Seminars in neurology
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Seminars in neurology · Aug 2020
ReviewThe Neuropathology of Chronic Traumatic Encephalopathy: The Status of the Literature.
Chronic traumatic encephalopathy (CTE) is a tauopathy associated with repetitive mild head trauma, including concussion and asymptomatic subconcussive impacts. CTE was first recognized in boxers almost a century ago and has been identified more recently in contact sports athletes, military veterans exposed to blast, and victims of domestic violence. Like most neurodegenerative diseases, CTE is diagnosed conclusively by a neuropathological examination of brain tissue. ⋯ Some authors consider β-amyloid (Aβ) to be a primary feature of CTE, yet the data indicate that CTE is a primary tauopathy, with Aβ deposition a function of age and inheritance of the ApoEe4 allele. Some authors also question the progressive nature of CTE pathology, although there is clear evidence in most individuals that p-tau pathology increases in density and affects more brain regions with survival. This review is intended to outline the status of the evidence-based literature regarding CTE neuropathology and to address the misrepresentations and confusions that have arisen in recent reviews and a letter of correspondence.
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Seminars in neurology · Aug 2020
ReviewRepetitive Head Trauma Induces Chronic Traumatic Encephalopathy by Multiple Mechanisms.
Exposure to repetitive neurotrauma increases lifetime risk for developing progressive cognitive deficits, neurobehavioral abnormalities, and chronic traumatic encephalopathy (CTE). CTE is a tau protein neurodegenerative disease first identified in boxers and recently described in athletes participating in other contact sports (notably American football, ice hockey, rugby, and wrestling) and in military veterans with blast exposure. Currently, CTE can only be diagnosed by neuropathological examination of the brain after death. ⋯ This review will explore two important areas of CTE pathobiology. First, we will review what is known about the biomechanical properties of RHI that initiate CTE-related pathologies. Second, we will provide an overview of key features of CTE neuropathology and how these contribute to abnormal tau hyperphosphorylation, accumulation, and spread.
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Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PD-D) are Lewy body-related neurodegenerative disorders sharing common clinical and neuropathological findings. The clinical features of both conditions include cognitive impairment, behavioral symptoms, autonomic dysfunction, sleep disorders, and parkinsonism. The cognitive profile of both disorders is characterized by particularly severe deficits in executive and visuospatial functions as well as attention. ⋯ Although the diagnosis is basically clinical, structural and functional neuroimaging as well as cerebrospinal fluid biomarkers may help the clinician in the diagnosis. Placebo-controlled randomized trials of the cholinesterase inhibitors have shown modest but significant benefits in cognition, global function, and neuropsychiatric symptoms in both disorders. Behavioral symptoms such as hallucinations and delusions should be treated with caution with antipsychotics, as they have the potential to worsen motor and cognitive symptoms.
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Dizziness is a common chief complaint with an extensive differential diagnosis that includes both benign and serious conditions. Physicians must distinguish the majority of patients who suffer from self-limiting conditions from those with serious illnesses that require acute treatment. The preferred approach to the diagnosis of an acutely dizzy patient emphasizes different aspects of the history to guide a focused physical examination, with the goal of differentiating benign peripheral vestibular conditions from dangerous posterior circulation strokes. ⋯ A better approach categorizes patients into three groups based on timing and triggers. Each category has its own differential diagnosis and targeted bedside approach: (1) acute vestibular syndrome, where bedside physical examination differentiates vestibular neuritis from stroke; (2) spontaneous episodic vestibular syndrome, where associated symptoms help differentiate vestibular migraine from transient ischemic attack; and (3) triggered episodic vestibular syndrome, where the Dix-Hallpike and supine roll test help differentiate benign paroxysmal positional vertigo from posterior fossa structural lesions. The "timing and triggers" diagnostic approach for the acutely dizzy derives from current best evidence and offers the potential to reduce misdiagnosis while simultaneously decreasing diagnostic test overuse, unnecessary hospitalization, and incorrect treatments.
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Neck and back pain are common reasons for seeking evaluation and treatment in the emergency department. Within both systems there exist several time-sensitive diagnoses that the emergency provider should be familiar with in order to prevent significant morbidity and mortality. In this article we provide a general overview of these complaints by discussing problems in a systems-based fashion as well as discussing the initial evaluation, work-up, and treatment options for these diagnoses.