Tetracycline-, Doxycycline-, Minocycline-Induced Pseudotumor Cerebri and Esophageal Perforation.

Tetracyclines are a class of broad-spectrum bacteriostatic antibiotics used to treat many infections, including methicillin-resistant Staphylococcus aureus (MRSA), acne, pelvic inflammatory disease, chlamydial infections, and a host of zoonotic infections. These drugs work by inhibiting protein synthesis in bacterial ribosomes, specifically by disallowing aminoacyl-tRNA molecules from binding to the ribosomal acceptor sites. While rare, tetracycline antibiotics, particularly minocycline and doxycycline, are associated with an increased risk of developing esophageal perforation and pseudotumor cerebri (PTC, or idiopathic intracranial hypertension). Since tetracyclines are a commonly prescribed class of medications, especially in adolescents for acne treatment, it is important for clinicians to appreciate significant side effects that can result in morbidity and mortality. This paper aims to consolidate and to emphasize current research on the association between tetracycline antibiotics and the development of esophageal perforation, and PTC. PTC is a neurological syndrome consisting of increased intracranial pressure, headache, and vision changes without evidence of the contributing source, such as mass lesion, infection, stroke, or malignancy. Esophageal perforation, while rare, can be the result of pill esophagitis. Pill-induced injuries occur when caustic medicinal pills dissolve in the esophagus rather than in the stomach. Most patients experience only self-limited pain (retrosternal burning discomfort, heartburn, dysphagia, or odynophagia), but hemorrhage, stricture, and perforation may occur. Tetracycline use can lead to pill esophagitis. In summary, clinicians should appreciate the potential risks of tetracycline compounds in clinical practice.

Benzodiazepines: Uses, Dangers, and Clinical Considerations.

Benzodiazepines (BZDs) are among one of the most widely prescribed drug classes in the United States. BZDs are a class of psychoactive drugs known for their depressant effect on the central nervous system (CNS). They quickly diffuse through the blood-brain barrier to affect the inhibitory neurotransmitter GABA and exert sedative effects. Related to their rapid onset and immediate symptom relief, BZDs are used for those struggling with sleep, anxiety, spasticity due to CNS pathology, muscle relaxation, and epilepsy. One of the debilitating side effects of BZDs is their addictive potential. The dependence on BZDs generally leads to withdrawal symptoms, requiring careful tapering of the medication when prescribed. Regular use of BZDs has been shown to cause severe, harmful psychological and physical dependence, leading to withdrawal symptoms similar to that of alcohol withdrawal. Some of these withdrawal symptoms can be life threatening. The current treatment for withdrawal is through tapering with clonazepam. Many drugs have been tested as a treatment for withdrawal, with few proving efficacious in randomized control trials. Future research is warranted for further exploration into alternative methods of treating BZD withdrawal. This call to action proves especially relevant, as those seeking treatment for BZD dependence and withdrawal are on the rise in the United States.

The Role of Parvalbumin Interneurons in Neurotransmitter Balance and Neurological Disease.

While great progress has been made in the understanding of neurological illnesses, the pathologies, and etiologies that give rise to these diseases still remain an enigma, thus, also making treatments for them more challenging. For effective and individualized treatment, it is beneficial to identify the underlying mechanisms that govern the associated cognitive and behavioral processes that go awry in neurological disorders. Parvalbumin fast-spiking interneurons (Pv-FSI) are GABAergic cells that are only a small fraction of the brain's neuronal network, but manifest unique cellular and molecular properties that drastically influence the downstream effects on signaling and ultimately change cognitive behaviors. Proper brain functioning relies heavily on neuronal communication which Pv-FSI regulates, excitatory-inhibitory balances and GABAergic disinhibition between circuitries. This review highlights the depth of Pv-FSI involvement in the cortex, hippocampus, and striatum, as it pertains to expression, neurotransmission, role in neurological disorders, and dysfunction, as well as cognitive behavior and reward-seeking. Recent research has indicated that Pv-FSI play pivotal roles in the molecular pathophysiology and cognitive-behavioral deficits that are core features of many psychiatric disorders, such as schizophrenia, autism spectrum disorders, Alzheimer's disease, and drug addiction. This suggests that Pv-FSI could be viable targets for treatment of these disorders and thus calls for further examination of the undeniable impact Pv-FSI have on the brain and cognitive behavior.