Physician distress: Where are we and what can be done.

Depression, suicidal ideation, burnout, and moral injury are on the rise among physicians. Depression and suicidal ideation are mental health disorders that result from multiple interacting factors including biological vulnerabilities and acute stressors. Medical treatment for depression and suicidal ideation is critical to interrupt the potentially deadly progression to suicide that occurs when one's ability to find hope and other solutions is clouded by despair. Yet, stigma and perceived stigma of seeking treatment for mental health disorders still plagues medical providers. Transitions during medical training and practice can be particularly vulnerable time periods, though newer evidence suggests that overall, physicians are not at an increased risk of suicide compared to the general population. While burnout and moral injury are common among rehabilitation physicians, unlike depression, they are not directly associated with suicidal ideation. Opportunities for continued improvement in mental health resources and institutional support exist across the spectrum from medical student to staff physician. With wellness now increasingly supported and promoted by various medical organizations and recognition of the importance of access to effective mental health treatment, regaining hope and positivity while restoring resiliency in physicians, trainees, and medical students is possible.

Serotonin Syndrome Precipitated by Amantadine in a Patient With Persistent Post Concussive Symptoms - A Case Report.

Symptoms after mild traumatic brain injury (MTBI) can persist for greater than 1 month in up to 20% of individuals, yet there are no current medications approved by the Food and Drug Administration for treatment of specific concussion related sequelae. Amantadine, a dopamine agonist and N-Methyl-D-aspartate antagonist, is increasingly being used as a treatment option for individuals with traumatic brain injury across the spectrum of injury severity. This case report describes a 22-year-old individual who sustained an MTBI without loss of consciousness or post-traumatic amnesia after striking their head against a metal cabinet. The individual was referred to an interdisciplinary outpatient brain rehabilitation program secondary to persistent symptoms after MTBI, was prescribed amantadine for post-traumatic headache 97 days after injury, and subsequently developed symptoms of serotonin syndrome (SS) within 10 days of medication initiation. While SS caused by amantadine has been described in individuals with renal failure, this case report is the first to describe amantadine precipitating SS - confirmed by a validated diagnostic criterion and successfully treated with lorazepam and cyproheptadine - in a patient with normal renal function already on duloxetine, bupropion, and gabapentin. This case report is important in elucidating potential contributions of amantadine to the development of SS and highlighting the important role clinicians have in assessing for polypharmacy when prescribing amantadine for individuals with traumatic and acquired brain injuries.

Management of Medical Complications During the Rehabilitation of Moderate-Severe Traumatic Brain Injury.

Brain injury specialists are experienced providers able to identify and treat the unique medical complications after moderate-severe traumatic brain injury, including posttraumatic seizures, paroxysmal sympathetic hyperactivity, spasticity, hydrocephalus, agitation, neuroendocrine dysfunction, heterotopic ossification, venous thromboembolism, and cranial nerve dysfunction. Owing to the potential negative impact on outcome if left untreated, identification and appropriate treatment is essential. An additional role of the brain injury specialist is to educate family about potential medical complications and anticipated outcomes after brain injury. The provider, patient, and family work together to identify and treat any potential sequelae of the moderate-severe brain injury.

Measure of functional independence dominates discharge outcome prediction after inpatient rehabilitation for stroke.

BACKGROUND AND PURPOSE: Identifying clinical data acquired at inpatient rehabilitation admission for stroke that accurately predict key outcomes at discharge could inform the development of customized plans of care to achieve favorable outcomes. The purpose of this analysis was to use a large comprehensive national data set to consider a wide range of clinical elements known at admission to identify those that predict key outcomes at rehabilitation discharge. METHODS: Sample data were obtained from the Uniform Data System for Medical Rehabilitation data set with the diagnosis of stroke for the years 2005 through 2007. This data set includes demographic, administrative, and medical variables collected at admission and discharge and uses the FIM (functional independence measure) instrument to assess functional independence. Primary outcomes of interest were functional independence measure gain, length of stay, and discharge to home. RESULTS: The sample included 148,367 people (75% white; mean age, 70.6±13.1 years; 97% with ischemic stroke) admitted to inpatient rehabilitation a mean of 8.2±12 days after symptom onset. The total functional independence measure score, the functional independence measure motor subscore, and the case-mix group were equally the strongest predictors for any of the primary outcomes. The most clinically relevant 3-variable model used the functional independence measure motor subscore, age, and walking distance at admission (r(2)=0.107). No important additional effect for any other variable was detected when added to this model. CONCLUSIONS: This analysis shows that a measure of functional independence in motor performance and age at rehabilitation hospital admission for stroke are predominant predictors of outcome at discharge in a uniquely large US national data set.

Assessment and treatment of common persistent sequelae following blast induced mild traumatic brain injury.

The ongoing wars in Iraq and Afghanistan and terrorist activity worldwide have been associated with an increased incidence of blast injuries. While blast injuries share similarities with blunt or penetrating traumatic injuries, there are unique mechanistic elements of blast injury that create increased vulnerability to damage of specific organs. This review highlights the mechanism of blast-related injury, describes the common sequelae of blast exposure that may impact rehabilitation care, and summarizes the intervention strategies for these blast-related sequelae.

Recovery and rehabilitation after stroke.

Most individuals survive stroke and age with its consequences. Rehabilitation becomes the dominant medical need soon after onset, and coordinated rehabilitation services using evidence-based interventions determined by patient need are of primary importance in affecting outcome and quality of life. This discussion will focus on the natural history of recovery after stroke and the changes in brain organization that support behavioral improvement during recovery, then review established and emerging therapeutic approaches directed at improving independent functional performance and quality of life.

Inhibition of bovine phenol sulfotransferase (bSULT1A1) by CoA thioesters. Evidence for positive cooperativity and inhibition by interaction with both the nucleotide and phenol binding sites.

Previous work with the bovine phenol sulfotransferase (bSULT1A1, EC ) demonstrated inhibition by CoA that was competitive with respect to the sulfuryl donor substrate, 3'-phosphoadenosine-5'-phosphosulfate (PAPS) (Leach, M., Cameron, E., Fite, N., Stassinopoulos, J., Palmreuter, N., and Beckmann, J. D. (1999) Biochem. Biophys. Res. Commun. 261, 815-819). Here we report that long chain acyl-CoAs are more potent inhibitors of bSULT1A1 and also of human dopamine sulfotransferase (SULT1A3) when compared with unesterified CoA and short chain-length acyl-CoAs. A complex pattern of inhibition was revealed by systematic variation of palmitoyl-CoA, PAPS, and 7-hydroxycoumarin, the acceptor substrate. Convex plots of apparent K(m)/V(max) versus [palmitoyl-CoA] were adequately modeled using an ordered rapid equilibrium scheme with PAPS as the leading substrate and by accounting for the possible binding of two equivalents of inhibitor to the dimeric enzyme. Interestingly, the first K(i) of 2-3 microm was followed by a second K(i) of only 0.01-0.05 microm, suggesting that positive subunit cooperativity enhances binding of long chain acyl-CoAs to this sulfotransferase. Simultaneous interaction of palmitoyl-CoA with both the nucleotide and phenol binding sites is suggested by two experiments. First, the acyl-CoA displaced 7-hydroxycoumarin from the highly fluorescent bSULT1A1.PAP.7-HC complex in a cooperative manner. Second, palmitoyl-CoA prevented the quenching of bSULT1A1 fluorescence observed with pentachlorophenol. Finally, titrations of bSULT1A1-pentachlorophenol complex with palmitoyl-CoA caused the return of protein fluorescence, and the binding of palmitoyl-CoA was highly cooperative (Hill constant of 1.9). Overall, these results suggest a model of sulfotransferase inhibition in which the 3'-phosphoadenosine-5'-diphosphate moiety of CoA docks to the PAPS domain, and the acyl-pantetheine group docks to the hydrophobic phenol binding domain.