained a mild TBI. Functional impairment, rather than mild TBI, was associated with psychiatric illness.
A significant range of psychiatric disorders occur after traumatic injury. The identification and treatment of a range of psychiatric disorders are important for optimal adaptation after traumatic injury.
Traumatic injuries affect millions of patients each year, and resulting post-traumatic stress disorder (PTSD) significantly contributes to subsequent impairment.
To map the distinctive long-term ...trajectories of PTSD responses over 6 years by using latent growth mixture modelling.
Randomly selected injury patients (n = 1084) admitted to four hospitals around Australia were assessed in hospital, and at 3, 12, 24 and 72 months. Lifetime psychiatric history and current PTSD severity and funxctioning were assessed.
Five trajectories of PTSD response were noted across the 6 years: (a) chronic (4%), (b) recovery (6%), (c) worsening/recovery (8%), (d) worsening (10%) and (e) resilient (73%). A poorer trajectory was predicted by female gender, recent life stressors, presence of mild traumatic brain injury and admission to intensive care unit.
These findings demonstrate the long-term PTSD effects that can occur following traumatic injury. The different trajectories highlight that monitoring a subset of patients over time is probably a more accurate means of identifying PTSD rather than relying on factors that can be assessed during hospital admission.
Summary A bomb blast may cause the full severity range of traumatic brain injury (TBI), from mild concussion to severe, penetrating injury. The pathophysiology of blast-related TBI is distinctive, ...with injury magnitude dependent on several factors, including blast energy and distance from the blast epicentre. The prevalence of blast-related mild TBI in modern war zones has varied widely, but detection is optimised by battlefield assessment of concussion and follow-up screening of all personnel with potential concussive events. There is substantial overlap between post-concussive syndrome and post-traumatic stress disorder, and blast-related mild TBI seems to increase the risk of post-traumatic stress disorder. Post-concussive syndrome, post-traumatic stress disorder, and chronic pain are a clinical triad in this patient group. Persistent impairment after blast-related mild TBI might be largely attributable to psychological factors, although a causative link between repeated mild TBIs caused by blasts and chronic traumatic encephalopathy has not been established. The application of advanced neuroimaging and the identification of specific molecular biomarkers in serum for diagnosis and prognosis are rapidly advancing, and might help to further categorise these injuries.
Little is understood about how the symptoms of posttraumatic stress develop over time into the syndrome of posttraumatic stress disorder (PTSD).
To use a network analysis approach to identify the ...nature of the association between PTSD symptoms in the acute phase after trauma and the chronic phase.
A prospective cohort study enrolled 1138 patients recently admitted with traumatic injury to 1 of 4 major trauma hospitals across Australia from March 13, 2004, to February 26, 2006. Participants underwent assessment during hospital admission (n = 1388) and at 12 months after injury (n = 852). Networks of symptom associations were analyzed in the acute and chronic phases using partial correlations, relative importance estimates, and centrality measures of each symptom in terms of its association strengths, closeness to other symptoms, and importance in connecting other symptoms to each other. Data were analyzed from March 3 to September 5, 2016.
Severity of PTSD was assessed at each assessment with the Clinician-Administered PTSD Scale.
Of the 1138 patients undergoing assessment at admission (837 men 73.6% and 301 women 26.4%; mean SD age, 37.90 13.62 years), strong connections were found in the acute phase. Reexperiencing symptoms were central to other symptoms in the acute phase, with intrusions and physiological reactivity among the most central symptoms in the networks in terms of the extent to which they occur between other symptoms (mean SD, 1.2 0.7 and 1.0 0.9, respectively), closeness to other symptoms (mean SD, 0.9 0.3 and 1.1 0.9, respectively), and strength of the associations (mean SD, 1.6 0.3 and 1.5 0.3 respectively) among flashbacks, intrusions, and avoidance of thoughts, with moderately strong connections between intrusions and nightmares, being upset by reminders, and physiological reactivity. Intrusions and physiological reactivity were central in the acute phase. Among the 852 patients (73.6%) who completed the 12-month assessment, overall network connectivity was significantly stronger at 12 months than in the acute phase (global strength values, 6.57 vs 7.60; paired difference, 1.03; P < .001). The network associations among the reexperiencing symptoms were strengthened at 12 months, and physiological reactivity was strongly associated with the startle response, which was also associated with hypervigilance. Strong connectivity among emotional numbing, detachment from others, and disinterest in activities as well as moderately strong links among irritability (anger), concentration deficits, and sleep disturbance were found.
As time elapses after trauma, fear circuitry and dysphoric PTSD symptoms appear to emerge as connected networks. Intrusive memories and reactivity are centrally associated with other symptoms in the acute phase, potentially pointing to the utility of addressing these symptoms in early intervention strategies.
Delayed-onset posttraumatic stress disorder (PTSD) accounts for approximately 25% of PTSD cases. Current models do not adequately explain the delayed increases in PTSD symptoms after trauma exposure.
...To test the roles of initial psychiatric reactions, mild traumatic brain injury (MTBI), and ongoing stressors on delayed-onset PTSD.
In this prospective cohort study, patients were selected from recent admissions to 4 major trauma hospitals across Australia. A total of 1084 traumatically injured patients were assessed during hospital admission from April 1, 2004, through February 28, 2006, and 785 (72.4%) were followed up at 3, 12, and 24 months after injury.
Severity of PTSD was determined at each assessment with the Clinician-Administered PTSD Scale.
Of those who met PTSD criteria at 24 months, 44.1% reported no PTSD at 3 months and 55.9% had subsyndromal or full PTSD. In those who displayed subsyndromal or full PTSD at 3 months, PTSD severity at 24 months was predicted by prior psychiatric disorder, initial PTSD symptom severity, and type of injury. In those who displayed no PTSD at 3 months, PTSD severity at 24 months was predicted by initial PTSD symptom severity, MTBI, length of hospitalization, and the number of stressful events experienced between 3 and 24 months.
These data highlight the complex trajectories of PTSD symptoms over time. This study also points to the roles of ongoing stress and MTBI in delayed cases of PTSD and suggests the potential of ongoing stress to compound initial stress reactions and lead to a delayed increase in PTSD symptom severity. This study also provides initial evidence that MTBI increases the risk of delayed PTSD symptoms, particularly in those with no acute symptoms.
Post-traumatic stress disorder Yehuda, Rachel; Hoge, Charles W; McFarlane, Alexander C ...
Nature reviews. Disease primers,
10/2015, Letnik:
1
Journal Article
Recenzirano
Post-traumatic stress disorder (PTSD) occurs in 5-10% of the population and is twice as common in women as in men. Although trauma exposure is the precipitating event for PTSD to develop, biological ...and psychosocial risk factors are increasingly viewed as predictors of symptom onset, severity and chronicity. PTSD affects multiple biological systems, such as brain circuitry and neurochemistry, and cellular, immune, endocrine and metabolic function. Treatment approaches involve a combination of medications and psychotherapy, with psychotherapy overall showing greatest efficacy. Studies of PTSD pathophysiology initially focused on the psychophysiology and neurobiology of stress responses, and the acquisition and the extinction of fear memories. However, increasing emphasis is being placed on identifying factors that explain individual differences in responses to trauma and promotion of resilience, such as genetic and social factors, brain developmental processes, cumulative biological and psychological effects of early childhood and other stressful lifetime events. The field of PTSD is currently challenged by fluctuations in diagnostic criteria, which have implications for epidemiological, biological, genetic and treatment studies. However, the advent of new biological methodologies offers the possibility of large-scale approaches to heterogeneous and genetically complex brain disorders, and provides optimism that individualized approaches to diagnosis and treatment will be discovered.
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