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Altered Mental Status clinical trials

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NCT ID: NCT04929704 Active, not recruiting - Clinical trials for Altered Mental Status

Diagnostic Yield and Influence on Length of Stay of Brain Computed Tomography for Elderly Patients With Altered Mental Status in an Emergency Setting

DISCUSS-CT
Start date: June 11, 2021
Phase:
Study type: Observational

The confusional syndrome is defined by the acute or subacute onset of a deficit syndrome (temporo-spatial disorientation, memory and concentration disorders, abnormal behavior, impairment of intellectual efficiency, fluctuation of disorders with an increase in the evening) that may be associated with a productive syndrome (visual or auditory hallucinations, delusional elements) (French College of Neurology). It is a frequent, serious and costly problem in hospitalized patients and in emergency rooms. Its prevalence is between 10 and 31% of cases in emergency rooms and concerns up to one out of two elderly patients during a hospitalization. The potential morbidity and mortality of the confusional syndrome is due in part to the difficulty of identifying and treating rapidly the triggering and aggravating factors that are often interrelated in the elderly. Most often, these are drug effects, metabolic disorders, infections, consequences of prolonged immobilization or physical restraint. The lack of rapid treatment of these causes increases the risk of medium and long-term cognitive problems. Because of the aging population, this is an increasingly expensive problem. In 2012, the World Health Organization Regional Office for Europe study conducted in 18 European countries combined estimated its cost at $182 billion per year. The management of confusional syndrome in the elderly is now a major public health issue. It is a targeted indicator of the safety and quality of care for the elderly.

NCT ID: NCT03133208 Active, not recruiting - Sepsis Clinical Trials

Sepsis Associated Encephalopathy (SAE) Biomarkers

Start date: June 1, 2017
Phase:
Study type: Observational

Sepsis associated encephalopathy (SAE) is a poorly understood acute cerebral dysfunction that frequently appears in the setting of sepsis induced systemic inflammation. In fact, altered mentation is recognized as an independent predictor of death and poor outcomes in patients with sepsis. SAE may be manifested by a number of symptoms characterized by a change in baseline behavior, attention, alertness, cognition, or executive functioning. It occurs in the absence of direct Central Nervous System (CNS) infection, and the exact pathophysiology is of SAE is unknown, but theoretically seems to encompass a constellation of mechanisms such as impairment of the blood brain barrier (BBB), endothelial dysfunction, alteration in cerebral blood flow and neurotransmission, circulating inflammatory mediators, cellular hypoxia, and metabolic disturbances, that ultimately result in neuronal dysfunction and cell death. SAE is characterized by an altered mental status (AMS) that ranges from delirium to coma, and can lead to long-term cognitive impairment. SAE may appear early in the course of sepsis, and is often underestimated as an independent factor of mortality, yet the pathophysiology of SAE remains unknown, and there is a lack of specific investigations available to clinicians. Studies have evaluated biomarkers as prognostic tools. The Investigator propose to measure neuron specific enolase (NSE), S-100B, glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase L1 (UCH-L1), Tau protein, Copeptin, spectrin breakdown products (SBDP 145, SBDP150), αII-spectrin N-terminal fragment (SNTF), neurofilament light and heavy chains (NF-L, NF-H), myelin basic protein (MBP), secretoneurin (SN), and other peptide levels in the serum of sepsis patients who develop altered mental status, to evaluate the kinetics of said biomarkers for 72 hours. The Investigator will monitor the course of the patients' hospitalization to determine whether there are biomarker correlates with survival and outcomes, including neurologic impairment. Finally, this investigation may provide a mechanistic pathway that defines the development of AMS in septic patients.