Hinsonjosephsen8739
Almost half (42.5%) explicitly self-reported history of HI. Compared to clients who did not report HI, clients with HI were older and more likely to report a history of headache, physical abuse, physical trauma, concussion, and loss of consciousness. After adjustment for demographic and clinical characteristics, clients with HI had greater odds for neuropsychological sequelae such as headache (odds ratio [OR] 4.2, 95% confidence interval [CI] 2.0-8.7) and depression (OR 2.5, 95% CI 1.1-5.7).
We observed a high prevalence of HI in asylum seekers. Comprehensive screening for HI and neuropsychiatric comorbidities is encouraged when evaluating asylum seekers.
We observed a high prevalence of HI in asylum seekers. Comprehensive screening for HI and neuropsychiatric comorbidities is encouraged when evaluating asylum seekers.
To empirically test whether apathy and impulse control disorders (ICDs) represent independent, opposite ends of a motivational spectrum.
In this single-center, cross-sectional study, we obtained retrospective demographics and clinical data for 887 patients with idiopathic Parkinson disease (PD) seen at a tertiary care center. Mood and motivation disturbances were classified using recommended cutoff scores from self-reported measures of apathy, ICD, anxiety, and depression.
Prevalence rates included 29.0% of patients with PD with depression, 40.7% with anxiety, 41.3% with apathy, 27.6% with ICDs, and 17.0% with both apathy and ICD. The majority (61.6%) of people reporting clinically significant ICDs also reported clinically significant apathy, and more than a third of patients with apathy (41.3%) also reported elevated ICD. Anxiety and depression were highest in patients with both apathy and ≥1 ICDs. Dopamine agonist use was higher in people with only ICD compared to people with only apathy. Mood significantly interacted with demographic variables to predict motivational disturbances.
Motivational disturbances are common comorbid conditions in patients with PD. In addition, these complex behavioral syndromes interact with mood in clinically important ways that may influence the design of future clinical trials and the development of novel therapies. This study challenges the concept of apathy and ICD in PD as opposite ends of a spectrum.
Motivational disturbances are common comorbid conditions in patients with PD. In addition, these complex behavioral syndromes interact with mood in clinically important ways that may influence the design of future clinical trials and the development of novel therapies. This study challenges the concept of apathy and ICD in PD as opposite ends of a spectrum.
To explore whether hospitalized patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and neurologic symptoms have evidence of CNS infection, inflammation, and injury using CSF biomarker measurements.
We assessed CSF SARS-CoV-2 RNA along with CSF biomarkers of intrathecal inflammation (CSF white blood cell count, neopterin, β
-microglobulin, and immunoglobulin G index), blood-brain barrier integrity (albumin ratio), and axonal injury (CSF neurofilament light chain protein [NfL]) in 6 patients with moderate to severe coronavirus disease 2019 (COVID-19) and neurologic symptoms who had undergone a diagnostic lumbar puncture. Neurologic symptoms and signs included features of encephalopathies (4 of 6), suspected meningitis (1 of 6), and dysgeusia (1 of 6). SARS-CoV-2 infection was confirmed by real-time PCR analysis of nasopharyngeal swabs.
SARS-CoV-2 RNA was detected in the plasma of 2 patients (cycle threshold [Ct] value 35.0-37.0) and in CSF at low levels (Ct 37.2, 38.0, 39.0) in 3 e markers were increased but white cell response and other immunologic features typical of CNS viral infections were absent. While our initial hypothesis centered on CNS SARS-CoV-2 invasion, we could not convincingly detect SARS-CoV-2 as the underlying driver of CNS inflammation. These features distinguish COVID-19 CSF from other viral CNS infections and raise fundamental questions about the CNS pathobiology of SARS-CoV-2 infection.Brain arteriovenous malformations (AVMs) are anomalous direct shunts between cerebral arteries and veins that convalesce into a vascular nidus. The treatment strategies for AVMs are challenging and variable. Intracranial hemorrhage and seizures comprise the most common presentations of AVMs. selleck kinase inhibitor However, incidental AVMs are being diagnosed with increasing frequency due to widespread use of noninvasive neuroimaging. The balance between the estimated cumulative lifetime hemorrhage risk vs the risk of intervention is often the major determinant for treatment. Current management options include surgical resection, embolization, stereotactic radiosurgery (SRS), and observation. Complete nidal obliteration is the goal of AVM intervention. The risks and benefits of interventions vary and can be used in a combinatorial fashion. Resection of the AVM nidus affords high rates of immediate obliteration, but it is invasive and carries a moderate risk of neurologic morbidity. AVM embolization is minimally invasive, but cure can only be achieved in a minority of lesions. SRS is also minimally invasive and has little immediate morbidity, but AVM obliteration occurs in a delayed fashion, so the patient remains at risk of hemorrhage during the latency period. Whether obliteration can be achieved in unruptured AVMs with a lower risk of stroke or death compared with the natural history of AVMs remains controversial. Over the past 5 years, multicenter prospective and retrospective studies describing AVM natural history and treatment outcomes have been published. This review provides a contemporary and comprehensive discussion of the natural history, pathobiology, and interventions for brain AVMs.Inborn errors of metabolism (IEMs) are inherited defects in a metabolic pathway resulting in clinical disease. The overall goal of therapy is to restore metabolic homeostasis while minimizing the deleterious effects of the interruption. Conventional treatments focus on decreasing substrate, providing product, and replacing deficient enzyme or cofactor. We discuss examples of established, novel, and emerging therapies to provide a framework for understanding the principles of management for patients with IEMs.