Peripubertal PTSD-like stress in rats induces transient behavioral but lasting metabolic and inflammatory alterations: Limited fluoxetine efficacy.

The purpose of this study was to determine whether anterior limbic and paralimbic regions of the brain are differentially activated during the recollection and imagery of traumatic events in trauma-exposed individuals with and without posttraumatic stress disorder (PTSD). Positron emission tomography (PET) was used to measure normalized regional cerebral blood flow (CBF) in 16 women with histories of childhood sexual abuse: eight with current PTSD and eight without current PTSD. In separate script-driven imagery conditions, participants recalled and imagined traumatic and neutral autobiographical events. Psychophysiologic responses and subjective ratings of emotional state were measured for each condition. In the traumatic condition versus the neutral control conditions, both groups exhibited regional CBF increases in orbitofrontal cortex and anterior temporal poles; however, these increases were greater in the PTSD group than in the comparison group. The comparison group exhibited regional CBF increases in insular cortex and anterior cingulate gyrus; increases in anterior cingulate gyrus were greater in the comparison group than in the PTSD group. Regional CBF decreases in bilateral anterior frontal regions were greater in the PTSD group than in the comparison group, and only the PTSD group exhibited regional CBF decreases in left inferior frontal gyrus. The recollection and imagery of traumatic events versus neutral events was accompanied by regional CBF increases in anterior paralimbic regions of the brain in trauma-exposed individuals with and without PTSD. However, the PTSD group had greater increases in orbitofrontal cortex and anterior temporal pole, whereas the comparison group had greater increases in anterior cingulate gyrus.

This study examined the prevalence of lifetime traumatic events and current symptoms of posttraumatic stress disorder (PTSD) among treatment-seeking cocaine-dependent outpatients and compared patients with and without PTSD on current substance use, psychopathology, and sociodemographic characteristics. The subjects were 122 adult cocaine-dependent outpatients participating in a treatment outcome study of psychosocial therapy. In addition to standard self-report and interview measures of psychopathology and substance use, the subjects completed the Trauma History Questionnaire and the PTSD Checklist before entering treatment. These patients experienced a large number of lifetime traumatic events (mean = 5.7); men experienced more general disasters and crime-related traumas than women, and women experienced more physical and sexual abuse than men. According to self-report measures, 20.5% of the subjects currently met the DSM-III-R criteria for PTSD; the rate of PTSD was 30.2% among women and 15.2% among men. Patients with PTSD had significantly higher rates of co-occurring axis I and axis II disorders, interpersonal problems, medical problems, resistance to treatment, and psychopathology symptoms than patients without PTSD. Psychopathology symptoms represented the most consistent difference between the two groups and provided the best prediction of PTSD status in a logistic regression. However, the groups did not differ significantly in current substance use or sociodemographic characteristics. These findings underscore the value of screening substance abusers for PTSD, because it can identify a small but substantial number who might require additional treatment. Further studies of the relationship between PTSD and substance abuse appear warranted.

The authors aim to delineate cognitive dysfunction associated with posttraumatic stress disorder (PTSD) by evaluating a well-defined cohort of former World War II prisoners of war (POWs) with documented trauma and minimal comorbidities. The authors studied a cross-sectional assessment of neuropsychological performance in former POWs with PTSD, PTSD with other psychiatric comorbidities, and those with no PTSD or psychiatric diagnoses. Participants who developed PTSD had average IQ, while those who did not develop PTSD after similar traumatic experiences had higher IQs than average (approximately 116). Those with PTSD performed significantly less well in tests of selective frontal lobe functions and psychomotor speed. In addition, PTSD patients with co-occurring psychiatric conditions experienced impairment in recognition memory for faces. Higher IQ appears to protect individuals who undergo a traumatic experience from developing long-term PTSD, while cognitive dysfunctions appear to develop with or subsequent to PTSD. These distinctions were supported by the negative and positive correlations of these cognitive dysfunctions with quantitative markers of trauma, respectively. There is a suggestion that some cognitive decrements occur in PTSD patients only when they have comorbid psychiatric diagnoses.

Disturbed sleep is a hallmark feature of posttraumatic stress disorder (PTSD). However, few studies have examined sleep objectively in individuals with PTSD compared to trauma-exposed controls. This study used wrist actigraphy to measure and compare sleep patterns in trauma-exposed Australian Vietnam veterans (VV) with and without PTSD. Trauma-exposed Australian VV with and without PTSD were recruited from the PTSD Initiative. VV wore wrist accelerometers over 14 days and completed daily sleep diaries. Sleep parameters were compared between groups including sleep latency (SL), time in bed (TIB), total sleep time (TST), wake after sleep onset (WASO), and movement index (MI). Night-to-night and overall within-individual variability were assessed by root mean squared successive differences and comparison of individual standard deviations. Correlations between sleep diary (self-reported) and wrist actigraphy (objective) variables were also assessed. A total of 40 male VV (20 with PTSD) participated in the study. We found no difference in sleep patterns determined by wrist actigraphy between groups with the exception of reduced SL in VV with PTSD (3.9 ± 0.9 versus 4.9 ± 1.4 minutes, P < .05). Overall within-individual variability was significantly greater in VV with PTSD for TIB, TST, WASO, and MI. Self-reported and objective TST and WASO were more strongly correlated in VV without PTSD than those with PTSD. Although there were no significant differences in sleep parameters, VV with PTSD had increased within-individual overall sleep variability and reduced correlation between self-reported and objective sleep parameters compared to trauma-exposed controls. Further evaluation of extended sleep patterns by actigraphy in VV with PTSD is warranted.

Changes in Relative Glucose Metabolic Rate Following Cortisol Administration in Aging Veterans with Posttraumatic Stress Disorder: An FDG-PET Neuroimaging Study

Few case series studies have addressed the issue of treatment response in patients with obsessive-compulsive disorder (OCD) and comorbid post-traumatic stress disorder (PTSD), and there are no prospective studies addressing response to conventional treatment in OCD patients with a history of trauma (HT). The present study aimed to investigate, prospectively, the impact of HT or PTSD on two systematic, first-line treatments for OCD. Two hundred and nineteen non-treatment-resistant OCD outpatients were treated with either group cognitive-behavioral therapy (GCBT n = 147) or monotherapy with a selective serotonin reuptake inhibitor (SSRI n = 72). Presence of HT and PTSD were assessed at intake, as part of a broader clinical and demographical baseline characterization of the sample. Severity and types of OCD symptoms were assessed with the Yale-Brown Obsessive-Compulsive Scale (YBOCS) and the Dimensional YBOCS (DYBOCS), respectively. Depression and anxiety symptoms were measured with the Beck Depression Inventory (BDI) and the Beck Anxiety Inventory (BAI). Both treatments had 12-week duration. Treatment response was considered as a categorical [35% or greater reduction in baseline YBOCS scores plus a Clinical Global Impression-Improvement rating of better (2) or much better (1)] and continuous variable (absolute number reduction in baseline YBOCS scores). Treatment response was compared between the OCD + HT group versus the OCD without HT group and between the OCD + PTSD group versus the OCD without PTSD group. Parametric and non-parametric tests were used when indicated. Data on HT and PTSD were available for 215 subjects. Thirty-eight subjects (17.67% of the whole sample) had a positive HT (OCD + HT group) and 22 subjects (57.89% of the OCD + HT group and 10.23% of the whole sample) met full DSM-IV criteria for PTSD. The OCD + HT and OCD without HT groups presented similar response to GCBT (60% of responders in the first group and 63% of responders in the second group, p = 1.00). Regarding SSRI treatment, the difference between the response of the OCD + HT (47.4%) and OCD without HT (22.2%) groups was marginally significant (p = 0.07). In addition, the OCD + PTSD group presented a greater treatment response than the OCD without PTSD group when treatment response was considered as a continuous variable (p = 0.01). The age when the first trauma occurred had no impact on treatment response. In terms of specific OCD symptom dimensions, as measured by the DYBOCS, OCD treatment fostered greater reductions for the OCD + PTSD group than for the OCD without PTSD group in the scores of contamination obsessions and cleaning compulsions, collecting and hoarding and miscellaneous obsessions and related compulsions (including illness concerns and mental rituals, among others). The OCD + PTSD group also presented a greater reduction in anxiety scores than the OCD without PTSD group (p = 0.003). The presence of HT or PTSD was not related to a poorer treatment response in this sample of non-treatment-resistant OCD patients. Unexpectedly, OCD patients with PTSD presented a greater magnitude of response when compared with OCD without PTSD patients in specific OCD symptom dimensions. Future studies are needed to clarify if trauma and PTSD have a more significant impact on the onset and clinical expression of OCD than on the conventional treatment for this condition, and whether OCD stemming from trauma would constitute a subtype of OCD with a distinct response to conventional treatment.

Clinical Characteristics and Health Service Use of Veterans With Comorbid Bipolar Disorder and PTSD

Posttraumatic stress disorder (PTSD) is one of the few psychiatric conditions in which a subjective decrease in emotional range serves as a diagnostic criterion. In order to investigate whether veterans with chronic PTSD also experienced objective limitations in emotional perception, the authors administered the Aprosodia Battery to a group of 11 veterans with chronic PTSD, nine subjects with right hemisphere damage, seven subjects with left hemisphere damage, and 12 comparison subjects. The patients with PTSD displayed significant deficiencies in the comprehension and discriminative components of affective speech, similar in severity and performance profile on the Aprosodia Battery to the individuals with focal right hemisphere damage due to ischemic infarction.

BackgroundOn February 6, 2023, a series of earthquakes resulted in approximately 60,000 deaths and 120,000 injuries in Turkey and Syria. These earthquakes caused serious psychological problems in addition to their social and economic effects. Post-traumatic stress disorder (PTSD) is one of the most frequently reported psychiatric disorder among the survivors of earthquakes. The aim of this study is to investigate the hemispheric asymmetries and volumes of hippocampus and amygdala of survivors under treatment with a diagnosis of earthquake-exposed PTSD (PTSD group) with earthquake-exposed subjects without a diagnosis of PTSD (non-PTSD group) one year after the Kahramanmaraş earthquakes.MethodsPTSD subjects (n = 39, 17 females and 22 males) who had been using antidepressants for 6–12 months and matched (age, gender, education, smoking, menstrual cycle phase) non-PTSD subjects (n = 42, 21 females and 21 males) from hospital staff were retrospectively included in the study based on filtering criteria. Sociodemographic and clinical data were obtained through the patient registration system. The scores of the PTSD Checklist for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Beck Depression Inventory, and Beck Anxiety Inventory administered to PTSD subjects and the Symptom Checklist-90-Revised (SCL-90-R) administered to all subjects at admission were recorded. Imaging of hippocampus and amygdala was performed with a 1.5-tesla MRI scanner and loaded into software that automatically analysed the segments. SPSS version 26.0 was used for the statistical analysis (descriptive, regression, correlation, receiver operating characteristic, multiple testing correction). A value less than 0.05 was considered statistically significant.ResultsWhile the groups were similar regarding history of major depressive disorder (p = 0.850) and anxiety disorder (p = 0.590), PTSD history in 1st degree relative (p = 0.005) and loss or injury of 1st degree relative in earthquake (p = 0.002) was higher in the PTSD group. The severity of psychiatric symptoms assessed with SCL-90-R was higher in the PTSD group than in the non-PTSD group (p < 0.001). Hippocampus and amygdala asymmetry was in favor of the left side in the PTSD group, while amygdala asymmetry was in favor of the right side in the non-PTSD group. After controlling for the effect of age in the PTSD group, a significant correlation was detected between total hippocampus volume and PCL-5 (r=-0.740, p < 0.001), SCL-90-R (r=-0.670, p < 0.001). According to the hierarchical binary logistic regression analysis, the sensitivity of age, gender, smoking status (block one) plus total hippocampus volume, amygdala asymmetry, loss or physical injury of 1st degree relative (block two) related to the determining the participants who was involved in PTSD and non-PTSD groups was 66.7%, and the specificity was 81.0% (Nagelkerke R2 0.363; Constant p = 0.040).ConclusionsThis study provides various results that volume and asymmetry parameters of hippocampus and amygdala may be associated with the presence of PTSD. Our study supports the information that stress exposure results in changes in hippocampus structure in PTSD. Longitudinal studies are needed to elucidate possible mechanisms.

INTRODUCTION Psychiatric disorders are common after stroke and traumatic brain injury (TBI) both in the short term and long term. They can be caused by regional disruption of neuronal network, impairment of regional cerebral blood flow, impaired cerebral metabolism, axonal injury, and pressure effect of intracranial bleed. Around 16 million people each year experience first ever stroke. Of these patients, 5 million become disabled and 5.7 million dies.[1] Traumatic brain injuries are also common and pose an enormous burden on families and caregivers because of the associated neuropsychiatric complications.[2] However, these neuropsychiatric complications are often remained unaddressed or not adequately treated because of the treating doctor's preoccupation with other severe physical disabilities, whereas treating these neuropsychiatric complications can improve the overall outcome of the patients to a considerable extent. In this clinical practice guideline (CPG), the assessment of psychiatric disorders following stroke and TBI is discussed together, while the management of psychiatric disorders following stroke and TBI is discussed separately under the two broad subheadings. This CPG mostly focused on the most common neuropsychiatric consequences of stroke and TBI, namely depression, psychosis, anxiety, posttraumatic stress disorders (PTSD), mania, emotional lability, fatigue, apathy, and personality changes. There is substantial overlap between neuropsychiatric disorders following stroke and TBI and repetitions will be avoided. This CPG does not include the cognitive consequences of stroke and TBI. We included researches both on ischemic stroke and intracerebral hemorrhage. However, we did not include dementia. CATEGORIES OF EVIDENCE AND STRENGTH OF RECOMMENDATIONS While writing this CPG, we ensured compliance with AGREE II instrument. We marked available evidences from Ia to IV and strengths of recommendations from A to D as per the prevailing norms.[3] Categories of evidence Ia: Evidence from meta-analysis of randomized controlled trials (RCTs) Ib: Evidence from at least one RCT IIa: Evidence from at least one controlled study without randomization IIb: Evidence from at least one quasi-experimental study III: Evidence from nonexperimental descriptive studies, such as correlation studies comparative studies, and case − control studies IV: Evidence from opinions and/or clinical experience of respected authorities or expert committee reports. Strength of recommendations A: Directly based on Category I evidence B: Directly based on Category II evidence or extrapolated recommendation from Category I evidence C: Directly based on Category III evidence or extrapolated recommendation from category I or II evidence D: Directly based on Category IV evidence or extrapolated recommendation from Category I, II or III evidence S: Standard of care. GENERAL ASSESSMENT OF PSYCHIATRIC DISORDERS FOLLOWING STROKE AND TRAUMATIC BRAIN INJURY As a referral physician, psychiatrists have the role to make thorough assessment of a patient following stroke and TBI to rule in/out the presence of any psychiatric disorders in a busy emergency room or inpatient department or intensive care unit (ICU). To assess the consciousness level of the patient, Glasgow Come Scale still remains the gold standard. It is usually very difficult to conduct a psychiatric assessment on a semi-comatose patient or a patient who is uncooperative. In that case, one can use Kirby's pro forma for examining uncooperative patients. The attending psychiatrist should examine the patient in a calm environment with not too many people around. However, the presence of primary caregiver can be allowed if the patient cannot give reliable and valid information which is more often the case. The demeanor of the treating doctor should be nonthreatening. He should talk in a clear voice with every word being uttered with due stress to reach the patient who usually have some or the other sensory impairment. If in delirium, psychiatrist should revisit the patient at a later date and time. Psychiatrist should also take the pain to bring forth the history of substance use disorders which are commonly associated with road traffic accidents and resultant TBI [Box 1].Box 1: Checklist for treating psychiatrist while evaluating post stoke and posttraumatic brain injury psychiatric disordersThe treating psychiatrist should go through the clinical records very carefully and if needed should corroborate the clinical history from the primary caregiver or the eye witnesses. Patient's past psychiatric history is of immense importance as it has some correlation with development of poststroke depression (PSD) and other psychiatric disorders. Psychiatrist should also go through the laboratory reports carefully and look for underlying infection, blood loss, electrolyte disturbances, endocrine dysfunction, and other systemic comorbid conditions which are reflected in complete blood count, urine culture and sensitivity, cerebrospinal fluid study, hemoglobin level, serum sodium, serum potassium, serum chloride, serum thyroid-stimulating hormone, serum parathyroid hormone, fasting blood sugar, liver function test, serum creatinine, etc. If needed and when in doubt, the referral psychiatrist should order for more biochemical investigation to rule out organic condition. The psychiatrist should also pay attention to the neuroimaging reports (computed tomography scan, magnetic resonance imaging, etc.,) to decipher a possible connection between the neurological insult and psychiatric disorder. Electroencephalography should be ordered to rule out subconvulsive status epilepticus which can mimic a psychiatric disorder. A detailed scrutiny of the medications already received should be done to rule out any iatrogenic psychiatric disorder. If needed, the psychiatrist should talk to treating neurologist or the neurosurgeon regarding stoppage of medicine, replacing the offending drug, or possible dose adjustment. A detailed mental status examination should be done with particular focus on obtaining an adequate speech sample, looking for the predominant affect, presence of any delusion or hallucination, and assessment of cognitive function, particularly judgment, abstract thinking, and lobar functions. There are provisions to diagnose various psychiatric disorders following stroke, transient ischemic attack (TIA), and brain injury in DSM 5 and ICD10. The diagnosis of poststroke and post-TBI psychiatric disorders depends on structured clinical interview and using of a screening instrument. There is no universally accepted screening instrument for diagnosing psychiatric disorders following stroke or TBI. For the diagnosis of PSD, Beck Depression Inventory, Hamilton Depression Rating Scale, Nine-item Patient Health Questionnaire-9, Hospital Anxiety Depression Scale, Geriatric Depression Scale, and the Center for Epidemiological Studies Depression (CES-D) Scale have been used. Anxiety disorders can be screened by Hospital Anxiety and Depression Scale-Anxiety Subscale and Hamilton Anxiety Scale. For screening of PTSD, psychiatrist can use clinician administered PTSD Scale, PTSD checklist for a stressor, TIA or stroke as stressor; Post-Traumatic Stress Diagnostic Scale; Impact of Events Scale-Revised. Brief Psychiatric Rating Scale can be used for screening of psychosis and Young's Mania Rating Scale can be used for screening of mania. For the assessment of personality disorders or personality changes, a detailed psychological evaluation with Eysenck's Personality Questionnaire, Minnesota Multiphasic Personality Inventory, International Personality Disorder Examination, or Iowa Personality Disorder Screen may be needed [Table 1].Table 1: Screening tools and management of various psychiatric disorders following stroke/traumatic brain injuryMANAGEMENT OF POSTSTROKE PSYCHIATRIC DISORDERS Poststroke depression PSD is the one of the most commonly reported neuropsychiatric conditions following stroke. Often undiagnosed, PSD is a treatable condition. PSD can occur within 1–18 months following stroke and its prevalence vary considerably over time (reported prevalence at 1, 3, 6, 12, and 18 months were 24.5%, 27.1%, 28.3%, 19.8%, and 26.3%, respectively).[4] PSD is believed to be associated with worse functional outcome following stroke. A meta-analysis showed that, PSD had a adverse impact on survival rates following stroke and it affected short-term mortality more than long-term mortality.[5] Various meta-analysis and systematic review have looked into the role of prophylactic antidepressant treatment to reduce the chance of developing PSD.[6789] Many of them found that, selective serotonin reuptake inhibitors (SSRIs), cognitive behavioral therapy (CBT), and physical exercise improved mood symptoms in PSD. A Cochrane review which included 63 RCTs and over 9000 participants and specifically looked into the role of SSRIs in PSD found that, SSRIs should not be used routinely to promote recovery after stroke as they do not improve recovery after stroke (A).[10] In the Effect of fluoxetine on functional outcomes after acute stroke trial, eligible patients with stroke were recruited and randomly given fluoxetine (20 mg daily) or placebo for 6 months, starting after 2 − 15 days of stroke. After 12 months of follow-up, fluoxetine was found to improve the neuropsychological scale score but not other variables. Therefore, it did not support the routine use of prophylactic fluoxetine in PSD (A).[11] Similar was the finding from the efficacy of citalopram treatment in acute stroke (TALOS study) (A).[12] The efficacy of CBT on PSD remains undetermined due to low quality of the studies and high degree of heterogeneity among them as found by one meta-analysis (A).[13] Neuromodulation techniques such as transcranial direct current stimulation and transcranial magnetic stimulation can offer some benefit, but there are the lack of high quality RCTs (B).[14] SSRIs and SNRIs are often used in conjunction with anti-platelet medication such as clopidogrel in PSD. Fluoxetine and fluvoxamine (CYP2C19 inhibiters) can reduce the efficacy of clopidogrel and can increase the risk of ischemic disease.[15] There have been concerns regarding intracranial bleed following the use of SSRIs also. Studies have suggested that, if given before stroke, SSRIs were associated with severity and mortality in patients with hemorrhagic stroke.[16] However, one recent review pointed out the lack of evidence in support of SSRIs alone increasing the risk of spontaneous intracranial bleed. Therefore, it can be concluded that, SSRIs should not be prescribed prophylactically in all poststroke patients. Rather, they should be screened for PSD and if diagnosed, then only SSRIs and SNRIs can be prescribed as needed (S) with some sort psychological intervention (CBT) (B). Both neurologists and psychiatrists need to be aware of drug-drug interaction which can be potentially life threatening in such group of patients (S). Poststroke psychosis The symptoms of PSP include delusions, hallucinations, psychomotor agitation, irrelevant and incoherent speech, catatonic symptoms, and sleep cycle disturbances. These symptoms usually manifest within a week following stroke but may manifest several weeks later also. Studies form the early 90s indicated that PSP is relatively rare and after 9 years' follow-up only 5 patients developed PSP.[17] A recent meta-analysis found the prevalence of PSP to be around 4.86%.[18] Literature on the management of PSP is sparse compared to PSD or poststroke anxiety (PSA). RCTs on the management of PSP are lacking. The treatment usually follows same principles which are followed for the management and treatment of primary psychotic disorders. Secondgenerationantipsychotics(SGAs), for example, quetiapine, risperidone, andolanzapinearemostcommonlyusedtotreatPSP (D). However, their safety in patients with stroke is highly debatable. Olanzapine can have deleterious effect of plasma glucose and lipids which are not welcome in patients with stroke. Quetiapine can cause postural hypotension, whereas risperidone can cause extra-pyramidal side effects. The concern of anti-psychotics being associated with high incidences stroke has been refuted by a large case − control study.[192021] TheusualpracticeistostartlowandgoslowincaseoftreatmentofPSP(S). However, incertaincases(agitatedandviolentpatients)injectablesmightberequiredandinthatcaseinjectableolanzapineorinjectablehaloperidolcanbeused(D). Asinpatientswithprimarypsychoticdisorders, CBTforhallucinationordelusioncanbebeneficialinPSP(S).[22] Poststroke anxiety disorders PSA is common and only second to PSD in terms of prevalence. All kind of anxiety disorders can be seen following stroke but the core symptoms remain the same – palpitation, psychic and physical restlessness, excessive worry and fear, feeling of nervousness, pseudo neurological symptoms, for example, dizziness, blurring of vision, tingling and numbness of hands and feet, fine tremors, etc. Sensory impairment, ICU admission, painful physical conditions, communication difficulties, and sleep disturbance can lead to the development of PSA. A meta-analysis found the prevalence of PSA to vary between 20% to 24% depending on the time elapsed following stroke.[23] SSRIs, SNRIs, Tri-CyclicAntidepressants(TCAs), Mirtazapine, Buspirone, Benzodiazepines, and Z-drugsallhavebeenusedinthetreatmentofPSAintheabsenceofanydefiniteguideline(D).[24] Meta-analyses conducted by Chun etal. reported beneficial effect of pharmacotherapy (paroxetine, imipramine, and buspirone) and psychotherapy compared to control. However, the studies were of low quality and highly heterogeneous, and therefore, the positive conclusion could be due to bias.[25] Cochrane review in this area also highlighted lack of quality studies and emphasized the need of large scale RCTs.[24] Nonpharmacologicalmanagements, for example, Yoga, Tai-Chi, Self-helpmindfulness, andrelaxationtechniquescanoffersomebenefitinthemanagementofPSA(C).[2627] Therefore, SSRIs, SNRIs, andevenTCAscanbeusedinthetreatmentofPSA(S, D)alongwithnon-pharmacologicalinterventions(C). However, as in case of PSD, psychiatrists and neurologists should be aware of potential drug-drug interactions. Posttraumatic stress disorder following stroke PTSD develops following an event which pose actual or imagined threat to physical and psychological integrity of an individual and stroke is no less than a catastrophe. Symptoms of PTSD include intrusive flashbacks/memories, autonomic arousal, emotional numbness, and avoidance behavior. Poststroke PTSD often has associated PSD and PSA (in up to 40% of the cases).[28] A meta-analysis reported 1-year prevalence of poststroke PTSD to be around 23%.[29] Furthermore, persons with PTSD have higher risk of developing stroke compared to people without PTSD.[30] There is dearth of RCTs in treatment of PTSD. SSRIs, SNRIs, andTCAscanbetried(D). Othermedications, e.g., antipsychotics, anticonvulsants, andanxiolyticshavealsobeentried(D).[31] Psychotherapeutic approaches, e.g., trauma-focused therapies, CBT, and exposure therapy appears to be helpful in resolution of symptoms but they need to be tested in large scale studies (D).[32] Poststroke mania Prevalence of poststroke mania (PSM) is rather low (<2%).[33] Most of the data in this area are in the form of case report or case series.[33] Majority of the subject developed PSM between 1 day to 24 months after stroke.[34] In 1978, Kraut-hammer and Klerman gave the concept of secondary mania in which a manic episode is produced by metabolic, neurological, or toxic disorder.[34] The criteria of secondary mania (PSM in this case) are as follows: (1) symptoms lasting for at least 1 week; (2) presence of elevated or irritable mood; and (3) presence of at least two symptoms out of the followings: Pressured speech, grandiosity, hyperactivity, flight of ideas, distractibility, lack of judgment, and decreased sleep; and (4) no history of affective illness or delirium co-occurring with the mania. Lesions responsible for PSM are usually found in the caudate nucleus, parietal, temporal, and frontal lobes and thalamus. Mania is more common with right-sided lesions, although left sided lesions have also been reported.[3536] Treatment of PSM is in line with treatment of an acute manic episode. Moodstabilizers, e.g., valproate, carbamazepine, oxcarbazepine, etc.;antipsychotics, e.g., olanzapine, quetiapine, risperidone, etc.;andbenzodiazepinesarethemainstayoftreatment(S. D). It is better to avoid lithium in this population because of the presence of multiple comorbidities and potential drug-drug interactions. Furthermore, choosing a mood stabilizer which allows antiepileptic coverage is beneficial. Poststroke emotional lability Poststroke emotional lability is also known by various other names, for example, pathological laughter/crying, emotional incontinence, hyperemotionality, pseudobulbar affect, etc. The symptoms appeared to be dramatic but transient. Patients can present with sudden onset laughter or crying while speaking on a rather inconspicuous matter. Sometimes, it may be difficult to differentiate it from depression. If symptoms are long-lasting, it may result in distress, depression, social avoidance, and embarrassment. The prevalence of poststroke emotional lability varies between 8% to 32%.[37] Quality research in the management of poststroke emotional lability is lacking, thereby precluding any meaningful recommendation. ACochranereviewwithtotal293participantsreported, antidepressantsreducedthefrequencyoflaughingandcryingepisodesbutthequalityofevidencewaslow(A). The effect was not specific to any particular drug or class of drugs. The review pointed our several methodological deficiencies.[38] Poststroke fatigue Poststroke fatigue (PSF) is common sequalae of both ischemic and hemorrhagic stroke. Nearly half of the stroke survivors suffer from PSF. A systematic review put the prevalence of PSF between 25% and 85%.[39] Uniform definition of PSF is lacking. Most commonly PSF is described as, subject lack of mental and physical energy which interferes with individual's day to day activities. PSF has been found to be associated with old age, neurological deficits, diabetes, hypertension, heart failure, kidney disease, pain, anxiety, depression, sleep disturbances, prestroke fatigue, and cognitive impairment.[40] Few studies have pointed to a link between PSF and subcortical and infra-tentorial infarcts.[40] Considering the multifactorial causation of PSF, any one particular pharmacological agent is unlikely to provide any benefit. Modafinil, amoodawakenerhasbeenfoundtobeusefulinPSFfollowingbrainstem-diencephalicstrokebecauseofitseffectonreticularactivatingsystem(C).[41] A small RCT also favoured the use of Modafinil up to a dose of 400 mg/day (B).[42] SSRIs including fluoxetine, escitalopram, sertraline and SNRI, duloxetine has been studied in PSF but none were proven beneficial except for anxiety symptoms.[4344] Clinicians often try vitamin supplementations in PSF. Vitamin B12, Vitamin B1, and idebenone, a synthetic coenzyme Q10 analog have all been studied, but results are inconclusive (C).[454647] JointAmericanStrokeAssociationandAmericanHeartAssociationstatementencouragesregularphysicalexercisetoreducePSF(D, S).[48] A Cochrane review which included two nonpharmacological interventions, mindfulness-based stress reduction program and a fatigue education program found no conclusive evidence of any intervention having any efficacy to treat PSF (A).[49] Poststroke apathy Post-stroke apathy is of stroke. It is by a lack of with and criteria for poststroke apathy for weeks or and two other symptoms cognitive or and functional There are conditions, particularly depression, which can mimic poststroke In that case, should be put on of cognitive symptoms of depression, for example, low lack of attention and ideas, etc. prevalence of poststroke apathy was in a large Poststroke apathy is more common in less and in of and depression in 40% of Patients with poststroke apathy have been found to have higher risk of depression and worse functional Quality evidence for the treatment of poststroke apathy is lacking. There is one RCT with mg and mg which in in Scale score and more There are Poststroke personality disorders There can be of personality or patient can personality after a stroke. There are that patient and/or Personality are more in case of frontal Studies have put the prevalence of and at and The in the prevalence was because of the in which the study was population of stroke, and used to assess personality changes. There are very RCTs which have looked into the treatment of poststroke personality disorders have been extrapolated from studies conducted in SSRIs, for example, in this group of patients OF PSYCHIATRIC DISORDERS FOLLOWING TRAUMATIC BRAIN INJURY For management of psychiatric disorders following TBI, we are not to the same for stroke for of this Rather, we will management and treatment evidences as The first report of psychiatric disorder following TBI was of a who an in when an and frontal which personality form a responsible to and not to take A of psychiatric disorders can be seen following TBI. Posttraumatic agitation, and are common in Posttraumatic has been to posttraumatic consciousness and in cognitive The of posttraumatic varies between to sleep and underlying delirium can promote can be physical and and often than not is sudden and in The of is the severity of injury and of The of in TBI varies between 25% to is although a rather form compared to and it is common in post-TBI patients which as excessive with The of post-TBI varies between to as per the of the studies consequences of TBI are apathy, and We have discussed apathy in in the of psychiatric disorders following stroke. The prevalence of post-TBI apathy varies between 20% to As discussed it may be difficult to differentiate apathy from depression. Furthermore, apathy can to available pharmacological anxiety, and psychosis are other common psychiatric disorders following TBI. The prevalence of depression after TBI was higher compared to population and was put at having depression at the time of injury, cognitive deficits, of left and and pain was associated with depression in TBI All of anxiety for example, anxiety social anxiety and PTSD are common in TBI patients. The prevalence of anxiety disorders varies between and following between psychosis and TBI is less A meta-analysis suggested that, risk of was in TBI group as compared to the control but of studies included any meaningful and are higher in TBI group as compared to the population and some have found it to be as high as Around 20% participants with TBI all of for example, mood antipsychotics, and have been used in the treatment of psychiatric disorders following TBI [Table but in the of study and large of the studies recommendations are difficult to In clinical many of these alone or in There is evidence in of nonpharmacological Cochrane review did not any evidence in of any nonpharmacological for example, mindfulness-based cognitive therapy or CBT for depression following There are a psychiatrist should be aware while such patients, for example, level of cognitive function, neuroimaging done or presence or of clinical subconvulsive status medications received by the patient, drug-drug etc. [Box of medications for should be prescribed to improve patient compliance (S). or should be used because of risk of and cognitive (S). but not the attending psychiatrist should also use depending on of comorbid physical conditions 1].Table used to treat psychiatric disorders following traumatic brain injury and their of to for treating psychiatrist in patients with traumatic brain 1: of psychiatric management of a patient with traumatic brain Psychiatric disorders following stroke and TBI present for the treating a who is with brain psychiatrists of should in of brain and its the other being a behavioral should be the of the patient, the need of the and the emotional need of The link between psychiatric disorders following stroke and TBI is not an Therefore, treatment also to be one drug for Psychiatrist often has to do and before the As already been there is dearth of large scale RCTs for most of the conditions and treatment recommendations are often extrapolated from primary disorders. 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Toward the Predeployment Detection of Risk for PTSD

Background: Previous studies have suggested that sexual dysfunction may be associated with posttraumatic stress disorder (PTSD). Yet such studies have not examined a full range of sexual functioning and have not accounted for the possibility that medication used to treat PTSD may contribute to sexual dysfunction. Objective: The current study compares the various components of sexual functioning among three groups of males: (1) untreated PTSD patients (n = 15), (2) PTSD patients currently treated with selective serotonin reuptake inhibitor (SSRI) agents (n = 27) and (3) a group of normal controls (n = 49). Methods: All participants completed an 18-item questionnaire for assessment of sexual functioning. Those with PTSD also completed the Impact of Events Scale and the Symptom Check List-90 (SCL-90). Results: Untreated and treated PTSD patients had significantly poorer sexual functioning in all domains (desire, arousal, orgasm, activity and satisfaction) as compared to normal controls. Those treated with SSRI had greater impairment in desire, arousal and frequency of sexual activity with a partner. There was a high correlation between sexual dysfunction among the PTSD group and the anger-hostility subscale of the SCL-90. Conclusions: PTSD appears to be associated with pervasive sexual dysfunction that is exacerbated by treatment with SSRIs. PTSD may represent a heterogeneous syndrome. Patients with PTSD have a high rate of comorbid panic disorder, major depression and anxiety, and it could thus be argued that these comorbid disorders, rather than PTSD, accounted for the observed result. Future research aimed at understanding comorbidity and heterogeneity should help to illuminate the psychobiology of PTSD and eventually guide both medication and psychosocial treatments.

Veterans with posttraumatic stress disorder (PTSD) often report suboptimal sleep quality, often described as lack of restfulness for unknown reasons. These experiences are sometimes difficult to objectively quantify in sleep lab assessments. Here, we used a streamlined sleep assessment tool to record in-home 2-channel electroencephalogram (EEG) with concurrent collection of electrodermal activity (EDA) and acceleration. Data from a single forehead channel were transformed into a whole-night spectrogram, and sleep stages were classified using a fully automated algorithm. For this study, 71 control subjects and 60 military-related PTSD subjects were analyzed for percentage of time spent in Light, Hi Deep (1–3 Hz), Lo Deep (<1 Hz), and rapid eye movement (REM) sleep stages, as well as sleep efficiency and fragmentation. The results showed a significant tendency for PTSD sleepers to spend a smaller percentage of the night in REM (p < 0.0001) and Lo Deep (p = 0.001) sleep, while spending a larger percentage of the night in Hi Deep (p < 0.0001) sleep. The percentage of combined Hi+Lo Deep sleep did not differ between groups. All sleepers usually showed EDA peaks during Lo, but not Hi, Deep sleep; however, PTSD sleepers were more likely to lack EDA peaks altogether, which usually coincided with a lack of Lo Deep sleep. Linear regressions with all subjects showed that a decreased percentage of REM sleep in PTSD sleepers was accounted for by age, prazosin, SSRIs and SNRIs (p < 0.02), while decreased Lo Deep and increased Hi Deep in the PTSD group could not be accounted for by any factor in this study (p < 0.005). Linear regression models with only the PTSD group showed that decreased REM correlated with self-reported depression, as measured with the Depression, Anxiety, and Stress Scales (DASS; p < 0.00001). DASS anxiety was associated with increased REM time (p < 0.0001). This study shows altered sleep patterns in sleepers with PTSD that can be partially accounted for by age and medication use; however, differences in deep sleep related to PTSD could not be linked to any known factor. With several medications [prazosin, selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs); p < 0.03], as well as SSRIs were associated with less sleep efficiency (b = -3.3 ± 0.95; p = 0.0005) and more sleep fragmentation (b = -1.7 ± 0.51; p = 0.0009). Anti-psychotics were associated with less sleep efficiency (b = -4.9 ± 1.4; p = 0.0004). Sleep efficiency was negatively impacted by SSRIs, antipsychotic medications, and depression (p < 0.008). Increased sleep fragmentation was associated with SSRIs, SNRIs, and anxiety (p < 0.009), while prazosin and antipsychotic medications correlated with decreased sleep fragmentation (p < 0.05).

Post-traumatic stress disorder (PTSD) is characterized by re-experiencing of a traumatic event, avoidance of trauma-associated stimulation, general changes in mood and cognition, and hyper arousal symptoms. Cyclooxygenase is involved in the production of prostaglandins and thromboxanes, and its inducible form cyclooxygenase-2(COX-2), an important mediator of cell injury in inflammation, is primarily expressed in leukocytes and brain cells. The present study investigated the expression of COX-2 in the hippocampi of rats with PTSD and evaluated the effect of COX-2 inhibition on PTSD. Adult male Wistar rats were randomly divided into three groups: Control (n=20), PTSD (n=20) and intervention group (PTSD+COX-2 inhibitor treatment, n=20). The expression of COX-2 was detected by immunohistochemistry, reverse transcription-quantitative polymerase chain reaction and western blotting. Terminal deoxynucleotidyl transferase mediated dUTP nick end labeling staining was used to observe the apoptosis of rat hippocampal neurons. Tumor necrosis factor α (TNF-α), interleukin (IL)-6 and prostaglandin E2 (PGE2) levels were analyzed by ELISA. Nitric oxide (NO) was detected using the Griess test. The behavioral and cognitive function of rats in the PTSD group was significantly decreased compared with the control group, while the behavioral and cognitive function of rats in the intervention group were improved. The COX-2 mRNA and protein expression levels in hippocampi of rats in the PTSD group were higher than in the control and intervention group. The apoptosis of hippocampus in rats with PTSD was significantly increased compared with the control group and following treatment with COX-2 inhibitor, apoptosis was decreased. In addition, compared with the control group and intervention group, the levels of TNF-α, IL-6, PGE2 and NO in hippocampi of rats were increased in the PTSD group. The present study indicated that COX-2 may be involved in the pathogenesis of PTSD, and inhibition of its expression serves a neuroprotective role in hippocampi of PTSD rats.

Reduced gamma-amino butyric acid (GABA) and glutamine in the anterior cingulate cortex (ACC) of veterans exposed to trauma