Background COVID-19 is a virus pandemic. According to the first obtained data, COVID-19 has defined with findings such as cough, fever, diarrhea, and fatigue although neurological symptoms of patients with COVID-19 have not been investigated in detail. This study aims to investigate the neurological findings via obtained face-to-face anamnesis and detailed neurological examination in patients with COVID-19. Methods Two hundred thirty-nine consecutive inpatients with COVID-19, supported with laboratory tests, were evaluated. Detailed neurological examinations and evaluations of all patients were performed. All evaluations and examinations were performed by two neurologists who have at least five-year experience. Results This study was carried out 239 patients (133 male + 106 female) with diagnosed COVID-19. Neurological findings were present in 83 of 239 patients (34.7%). The most common neurological finding was a headache (27.6%). D-dimer blood levels were detected to be significantly higher in patients with at least one neurological symptom than patients without the neurological symptom (p < 0.05). IL-6 level was found to be significantly higher in patients with headache than without headache (p < 0.05). Creatine kinase (CK) level was detected to be significantly higher in patients with muscle pain (p < 0.05). Conclusion Neurological symptoms are often seen in patients with COVID-19. Headache was the most common seen neurological symptom in this disease. Dizziness, impaired consciousness, smell and gustation impairments, cerebrovascular disorders, epileptic seizures, and myalgia were detected as other findings apart from the headache. It is suggested that determining these neurological symptoms prevents the diagnosis delay and helps to prohibit virus spread.

Background and objective Clinical studies on COVID-19 headache are limited. This prospective study aimed to define headache characteristics, associated clinical and laboratory factors, and treatment response in COVID-19. Methods Cross-sectional study enrolled 287 patients diagnosed with COVID-19 and hospitalized on a regular ward during the pandemic. All patients were examined face to face and followed by a neurologist during their stay in the hospital. The characteristics, concomitant symptoms, treatment responses, and laboratory findings of COVID-19-associated headaches were recorded. Results Eighty-three COVID-19 patients reported headache (28.9%), in which 85.5% had no prior headaches. Mean age was 48.40 ± 15.90 and 58% was men. Compared to COVID-19 patients without headache ( n = 204), patients with headache showed significantly higher frequency of pulmonary involvement (76%) and increased D-dimer levels. Fifty-nine percent of headaches responded iv paracetamol 1000 mg, and 85% of the paracetamol unresponsive headaches were relieved by greater occipital nerve (GON) blocks. Latent class cluster analysis identified 2 distinct class of bilateral, frontal, throbbing headaches: severe (VAS > 84), longer (> 14 h), frequent (> 7 headache days), paracetamol unresponsive-GON responsive headaches (85%), with pulmonary involvement (100%), and higher IL-6 levels (> 90 pg/mL) were classified in cluster 1. Cluster 2 included moderately affected patients (VAS > 54, > 6 h, > 4 days, 60% pulmonary involvement, > 20 pg/mL IL-6) and paracetamol responsive headaches (96%). VAS scores showed positive linear correlation with IL-6 levels ( p < 0.001; r = 0.567). Conclusion The intensity, duration, frequency, bilateral frontal location, and treatment response of COVID-19 headache was related to pulmonary involvement and IL-6 levels, which indicated a role of inflammation in determining the headache manifestations in moderately affected hospitalized patients. ROC curve cutoff values pointed that VAS > 70 severity, > 9 h duration, > 5 headache days, and IL-6 > 43 pg/mL levels can be diagnostic for COVID-19 headache. GON blocks can effectively abort headache when patients are unresponsive to paracetamol, and other NSAIDs are avoided during the SARS-CoV-2 infection.

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Introduction Even though lifelong premature ejaculation (PE) is highly prevalent, few studies have investigated the neural mechanisms underlying PE. Aim This study aimed to investigate whether patients with lifelong PE exhibit macrostructural or microstructural alterations of the parts of the brain involved in the male sexual response. Materials and Methods We enrolled 42 healthy participants and 54 lifelong PE patients. Lifelong PE was diagnosed according to the Premature Ejaculation Diagnostic Tool (PEDT) and intravaginal ejaculation latency time (IELT). We compared measures of cortical morphology, such as volumes of gray matter, white matter, cerebellum volumes, and subcortical structures (ie, amygdala, caudate, hippocampus, globus pallidus, putamen, and thalamus) between the groups using a voxel-based morphometry method from whole-brain T1-weighted magnetic resonance imaging. Moreover, we evaluated the relationships between the relevant cerebral alterations and the severity of symptoms obtained from participants via self-reported questionnaires. Main Outcome Measures Cerebral macrostructural and microstructural alterations were assessed in PE patients and controls, along with the correlation of caudate nucleus changes in PE patients with clinical data (including the PEDT and the IELT). Results The mean volume of the caudate nucleus was significantly larger in the lifelong PE patients compared with healthy controls (P = .048). Moreover, caudate nucleus volume was positively correlated with PEDT score (r = 0.621; P = .0179) and negatively correlated with the IELT (r = −0.592; P = .0101). However, cortex morphology and the other subcortical volumes were not significantly different between the 2 groups (P &gt; .05). Clinical Implications Microstructural alterations in deep gray matter nuclei might be a useful parameter for studying the mechanism of the neurobiology underlying PE. Strengths and Limitations There are few studies examining microstructural changes in PE patients. This study furthers our understanding of the etiology of PE. Limitations include the small sample, which limits our ability to make an absolute determination as to whether such subcortical changes are the cause or the consequence of lifelong PE. Conclusions We found a significant difference in caudate nucleus volume between patients with PE and healthy controls. In addition, the caudate nucleus volume was positively associated with the severity of PE symptoms. More extensive and possibly longitudinal studies are needed to improve our understanding of the mechanism of the neurobiology underlying PE.

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