Prospective comparative study on enhancing geometrical mental representation and anatomical learning in medical students through modeling clay as an assessment tool.

While traditional anatomy education often emphasizes passive learning and rote memorization, it seldom employs constructivist theories that focus on active, hands-on experiences for effective learning. This study tests the hypothesis that tactile experiences with modeling clay enhance geometric mental representation more effectively than verbal descriptions. We examine the potential of clay modeling to reflect and evaluate students' mental representation of anatomical structures. Utilizing a prospective randomized, open, blind endpoint (PROBE) design, we engaged 36 participants divided into three groups: blind, visually impaired, and a control group. The primary outcome measure was the difference between post-touch score and pre-touch score, which gauged the efficacy of tactile intervention in enhancing the participants' capacity to mentally reconstruct a well-designed anatomical fiction structure. Scoring was executed using a double-blind double-evaluation methodology, positioning clay model reconstruction as both an objective reliable assessment and a pedagogical tool. The analysis demonstrated a pronounced improvement in mental representation of anatomical structures, particularly in spatial comprehension and detailed textural discernment, with the mean score soaring from 47.81 pre-touch to 85.09 post-touch. Distinct cognitive processing adaptations were evident across groups, with the blind group excelling in tactile acuity and the visually impaired group showing the most significant gains in spatial understanding post-intervention (Cohen's d = 2.74). The application of modeling clay as a tactile intervention tool can significantly improve the learning of anatomy among medical students. The study underscores the value of active, multisensory engagement and customized teaching strategies for effective anatomy education among this demographic.

CT-Guided Aspiration of a Hemorrhagic Tarlov Cyst for the Treatment of a Post-Partum Sciatica: A Case Report and a Review of the Literature.

Background: Tarlov or perineural cysts are dilations of nerve roots resulting from a pathologically increased cerebrospinal fluid pressure. Although it is very common in the general population, most of these cysts remain asymptomatic. In some cases, they can evolve and exert pressure on neural elements, independently from their initial size. Case report: In this paper, we describe the case of a 33-year-old female known to have asymptomatic multiple and large radicular and pelvic Tarlov cysts. One cyst located in the right pelvic space progressed acutely after delivery, inducing a painful sciatica without neurological deficit. The intracystic bleeding can be a direct consequence of the delivery, leading to an acute and mechanical local compression of the right S1 root. A CT-guided puncture and aspiration allowed a complete recovery. This case report was completed by a review of the literature of these rare intracystic Tarlov bleedings. Conclusions: Intracystic hemorrhage is a rare complication of Tarlov cysts. Delivery-induced cyst bleeding was not described before. Patients known to have large and multiple Tarlov cysts should be monitored in post-partum, as their presence is considered a risk factor. Percutaneous cyst aspiration seems to be an effective and safe treatment to relieve symptoms.

Electrophysiological Evidence for Anti-epileptic Property of Taurine.

Taurine, 2-aminoethanesulfonic acid, is one of the most abundant free amino acids especially in excitable tissues, with wide physiological actions. Several lines of evidence suggest that taurine may function as a potent inhibitory neuromodulator that regulate neuronal activity in many cerebral areas. Parenteral injection of kainic acid (KA), a glutamate receptor agonist, causes severe and stereotyped behavioral convulsions in mice and is used as a rodent model for human temporal lobe epilepsy. In the adult brain, inhibitory GABAergic interneurons modulate the activity of principal excitatory cells via their GABAA receptors and thus adjust excitatory output of neuronal circuits. The goal of this study was to examine the potential anti-convulsive effects of the neuro-active amino acid taurine, in the mouse model of limbic seizures. We used the glutamic acid decarboxylase (GAD) inhibitor isoniazid (100 mg.kg-1, s.c.) which induces seizures by interfering with GABA synthesis through inhibition of GAD activity followed by kainic acid (5 mg.kg-1, s.c.) a glutamate receptor agonist which is commonly used to induce limbic seizures.Using intracerebral recordings of field potentials found that taurine (43 mg.kg-1, s.c.) had a significant anti-epileptic effect when injected prior to isoniazid and KA. Furthermore, injection of taurine to a mouse undergoing limbic seizure completely stopped burst population spikes and restored neuronal firing to its baseline. Therefore, taurine is potentially capable of treating seizure-associated brain damage.

Hyperreflexia and enhanced ripple oscillations in the taurine-deficient mice.

In this study, we examined neuronal excitability and skeletal muscle physiology and histology in homozygous knockout mice lacking cysteine sulfonic acid decarboxylase (CSAD-KO). Neuronal excitability was measured by intracerebral recording from the prefrontal cortex. Skeletal muscle response was measured through stretch reflex in the ankle muscles. Specifically, we measured the muscle tension, amplitude of electromyogram and velocity of muscle response. Stretch reflex responses were evoked using a specialized stretching device designed for mice. The triceps surae muscle was stretched at various speeds ranging from 18 to 18,000° s-1. A transducer recorded the muscle resistance at each velocity and the corresponding EMG. We also measured the same parameter in anesthetized mice. We found that at each velocity, the CSAD-KO mice generated more tension and exhibited higher EMG responses. To evaluate if the enhanced response was due to neuronal excitability or changes in the passive properties of muscles, we anesthetize mice to eliminate the central component of the reflex. Under these conditions, CSAD-KO mice still exhibited an enhanced stretch reflex response, indicating ultrastructural alterations in muscle histology. Consistent with this, we found that sarcomeres from CSAD-KO muscles were shorter and thinner when compared to control sarcomeres. Neuronal excitability was further investigated using intracerebral recordings of brain waves from the prefrontal cortex. We found that extracellular field potentials in CSAD-KO mice were characterized by reduced amplitude of low-frequency brain waves (delta, theta, alpha, beta and gamma) and increased in the high low-frequency brain waves (slow and fast ripples). Increased slow and fast ripple rates serve as a biomarker of epileptogenic brain. We have previously shown that taurine interacts with GABAA receptors and induces biochemical changes in the GABAergic system. We suggest that taurine deficiency leads to alterations in the GABAergic system that contribute to the enhanced stretch reflex in CSAD-KO mice through biochemical mechanisms that involve alterations not only at the spinal level but also at the cortical level.

Neuroinvasion, neurotropic, and neuroinflammatory events of SARS-CoV-2: understanding the neurological manifestations in COVID-19 patients.

Respiratory viruses are opportunistic pathogens that infect the upper respiratory tract in humans and cause severe illnesses, especially in vulnerable populations. Some viruses have neuroinvasive properties and activate the immune response in the brain. These immune events may be neuroprotective or they may cause long-term damage similar to what is seen in some neurodegenerative diseases. The new "Severe Acute Respiratory Syndrome Coronavirus 2" (SARS-CoV-2) is one of the Respiratory viruses causing highly acute lethal pneumonia coronavirus disease 2019 (COVID-19) with clinical similarities to those reported in "Severe Acute Respiratory Syndrome Coronavirus"(SARS-CoV) and the "Middle East Respiratory Syndrome Coronavirus"(MERS-CoV) including neurological manifestation. To examine the possible neurological damage induced by SARS-CoV-2, it is necessary to understand the immune reactions to viral infection in the brain, and their short- and long-term consequences. Considering the similarities between SARS-CoV and SARS-CoV-2, which will be discussed, cooperative homological and phylogenetical studies lead us to question if SARS-CoV-2 can have similar neuroinvasive capacities and neuroinflammatiory events that may lead to the same short- and long-term neuropathologies that SARS-CoV had shown in human and animal models. To explain the neurological manifestation caused by SARS-CoV-2, we will present a literature review of 765 COVID-19 patients, in which 18% had neurological symptoms and complications, including encephalopathy, encephalitis and cerebrovascular pathologies, acute myelitis, and Guillain-Barré syndrome. Clinical studies describe anosmia or partial loss of the sense of smell as the most frequent symptom in COVID19 patients, suggesting that olfactory dysfunction and the initial ultrarapid immune responses could be a prognostic factor.