No abstract

<b><i>Introduction:</i></b> Since 2019, COVID-19 pneumonia caused by SARS-CoV-2 virus has led to a worldwide pandemic. Since then, various neurological manifestations of COVID-19 pneumonia have been reported. Neurological manifestations include headache, anosmia, seizures, and altered mental status. In some cases, it presents as stroke, encephalitis, and neuropathy. Artery of Percheron (AOP) is a variant in the posterior circulation. Here, a single artery arises from the posterior cerebral artery p1 segment. It supplies bilateral thalamus with or without midbrain. Thrombosis in this artery leads to clinical symptoms like reduced level of consciousness, altered mental status, and memory impairment. <b><i>Case Report:</i></b> Here, we present a case who presented with fever and altered sensorium without any focal neurological deficits and without known risk factors for stroke. His COVID-19 PCR was positive. He was initially diagnosed as COVID-19 pneumonia with encephalitis and was started on treatment for the same. His initial CT brain and lumbar puncture were normal. The next day, when MRI brain with and without contrast was done, the thalamic stroke due to AOP infarction was diagnosed and appropriate treatment for stroke was initiated. <b><i>Discussion:</i></b> Many patients miss the window for thrombolysis because of variable presentation in clinical symptoms with negative imaging. It is also difficult to assess the time of onset of stroke in this varied presentation. Our patient had fever and cough for 2 days and had altered mental status since the morning of admission. During hospital stay, he developed bilateral third nerve palsy. This case also highlights the importance of detailed evaluation in COVID-19 patients with neurological complaints. This helps to avoid delays in treatment and to improve clinical outcomes. As our knowledge of COVID-19 and its varied neurological manifestations evolve, we need to be prepared for more atypical presentation to facilitate timely interventions.

The impact of financial access barriers to health care on the quality of life of patients with cognitive impairment is unknown. We aimed to estimate the association between the financial access barriers to health care and the quality of life among patients with cognitive impairment. Methods: We used a retrospective pooled cross-sectional study with the data from the 2010 to 2017 National Health Interview Survey (NHIS). Measurement of financial access barriers was based on respondents' "yes" to any of the following survey prompts: "couldn't afford medical care," couldn't afford dental care," "couldn't afford eyeglasses," "couldn't afford mental health care," "couldn't afford follow-up care," or "couldn't afford specialists."

The term “placebo” lives in infamy in the history of medicine and medical research because of its association with fraud, fakery, coercion, and abuse and has promulgated progressively stricter regulations and guidelines. Opposition to using placebo control in clinical trials is based on the principles of biomedical ethics: beneficence, non-maleficence, justice, and autonomy. Many psychiatric disorders affect thinking, ability to reason, and judgment to act in one’s best interests, and many patient volunteers are not aware that their participation does not ensure getting the desired treatment. The Declaration of Helsinki requires that every patient in a clinical trial receive the best-proven diagnostic and therapeutic method for the condition under study — a concept that just about rules out using placebo control in clinical and investigational drug research. The U.S. Food and Drug Administration does not require placebo control in randomized, controlled trials but points out non-superiority of active comparator trials in psychiatric disorders and suggests that placebos can be used when “risk of death or serious harm is not at stake,” as they are not in many psychiatric conditions. Many physicians fail to recognize the potential harm of using negative language in their clinical dialogue with patients. In everyday practice, the catch-22 inherent in information disclosure must be minimized. Too little information is antithetical to obtain informed consent and harms patient’s autonomy for decision-making. Too much information, especially about side effects, increases the possibility of nocebo effects and resulting nonadherence to treatment. “Positive framing” of information and tactfulness are the great allies of the physician.

Placebo responses are complex and work through several neurobiological mechanisms. The neurotransmitters implicated thus far are dopamine (DA), gamma-aminobutyric acid (GABA), cholecystokinin (CCK), opioids, serotonin, and endocannabinoids. Both conscious expectations and unconscious conditioning can bring about molecular changes using the above neurotransmitters along the distributed biological systems, subserving cognition, emotions, pain control, reward, and learning. Expectations can enhance DA secretion in the reward circuitry of the brain, which has a nucleus accumbens at its epicenter. The prefrontal cortex (PFC), which controls attention and emotional memories, negotiates the path to the reward. The nucleus accumbens (NAc), after capturing the sole attention of the PFC, is able to modulate arousal, emotional tone, and autonomic tone to make the brain seek reward of therapeutic benefit, even when no active treatment is offered. Both DA and endogenous opioids play a key role in modulation of placebo responsiveness. The negative expectations of the person regarding treatment or negative suggestions given by the treater can amplify anxiety and pain by activating several brain regions, such as the anterior cingulate cortex (ACC), PFC, and the insula. Thus, anticipatory anxiety generated acts on two independent pathways: the hypothalamic pituitary adrenal (HPA) axis and the CCKergic pro-nociceptive system. By acting on anxiety, benzodiazepines can block both pathways and reduce pain. But CCK antagonists such as proglumide can only prevent nocebo hyperalgesia, and have no effect on HPA hyperactivity. The ebb and the flow of opioid/CCKergic systems produce the opposing effects of placebo/nocebo. The activation/deactivation between endogenous opioids/DA in NAc helps us understand both placebo and nocebo responses. There are parallels between the placebo response and classical conditioning. Endocrine, immune, and autonomic responses can be conditioned by placebos. Both the expectancy and conditioning mechanisms mediate placebo responses contingent upon previous experiences and social observational learning.