Whole-Brain Permeability Analysis on Admission Improves Prediction of Delayed Cerebral Ischemia Following Aneurysmal Subarachnoid Hemorrhage

PurposeTo evaluate the changes of blood-brain barrier permeability (BBBP) after aneurysmal subarachnoid hemorrhage (aSAH) and find out whether BBBP within 24 h after onset can further improve prediction of delayed cerebral ischemia (DCI).MethodsCT perfusion (CTP) was performed within 24 h after onset and in the DCI time window (DCITW). Whole brain average values of flow extraction product (mK^trans), qualitative and quantitative CTP parameters, and clinical data were compared between DCI and non-DCI groups. The changes of mK^trans were analysed using a Paired t test. Multivariate logistic regression analysis and ROC analyses were performed to identify predictors of DCI and evaluate the predictive performance.ResultsOne hundred and forty of 179 consecutive patients were included, 45 of whom (32%) developed DCI. mK^trans was higher in the DCI group both on admission and in the DCITW (P<0.001). mK^trans decreased significantly in the non-DCI group (P=0.003), but not in DCI group (P=0.285). Multivariate logistic regression analysis showed that mK^trans (OR=1.07, 95%CI: 1.03-1.11, P<0.001), World Federation of Neurosurgery Scale (OR=6.73, 95%CI: 1.09-41.41, P=0.040), Hunt-Hess grade (OR=0.16, 95%CI: 0.02-1.19, P=0.073), modified Fisher Score (OR=3.74, 95%CI: 1.30-10.75, P=0.014), and qualitative CTP (OR=4.31, 95%CI: 1.49-12.47, P=0.007) were independent predictors of DCI. The model with K^trans produced a larger AUC of 0.88 (95%CI: 0.81-0.95), with corresponding sensitivity and specificity of 84% and 86%, respectively.ConclusionBBBP measurement within 24 h after onset can improve the prediction of DCI. Early moderate BBB disruption may be reversible, whereas severe BBBP disruption indicates the risk of DCI.     

A Single Immediate Use of the Cathodal Transcranial Direct Current Stimulation Induces Neuroprotection of Hippocampal Region Against Global Cerebral Ischemia

ObjectivesGlobal cerebral ischemia (CI) causes severe neuronal injury, mainly in the hippocampal CA1 region. This study aimed to investigate an immediate using transcranial direct current stimulation (tDCS) in reducing neuronal injury induced by CI.Materials and methodsThe 32 Wistar male rats were randomly divided into four groups (n=8 per group). In the ischemia group (I), CI was induced via the 4-vessel occlusion model. In the sham group (Sh), rats did not receive any intervention. In the ischemia+cathodal group (I+c/tDCS), the cathodal current was applied during CI. In the ischemia+anodal group (I+a/tDCS), the anodal current was applied. The current intensity of 400 μA was applied for 15-min during the ischemia. Hippocampal tissue was used to assess levels of NMDAR, IL-1β, TNF-α, MDA, SOD, NOS, and apoptosis markers. Histological assessment and TUNEL staining were performed in CA1 hippocampal region.ResultsThe c/tDCS significantly decreased the levels of IL-1β and TNF-α than the I and a/tDCS groups. The c/tDCS significantly reduced MDA and NOS levels, while increasing the level of SOD than the I and a/tDCS. The c/tDCS caused a significant decrease in NMDAR level than the a/tDCS. Using c/tDCS significantly reduced the Bax and Caspase-3 expressions, while increasing the Bcl-2 expression than the I group. In the c/tDCS group, DNA fragmentation and neuronal death were significantly lower than the I and a/tDCS groups.ConclusionUsing cathodal a direct current could attenuate primary pathophysiological pathways induced by CI, and it eventually reduced neurons death and apoptosis in the CA1 hippocampal region.     

Cerebral fat embolism syndrome at a single trauma center

ObjectivesBased on a 16-year case series, we sought lessons about diagnosis and treatment of cerebral fat embolism syndrome.Materials and methodsUsing discharge codes at a Level 1 Trauma Center, we performed a retrospective chart review of clinical characteristics, diagnostic studies, treatments, and outcome in cerebral fat embolism syndrome.ResultsThirty-nine (40%) of 97 patients with fat embolism syndrome were diagnosed with cerebral fat embolism syndrome, with 29 (74%) presenting with coma. All had abnormal brain magnetic resonance imaging, with scattered cytotoxic edema (starfield pattern) in 29 (74%). All but two of the 21 patients with dilated fundoscopy showed retinal embolism. Among 29 patients with transcranial Doppler, the presence of microembolic signals in 15 (52%) was associated with fever (p = 0.039), right-to-left intracardiac shunting (p = 0.046) and a trend towards initial coma. In 11 patients with serial transcranial Dopplers and treatment with high-intensity statin therapy, the frequency of microembolic signals tended to decrease after therapy was initiated. Of the 28 (72%) of the 39 patients discharged, 16 (57%) had mild to moderate disability at last follow up.ConclusionsThe recognition of cerebral fat embolism syndrome may be improved with routine inclusion of brain magnetic resonance imaging, dilated fundoscopy, and transcranial Doppler. We share our empiric management algorithm for cerebral fat embolism syndrome using these studies and with consideration of experimental therapies in select patients to prevent ongoing cerebral injury.     

Electroacupuncture Pretreatment Alleviates Cerebral Ischemia-Reperfusion Injury by Regulating Mitophagy via mTOR-ULK1/FUNDC1 Axis in Rats

Objective: Electroacupuncture (EA) pretreatment has been shown to alleviate cerebral ischemia-reperfusion (I/R) injury; however, the underlying mechanism remains unclear. To investigate the involvement of mTOR signaling in the protective role of EA in I/R-induced brain damage and mitochondrial injury. Methods: Sprague-Dawley male rats were pretreated with vehicle, EA (at Baihui and Shuigou acupoints), or rapamycin + EA for 30 min daily for 5 consecutive days, followed by the middle cerebral artery occlusion to induce I/R injury. The neurological functions of the rats were assessed using the Longa neurological deficit scores. The rats were sacrificed immediately after neurological function assessment. The brains were obtained for the measurements of cerebral infarct area. The mitochondrial structural alterations were observed under transmission electron microscopy. The mitochondrial membrane potential changes were detected by JC-1 staining. The alterations in autophagy-related protein expression were examined using Western blot analysis. Results: Compared with untreated I/R rats, EA-pretreated rats exhibited significantly decreased neurological deficit scores and cerebral infarct volumes. EA pretreatment also reversed I/R-induced mitochondrial structural abnormalities and loss of mitochondrial membrane potential. Furthermore, EA pretreatment downregulated the protein expression of LC3-II, p-ULK1, and FUNDC1 while upregulating the protein expression of p-mTORC1 and LC3-I. Rapamycin effectively blocked the above-mentioned effects of EA. Conclusion: EA pretreatment at Baihui and Shuigou alleviates cerebral I/R injury and mitochondrial impairment in rats through activating the mTORC1 signaling. The suppression of autophagy-related p-ULK1/FUNDC1 pathway is involved in the neuroprotective effects of EA.     

First Report of Cerebral Venous Thrombosis Following Inactivated-Virus Covid Vaccination (Sinopharm and Sinovac)

Cerebral venous thrombosis (CVT) is an uncommon cerebrovascular disease, which has been reported with covid infection as well as covid vaccines, particularly AstraZeneca and Janssen vaccines. We present four consecutive cases of CVT after receiving either Sinopharm or Sinovac vaccine, both of which are composed of an inactivated-virus. All the patients recovered well with anticoagulation and discharged with a good functional outcome. This is the first case series reporting CVT following the administration of these vaccines.     

Outcomes of Medical Management Alone for Adult Patients with Cerebral Misery Perfusion Due to Ischemic Moyamoya Disease

ObjectivesAlthough revascularization surgery is recommended for adult patients with moyamoya disease (MMD) who present with ischemic symptoms due to hemodynamic compromise, the clinical course of such patients who are treated with medical management alone remains unclear. Here, we report outcomes of adult patients with cerebral misery perfusion due to ischemic MMD who received medical management alone.Materials and MethodsWe prospectively followed up patients who showed misery perfusion in the symptomatic cerebral hemisphere on ¹⁵O gas positron emission tomography (PET) and received strict medical management alone after refusing revascularization surgery.ResultsOf 57 patients who showed symptomatic misery perfusion on ¹⁵O gas PET, three (5%) were included into the present study. Two of these patients suffered further ischemic events at 7 and 8 months after inclusion, after which, their modified Rankin disability scale scores deteriorated. In the remaining patient, fatal intracerebral hemorrhage developed at 10 months after inclusion.ConclusionsThese findings suggest that receiving medical management alone is associated with considerably poor outcomes for adult patients with cerebral misery perfusion due to ischemic MMD.     

Brain maturation in the first 3 months of life,measured by electroencephalogram: A comparison between preterm and term-born infants

ObjectivePreterm infants are at risk for altered brain maturation resulting in neurodevelopmental impairments. Topographical analysis of high-density electroencephalogram during sleep matches underlying brain maturation. Using such an EEG mapping approach could identify preterm infants at risk early in life.Methods20 preterm (gestational age < 32 weeks) and 20 term-born infants (gestational age > 37 weeks) were recorded by 18-channel daytime sleep-EEG at term age (GA 40 weeks for preterm and 2–3 days after birth for term infants) and 3 months (corrected age for preterm infants).ResultsPreterm infant’s power spectrum at term age is immature, leveling off with term infants at 3 months of age. Topographical distribution of maximal power density however, reveals qualitative differences between the groups until 3 months of age. Preterm infants exhibit more temporal than central activation at term age and more occipital than central activation at 3 months of age. Moreover, being less mature at term age predicts being less mature at 3 months of age.ConclusionTopographical analysis of sleep EEG reveals changes in brain maturation between term and preterm infants early in life.SignificanceIn future, automated analysis tools using topographical power distribution could help identify preterm infants at risk early in life.     

Characterization of Moyamoya and Middle Cerebral Artery Diseases by Carotid Canal Diameter and RNF213 p.R4810K Genotype

ObjectivesIt is sometimes difficult to differentiate middle cerebral artery disease from moyamoya disease because the two can present similarly yet have different treatment strategies. We investigated whether the presence of a narrow carotid canal and the RNF213 mutation can help differentiate between the two phenotypes.Population and MethodsWe analyzed 78 patients with moyamoya disease, 27 patients with middle cerebral artery disease, and 79 controls from 2 facilities. The carotid canal diameter was measured using computed tomography. The p.R4810K mutation was genotyped by TaqMan assay. A receiver operating characteristics analysis was performed to assess the significance of the carotid canal diameter for the accurate diagnosis of moyamoya disease.ResultsThe carotid canal diameter was significantly narrower in patients with moyamoya disease than in controls. The optimal cutoff values were 5.0 mm for adult males and 4.5 mm for adult females and children (sensitivity: 0.82; specificity: 0.92). Among the patients with middle cerebral artery disease, 18.5% and 25.0% of the affected hemispheres had the p.R4810K mutation and narrow canal (i.e., below the cutoff), respectively, whereas only 3.1% of those had both. Contrastingly, 68.8% of the affected hemispheres in patients with moyamoya disease had both these characteristics. Among the patients with moyamoya disease, those with the p.R4810K mutation tended to have narrower carotid canals.ConclusionsAlthough the presence of a narrow carotid canal or the p.R4810K mutation alone could not be used to distinguish those with moyamoya disease from those with middle cerebral artery disease, the combination of these factors could better characterize the two phenotypes.     

Cerebral Infarction due to Severe ADAMTS-13 Deficiency with Normal Hematological Parameters: A Cause of Cryptogenic Stroke

ObjectivesThrombotic thrombocytopenic purpura (TTP) is a microangiopathy resulting from an inherited or acquired severe deficiency in a disintegrin and metalloproteinase called ADAMTS-13. Acquired or immune TTP is classically described as a pentad of microangiopathic hemolytic anemia (MAHA), thrombocytopenia, fever, renal insufficiency and neurological symptoms. Thrombotic thrombocytopenic purpura has been linked to stroke with the presence of hematologic abnormalities but whether or not severe ADAMTS-13 deficiency can cause stroke without hematological abnormalities is unknown.Materials and MethodsAs part of routine clinical care, we identified four cases of recurrent stroke attributed to severe deficiency of ADAMTS-13. We also conducted a search of a centralized electronic health record database including all inpatients and outpatient charts at a single academic medical center over the last ten years in an attempt to identify additional cases.ResultsHere we present four cases of stroke and severe ADAMTS-13 deficiency where stroke episodes occurred without microangiopathic hemolytic anemia or severe thrombocytopenia. These cases show the need to consider severe ADAMTS-13 deficiency in the setting of recurrent cryptogenic stroke in young patients.Conclusions and RelevanceTTP directed therapies may be considered for patients with recurrent stroke who have extremely low ADAMTS-13 levels, even when platelet and hemoglobin values are normal.     

Prevalence and Risk Factors of Silent Cerebral Microbleeds in Patients with Coronary Artery Disease

ObjectivesCerebral microbleeds (CMBs), which can be detected by gradient-echo T2*-weighted magnetic resonance imaging (MRI), represent small chronic brain hemorrhages caused by structural abnormalities in cerebral small vessels. CMBs are known to be a potential predictor of future stroke, and are associated with age, various cardiovascular risk factors, cognitive impairment, and the use of antithrombotic drugs. Patients with coronary artery disease (CAD) are at potentially high risk of CMBs due to the presence of coexistent conditions. However, little is known about CMBs in patients with CAD. We aimed to identify the factors associated with the presence of CMBs among patients with CAD.MethodsWe evaluated 356 consecutive patients [mean age, 72 ± 10 years; men = 276 (78%)] with angiographically proven CAD who underwent T2*-weighted brain MRI. The brain MRI was assessed by researchers blinded to the patients’ clinical details.ResultsCMBs were found in 128 (36%) patients. Among 356 patients, 119 (33%) had previously undergone percutaneous coronary intervention (PCI), and 26 (7%) coronary artery bypass grafting (CABG). There was no significant relationship between CMBs and sex, hypertension, dyslipidemia, diabetes mellitus, anticoagulation therapy, antiplatelet therapy, or prior PCI. CMBs were significantly associated with advanced age, previous CABG, eGFR, non-HDL cholesterol, carotid artery disease, long-term antiplatelet therapy, and long-term dual antiplatelet therapy (DAPT) using univariate logistic regression analysis. The multivariate logistic regression analysis showed that long-term antiplatelet therapy (odds ratio, 1.73; 95% CI, 1.06 – 2.84; P = 0.03) or long-term DAPT (odds ratio, 2.92; 95% CI, 1.39 – 6.17; P = 0.004) was significantly associated with CMBs after adjustment for confounding variables.ConclusionsCMBs were frequently observed in patients with CAD and were significantly associated with long-term antiplatelet therapy, especially long-term DAPT.     

Review of synthetic MRI in pediatric brains: Basic principle of MR quantification,its features,clinical applications,and limitations

Quantitative magnetic resonance imaging (MRI) with multislice, multi-echo, and multi-delay acquisition enables simultaneous quantification of R₁ and R₂ relaxation rates, proton density, and the B₁ field in a single acquisition, and requires only about 6 minutes for full-head coverage. Using dedicated SyMRI software, radiologists can generate any contrast-weighted image by manipulating the acquisition parameters, including repetition time, echo time, and inversion time. Moreover, automatic brain tissue segmentation, volumetry, and myelin measurement can also be performed. Using the SyMRI approach, a shorter scan time, an objective examination, and personalized MR imaging parameters can be obtained in daily clinical pediatric imaging. Here we summarize and review the use of SyMRI in imaging of the pediatric brain, including the basic principles of MR quantification along with its features, clinical applications, and limitations.     

Effect of early mobilization in patients with stroke and severe disturbance of consciousness: Retrospective study

ObjectivesThis study aimed to investigate the effectiveness and safety of early mobilization with a physiatrist and registered therapist Operating rehabilitation (PROr) for patients with stroke and severe disturbance of consciousness (DoC).Materials and methodsWe retrospectively screened records from patients with stroke admitted to our hospital from January 2015 to June 2021. Eligible patients with severe DoC were classified into two groups: patients who received standard rehabilitation (control group) and patients who received PROr (PROr group). We studied longitudinal change in the level of consciousness using the Japan Coma Scale (JCS) during hospital stay and compared in-hospital mortality, the incidence of respiratory complication, and modified Rankin Scale of discharge between the two groups.ResultsAmong the 2191 patients screened for inclusion, 16 patients were included in the PROr group, and 12 patients were included in the control group. Early mobilization was more promoted in the PROr group compared to the control group, but there were no significant differences in in-hospital mortality, the incidence of respiratory complication, or modified Rankin Scale at discharge between the two groups. In patients who survived during their hospital stay, JCS scores 2 weeks after the onset of stroke and JCS scores at discharge significantly improved from the start of rehabilitation in the PROr group, but not in the control group.ConclusionsEarly mobilization provided with the PROr program appears to be a safe treatment and may contribute to the improvement of consciousness level for patients with acute stroke and severe DoC.     

Diabetes is an Independent Growth Factor of Ischemic Stroke During Reperfusion Phase Leading to Poor Clinical Outcome

ObjectivesDespite the success of recanalization by bridging therapy, about half of treated stroke patients remain disabled. While numerous reports propose clinical predictors of stroke clinical outcome in this context, we originally aimed to study pre-therapeutic factors influencing infarct growth (IG) and poor clinical outcome in strokes due to large vessel occlusion (LVO) successfully recanalized.Materials and methodsWe enrolled 87 consecutive successfully recanalized patients (mTICI: 2b/2c/3) by mechanical thrombectomy (±rt-PA) after stroke due to middle cerebral artery (M1) occlusion within 6 h according to AHA guidelines. IG was defined by subtracting the initial DWI volume to the final 24 h-TDM volume. Statistical associations between poor clinical outcome (mRS≥2), IG and pertinent clinico-radiological variables, were measured using logistic and linear regression models.ResultsAmong 87 enrolled patients (Age(y): 68.4 ± 17.5; NIHSS: 16.0 ± 5.4), 42/87 (48,28%) patients had a mRS ≥ 2 at 3 months. Diabetic history (OR: 3.70 CI95%[1.03;14.29] and initial NIHSS (/1 point: OR: 1.16 CI95%[1.05;1.27]) were independently associated with poor outcome. IG was significantly higher in stroke patients with poor outcome (+7.57 ± 4.52 vs ?7.81 ± 1.67; p = 0.0024). Initial volumes were not significantly different (mRS≥2: 16.18 ± 2.67; mRS[0–1]: 14.70 ± 2.30; p = 0.6771). Explanatory variables of IG in linear regression were diabetic history (β: 21.26 CI95%[5.43; 37.09]) and NIHSS (β: 0.83 CI95%[0.02; 1.64]). IG was higher in diabetic stroke patients (23.54 ± 1.43 vs ?6.20 ± 9.36; p = 0.0061).ConclusionsWe conclude that diabetes leads to continued IG after complete recanalization, conditioning clinical outcome in LVO strokes successfully recanalized by bridging therapy. We suggest that poor tissular reperfusion by diabetic microangiopathy could explain this result.     

Bradykinesia in Alzheimer’s disease and its neurophysiological substrates

ObjectiveAlzheimer’s disease is primarily characterized by cognitive decline; recent studies, however, emphasize the occurrence of motor impairment in this condition. Here, we investigate whether motor impairment, objectively evaluated with kinematic techniques, correlates with neurophysiological measures of the primary motor cortex in Alzheimer’s disease.MethodsTwenty patients and 20 healthy subjects were enrolled. Repetitive finger tapping was assessed by means of a motion analysis system. Primary motor cortex excitability was assessed by recording the input/output curve of the motor-evoked potentials and using a conditioning-test paradigm for the assessment of short-interval intracortical inhibition and short-latency afferent inhibition. Plasticity-like mechanisms were indexed according to changes in motor-evoked potential amplitude induced by the intermittent theta-burst stimulation.ResultsPatients displayed slowness and altered rhythm during finger tapping. Movement slowness correlated with reduced short-latency afferent inhibition in patients, thus suggesting that degeneration of the cholinergic system may also be involved in motor impairment in Alzheimer’s disease. Moreover, altered movement rhythm in patients correlated with worse scores in the Frontal Assessment Battery.ConclusionThis study provides new information on the pathophysiology of altered voluntary movements in Alzheimer’s disease.SignificanceThe study results suggest that a cortical cholinergic deficit may underlie movement slowness in Alzheimer’s disease.     

Stroke and stroke risk factors in women of reproductive age with a history of metabolic or bariatric surgery

ObjectiveTo determine the odds of stroke in women of reproductive age who have had metabolic or bariatric surgery (MBS).MethodsWe used the National Inpatient Sample (NIS), a publicly available dataset that samples 20% of hospital discharges. The study population includes women between the ages of 20 and 44 without a maternal admission code. Weighted logistic regression analyses were conducted to assess the odds of stroke in women with history of MBS compared to other women of reproductive age. Adjustment of odds was done for the following covariates: age, race, primary payer, severity of illness, depression, and obesity.ResultsWomen with a history of MBS had 52% lower adjusted odds of having a stroke than women who did not have MBS (OR = 0.48, 95%CI = 0.42-0.55). Additionally, women who had MBS had lower odds of risk factors for stroke, including diabetes (OR = 0.61, 95%CI = 0.59-0.63), hypertension (OR = 0.82, 95%CI = 0.81-0.84), hypercholesterolemia (OR=0.72, 95%CI =0.68-0.77), and migraine with aura (OR = 0.86, 95%CI = 0.74-0.99).ConclusionsAmong women of reproductive age with a history of MBS, there were lower odds of having a stroke and stroke risk factors when compared to women who did not have MBS. Additionally, this study showed a modest decrease in the odds of stroke among women with obesity when adjusted for other risk factors. Future research should focus on examining this finding further, with a focus on the moderation of the impact of having obesity on stroke risk independent of other stroke risk factors.     

Cognitive deficits and rehabilitation mechanisms in mild traumatic brain injury patients revealed by EEG connectivity markers

ObjectiveTo explore the multiple specific biomarkers and cognitive compensatory mechanisms of mild traumatic brain injury (mTBI) patients at recovery stage.MethodsThe experiment was performed in two sections. In Section I, using event-related potential, event-related oscillation and spatial phase-synchronization, we explored neural dynamics in 24 volunteered healthy controls (HC) and 38 patients at least 6 months post-mTBI (19 with epidural hematoma, EDH; 19 with subdural hematoma, SDH) during a Go/NoGo task. In Section II, according to the neuropsychological scales, patients were divided into sub-groups to assess these electroencephalography (EEG) indicators in identifying different rehabilitation outcomes of mTBI.ResultsIn Section I, mean amplitudes of NoGo-P3 and P3d were decreased in mTBI patients relative to HC, and NoGo-theta power in the non-injured hemisphere was decreased in SDH patients only. In Section II, patients with chronic neuropsychological defects exhibited more serious impairments of intra-hemispheric connectivity, whereas inter-hemispheric centro-parietal and frontal connectivity were enhanced in response to lesions.ConclusionsEEG distinguished mTBI patients from healthy controls, and estimated different rehabilitation outcomes of mTBI. The centro-parietal and frontal connectivity are the main compensatory mechanism for the recovery of mTBI patients.SignificanceEEG measurements and network connectivity can track recovery process and mechanism of mTBI.     

Inter-ictal network of focal epilepsy and effects of clinical factors on network activity

ObjectiveAim of the study was to explore the inter-ictal, resting-state EEG network in patients with focal epilepsy (FE) and to specify clinical factors that influence network activity.MethodsFunctional EEG connectivity (EEGfC) differences were computed between 232 FE patients (FE group) and 77 healthy controls. EEGfC was computed among 23 cortical regions within each hemisphere, for 25 very narrow bands from 1 to 25 Hz. We computed independent effects for six clinical factors on EEGfC in the FE group, by ANOVA and post-hoc t-statistics, corrected for multiple comparisons by false discovery rate method.ResultsRobust, statistically significant EEGfC differences emerged between the FE and the healthy control groups. Etiology, seizure type, duration of the illness and antiepileptic treatment were independent factors that influenced EEGfC. Statistically significant results occurred selectively in one or a few very narrow bands and outlined networks. Most abnormal EEGfC findings occurred at frequencies that mediate integrative and motor activities.ConclusionsFE patients have abnormal resting-state EEGfC network activity. Clinical factors significantly modify EEGfC.SignificanceDelineation of the FE network and modifying factors can open the way for targeted investigations and introduction of EEGfC into epilepsy research and practice.     

Effect of partial and total sleep deprivation on serum testosterone in healthy males: a systematic review and meta-analysis

BackgroundCurrently, there is no consensus on the effect of sleep deprivation on male serum testosterone. This systematic review and meta-analysis aimed to determine the association between partial/total sleep deprivation and male serum testosterone level.MethodsThe literature related to sleep deprivation and male serum testosterone in the PubMed, Embase, and Cochrane Library databases were searched from their inception to July 15, 2021. Data were pooled using the Stata 15 software. The results were presented as standard mean differences (SMDs) with their 95% confidence intervals (CIs).ResultsEighteen studies involving 252 men were included in the systematic review and meta-analysis. The findings revealed that short-term partial sleep deprivation had no significant effect on male serum testosterone (SMD = −0.22; 95% CI: −0.5, 0.06; P = 0.13), while total sleep deprivation reduced the male testosterone levels (SMD = −0.64; 95% CI: −0.87, −0.42; P < 0.001). According to the intervention duration of total sleep deprivation, subgroup analysis was conducted by a fixed-effects model. The results revealed that the serum testosterone was significantly decreased after 24 h total sleep deprivation (SMD = − 0.67; 95% CI = − 0.93, −0.42, P < 0.001), as well as 40–48 h total sleep deprivation (SMD = − 0.74; 95% CI = − 1.22, −0.26, P = 0.002).ConclusionsThis meta-analysis revealed that total sleep deprivation (more than or equal to 24 h) reduces the male testosterone levels, while short-term partial sleep deprivation has no significant effect on male serum testosterone. Sleep duration plays a pivotal role in maintaining male serum testosterone levels.