The patient in this scenario has minimally formed values, but the

The patient in this scenario has minimally formed values, but the selleck chemicals llc physician works with the patient to discover and develop these values. The physician presents carefully selected medical information to the patient. Decision-making is a shared effort, but the physician encourages specific recommendations based on an interpretation of established health-related values. Continuing in the direction of greater patient involvement is the interpretive scenario,

in which the patient has inchoate values regarding the situation which the physician helps to elucidate. Substantial Inhibitors,research,lifescience,medical dialogue regarding the condition and interventions is exchanged between physician and patient. Once presented with the pertinent information, the patient makes the decision, with the physician acting mainly as a counselor. Lastly is the informative scenario, where patient autonomy Inhibitors,research,lifescience,medical is high and the patient has well-formed values; the patient alone takes on decision-making responsibilities. The physician’s role is as a conduit of all relevant medical information. In the Emanuel and Emanuel system of

understanding the patient–physician interaction, the prior formation of patient values, the extent of autonomy, and the amount of medical information provided to the patient by the physician are all coupled and change simultaneously. Thus Inhibitors,research,lifescience,medical the paternalistic model is characterized by low values formation, low autonomy, Inhibitors,research,lifescience,medical and low information disclosure, while high values formation, high autonomy, and high information delivery are found in the informative model. In the intervening decades, additional models of patient–physician interaction have examined aspects more or less addressed in the Emanuel and Emanuel model. To this end, Charles and colleagues

created a model examining the interplay of patient autonomy and information exchange, stressing that the combination of these and other variables exists on a continuum, rather than at the discrete points suggested by Emanuel and Emanuel.17 Bradley and colleagues, recognizing the likely influence of family and friends in decision-making, developed a model where the key players Inhibitors,research,lifescience,medical in decision-making served as central variables.9 Humphrey et al. developed a model incorporating physician interaction style and patient coping ability, while others have further examined the role of injury severity on interaction, or studied the clinical encounter because through a complex interplay of cognitive, emotional, and reflective demands.18–20 UNDERSTANDING PATIENT VALUES AND AUTONOMY Patient values and patient autonomy are central variables in many models of patient–physician interaction. To assist in understanding exactly why this is the case, and to facilitate further discussion, it would be helpful to first consider definitions of these terms. The term value itself is generally defined as the beliefs or principles of a person or group that are used to guide decisions and way of life.

In the intent-to-treat population of one study of gefitinib in co

In the intent-to-treat population of one study of gefitinib in combination with capecitabine and oxaliplatin, three patients had a complete response, 14 had a partial response, and 11 had stable disease (55). Furthermore, in a phase II study of gefitinib in combination with the standard treatment option FOLFOX-4 in patients with advanced disease, 31 of 43 patients had a complete or partial response (54). While studies in advanced NSCLC have found no difference in response rates between 250 and 500 mg/day doses of gefitinib (56,57), data from 75

patients with advanced GI cancers have indicated that the higher dose may be more effective, with disease control achieved in 13.9% and Inhibitors,research,lifescience,medical 22.9% of patients randomized

to receive Inhibitors,research,lifescience,medical gefitinib 250 and 500 mg/day, respectively; median TTP was 0.9 and 1.6 months, respectively (30). While there were no statistically significant differences between the groups for either parameter, further investigations into the most appropriate dose for gefitinib to treat patients with advanced GI tumors are warranted. In summary, this pilot, open-label, exploratory trial investigated Inhibitors,research,lifescience,medical the use of gefitinib plus celecoxib, a novel treatment combination, in patients with advanced GI tumors. The results of this study are encouraging for a population in whom care is generally palliative, and several other studies have shown promising activity with gefitinib in this setting. Nevertheless, there is still much to understand about the mode of action of EGFR and COX-2 inhibitors and how

best to combine the agents with existing chemotherapeutic regimens. Moreover, the optimal dose for gefitinib in this setting remains undetermined and Inhibitors,research,lifescience,medical a definitive outcome regarding the long-term safety issues with COX-2 inhibitors is awaited. Acknowledgements We thank Fiona Boswell and Hannah FitzGibbon from Complete Medical Communications who provided editorial support funded by AstraZeneca. Iressa® is a trademark of the AstraZeneca Inhibitors,research,lifescience,medical group of companies. Celebrex® is a registered trademark of Pfizer, Inc. Funding: No external funding was used to support this Carnitine palmitoyltransferase II work. Editorial support for the preparation of this manuscript was funded by AstraZeneca. Disclosure: The authors declare no conflict of interest.
An 87-year-old Hispanic male presented at an outside institution with a one month history of fatigue, 10-pound weight loss, and melena. He was found to have severe anemia (Hgb 6.7) requiring transfusion. Initial CT of the abdomen and pelvis showed a possible gastric mass. Esophagogastroduodenoscopy (EGD) was performed revealing an 8 cm pedunculated mass at the greater curvature of the stomach, partly black, partly green, partly white. Endoscopic ultrasound showed an isohypoechoic heterogenous mass with visible stalk.

Obsessive-compulsive disorder The serendipitous discovery that cl

Obsessive-compulsive disorder The serendipitous discovery that clomipramine (CMI), a more serotonergic tricyclic, is effective for obsessive-compulsive disorder (OCD) was important in giving impetus to a serotonin hypothesis of OCD.47 Subsequent work found that the more selective SSRIs were not only efficacious but also well-tolerated.48 More recent psychobiological Inhibitors,research,lifescience,medical research has focused on

delineating the role of neurotransmitters other than serotonin; dopaminergic augmentation strategies have been used clinically for some time now,49 and a range of other molecular treatment targets are being pursued.50,51 clinical trial Anecdotal reports of the efficacy of CMI in OCD were followed by rigorous randomized controlled trials. Such work demonstrated Inhibitors,research,lifescience,medical that clomipramine was more efficacious than both placebo and noradrenergic tricyclic agents such as desipramine, and that it was efficacious in both adults as well as in children and adolescents with OCD.52 Such work led to the first FDA approval for OCD pharmacotherapy.15 The use of intravenous (IV) CMI for refractory OCD has also been investigated,53,54 as this route of administration avoids first-pass hepatic metabolism which breaks CMI down to its less potent form, desmethyl-clomipramine. Inhibitors,research,lifescience,medical With the introduction of the SSRIs, several studies of these

agents were undertaken in OCD, and these generally showed efficacy and safety.55 Fluoxetine, fluvoxamine, paroxetine, and sertraline have all been FDA-approved for OCD.56 While several meta-analyses have suggested that CMI may be more effective Inhibitors,research,lifescience,medical than SSRIs (Table II),57 this finding may reflect the fact that earlystudies were characterized by a lower placebo response rate. Flead-to-head comparisons of CMI and SSRIs have shown equal efficacy and superior tolerability for the SSRIs.58 Thus, the SSRIs are now typically viewed as the first-line choice for OCD.8,9,11,56,59 Table II. Selected meta-analyses of obsessive-compulsive disorder treatment. CMI, clomipramine; SSRI, selective serotonin reuptake Inhibitors,research,lifescience,medical inhibitor;

OCD, obsessive-compulsive disorder A meta-analysis of medication dosage findings in OCD suggests that patients who fail to respond to low-dose therapy should be increased to a higher SB-3CT dose.60 An adequate trial in OCD should be at least 12 weeks in length.61 Although there is less published work on the longer-term treatment of OCD, a number of studies have demonstrated that early discontinuation often leads to relapse.58 Guidelines therefore suggest that patients who respond to initial acute treatment should then be continued for at least 1 year, and withdrawn gradually.8,9,56,59 It has been suggested that efficacy can be maintained even after a reduction in dosage of long-term treatment, with the benefits of improved tolerability and adherence.

In the 15q13 3 deletion region, the alpha 7 subunit of the nicoti

In the 15q13.3 deletion region, the alpha 7 subunit of the nicotinic receptor gene (CHRNA7) is present. This receptor is targeted to axons by NRG1, and has been implicated in schizophrenia and mental retardation.107 In the study from the International Schizophrenia Consortium,108 a genome -wide survey of 3391 patients with schizophrenia and in 3181 ancestrally matched controls using SNP arrays revealed 6753 rare CNVs. These rare CNVs, observed in less than 1% of the sample and more than 100Kb in length, were 1.15-fold increased in patients with schizophrenia in comparison with controls. They also observed deletions on 1q21.1

Inhibitors,research,lifescience,medical (0.29%, OR=6.6), 2p16.3 (0.12%, NRXN1), 7q35 (0.09%, CNTNAP2), 12p11.23 (0.12%), 15q13.3 (0.03%, APBA2), 15q13.3 (0.27%, CHRNA7, OR=17.9), 16p12.2-12.1, Inhibitors,research,lifescience,medical (0.12%) and 22q11.2 (VCFS region, 0.38%, OR=21.6). Further support for the role of rare CNVs in schizophrenia came from a recent study that analysed 471 patients with schizophrenia or schizoaffective disorder and 2792 controls.110 Kirov et al observed an excess of rare CNVs larger than 1Mb in cases (OR=2.26, P=0.00027) compared with controls. The associations were stronger with deletions

(OR=4.53, P=0.00013) than with duplications (OR=1.71, P=0.04). Similar to the abovementioned Inhibitors,research,lifescience,medical studies, these investigators also observed deletion at 22q11.2 in two schizophrenia patients. A deletion at 17p12 was also observed in two patients Inhibitors,research,lifescience,medical but not in controls. Unlike the ISC study,108 Kirov et al110 did not observe an overall excess burden of rare CNVs in their investigation. However, rare CNVs >500kb were also enriched in schizophrenia cases (OR=2.18). On combining their results with the ISC and the SGENE study,107 Kirov et al observed that the 17p12 deletion was more common in cases than controls (OR~10, 0.15% vs 0.015%) and also observed the deletion at 15q11.2 (OR=2.8, 0.62% vs 0.22). A duplication Inhibitors,research,lifescience,medical observed at 16p13.1, which includes the DISC1 interacting gene NDE1, was more common in cases than controls in the Kirov study as well as the ISC inhibitors purchase study108 Need et al100 in their GWAS investigation, analysed a subset of patients for presence of copy number variations, and they

identified large deletions (>2Mb) in eight cases but not in controls. Of these four CNVs, one was at 22q11.2, one at 16p13.11-p12.4 (includes the gene NDE1 a binding partner for DISC1), one at 8p22 and two CYTH4 at 1q21.1 (these are same as that reported by Stone et al108 and Stefansson et al107). Overall, similarly to Kirov et al,110 they did not observe an excess of rare CNVs (>100kb) in schizophrenia cases. Unlike Walsh et al111 they did not observe an excess of rare CNVs disrupting genes from the neurodevelopmental pathways. An important difference may have been that the primary investigation samples in the study by Walsh et al were child-onset schizophrenia patients. Similar observations have also been reported in Japanese schizophrenic patients.

Also of interest is the observed reduction in anxiety observed in

Also of interest is the observed reduction in anxiety observed in mice with a mutation of the Clock gene. For example, Clock mutant animals are much more likely to spend time in open spaces, which normal mice avoid.63 However, as these mice also showed behaviors associated with mania, it is unclear how to best classify this phenotype. Bipolar disorder Sleep disturbances have been observed in BPD and often precede relapses into depression or mania.46,64-67 Insomnia or hypersomnia, early-morning awakenings, reduced Inhibitors,research,lifescience,medical sleep efficiency, and reduced RL are the most consistently reported changes.

Irregularities in the sleep-wake cycle and daily activities can be important contributing factors in mood disruption.68 The relationship between the sleep-wake cycle and changes in mood appears to be important in patients with frequent Inhibitors,research,lifescience,medical and rapid changes in mood state, so-called “rapid cyclers,” with the switch from mania/hypomania to depression/euthymia occurring during or after sleep, while positive changes in mood from depression to hypomania/mania are more likely to occur after a period of wakefulness.69,70 Circadian disturbances have

been Inhibitors,research,lifescience,medical reported in BPD that suggest a phase advance of the master clock, including a phase advance of the diurnal rhythm of plasma Inhibitors,research,lifescience,medical Cortisol,71 although negative results have

been reported.72 Much of the work attempting to link BPD to clock genes has focused on the 3111T/C polymorphism of the human CLOCK gene.73-76 The C/C allele of CLOCK has been associated with greater severity of insomnia during antidepressant treatment76 and a higher recurrence rate of bipolar Inhibitors,research,lifescience,medical episodes,74 and reduced need for sleep.75 Support for a role of Clock mutation in BPD has recently come from the animal literature, where behavioral studies using CLOCK mutant mice suggest a phenotype similar to mania, with an increase in the reward value Endonuclease of appetitive stimuli and reduced depressive and anxiety-like behaviors.63 An analysis of 46 single nucleotide polymorphisms (SNP) in eight clock genes (BMAL1, CLOCK, PER 1, 2, 3 CRY 1,2, TIMELESS) using family-based samples with BPD or schizophrenia has been reported.77 A Mendelian transmission distortion analysis chemical structure revealed association of BMAL1 (ARNTL) and TIMELESS with BPD. However, these were modest associations found using a very liberal analysis. Interestingly, an independent study using haplotype analysis seems to confirm the association with BMAL1 (ARNTL) and also finds one with PER3 (TIMELESS was not studied).

The authors recommend a short “drug holiday” to assess medication

The authors recommend a short “drug holiday” to assess medication

efficacy. Another therapeutic alternative is the anticholinergic compounds. There have been several open, nonrandomized studies indicating beneficial effects in therapy-resistant children with enuresis. This has been corroborated by a recent randomized, placebo-controlled study by Austin and colleagues examining combination desmopressin and anticholinergic medication for nonresponders to desmopressin.7 The authors note that, once beginning anticholinergic therapy, the antienuretic effects should appear within 2 Inhibitors,research,lifescience,medical months or sooner. Parents should be warned to watch for constipation and should return within 4 to 6 weeks for a postvoid residual and urinalysis

when using these medications. They also discuss the use of tricyclic antidepressants. These drugs are thought to be third-line therapy at tertiary care centers because there have been safety concerns in the past. A 50% response rate has been shown in some children. Usually imipramine 25 to 50 mg is Inhibitors,research,lifescience,medical administered at bedtime and larger doses are given to children older than age 9 years. After 1 month, the child is reevaluated. If there is partial response, desmopressin may be added. Tolerance of this drug can occur so a drug holiday of at least 2 weeks interspersed every third month is recommended to inhibitors lessen this risk. The authors suggest an electrocardiogram (EKG) prior to imipramine treatment, especially Inhibitors,research,lifescience,medical in those children with a history of palpitations or syncope or any sudden cardiac death or unstable arrhythmia in the family. I always obtain a pretreatment EKG and this is reassuring to parents Inhibitors,research,lifescience,medical once they learn of the potential cardiac side effects. The authors note mood change, nausea, and insomnia as side effects that may occur before nocturnal

continence is attained. Other therapies have included acupuncture, treatment of hypercalciuria, and noncardiotoxic alternatives to imipramine. At a recent pediatric urology meeting, hypnosis for MNE was discussed as a successful therapeutic alternative, and provides a concise guideline for practitioners for the treatment of MNE. Inhibitors,research,lifescience,medical Vesicoureteral Reflux Cannon and the investigators from Children’s Hospital in Boston determined whether improvement in reflux on serial imaging predicts resolution of vesicoureteral reflux.8 They evaluated 965 children who had a minimum of 2 years of follow-up. They noted the initial reflux grade and the grade on serial GBA3 imaging up to 5 years following diagnosis. The authors found several factors that were predictive of reflux resolution. Multivariant analysis showed that male sex, age younger than 1 year at diagnosis, lower grade at presentation, and unilateral reflux were independent predictors of reflux resolution. Additional independent predictors of reflux resolution were reflux improvement on imaging 1 year after diagnosis or improvement from the previous year at any point during follow-up.

Likewise, Harrison and Weinberger51 have pointed out that “schiz

Likewise, Harrison and Weinberger51 have pointed out that “schizophrenia genes” and their expression may converge on critical neuronal synaptic

and glial populations in crucial brain areas, such as the hippocampus, dorsal thalamus, and dorsolateral prefrontal cortex. These structures are all part of the cortico-striato-pallido-thalamic (CSPT) circuitry. This CSPT circuitry involves complex loops and connections that are Inhibitors,research,lifescience,medical derived from Penney and Young’s56 examination of the neural substrate of motor functions. The finding of distributed neural network abnormalities in the CSPT circuitry was described in psychiatric populations in a definitive manner by Swerdlow and Koob57 and has led to many neurophysiological and “brain connectivity” hypotheses. These hypotheses include Andreason’s concept of cognitive Inhibitors,research,lifescience,medical dysmetria,58 which attempts to “connect the dots” of brain dysfunction in schizophrenia patients,59 and the evolution

of corticocortical coherence measures to assess functional connectivity deficits to probe the multiple cognitive deficits of Inhibitors,research,lifescience,medical schizophrenia patients.60 As Harrison and Weinberger point out, “a way forward is provided by the recent identification of several putative susceptibility genes including neuroregulin, dysdindin, COMT, DISCI, RGS4, GRN3, G72.”51 These authors discuss the evidence for these and other genes as vulnerability vectors along dimensions of their expression profiles and neurobiological roles. While the evidence for genetic abnormalities in these critical genes with their Inhibitors,research,lifescience,medical important integrative functions is attractive, the causative allele or mechanism that results in the development of schizophrenia is unknown. Harrison and Weinberger51 Inhibitors,research,lifescience,medical also point out that COMT may be an exception where

a causative allele may have been identified. Nevertheless, in the area of brain connectivity and synaptic plasticity, they have proposed that the genes cited above may all converge functionally via an signaling pathway influence upon synaptic plasticity and the development and stabilization of functionally important cortical microcircuitry.51 Thus, at the most basic level, these neurodevelopmental genes may oxyclozanide characterize a molecular biological basis for a genetic cytoarchitecture that has the potential to incrementally advance our understanding of schizophrenia. Neurophysiological endophenotypes: gating abnormalities Many neurophysiological endophenotypes have undergone extensive study and analysis (Table I).15-47 These endophenotypic measures include antisaccade oculomotor functioning, smooth pursuit eye movement, P50 suppression, prepulse inhibition (PPI) of the startle response, P300 ERPs, and visual backward masking.

Surviving individuals with significant, vascular or depressive pa

Surviving individuals with significant, vascular or BMS-907351 chemical structure depressive pathology might, actually be expected to possess protective biopsychosocial factors which interrupt the positive bidirectional relationship described above. Strong supporting evidence for the notion that vascular disease contributes to late-life depression comes from structural MRI studies showing a robust association between ischemic brain lesions and depression diagnosis or selfreported symptoms in older persons.92 Large communitybased studies have demonstrated independent cross-sectional relationships between late-life depression and small basal ganglia lesions93

and white matter Inhibitors,research,lifescience,medical abnormalities visualized as hyperintense regions on T2-weighted M’RI (WMHs) in deep or subcortical areas.94,95 Longitudinal Inhibitors,research,lifescience,medical studies suggest white matter changes may both predate and independently predict late-life depression.96,97 The ischemic etiology of WMHs is suggested by several lines of evidence, including post-mortem histopathologic studies in patients with late-life depression98,99 and in the general population, Inhibitors,research,lifescience,medical correlating WMHs with both evidence of cerebrovascular disease100,101 and systemic hypotensive,102 or hypoxemic disease.101,103 Ischemic damage to frontostriatal brain regions may explain the executive dysfunction, psychomotor slowing and resistance to treatment common in late-life depression.104 The few studies examining

WMHs and cognition in late-life depression have found associations with psychomotor slowing,105,106 memory, language, and executive functioning.107,108 The

relationship between WMHs and executive Inhibitors,research,lifescience,medical function may be particularly strong in individuals with late-onset depression.106,109,110 Taken together, these studies suggest a relationship among late-onset depression, ischemic WMHs (especially in the frontostriatal region) and executive dysfunction, raising the possibility Inhibitors,research,lifescience,medical that ischemic structural changes in the brain are a common etiologic factor of both the depression and the associated cognitive dysfunction. The cognitive impairment related to this ischemic damage may be severe enough to culminate in a clinical diagnosis of dementia. Vascular dementia, alone or in combination with AD, occurs at. high prevalence in the population (up to 44% of all dementia).111 In Dipeptidyl peptidase accordance with the bidirectional relationship described here, prior depression independently predicts subsequent vascular dementia (OR =2.1 5112) and individuals with late-life depression who develop clinical AD have high rates of cerebrovascular pathology upon postmortem examination.1 Indeed, prospective community-based studies report associations between baseline systemic vascular disease/risk and both higher rates of incident AD,113 and more rapid cognitive decline in established AD.114 Moreover, rapid progression of cerebrovascular disease as inferred from serial MRI predicts subsequent dementia diagnosis.

Next, empirical evidence for the immunologic and neuroimaging asp

Next, empirical evidence for the immunologic and neuroimaging aspects of bereavement, and of CG specifically, will be reviewed. Finally, the article ends with a summary of some of the gaps in knowledge of the neurobiological and immunological aspects of CG. Bereavement models and theories Why investigate the immunological and neuroimaging biomarkers of CG? Certainly there is value in the mere evidence of these biomarkers, but in addition, the physiological

components or correlates Inhibitors,research,lifescience,medical of CG may help us to understand how CG arises, predict who it may affect, and CT99021 in vitro provide suggestions for how to treat it. However, these latter reasons are best served when there is a clear theory behind

the study of the biomarkers. Theory points us in the direction for study, and the results of the studies inform and refine Inhibitors,research,lifescience,medical our theories. The following section reviews cognitive stress theory, attachment theory, and the biopsychosocial model of CG. Cognitive stress theory suggests that the death of a loved one is stressful Inhibitors,research,lifescience,medical because it is a disruptive event requiring a great deal of adjustment.2 In addition, at exactly the moment when one must cope with a significant stressor, a primary source of support may be absent (ie, the deceased), reducing one’s emotional and instrumental resources. This is one definition of stress: the perceived demands of the situation tax or exceed the individual’s perceived coping resources.3 Attachment Inhibitors,research,lifescience,medical theory states that the bonds between parent and child, and romantic partners, is a product of behavioral conditioning whereby an association is developed between the attachment figure and: (i) a reduction in distress; and (ii) the generation of pleasure.4 Inhibitors,research,lifescience,medical This conditioning explains a variety of behaviors, such as the maintenance of close proximity between bonded individuals, the development of mental schemas, or working models, that provide comfort during absence of the attachment figure, and distress that is generated upon separation

from the attachment figure. For bereavement, attachment theory has specific predictions. Bereavement Digestive enzyme includes a gradual extinction of this conditioning, in which the regulatory benefits conferred by mental representations of the attachment figure diminish slowly over time. Bowlby4 described the end point of successful mourning as a psychological reorganization of one’s thoughts and feelings about a deceased attachment figure (for review, see ref 5). In a very elegant study comparing cognitive stress theory and attachment theory, Stroebe and colleagues2 examined a prospective dataset of older adults. At the baseline, both members of the couple were alive. At the second time point, one of the spouses had died.

8 times more likely to develop a psychiatric disorder than patien

8 times more likely to develop a psychiatric disorder than patients with no TBI history.77 In a large military survey, whereas 16% of troops who sustained a bodily injury indicated PTSD, 44% of those with MTBI screened positive for

PTSD.59 Further, a large civilian study that employed rigorous clinical interviews found that sustaining a MTBI significantly increased the risk for PTSD.78 This development is in stark contrast to previously held views that TBI was protective of PTSD Inhibitors,research,lifescience,medical development. This observation may have several possible explanations. The prevailing neurobiological model posits that PTSD involves exaggerated amygdala response associated with impaired regulation by the medial prefrontal cortex.79 The amygdala appears to be pivotal to development and expression of conditioned fear reactions in human and animal studies, and that learning to inhibit these fear reactions (extinction learning) involves inhibition by the Inhibitors,research,lifescience,medical ventral medial prefrontal cortex.80 Consistent with this model, numerous 3-MA manufacturer studies have reported that patients with PTSD have diminished

medial prefrontal cortex during processing of fear.81 It is possible that MTBI enhances risk Inhibitors,research,lifescience,medical for PTSD because neural damage sustained in the injury compromises the critical neural circuitry required to regulate fear following the traumatic experience.82 Alternately, the management of post-traumatic stress, as well as problems caused by ongoing stressors in one’s environment, requires adequate working memory Inhibitors,research,lifescience,medical and cognitive resources83; it is possible that TBI depletes these resources to some extent, and this may contribute to increased PTSD risk. There is much evidence that PTSD is influenced by the compounding effects of stressors that occur following the precipitating trauma.84,85 Pain, medical procedures, loss

of employment, legal issues, and interpersonal conflict are commonplace following MTBI, and Inhibitors,research,lifescience,medical it is possible that the marginal deficits that may be attributed to MTBI could limit optimal management of these stressors. Although MTBI does appear to increase the risk of PTSD, it needs to be remembered that the association Clinical Microbiology Reviews between TBI and PTSD is complex, and much is not understood. There is evidence of an inverse relationship between extent of one’s memory of the traumatic experience and the occurrence of re-experiencing memories. One study of 228 motor vehicle accident survivors indexed the extent to which patients with MUM recalled details of the traumatic accident,87 and found that the less patients recalled of their traumatic event, the less likely they were to develop PTSD. Another study assessed 1167 traumatic injury patients in hospital (459 with mild TBI and 708 with no TBI) for post-traumatic amnesia and PTSD in hospital immediately, and subsequently reassessed them for PTSD 3 months later.