Posterior reversible encephalopathy syndrome (PRES) is associated with seizures, visual disturbances, headache, and altered mental status. Given its presentation, the diagnosis can be mistaken for other severe conditions. Palliative medicine consultants should be aware of PRES and be prepared to counsel families on the treatment and prognosis of this syndrome.

The use of valproic acid (VPA) (also known as Depakote, Depakene, and others) frequently results in elevated plasma ammonia. In some people, hyperammonemia may be clinically significant, resulting in hyperammonemic encephalopathy, which may be severe. Valproic acid-induced hyperammonemic encephalopathy may occur in people with normal liver function, despite normal doses and serum levels of VPA. We describe 2 cases of valproic acid-induced hyperammonemic encephalopathy in patients with supratherapeutic VPA levels, although the condition has been described in people with normal VPA levels. With the increasing indications and off-label uses of VPA, family physicians should be aware of this potential complication of VPA and check ammonia levels in patients taking VPA who present with alterations in mental status. Treatment with L-carnitine may be beneficial in reducing ammonia levels. Valproic acid (VPA) is effective in the treatment of seizure disorders, bipolar disorder, migraine headache prophylaxis, neuropathic pain, restless legs syndrome, dementia-related agitation, and social anxiety disorder, among other conditions. VPA has numerous drug interactions and toxicities; severe toxicities include hepatic damage, pancreatitis, teratogenicity, thrombocytopenia, and hyperammonemia. Here we depict 2 case reports of VPA-induced hyperammonemic encephalopathy (VHE), both occurring in patietns with no history of underlying liver disease. In one instance, the patient was able to function, but with significant cognitive limitations. In the second case, the patient was comatose. Both of the patients we describe also had supratherapeutic VPA levels, but VHE is a well-documented potential complication of the use of VPA in the medical literature, and it may occur in people with normal VPA levels.1 Because of the wide spectrum of symptoms associated with VHE, physicians should consider hyperammonemia in the differential diagnosis of any patient taking VPA who shows changes in behavior, cognition, or orientation

With the advancement of protective gear and medical aid, soldiers are now surviving traumatic experiences that were once fatal. As a result, the prevalence of brain injury and posttraumatic stress disorder in military service members has grown. Those who have obtained brain injury are at risk of developing chronic traumatic encephalopathy, a neurodegenerative syndrome. To date, there is no cure, treatment, or diagnostic method (besides autopsy) for chronic traumatic encephalopathy. Because chronic traumatic encephalopathy and posttraumatic stress disorder present many of the same symptoms and have the possibility of deriving from the same traumatic experience, an investigation of a potential link is necessary. This study explores the possibility of chronic traumatic encephalopathy being misdiagnosed as posttraumatic stress disorder. This is done by analyzing the frequency of brain injury along with the comorbidity of posttraumatic stress disorder and brain injury. This thesis also proclaims the need for research that attempts to develop diagnostic criterion and treatment methods for chronic traumatic encephalopathy.

Posterior reversible encephalopathy syndrome (PRES) is a clinical-radiographic syndrome that presents with neurological manifestations, including seizures, headache, or confusion, and is associated with posterior cerebral white matter edema on imaging. PRES is typically a benign and reversible condition. However, PRES can be fatal or associated with permanent deficits. Numerous conditions are associated with PRES, including hypertensive encephalopathy, renal diseases, and cytotoxic or immunosuppressant drugs. Recently, many case reports described the association between PRES and chemotherapeutic agents. However, trastuzumab-associated PRES is rarely reported. Herein, we report a case of a 51-year-old female with a history of metastatic gastric cancer who developed seizures while being treated with trastuzumab, and neuroimaging confirmed the diagnosis of PRES.

Background: According to the Center for Disease Control and Prevention, approximately 1.6 to 3.8 million Americans suffer a sports related concussion each year. Concussion is defined as a transient alteration of the brain structure caused by a direct or indirect force. During the last decade, a vast amount of clinical research on the long term effects of repetitive head trauma has occurred, especially on the subject of chronic traumatic encephalopathy (CTE), depression and dementia. Objective: The purpose of this literature review is to examine the literature pertaining to multiple concussion and the long-term effects of multiple concussion such as neurodegenerative diseases and psychological. Methods: A literature review was conducted using an electronic search of the following databases: MEDLINE, Cochrane Database of Systematic Reviews, and SportDiscus. The key search terms included were concussion, "sport concussion" and "sports concussion". One of the above three terms needed to be in conjunction with one of the following key search terms: depression, dementia, "mild cognitive impairment", "chronic traumatic encephalopathy" (CTE), or "psychological disorder". Additional inclusion criteria also included studies that targeted the adult athlete population who had sustained more than one concussion. Studies only were included if they were peer-reviewed, in the English language, and were published after 1990. To be included in the review, the study must have examined the long term effects of repetitive concussion. Results: The research completed to date suggests there is a strong correlation between the number of concussions an athlete suffers and the long-term ramifications of neurodegenerative and psychological disorders. However, more research is needed.

No description available.

Over 15 million contact sports players and military veterans are at risk for the development of chronic traumatic encephalopathy (CTE), a neurodegenerative disease associated with exposure to repetitive head impacts (RHI) that sometimes presents with parkinsonian motor symptoms, although very little is understood about how these individuals develop parkinsonism. CTE is characterized by accumulation of hyperphosphorylated tau protein (p-tau), and diagnosis requires the presence of neuronal tau in the form of neurofibrillary tangles at the depth of cortical sulci. We performed quantitative immunoassays for markers of neurovascular inflammation within the postmortem dorsolateral frontal cortex of participants with and without a history of RHI and CTE (n = 156), and tested for associations with RHI, microgliosis, and tau pathology measures. Levels of vascular injury-associated markers were increased in CTE compared to RHI-exposed and -naïve controls. Markers increased with RHI exposure duration and were associated with increased microglial density and tau pathology. Histologically, there was significantly increased ICAM1 staining of the microvasculature, extracellular space, and astrocytes at the sulcal depths in high stage CTE compared to both low stage CTE and controls. Multifocal perivascular immunoreactivity for serum albumin was present in all RHI-exposed individuals. These findings demonstrate that vascular injury markers are associated with RHI exposure, duration, and microgliosis, are elevated in CTE, and increase with disease severity. We next performed a cross-sectional analysis of all brain donors with CTE and without comorbid neurodegenerative disease (n=495) in the UNITE Brain Bank. Participants with parkinsonism (CTE-p, n=119) had a higher mean age at death (71.5 years (y)) than participants without parkinsonism (CTE-np, n=362, 54.1 y) and exhibited a higher rate of dementia than CTE-np participants. CTE-p participants had a more severe CTE stage and nigral pathology (NFTs, neuronal loss, and more frequent Lewy bodies), though the majority of cases were negative for nigral Lewy bodies. In American football players, simultaneous regression analysis demonstrated that nigral NFTs and neuronal loss mediate a connection between years of play and parkinsonism in CTE. In this cross-sectional study of contact sports athletes with CTE, years of contact sports participation was associated with SN proteinopathy and neuronal loss, and these pathologies were associated with parkinsonism. Finally, in a postmortem cohort (n=392) of brain donors with CTE without comorbid neurodegenerative disease, we used linear regression modelling to analyze the associations between isodendritic core nuclei pathology (semiquantitative neurofibrillary tangles (NFTs), neurites, and neuronal loss scores) and CTE disease severity, RHI exposure duration (years of contact sport play), and informant-reported cognitive and daily function as assessed by the Cognitive Difficulties Scale (CDS) and Functional Activities Questionnaire (FAQ), respectively. Overall, isodendritic core (IC) NFT scores increase with disease stage, Initially in the locus coeruleus and finally in the median raphe nuclei. Neuronal loss occurred at later disease stages than NFT accumulation. RHI exposure was associated with p-tau pathology for all IC regions. NFTs and neuronal loss in the substantial nigra were associated with increased CDS scores (i.e., worse cognitive function), and neuronal loss in the substantia nigra and locus coeruleus were associated with increased FAQ scores (i.e., worse daily function). We are able to show CTE is similar in distribution of p-tau pathology to progressive supranuclear palsy (PSP), a disease that is thought to primarily affect subcortical regions, especially by end stage disease. These results demonstrate the vulnerability of the isodendritic core nuclei to p-tau pathology and neuronal loss in CTE, and suggest that their involvement contributes to cognitive and functional symptoms during life. This work highlights the possible linkage between neuroinflammation leading to nigral p-tau accumulation and neuron loss which likely underlies the development and progression of parkinsonian motor symptoms in CTE.

No description available.

BSE was discovered in Canada in 2003. Research on the impacts of BSE indicates that cattle producers suffered significant economic losses, and that these may have reverberated into local communities, where industries connected to cattle production have sustained secondary impacts. Also, the desirability of different forms of agriculture may have shifted as a result of BSE. This study addresses the impacts of BSE in Alberta from a geographical perspective, examining the cattle industry, community economic structure, and regional agricultural economies. The spatial organization and structure of the cattle herd has changed as a result of BSE. Little evidence of a ripple effect was found in the geography of community economic structure. Spatial changes in regional agricultural economies may be tied to changes in the cattle industry resulting from BSE, but do not indicate significant agricultural restructuring. This study places limits on the spatial and economic impacts of BSE in Alberta. / x, 171 leaves ; maps ; 29 cm

12 month embargo; Available online 9 November 2016 / SCN8A encephalopathy is a severe, early-onset epilepsy disorder resulting from de novo gain-of-function mutations in the voltage-gated sodium channel Na(v)1.6. To identify the effects of this disorder on mRNA expression, RNA-seq was performed on brain tissue from a knock-in mouse expressing the patient mutation p.Asn1768Asp (N1768D). RNA was isolated from forebrain, cerebellum, and brainstem both before and after seizure onset, and from age-matched wildtype littermates. Altered transcript profiles were observed only in forebrain and only after seizures. The abundance of 50 transcripts increased more than 3-fold and 15 transcripts decreased more than 3 fold after seizures. The elevated transcripts included two anti-convulsant neuropeptides and more than a dozen genes involved in reactive astrocytosis and response to neuronal damage. There was no change in the level of transcripts encoding other voltage-gated sodium, potassium or calcium channels. Reactive astrocytosis was observed in the hippocampus of mutant mice after seizures. There is considerable overlap between the genes affected in this genetic model of epilepsy and those altered by chemically induced seizures, traumatic brain injury, ischemia, and inflammation. The data support the view that gain-of-function mutations of SCN8A lead to pathogenic alterations in brain function contributing to encephalopathy.