Fluoxetine use is associated with improved survival of patients with COVID-19 pneumonia: A retrospective case-control study.

BACKGROUND AND PURPOSE: We aimed to investigate the association between fluoxetine use and the survival of hospitalised coronavirus disease (COVID-19) pneumonia patients. METHODS: This retrospective case-control study used data extracted from the medical records of adult patients hospitalised with moderate or severe COVID-19 pneumonia at the Uzsoki Teaching Hospital of the Semmelweis University in Budapest, Hungary between 17 March and 22 April 2021. As a part of standard medical treatment, patients received anti-COVID-19 therapies as favipiravir, remdesivir, baricitinib or a combination of these drugs; and 110 of them received 20 mg fluoxetine capsules once daily as an adjuvant medication. Multivariable logistic regression was used to evaluate the association between fluoxetine use and mortality. For excluding a fluoxetine-selection bias potentially influencing our results, we compared baseline prognostic markers in the two groups treated versus not treated with fluoxetine. RESULTS: Out of the 269 participants, 205 (76.2%) survived and 64 (23.8%) died between days 2 and 28 after hospitalisation. Greater age (OR [95% CI] 1.08 [1.05-1.11], p<0.001), radiographic severity based on chest X-ray (OR [95% CI] 2.03 [1.27-3.25], p=0.003) and higher score of shortened National Early Warning Score (sNEWS) (OR [95% CI] 1.20 [1.01-1.43], p=0.04) were associated with higher mortality. Fluoxetine use was associated with an important (70%) decrease of mortality (OR [95% CI] 0.33 [0.16-0.68], p=0.002) compared to the non-fluoxetine group. Age, gender, LDH, CRP, and D-dimer levels, sNEWS, Chest X-ray score did not show statistical difference between the fluoxetine and non-fluoxetine groups supporting the reliability of our finding. CONCLUSION: Provisional to confirmation in randomised controlled studies, fluoxetine may be a potent treatment increasing the survival for COVID-19 pneumonia.

Epilepsy and vitamin D.

Several disorders, both systemic and those of the nervous system, have been linked with vitamin D deficiency. Neurological disorders with a vitamin D link include but are not limited to multiple sclerosis, Alzheimer and Parkinson disease, as well as cerebrovascular disorders. Epilepsy which is the second leading neurological disorder received much less attention. We review evidence supporting a link between vitamin D and epilepsy including those coming from ecological as well as interventional and animal studies. We also assess the literature on the interaction between antiepileptic drugs and vitamin D. Converging evidence indicates a role for vitamin D deficiency in the pathophysiology of epilepsy.

Are proprioceptive-induced reflex seizures epileptically-enhanced stretch reflex manifestations?

In reflex seizures induced by proprioceptive stimuli, the activated network may be identified as a single anatomo-functional circuit; the sensory-motor network. These seizures may be considered as epileptically-enhanced stretch reflexes. Proprioceptive reflex epilepsies are a good example of the so-called "system epilepsies". We present three cases discussing the clinical features of such epilepsies. [Published with videosequences].

Correction of vitamin D deficiency improves seizure control in epilepsy: a pilot study.

There is growing interest concerning the role of vitamin D in various medical conditions such as diabetes and oncological, cardiovascular and central nervous system disorders. Although vitamin D deficiency is known to be highly prevalent among epilepsy patients, only a single study, published nearly forty years ago, assessed the effect of vitamin D on seizure control. Here, we measured serum 25-hydroxy-vitamin D (25(OH)D) levels and normalized it by administration of vitamin D3 in 13 patients with pharmacoresistant epilepsy. To see if vitamin D3 has an impact on seizure frequency, we compared seizure numbers during a 90-day period before and after treatment onset. We found that seizure numbers significantly decreased upon vitamin D3 supplementation. Median seizure reduction was 40%. We conclude that the normalization of serum vitamin 25(OH)D level has an anticonvulsant effect.

Clinical experiences with Creutzfeldt-Jakob disease: three case studies.

The clinical picture, electroencephalographic, imaging and cerebrospinal fluid parameters as well as the molecular background of Creutzfeldt-Jakob disease have been well explored. The diagnostic criteria, offering clinicians a fair chance to identify these patients in vivo, have recently been updated. However, the diagnosis is still a challenge in everyday neurological routine. We report on three of our Creutzfeldt-Jakob patients for calling attention to the classical and the recently defined features of the disease. We conclude that based on the rapidly progressing neuropsychiatric syndrome Creutzfeldt-Jakob disease may be suspected; follow-up EEG may reveal the typical (pseudo)-periodic pattern with progressive deterioration of the background activity. In addition, diffusion-weighted brain MRI imaging (DWI) has high diagnostic value. Detection of 14-3-3 protein in the cerebrospinal fluid supports the in vivo diagnosis.

Late-life absence status epilepticus: a female disorder?

We report on three women and a review of the literature on absence status epilepticus over the age of 50 years. Our aim was to characterize the male-female ratio in this condition. Out of 16 studies on absence status epilepticus over the age of 50, including our cases, a female dominance was found in 15. We found altogether, 104 (71%) females and 42 (29%) males. This gender difference is highly significant (p < 0.00001). We conclude that absence status epilepticus over the age of 50 is predominantly a female disorder.

The risk of paradoxical levetiracetam effect is increased in mentally retarded patients.

PURPOSE: Incidental paradoxical antiepileptic effect of levetiracetam has been described. The aim of the present study was to identify the epilepsy patients at risk. METHODS: We performed a retrospective analysis in 207 patients treated with levetiracetam. This entailed evaluation of patient notes and patient interviews. A paradoxical effect was defined as an increased seizure frequency or the experience of more severe seizures including generalized tonic-clonic seizures (GTCS) within 1 month after starting levetiracetam (LEV). RESULTS: Thirty patients (14%) experienced a paradoxical effect. Eight of them (4%) developed de novo GTCS. We could not demonstrate any association between the paradoxical effect of levetiracetam and type of epilepsy or the antiepileptic comedication used. However we found that the paradoxical effect developed preferentially (p < 0.001) in mentally retarded patients. CONCLUSION: Because there is an increased risk of worsening epilepsy when starting levetiracetam treatment of mentally retarded epileptic patients, there is a need for caution and close observation during the first weeks of therapy.

[Genetic background of epilepsies]. / Az epilepszia genetikája.

In this article we review epilepsies with monogenic inheritance. Most of these diseases are caused by abnormal function of ligand- and voltage gated ion channels caused by a genetic defect, therefore belonging to the channelopathies. From the inherited epilepsies the genetics of the autosomal dominant partial epilepsies is clarified the best. Mutations of the nicotinic acetylcholine receptor subunits are found in familial nocturnal frontal lobe epilepsy, while defects in the voltage gated potassium channels (KCNQ2 and KCNQ3) have been identified in benign familial neonatal convulsions. Familial temporolateral epilepsy was associated with mutations of a tumor suppressor gene. From the generalized epilepsies, the syndrome of generalized epilepsy with febrile seizures plus (GEFS+) can be caused by mutations of the sodium channel subunits and of the GABAA receptor subunits. These important results would probably lead to new findings in the genetics of the more common forms of idiopathic generalized epilepsies, which have presumed polygenic origin. Although without definite conclusions, sodium channel and GABA receptor dysfunction is presumed. The accumulated knowledge about channelopathies enables insight to the cellular mechanism of epileptogenesis as well.