Deciphering the Great Imitator: Syphilis and Neurosyphilis.

Syphilis is an infectious disease caused by Treponema pallidum. Often known as the "great imitator," it has periods of active disease and periods of latency. Serologic syphilis testing can be divided into treponemal and non-treponemal tests, and multiple tests are required to prove infection. Standardized algorithms exist for syphilis testing and diagnosis. Neurosyphilis, which is often the result of the progression of untreated syphilis, can be life-threatening and requires intravenous antibiotics. Despite the significant challenge of diagnosing and treating neurosyphilis, there are no standardized testing algorithms available. Typically, the cerebral spinal fluid (CSF) venereal disease research laboratory (VDRL) test is considered the gold standard despite low sensitivity. The CSF fluorescent treponemal antibody absorption (FTA-ABS) test is more sensitive despite being less specific and is often the better testing option. This case illustrates a patient with a clinical presentation strongly suggestive of neurosyphilis despite negative initial lab testing and argues for the emergence of a standardized algorithm to guide clinicians.

A closer look to neural pathways and psychopharmacology of obsessive compulsive disorder.

The intricate neural pathways involved in obsessive-compulsive disorder (OCD) affect areas of our brain that control executive functioning, organization, and planning. OCD is a chronic condition that can be debilitating, afflicting millions of people worldwide. The lifetime prevalence of OCD in the US is 2.3%. OCD is predominantly characterized by obsessions consisting of intrusive and unwanted thoughts, often with impulses that are strongly associated with anxiety. Compulsions with OCD encompass repetitive behaviors or mental acts to satisfy their afflicted obsessions or impulses. While these factors can be unique to each individual, it has been widely established that the etiology of OCD is complex as it relates to neuronal pathways, psychopharmacology, and brain chemistry involved and warrants further exploration.

Exploring the role of inflammation in major depressive disorder: beyond the monoamine hypothesis.

Major depressive disorder affects approximately 8.4% of the United States population. The World Health Organization estimates that 280 million adults worldwide are suffering from depression. They have estimated that by 2030 it will be the second most serious condition. Current treatment relies on the monoamine hypothesis, however, one-third of patients with MDD do not respond to monoamine-based antidepressants. For years, it was hypothesized that the primary pathway of MDD involved serotonin as the main neurotransmitter. The monoamine hypothesis, a widely accepted theory, sought to explain the biological basis of MDD as being caused by the depletion of monoamine neurotransmitters, namely norepinephrine and serotonin. This hypothesis regarding monoamines as the pathophysiological basis of MDD led to the design and widespread use of selective serotonin reuptake inhibitors. However, given that only one-third of patients improve with SSRI it is reasonable to infer that the pathway involved is more complex than once hypothesized and there are more neurotransmitters, receptors, and molecules involved. The monoamine hypothesis does not explain why there is a delay in the onset of effect and action of SSRIs. Several studies have demonstrated that chronic stress is a risk factor for the development of MDD. Thus the monoamine hypothesis alone is not enough to fully account for the pathophysiology of MDD highlighting the need for further research involving the pathways of MDD. In this paper, we review the role of inflammation and cytokines on MDD and discuss other pathways involved in the development and persistence of depressive symptoms.

Levetiracetam-Induced Psychosis in the Setting of Intracranial Cavernomas.

Levetiracetam is a commonly used antiepileptic medication that has been associated with the development of psychosis. Cavernomas are vascular malformations that have been associated with psychosis as well, especially in the setting of hemorrhagic transformation. This case report describes a patient with cavernomas who developed psychotic symptoms after restarting her levetiracetam at a high dose (2000 mg twice a day) without gradual uptitration. Her symptoms improved upon the reduction of the levetiracetam as well as the initiation of paliperidone. This case highlights the importance of considering the biologic and medication-related factors for the development of psychosis, as well as the importance of gradual medication adjustments.

COVID-19 and its impact on the brain and Mind- A conceptual model and supporting evidence.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the novel coronavirus that is causing the ongoing coronavirus disease 2019 (COVID-19) pandemic, was first reported in late 2019. Since then, an unprecedented amount of new knowledge has emerged about this virus and its treatment. Although the reported symptoms of COVID-19 are primarily respiratory with acute respiratory distress syndrome, SARS-CoV-2 has also been shown to affect other organs, including brain, and there are growing reports of neuropsychiatric symptoms due to COVID-19. There are two suggested pathways for how COVID-19 can affect the brain and mind: the direct impact on the brain and impact mediated via stress. Direct impact on the brain is manifested as encephalitis/encephalopathy with altered mental status (AMS) and delirium. In this paper, we summarize evidence from studies of previous outbreaks and current data from the COVID-19 pandemic that describe how COVID-19 is associated with an increased prevalence of anxiety, stress, poor sleep quality, obsessive-compulsive symptoms, and depression among the general population during the pandemic. In addition, we summarize the current evidence that supports how COVID-19 can also impact the CNS directly and result in delirium, cerebrovascular events, encephalitis, unspecified encephalopathy, AMS, or peripheral neurologic disorders.