The COVID-19 (C-19) pandemic has highlighted the significance of understanding the long-term effects of this disease on the quality of life of those infected. Long COVID-19 (L-C19) presents as persistent symptoms that continue beyond the main illness period, usually lasting weeks to years. One of the lesser-known but significant aspects of L-C19 is its impact on neuropsychiatric manifestations, which can have a profound effect on an individual's quality of life. Research shows that L-C19 creates neuropsychiatric issues such as mental fog, emotional problems, and brain disease symptoms, along with sleep changes, extreme fatigue, severe head pain, tremors with seizures, and pain in nerves. People with cognitive problems plus fatigue and mood disorders experience great difficulty handling everyday activities, personal hygiene, and social interactions. Neuropsychiatric symptoms make people withdraw from social activity and hurt relationships, thus causing feelings of loneliness. The unpredictable state of L-C19 generates heavy psychological pressure through emotional suffering, including depression and anxiety. Neuropsychiatric changes such as cognitive impairment, fatigue, and mood swings make it hard for people to work or study effectively, which decreases their output at school or work and lowers their job contentment. The purpose of this narrative review is to summarize the clinical data present in the literature regarding the neuropsychiatric manifestations of L-C19, to identify current methods of diagnosis and treatment that lead to correct management of the condition, and to highlight the impact of these manifestations on patients' quality of life.

SARS-CoV-2 infection can affect any organ, including both the central nervous system (CNS) and peripheral nervous system (PNS). The aim of this study was to explore the outcome and risk factors associated with the involvement of either CNS or PNS in a cohort of hospitalized COVID-19 patients.

We performed a retrospective observational cohort study of hospitalized adult patients with COVID-19, between May 2020 and December 2022, presenting with new onset neurological disabilities any time after admission.

We included 115 patients, 72 with CNS manifestations and 43 with PNS involvement. The CNS manifestations were COVID-19-associated encephalopathy, headache, neurovascular events, and seizures in 80.5, 43, 31.9, and 11.1% of patients, respectively. The neurovascular events were ischemic stroke in 17 (23.6%) patients, hemorrhagic stroke in 6 (8.3%) patients, venous thrombosis in 1 (1.4%) patient, and subarachnoid hemorrhage in 1 (1.4%) patient. Cranial nerve involvement was the most frequent PNS manifestation in 34 (79%) cases, followed by mononeuritis in 5 (11.6%) patients and polyneuropathy in 4 (9.3%) patients. The affected cranial nerves were the vestibulocochlear nerve in 26 (60.5%) patients, the olfactory nerve in 24 (55.8%) patients, the oculomotor nerves in 5 (11.6%) patients, and the facial nerve in 1 (2.3%) patient. Two patients (9.3%) presented with polyneuritis cranialis. Older age (HR = 1.02, 95% CI: 1.003-1.037, p = 0.01), COVID severity (HR = 2.53, 95% CI: 1.42-4.5, p = 0.002), ischemic cardiac disease (HR = 2.42, 95% CI: 1.05-5.6, p = 0.03), and increased D-dimers (HR = 1.00, 95% CI: 1.00-1.00, p = 0.02) were independently associated with the development of CNS manifestations. The factors associated with in-hospital mortality were age (HR = 1.059, 95% CI: 1.024-1.096, p = 0.001), C-reactive protein (HR = 1.006, 95% CI: 1.00-1.011, p = 0.03), CNS involvement (HR = 9.155, 95% CI: 1.185-70.74, p = 0.03), and leucocyte number (HR = 1.053, 95% CI: 1.026-1.081, p < 0.001).

COVID-19-associated encephalopathy was the most common CNS manifestation in our study, but neurovascular events are also important considering the overlap between inflammatory and prothrombotic pathways, especially in severe cases. CNS involvement was associated with in-hospital all-cause mortality. PNS findings were various, involving mostly the cranial nerves, especially the vestibulocochlear nerve.

Observational studies have shown an association between COVID-19 and epilepsy. However, causality remains unproven. This study aimed to investigate the causative effect of genetically predicted COVID-19 phenotypes on epilepsy risk using a two-sample Mendelian randomization (MR) analysis.

We retrieved summary-level datasets for three COVID-19 phenotypes (COVID-19 susceptibility, COVID-19 hospitalization, and COVID-19 severity) and epilepsy from the genome-wide association studies conducted by the COVID-19 Host Genetics Initiative (COVID-19 HGI) and International League Against Epilepsy (ILAE) consortium, respectively. To analyze the final results, nine MR analytic methods were utilized. The inverse-variance weighted (IVW) method was chosen as the primary approach for data analysis to evaluate the potential causal effect. Other MR analytic methods (MR-Egger regression, weighted median estimator, mode based-estimator, and MR-PRESSO) were used as a supplement to IVW to ensure the robustness of the results.

The IVW approach demonstrated no causal association between any genetically predicted COVID-19 phenotype and the risk of epilepsy [COVID-19 susceptibility: odds ratio (OR) = 0.99, 95% confidence interval (CI) = 0.86-1.14, p = 0.92; COVID-19 hospitalization: OR = 1.00, 95% CI = 0.96-1.04, p = 0.95; COVID-19 severity: OR = 0.99, 95% CI = 0.96-1.01, p = 0.25]. Other MR complementary methods revealed consistent results. Additionally, no evidence for heterogeneity and horizontal pleiotropy was found.

This MR study revealed no genetically predicted causal relationship between COVID-19 phenotypes and epilepsy.

In 2017, one of us reviewed advances in epilepsy (Manford in J Neurol 264:1811-1824, 2017). The current paper brings that review up to date and gives a slight change in emphasis. Once again, the story is of evolution rather than revolution. In recognition that most of our current medications act on neurotransmitters or ion channels, and not on the underlying changes in connectivity and pathways, they have been renamed as antiseizure (ASM) medications rather than antiepileptic drugs. Cenobamate is the one newly licensed medication for broader use in focal epilepsy but there have been a number of developments for specific disorders. We review new players and look forward to new developments in the light of evolving underlying science. We look at teratogenicity; old villains and new concerns in which clinicians play a vital role in explaining and balancing the risks. Medical treatment of status epilepticus, long without evidence, has benefitted from high-quality trials to inform practice; like buses, several arriving at once. Surgical treatment continues to be refined with improvements in the pre-surgical evaluation of patients, especially with new imaging techniques. Alternatives including stereotactic radiotherapy have received further focus and targets for palliative stimulation techniques have grown in number. Individuals' autonomy and quality of life continue to be the subject of research with refinement of what clinicians can do to help persons with epilepsy (PWE) achieve control. This includes seizure management but extends to broader considerations of human empowerment, needs and desires, which may be aided by emerging technologies such as seizure detection devices. The role of specialist nurses in improving that quality has been reinforced by specific endorsement from the International League against Epilepsy (ILAE).

It is unclear whether patients with epilepsy are more susceptible to SARS-CoV-2 infection, whether they experience more severe manifestations of COVID-19, and whether seizures worsen after SARS-CoV-2 infection. Our study aims to explore these points and provide comprehensive and practical guidance for patients with epilepsy.

We designed a questionnaire to collect variables from epilepsy patients. We used the Chi-square test, Fisher's exact test, or Mann-Whitney U test to analyze differences between the two groups. Multiple logistic regressions were employed to determine the risk factors for relevant outcome variables.

We identified a total of 181 patients, with 74% (n = 134) reporting COVID-19. The patients' educational level was found to be a risk factor for COVID-19 (OR = 0.33, 95% CI 0.14-0.80, P = 0.013). When comparing seizure frequency changes between epilepsy patients with and without COVID-19, no statistically significant difference was observed (P > 0.05). However, an increase in seizure frequency was significantly associated with higher levels of anxiety (P < 0.001) and depression (P < 0.005).

The risk of COVID-19 infection may be increased in patients with epilepsy. COVID-19 infection does not seem to worsen seizures in epilepsy patients. Patients with epilepsy rarely develop more severe clinical manifestations of COVID-19 after SARS-CoV-2 infection. During the COVID-19 pandemic, patients with epilepsy who also suffer from anxiety and depression may experience an increase in the frequency of their seizures.

Neurological/neuropsychiatric symptoms are commonly reported by children/young people with long COVID, especially headache, fatigue, cognitive deficits, anosmia and ageusia, dizziness, mood symptoms, and sleep problems. However, reported prevalence estimates are highly variable due to study heterogeneity and often small sample size; most studies only considered short-term follow-ups; and, apart from mood and sleep problems, neuropsychiatric conditions have received less attention. Considering the potential debilitating effects of neurological/neuropsychiatric conditions, a comprehensive review of the topic is timely, and needed to support clinical recognition as well as to set the direction for future research.

The authors discuss neurological/neuropsychiatric manifestations of long COVID in pediatric populations, with a focus on prevalence, associated demographic characteristics, and potential pathogenetic mechanisms.

Children/young people may develop persistent neurological/neuropsychiatric symptoms following acute SARS-CoV-2 infection, which may affect daily functioning and well-being. Studies in larger samples with longer follow-ups are needed to clarify prevalence and symptom duration; as well as less investigated risk factors, including genetic predisposition, ethnicity, and comorbidities. Controlled studies may help separate infection-related direct effects from pandemic-related psychosocial stressors. Clarifying pathogenetic mechanisms is paramount to develop more targeted and effective treatments; whilst screening programs and psychoeducation may enhance early recognition.