Kaloyan Tanev

PTSD and TBI co-morbidity: Scope, clinical presentation and treatment options

Abstract Primary objective: To summarize the literature on post-traumatic stress disorder (PTSD) and traumatic brain injury (TBI) and their co-morbidity, focusing on diagnosis, clinical symptoms and treatment issues relevant to the clinician. Research design: Review of the literature. Methods and procedures: Pubmed searches were performed using the terms post-traumatic stress disorder, traumatic brain injury, sleep, cognitive, depression, anxiety, treatment and combinations of these terms. Those articles relevant to the objective were included. Main outcomes and results: This study presents pathophysiological, neuroimaging and clinical data on co-morbid PTSD and TBI. It reviews associated conditions, emphasizing the impact of cognitive and sleep problems. It summarizes the emerging literature on treatment effectiveness for co-morbid PTSD and TBI, including psychotherapy, pharmacotherapy and cognitive rehabilitation. Conclusions: Both PTSD and TBI commonly occur in the general population, both share some pathophysiological characteristics and both are associated with cognitive impairment and sleep disruption. PTSD and TBI present with a number of overlapping symptoms, which can lead to over-diagnosis or misdiagnosis. Both conditions are associated with co-morbidities important in diagnosis and treatment planning. More research is needed to elucidate what treatments are effective in PTSD and TBI co-morbidity and on factors predictive of treatment success.

Stress, PTSD, and dementia *

The physiological consequences of acute and chronic stress on a range of organ systems have been well documented after the pioneering work of Hans Selye more than 70 years ago. More recently, an association between exposure to stressful life events and the development of later‐life cognitive dysfunction has been proposed. Several plausible neurohormonal pathways and genetic mechanisms exist to support such an association. However, many logistical and methodological barriers must be overcome before a defined causal linkage can be firmly established. Here the authors review recent studies of the long‐term cognitive consequences of exposures to cumulative ordinary life stressors as well as extraordinary traumatic events leading to posttraumatic stress disorder. Suggestive effects have been demonstrated for the role of life stress in general, and posttraumatic stress disorder in particular, on a range of negative cognitive outcomes, including worse than normal changes with aging, Alzheimers disease, and vascular dementia. However, given the magnitude of the issue, well‐controlled studies are relatively few in number, and the effects they have revealed are modest in size. Moreover, the effects have typically only been demonstrated on a selective subset of measures and outcomes. Potentially confounding factors abound and complicate causal relationships despite efforts to contain them. More well‐controlled, carefully executed longitudinal studies are needed to confirm the apparent association between stress and dementia, clarify causal relationships, develop reliable antemortem markers, and delineate distinct patterns of risk in subsets of individuals.

Neuroimaging findings and brain-behavioral correlates in a former boxer with chronic traumatic brain injury

Chronic traumatic brain injury (CTBI) is associated with contact sports such as boxing. CTBI results from repetitive blows to the head rather than from a single impact. CTBI individuals present with motor symptoms (incoordination, spasticity, parkinsonism), cognitive impairment (executive dysfunction, memory deficits) and neuropsychiatric symptoms (irritability, affective disturbances). The structural and functional neuroimaging findings and clinical presentation of a CTBI case are described. We propose hypotheses about the pathophysiology of the observed neuroimaging findings and their relationship to the neuropsychiatric symptoms of the patients.

Evaluation and treatment of migraine in the emergency department: A review

Head pain is the fifth most common reason for emergency department (ED) visits. It is second only to focal weakness as the most common reason for neurological consultation in the ED. This manuscript reviews how patients with migraine, the most common primary headache disorder for which patients seek medical treatment, are managed in the ED. We discuss existing guidelines for head imaging in patients with migraine, recommended pharmacologic treatments, and current treatment trends. We also review studies evaluating the discharge care of migraine patients in the ED. With the goal of standardizing, streamlining, and optimizing ED‐based migraine care, we offer ideas for future research to improve the evaluation, treatment, and discharge care of patients who present to an ED with acute migraine.

Influence of psychiatric comorbidities in migraineurs in the emergency department.

OBJECTIVE To examine how psychiatric comorbidities in migraineurs in the emergency department (ED) affect healthcare utilization and treatment tendencies. METHOD This is a cross-sectional analysis of 2872 patients who visited our ED over a 10-year period and were given a principal diagnosis of migraine. RESULTS Compared to migraineurs without a psychiatric comorbidity, migraineurs with a psychiatric comorbidity had about three times more ED visits, six times more inpatient hospital stays and four times more outpatient visits. Migraineurs with psychiatric comorbidities received narcotics in the ED more often than migraineurs without psychiatric comorbidities (P<0.0001). In addition, migraineurs with psychiatric disorders were more likely to have a computed tomography scan of the head [Risk Ratio (RR) 1.42 (95% confidence interval (CI)=1.28-1.56, P<0.001)] or a magnetic resonance image of the brain [RR 1.53 (95% CI=1.33-1.76, P<0.001)] than patients without a psychiatric disorder when visiting our hospital center. CONCLUSIONS Migraineurs with psychiatric comorbidity who visit the ED have different healthcare utilization tendencies than migraineurs without psychiatric comorbidity who visit the ED. This is seen in the frequency of ED visits, outpatient visits and inpatient stays, in the medications administered to them and in the radiology tests they undergo.

An unusually presenting case of sCJD-The VV1 subtype

Creutzfeldt-Jakob disease (CJD) is a rapidly progressive neurodegenerative disease caused by prions. Typically CJD presents with a triad of rapidly progressive dementia, abnormal movements (e.g., myoclonus) and electroencephalographic (EEG) changes. Recently, CJD has been subdivided into subtypes based on host genetic polymorphisms and the characteristics of the pathological prion protein. Different subtypes likely have different clinical and laboratory presentations. We describe a case of sporadic CJD of the VV1 subtype. We describe our patients clinical symptoms, time course, laboratory workup, structural and functional neuroimaging data, EEG data and CJD biomarkers. Our patient presented with clinical symptoms atypical for CJD. Because of that, her clinical symptoms were initially attributed to psychiatric reasons. After extensive clinical and laboratory investigation, we concluded that the patient probably had CJD. Postmortem neuropathological results confirmed this clinical hypothesis. We compare our patients clinical, laboratory and neuroimaging data to the data on typical CJD as well as the data on the few CJD VV1 cases described in the literature. We discuss our cases relevance to the diagnosis of CJD.

Alcohol Dementia and Thermal Dysregulation: A Case Report and Review of the Literature

Wernickes encephalopathy and Korsakoffs psychosis in alcoholics are thought to be due to thiamine deficiency. When the process goes untreated, patients may develop alcohol-induced persisting dementia. We review the literature on thermal dysregulation and the place of thiamine treatment in Wernickes encephalopathy, Korsakoffs psychosis, and alcohol-induced persisting dementia. We describe a patient with alcohol-induced persisting dementia who showed thermal dysregulation which responded to parenteral but not oral thiamine. Subsequently, he developed aspiration pneumonia with associated fever reaction and expired. We describe the neuroimaging findings—diffuse cortical atrophy, ventricular dilatation, atrophy of the corpus callosum, hypothalamus, and medulla, and a probable arachnoid cyst in the left temporal tip. We conclude that thermal dysregulation was likely related to dysfunction of temperature regulatory brain centers, that thermal dysregulation was stabilized with parenteral but not oral thiamine, and that parenteral thiamine may have a role even in chronic cases of alcohol-induced persisting dementia.

Treatment of Meige's syndrome with ECT.

A 62-year-old woman with Meiges syndrome failed to respond to several pharmacologic interventions. Her dystonias improved significantly after treatment with bilateral electroconvulsive therapy (ECT). However, the effect was not durable, lasting < or = 72 h. ECT is an effective treatment for many movement disorders including dystonias of differing etiologies. Its efficacy for Meiges syndrome is questionable.

Cortical thickness alterations linked to somatoform and psychological dissociation in functional neurological disorders

Links between dissociation and functional neurological disorder (FND)/conversion disorder are well‐established, yet the pathophysiology of dissociation remains poorly understood. This MRI study investigated structural alterations associated with somatoform and psychological dissociation in FND. We hypothesized that multimodal, paralimbic cingulo‐insular regions would relate to the severity of somatoform dissociation in patients with FND.

Positive Association Between Nightmares and Heart Rate Response to Loud Tones: Relationship to Parasympathetic Dysfunction in Ptsd Nightmares

Abstract Seventy-three women with posttraumatic stress disorder (PTSD) resulting from rape or physical assault participated in a loud-tone procedure, while skin conductance (SC), heart rate, and electromyogram responses were recorded. Pearson correlations were examined between each psychophysiological response and Clinician-Administered PTSD Scale (CAPS) symptom scores. Significant correlations were adjusted for each remaining individual PTSD symptom score. Heart rate response (HRR) significantly correlated with CAPS total score and with CAPS nightmares. The relationship between HRR and nightmares remained significant after controlling for each of the other 16 individual PTSD symptoms, for the remaining reexperiencing cluster, and for CAPS total score. The zero-order correlations between SC response and nightmares and between electromyography response and nightmares were both not significant. The association of nightmares with larger HRR in the absence of an association with larger SC response likely reflects reduced parasympathetic tone. Thus, our findings indirectly support a role for reduced parasympathetic tone in PTSD nightmares.