Volume 32, Issue 3

The subicular complex (hereafter referred as subiculum), which is reciprocally connected with the hippocampus and rhinal cortices, exerts a major control on hippocampal outputs. Over the last three decades, several studies have revealed that the subiculum plays a pivotal role in learning and memory but also in pathological conditions such as mesial temporal lobe epilepsy (MTLE). Indeed, subicular networks actively contribute to seizure generation and this structure is relatively spared from the cell loss encountered in this focal epileptic disorder. In this review, we will address: (i) the functional properties of subicular principal cells under normal and pathological conditions; (ii) the subiculum role in sustaining seizures in in vivo models of MTLE and in in vitro models of epileptiform synchronization; (iii) its presumptive role in human MTLE; and (iv) evidence underscoring the relationship between subiculum and antiepileptic drug effects. The studies reviewed here reinforce the view that the subiculum represents a limbic area with relevant, as yet unexplored, roles in focal epilepsy.

Degenerative cervical myelopathy (DCM) presents insidiously during middle-age with deterioration in neurological function. It accounts for the most common cause of non-traumatic spinal cord injury in developed countries and disease prevalence is expected to rise with the aging population. Whilst surgery can prevent further deterioration, biological therapies may be required to restore neurological function in advanced disease. Cell replacement therapy has been inordinately focused on treatment of traumatic spinal cord injury yet holds immense promise in DCM. We build upon this thesis by reviewing the pathophysiology of DCM as revealed by cadaveric and molecular studies. Loss of oligodendrocytes and neurons occurs via apoptosis. The tissue microenvironment in DCM prior to end-stage disease is distinct from that following acute trauma, and in many ways more favourable to receiving exogenous cells. We highlight clinical considerations for cell replacement in DCM such as selection of cell type, timing and method of delivery, as well as biological treatment adjuncts. Critically, disease models often fail to mimic features of human pathology. We discuss directions for translational research towards clinical application.

Traumatic brain injury (TBI) represents a major health concern affecting the neuropsychological health; TBI is accompanied by drastic long-term adverse complications that can influence many aspects of the life of affected individuals. A substantial number of studies have shown that mood disorders, particularly depression, are the most frequent complications encountered in individuals with TBI. Post-traumatic depression (P-TD) is present in approximately 30% of individuals with TBI, with the majority of individuals experiencing symptoms of depression during the first year following head injury. To date, the mechanisms of P-TD are far from being fully understood, and effective treatments that completely halt this condition are still lacking. The aim of this review is to outline the current state of knowledge on the prevalence and risk factors of P-TD, to discuss the accompanying brain changes at the anatomical, molecular and functional levels, and to discuss current approaches used for the treatment of P-TD.

In recent decades, a significant body of evidence based on invasive clinical research has showed that high-frequency oscillations (HFOs) are a promising biomarker for localization of the seizure onset zone (SOZ), and therefore, have the potential to improve postsurgical outcomes in patients with epilepsy. Emerging clinical literature has demonstrated that HFOs can be recorded noninvasively using methods such as scalp electroencephalography (EEG) and magnetoencephalography (MEG). Not only are HFOs considered to be a useful biomarker of the SOZ, they also have the potential to gauge disease severity, monitor treatment, and evaluate prognostic outcomes. In this article, we review recent clinical research on noninvasively detected HFOs in the human brain, with a focus on epilepsy. Noninvasively detected scalp HFOs have been investigated in various types of epilepsy. HFOs have also been studied noninvasively in other pathologic brain disorders, such as migraine and autism. Herein, we discuss the challenges reported in noninvasive HFO studies, including the scarcity of MEG and high-density EEG equipment in clinical settings, low signal-to-noise ratio, lack of clinically approved automated detection methods, and the difficulty in differentiating between physiologic and pathologic HFOs. Additional studies on noninvasive recording methods for HFOs are needed, especially prospective multicenter studies. Further research is fundamental, and extensive work is needed before HFOs can routinely be assessed in clinical settings; however, the future appears promising.

Prolactin has been shown to favor both the activation and suppression of the microglia and astrocytes, as well as the release of inflammatory and anti-inflammatory cytokines. Prolactin has also been associated with neuronal damage in diseases such as multiple sclerosis, epilepsy, and in experimental models of these diseases. However, studies show that prolactin has neuroprotective effects in conditions of neuronal damage and inflammation and may be used as neuroprotector factor. In this review, we first discuss general information about prolactin, then we summarize recent findings of prolactin function in inflammatory and anti-inflammatory processes and factors involved in the possible dual role of prolactin are described. Finally, we review the function of prolactin specifically in the central nervous system and how it promotes a neuroprotective effect, or that of neuronal damage, particularly in experimental autoimmune encephalomyelitis and during excitotoxicity. The overall studies indicated that prolactin may be a promising molecule for the treatment of some neurological diseases.

Coronavirus disease 2019 (COVID-19), due to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged in Wuhan city, China in December 2019 and rapidly spread to other countries. The most common reported symptoms are fever, dry cough, myalgia and fatigue, headache, anorexia, and breathlessness. Anosmia and dysgeusia as well as gastrointestinal symptoms including nausea and diarrhea are other notable symptoms. This virus also can exhibit neurotropic properties and may also cause neurological diseases, including epileptic seizures, cerebrovascular accident, Guillian barre syndrome, acute transverse myelitis, and acute encephalitis. In this study, we discuss stroke as a complication of the new coronavirus and its possible mechanisms of damage.

The ongoing pandemic of Coronavirus disease 2019 (COVID-19) has infected more than 27 million confirmed cases and 8,90,000 deaths all around the world. Verity of viral infections can infect the nervous system; these viral infections can present a wide range of manifestation. The aim of the current study was to systematically review the COVID-19 associated central nervous system manifestations, mental and neurological symptoms. For that we conducted a comprehensive systematic literature review of four online databases, including Web of Science, PubMed, Scopus and Embase. All relevant articles that reported psychiatric/psychological symptoms or disorders in COVID-19 without considering time and language restrictions were assessed. All the study procedures were performed based on the PRISMA criteria. Due to the screening, 14 studies were included. The current study result indicated that, the pooled prevalence of CNS or mental associated disorders with 95% CI was 50.68% (6.68–93.88). The most prevalence symptoms were hyposmia/anosmia/olfactory dysfunction (number of study: 10) with 36.20% (14.99–60.51). Only one study reported numbness/paresthesia and dysphonia. Pooled prevalence of numbness/paresthesia and dysphonia was 5.83% (2.17–12.25) and 2.39% (10.75–14.22). The pooled prevalence of depression and anxiety was 3.52% (2.62–4.54) and 13.92% (9.44–19.08). Our findings demonstrate that COVID-19 has a certain relation with neurological symptoms. The hypsomia, anosmia or olfactory dysfunction was most frequent symptom. Other symptoms were headache or dizziness, dysgeusia or ageusia, dysphonia and fatigue. Depression, anxiety, and confusion were less frequent symptoms.