Transient Cognitive Impairment Research Articles

Patient Outcomes and Healthcare Practices Before and After COVID-19 Vaccination: A Comprehensive Analysis

Abstract: The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) unleashed a global pneumonia pandemic, causing significant harm to both physical and mental health. It emphasized the urgency for specialized therapies and protective measures. Approaches, including immunotherapy, antiviral drugs, and lifestyle improvements, like diet and exercise, have shown promise in controlling viral spread before widespread vaccination. However, COVID-19 vaccinations, while critical for reducing disease severity, have been associated with potential side effects, including transient cognitive impairment, rare renal disorders, physiologic anomalies, and dermatological reactions. The scientific community continues to rigorously study these issues to ensure the safety and efficacy of vaccination programs and to address the multifaceted impact of the pandemic.

CURRENT OVERVIEW OF CLINICAL AND RADIOLOGICAL FINDINGS ASSOCIATED WITH CEREBRAL AMYLOID ANGIOPATHY

Cerebral amyloid angipopathy (CAA), the second most common cause of spontaneous acute intracerebral hemorrhage after hypertension in the elderly population is characterized by brain parenchymal damage secondary to hemorrhage and ischemia caused by the accumulation of Aβ protein in the walls of small arteries and arterioles. Advanced age is the most significant risk factor for CAA. While the definitive diagnosis requires histopathological examination through autopsy/biopsy, the probable or possible diagnosis of CAA is based on clinical features as well as characteristic neuroimaging findings. With the increasing elderly population and the growing prevalence of succesibility-weighted magnetic resonance imaging sequences in routine, it becomes imperative to have a thorough understanding of the imaging spectrum associated with CAA. Early diagnosis is extremely critical in patients with CAA who have not yet developed intracranial hemorrhage. Furthermore, patients with CAA may present clinically transient focal neurological episodes or cognitive impairment, which can be mistaken for transient ischemic attacks caused by convexity subarachnoid hemorrhage. Additionally, before initiating newly introduced anti-amyloid monoclonal antibody drugs in Alzheimer's disease, it is necessary to exclude signs of CAA. Moreover, the anticipated side effects of these drugs often manifest imaging abnormalities resembling inflammation or bleeding associated with CAA, necessitating familiarity with the imaging findings of CAA. In this review, the pathophysiology, clinical manifestations, and radiological findings of sporadic CAA will be detailed.

Abstract WP219: Diffusion Weighted Imaging Characteristics in Deep White and Gray Matter Structures in Pediatric Patients With Moyamoya Disease

Background: Moyamoya Disease (MMD) is a steno-occlusive arteriopathy associated with transient ischemic attacks, stroke, and cognitive impairments. In adult MMD, normal-appearing deep gray and white matter structures (NADWM) show diffusion changes that are associated with cognitive impairments. Apparent diffusion coefficient [ADC] measures the mean diffusion and is sensitive to these changes. The association of ADC changes in NADWM in pediatric MMD is not clear. Our objective is to determine whether ADC is elevated in NADWM in pediatric MMD patients. Hypothesis: ADC values in NADWM will be elevated in MMD patients compared to controls. Methods: Twenty-nine MMD patients and no stroke and 7 healthy controls (HC) were included in a single center, retrospective study. Diffusion and T1-weighted images were analyzed. We constructed a script implementing a convolutional neural network (CNN) based approach to segment and binarize cortical regions of interest (ROI) and allow extraction of ADC values (units =[x10 -6 mm 2 /s]). Segmented ROIs included: 1) all white matter (WM), and NADWM including: 2) thalamus, 3) caudate, 4) putamen, 5) globus pallidus, 6) hippocampus. Mean ADC values were compared for: 1) all ROIs between MMD and controls, and 2) all ROIs in the MMD affected and the contralateral hemispheres within the MMD group. Results: Patients were on average 7.7 + 5.4 years at MMD diagnosis. In all WM, MMD patients had significantly higher ADC values than controls in the left (mean= 865.7 + 101.6 versus 762.4 + 21.6, p=0.01) and right hemispheres (mean= 869.9 + 104.9 versus 761.0 + 21.3, p=.01), respectively. In NADGM, there were no significant differences found between the MMD and control groups in any of the NADGM ROIs. In the NADGM of MMD patients, higher ADC values were found in the putamen (mean= 778.2 + 46.0, p=0.041), hippocampus (mean=1009.5 + 58.6, p=0.005) and all NAWM (mean= 860.3 + 57.0, p<0.0001) in the MMD affected compared to the contra-lesional hemisphere. Conclusions: In pediatric patients with MMD, we found elevated ADC values in deep gray and white matter structures in the diseased hemisphere indicating alterations in the underlying microstructure. Our future analysis will integrate hemodynamic profiles and cognitive outcomes.

Transient epileptic amnesia complex syndrome and epileptic cognitive impairment resembling Alzheimer's disease: Should the concept of epilepsy be extended?

Transient epileptic amnesia complex syndrome and epileptic cognitive impairment resembling Alzheimer's disease: Should the concept of epilepsy be extended?

A Patient with Severe Headache and Uncontrolled Blood Pressure in the Emergency Department: A Case Report

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a rare angiopathy inherited in an autosomal dominant manner. Because it manifests as nonspecific symptoms such as migraine with aura, ischemic stroke and transient ischemic attack, cognitive impairment, and dementia, the diagnosis may begin with a physician’s suspicion. Here, we describe a 69-year-old female patient with severe headaches and uncontrolled blood pressure at our emergency department and been diagnosed with CADASIL.

Wake slow waves in focal human epilepsy impact network activity and cognition

Slow waves of neuronal activity are a fundamental component of sleep that are proposed to have homeostatic and restorative functions. Despite this, their interaction with pathology is unclear and there is only indirect evidence of their presence during wakefulness. Using intracortical recordings from the temporal lobe of 25 patients with epilepsy, we demonstrate the existence of local wake slow waves (LoWS) with key features of sleep slow waves, including a down-state of neuronal firing. Consistent with a reduction in neuronal activity, LoWS were associated with slowed cognitive processing. However, we also found that LoWS showed signatures of a homeostatic relationship with interictal epileptiform discharges (IEDs): exhibiting progressive adaptation during the build-up of network excitability before an IED and reducing the impact of subsequent IEDs on network excitability. We therefore propose an epilepsy homeostasis hypothesis: that slow waves in epilepsy reduce aberrant activity at the price of transient cognitive impairment.

β-asarone improves cognitive impairment and alleviates autophagy in mice with vascular dementia via the cAMP/PKA/CREB pathway

BackgroundVascular dementia (VD) is the second most common type of dementia after Alzheimer's disease. β-asarone, a major component of Acorus tatarinowii Schott, is important in neurodegenerative and neurovascular diseases. Studies have confirmed that β-asarone can mitigate autophagy and reduce damage in hypoxic cells. We also reported that β-asarone improves learning and memory. This study further clarifies whether β-asarone attenuates cerebral ischaemic injury by acting through the cAMP/PKA/CREB pathway in VD model mice. MethodsHere, genes and potential pathways that may be targeted by β-asarone for the treatment of transient cerebral ischaemia (TCI) and cognitive impairment (CI) were obtained using network pharmacology. The two-vessel occlusion method was used to establish the VD model. The Morris water maze test was used to evaluate the effects on memory. Then, the protein levels of mitofusin-2 (Mfn2), brain-derived neurotrophic factor (BDNF), optic atrophy 1 (OPA1), cyclic adenosine monophosphate (cAMP), myelin basic protein (MBP), matrix metalloproteinase-9 (MMP9) and neuron specific enolase (NSE) were determined by ELISA. The levels of superoxide dismutase (SOD) and malonaldehyde (MDA) were measured using commercial kits. Then, qRT-PCR was employed to investigate the expression of the candidate genes screened from the protein-protein interaction (PPI) network. Furthermore, the expression of the autophagy-related proteins Beclin-1, (microtubule-associated protein light chain 3) LC3, p62, postsynaptic density protein 95 (PSD95), protein kinase A (PKA), pPKA, cyclic-AMP response binding protein (CREB), and pCREB was determined by western blotting. The expression of autophagy-related proteins, PSD95 and translocase of outer mitochondrial membrane 20 (TOM20) was determined by immunofluorescence analyses. ResultsThe network pharmacological analysis showed 234 targets related to β-asarone, 1,118 genes related to TCI and 2,039 genes associated with CI. Our results confirm that β-asarone treatment not only alleviated brain damage in the VD model by improving mitochondrial and synaptic function, reducing neuronal injury and upregulating the expression of antioxidants but also effectively improved the cognitive behaviour of VD model mice. Moreover, β-asarone downregulated VD-induced RELA and CCND1 mRNA expression. In addition, we validated that β-asarone increased the phosphorylation of PKA and CREB and upregulated cAMP protein expression. The results showed that the cAMP/PKA/CREB signalling pathway was upregulated. Moreover, β-asarone administration decreased the protein expression levels of Beclin-1 and LC3 and increased the expression levels of p62 in VD model mice. Conclusionsβ-asarone inhibits Beclin-1-dependent autophagy and upregulates the cAMP/PKA/CREB signalling pathway to attenuate mitochondrial and synaptic damage from cerebral ischaemia and improve learning and cognitive abilities in VD model mice.

Cognitive Impairment in MRI-Negative Epilepsy: Relationship between Neurophysiological and Neuropsychological Measures.

Epileptic patients frequently encounter cognitive impairment. Functions that are mostly affected involve memory, attention, and executive function; however, this is mainly dependent on the location of the epileptic activity. The aim of the present study is to assess cognitive functions in MRI-negative epilepsy patients by means of neurophysiological and neuropsychological measures, as well as study the concept of transient cognitive impairment in patients with epileptiform discharges during EEG acquisition. The patients were enrolled from an outpatient Epilepsy/Clinical Neurophysiology clinic over a time period of 6 months. The study sample comprised 20 MRI-negative epilepsy patients (mean age ± standard deviation (SD), 30.3 ± 12.56 years; age range, 16-60 years; average disease duration, 13.95 years) and 10 age-matched controls (mean age ± SD, 24.22 ± 15.39 years), who were also education-matched (p > 0.05). Patients with epileptogenic lesions were excluded from the study. Informed consent was obtained from all subjects involved in the study. Auditory ERPs and the cognitive screening tool EpiTrack were administered to all subjects. Latencies of P300 and slow waves were prolonged in patients compared to controls (p < 0.05). The ASM load and patients' performance in the EpiTrack maze subtest were the most significant predictors of P300 latency. A decline in the memory, attention, and speed of information processing was observed in patients with cryptogenic epilepsy compared to age-matched controls, as reflected by P300 latency and EpiTrack scores.

Perioperational management of elderly and senile patients based on a comprehensive geriatric assessment for endoprosthetics of large joint

Introduction. Due to the changing age structure of the world’s population, an increase in the number of geriatric patients undergoing endoprosthetics of large joints is to be expected in the future. Age-related frailty and existing comorbidities pose problems for the entire treatment team.The aim of the study was to determine the effectiveness of comprehensive geriatric management of elderly and senile patients before and after endoprosthetic of the hip and knee joints.Materials and methods. An analysis of publications on the use of comprehensive in endoprosthetic of large joints in elderly and senile patients with osteoarthritis was performed. Searched in the electronic databases and libraries Web of Science, Conchrane library, PubMed, eLibrary using the search words: comprehensive geriatric assessment.Results and discussion. There is an increasing incidence of large joints endoprosthetic in orthogeriatric patients with osteoarthritis. Anaesthesia and arthroplasty in this group of patients is an important issue, as well as ensuring immediate postoperative mobilization of the patient. An individualized patient preparation plan for surgical intervention and postoperative management, aimed at preventing the development of transient cognitive impairment and other complications associated with geriatric status, in particular falls, is a necessary organizational element of treatment.Conclusion. A comprehensive geriatric assessment plays a crucial role in the perioperative introduction of geriatric patients for endoprosthetic of large joints. Timely identification of geriatric patients during the preoperative phase eliminates risk factors.

Maresin1 ameliorates postoperative cognitive dysfunction in aged rats by potentially regulating the NF-κB pathway to inhibit astrocyte activation

Postoperative cognitive dysfunction (POCD) is one of the most serious postoperative complications in the elderly population. Perioperative central neuroinflammation is considered to be an important pathological mechanism of POCD, with the activation of astrocytes playing a key role in central neuroinflammation. Maresin1 (MaR1) is a specific pro-resolving mediator synthesized by macrophages in the resolution stage of inflammation, and provides unique anti-inflammatory and pro-resolution effects by limiting excessive neuroinflammation and promoting postoperative recovery. However, the question remains whether MaR1 can have a positive effect on POCD. The objective of this study was to investigate the protective effect of MaR1 on POCD cognitive function in aged rats after splenectomy. Morris water maze test and IntelliCage test showed that splenectomy could cause transient cognitive dysfunction in aged rats; however, the cognitive impairment of rats was significantly mitigated when MaR1 pretreatment was administered. MaR1 significantly alleviated the fluorescence intensity and protein expression of glial fibrillary acidic protein and central nervous system specific protein in the cornu ammonis 1 region of the hippocampus. Simultaneously, the morphology of astrocytes was also severely altered. Further experiments showed that MaR1 inhibited the mRNA and protein expression of several key proinflammatory cytokines–interleukin-1β, interleukin-6, and tumor necrosis factor-α in the hippocampus of aged rats following splenectomy. The molecular mechanism underlying this process was explored by evaluating expression of components of the nuclear factor κB (NF-κB) signaling pathway. MaR1 substantially inhibited the mRNA and protein expression of NF-κB p65 and κB inhibitor kinase β. Collectively, these results suggest that MaR1 ameliorated splenectomy-induced transient cognitive impairment in elderly rats, and this neuroprotective mechanism may occur through regulating the NF-κB pathway to inhibit astrocyte activation.

Transient cognitive impairment in the acute phase of stroke – prevalence, risk factors and influence on long-term prognosis in population of patients with stroke (research study – part of the PROPOLIS study)

BackgroundCognitive impairment is a common complication of the acute phase of stroke, which can be transient and resolve while still in the hospital. This study evaluated the prevalence and risk factors for transient cognitive impairment and their impact on long-term prognosis in a population of acute-phase stroke patients.MethodsConsecutive patients admitted to a stroke unit with acute stroke or transient ischemic attack were screened twice for cognitive impairment using the parallel version of Montreal Cognitive Assessment: the first time between the first and third day and the second time between the fourth and seventh day of hospitalization. If the second test score increased by two or more points, transient cognitive impairment was diagnosed. Patients were scheduled for follow-up visits three and 12 months after stroke. Outcome assessment included place of discharge, current functional status, dementia, or death.ResultsFour hundred forty-seven patients were included in the study, 234 (52.35%) were diagnosed with transient cognitive impairment. Delirium was the only independent risk factor for transient cognitive impairment (OR 2.417, 95%CI 1.096–5.333, p = 0.029). In the analysis of effects on three- and twelve-month prognosis, patients with transient cognitive impairment had a lower risk of hospital or institution stay 3 months after stroke compared with patients with permanent cognitive impairment (OR 0.396, 95%CI 0.217–0.723, p = 0.003). There was no significant effect on mortality, disability or risk of dementia.ConclusionsTransient cognitive impairment, which often occurs in the acute phase of stroke, does not increase the risk of long-term complications.

Distinct Associations Between Postdischarge Cognitive Change Patterns and 1-year Outcomes in Patients Hospitalized for Heart Failure

BackgroundThe patterns of patients’ cognitive function after hospital discharge for heart failure (HF), their prognostic implication and the predictors for new-onset cognitive impairment remain unknown. Methods and ResultsWe included 2307 patients (64 ± 14 years, 36.4% female sex) hospitalized for HF from a cohort who completed cognitive testing before discharge and after 1 month. Among 1658 patients with normal cognition before discharge, 229 (13.8%) and 1429 (86.2%) had new-onset cognitive impairment and normal cognition at 1 month, respectively. Of the 649 with cognitive impairment, 315 (48.5%) and 334 (51.5%) had transient and persistent cognitive impairment, respectively. Multivariable analyses showed that, compared with normal cognition, patients with new-onset cognitive impairment had an increased risk of cardiovascular death or HF rehospitalization (hazard ratio 1.35, 95% confidence interval 1.07–1.70); patients with persistent cognitive impairment showed an increased risk, but it was not statistically significant (hazard ratio 1.17, 95% confidence interval 0.95–1.44); patients with transient cognitive impairment had a similar risk (hazard ratio 0.91, 95% confidence interval 0.73–1.13). Older age, females, lower education level, prior atherosclerotic cardiovascular diseases, lower health status, and lower Mini-Cog score before discharge predicted new-onset cognitive impairment. ConclusionsAcute HF substantially affects short-term cognition. Patients who have developed new-onset cognitive impairment have an increased risk of adverse outcomes. Monitoring cognition is necessary, particularly in high-risk patients.

Possible causes of narcosis-like symptoms in freedivers

During deep-sea freediving, many freedivers describe symptoms fairly similar to what has been related to inert gas narcosis in scuba divers. This manuscript aims to present the potential mechanisms underlying these symptoms. First, known mechanisms of narcosis are summarized while scuba diving. Then, potential underlying mechanisms involving the toxicity of gases (nitrogen, carbon dioxide and oxygen) are presented in freedivers. As the symptoms are felt during ascent, nitrogen is likely not the only gas involved. Since freedivers are frequently exposed to hypercapnic hypoxia toward the end of the dive, it is proposed that carbon dioxide and oxygen gases both play a major role. Finally, a new “hemodynamic hypothesis” based on the diving reflex is proposed in freedivers. The underlying mechanisms are undoubtedly multifactorial and therefore require further research and a new descriptive name. We propose a new term for these types of symptoms: freediving transient cognitive impairment.

Interictal discharges delay target-directed eye movements and impair attentional set-shifting in children with epilepsy.

The theory of transient cognitive impairment in epilepsy posits that lapses in attention result from ephemeral disruption of attentional circuitry by interictal events. Eye movements are intimately associated with human attention and can be monitored in real time using eye-tracking technologies. Here, we sought to characterize the associations between interictal epileptiform discharges (IEDs), gaze, and attentional behavior in children with epilepsy. Eleven consecutive children undergoing invasive monitoring with stereotactic electrodes for localization-related epilepsy performed an attentional set-shifting task while tandem intracranial electroencephalographic signals and eye-tracking data were recorded. Using an established algorithm, IEDs were detected across all intracranial electrodes on a trial-by-trial basis. Hierarchical mixed-effects modeling was performed to delineate associations between trial reaction time (RT), eye movements, and IEDs. Hierarchical mixed-effects modeling revealed that both the presence of an IED (β±SE=72.74± 24.21 ms, p= .003) and the frequency of epileptiform events (β±SE=67.54± 17.30 ms, p< .001) were associated with prolonged RT on the attentional set-shifting task. IED occurrence at the time of stimulus presentation was associated with delays in gaze initiation toward the visual targets (p= .017). The occurrence of epileptiform activity in close temporal association with stimulus presentation is associated with delays in target-directed gaze and prolonged response time, hallmarks of momentary lapses in attention. These findings provide novel insights into the mechanisms of transient impairments in children and support the use of visual tracking as a correlate of higher order attentional behavior.

Structural Brain Network Reorganization Following Anterior Callosotomy for Colloid Cysts: Connectometry and Graph Analysis Results.

Introduction:The plasticity of the neural circuits after injuries has been extensively investigated over the last decades. Transcallosal microsurgery for lesions affecting the third ventricle offers an interesting opportunity to investigate the whole-brain white matter reorganization occurring after a selective resection of the genu of the corpus callosum (CC).MethodDiffusion MRI (dMRI) data and neuropsychological testing were collected pre- and postoperatively in six patients with colloid cysts, surgically treated with a transcallosal-transgenual approach. Longitudinal connectometry analysis on dMRI data and graph analysis on structural connectivity matrix were implemented to analyze how white matter pathways and structural network topology reorganize after surgery.ResultsAlthough a significant worsening in cognitive functions (e.g., executive and memory functioning) at early postoperative, a recovery to the preoperative status was observed at 6 months. Connectometry analysis, beyond the decrease of quantitative anisotropy (QA) near the resection cavity, showed an increase of QA in the body and forceps major CC subregions, as well as in the left intra-hemispheric corticocortical associative fibers. Accordingly, a reorganization of structural network topology was observed between centrality increasing in the left hemisphere nodes together with a rise in connectivity strength among mid and posterior CC subregions and cortical nodes.ConclusionA structural reorganization of intra- and inter-hemispheric connective fibers and structural network topology were observed following the resection of the genu of the CC. Beyond the postoperative transient cognitive impairment, it could be argued anterior CC resection does not preclude neural plasticity and may subserve the long-term postoperative cognitive recovery.

Revocable attention deficit hyperactivity disorder- An eye-opener

To highlight the clinical and electroencephalographic features, treatment strategies and outcome in atypical variant of benign childhood epilepsy with centrotemporal spikes (BECTS). Subject underwent video electroencephalograph (EEG), high-resolution magnetic resonance imaging (MRI), neuropsychological evaluation and language assessment and response to medication was followed up. In addition to sodium valproate, treatment with intravenous methylprednisolone (given as monthly bolus doses) was given as the seizures remained refractory to anti-seizure medications (ASM) alone. Earlier onset, increased frequency and duration of focal seizures compared to prototype Rolandic epilepsy are cardinal features suggestive of atypical variant of BECTS. Head drop and truncal sway due to axial or axiorhizomelic atonia occurring several times per day or week was the key manifestation. When the atypical seizures commenced, one or more of the following problems can occur: hyperactivity, attention deficit, and mild cognitive or language dysfunction. Child became seizure free on a combination of intravenous methylprednisolone, with sodium valproate and his hyperactivity reversed. BECTS in children with an early age of onset, frequent and prolonged seizures and scholastic decline pari passu with seizure onset are more likely to evolve into atonic-BECTS. Carbamazepine, oxcarbazepine and some benzodiazepines may worsen these seizures. They can become seizure free with immunomodulatory therapy, namely methylprednisolone (given as monthly bolus doses) or intravenous immunoglobulin (IVIG), and have complete resolution of the transient motor and cognitive impairment. Atonic-BECTS needs to be differentiated from Lennox–Gastaut syndrome since it is potentially treatable and children recover with no sequel.

The Cognitive Sequelae of Transient Ischemic Attacks—Recent Insights and Future Directions

There is now considerable evidence that Transient Ischemic Attack (TIA) carries important sequelae beyond the risk of recurrent stroke, particularly with respect to peri-event and post-event cognitive dysfunction and subsequent cognitive decline. The occurrence of a TIA could provide an important window in understanding the relationship of early mixed vascular-neurodegenerative cognitive decline, and by virtue of their clinical relevance as a “warning” event, TIAs could also furnish the opportunity to act preventatively not only for stroke prevention but also for dementia prevention. In this review, we discuss the current state of the literature regarding the cognitive sequelae associated with TIA, reviewing important challenges in the field. In particular, we discuss definitional and methodological challenges in the study of TIA-related cognitive impairment, confounding factors in the cognitive evaluation of these patients, and provide an overview of the evidence on both transient and long-term cognitive impairment after TIA. We compile recent insights from clinical studies regarding the predictors and mediators of cognitive decline in these patients and highlight important future directions for work in this area.

The anticholinergic burden is not associated with cognitive impairments in patients treated by electroconvulsive therapy for treatment-resistant depression

Electroconvulsive therapy (ECT) is the most effective non-pharmacological treatment for treatment-resistant depression (TRD) but can expose to transient cognitive impairments. Understanding factors underlying these cognitive side effects is important. This study investigated the impact of anticholinergic treatments on cognitive performances after ECT courses for TRD in naturalistic condition. Impact of anticholinergic burden (Anticholinergic Impregnation Scale, AIS) on cognitive changes (Montreal Cognitive Assessment, MoCA) adjusted on depression level (Montgomery and Asberg Depression Scale, MADRS) was investigated in 42 patients who received an ECT course between 2017 and 2020 for unipolar or bipolar TRD. Collection of daily treatments given during ECT was carried out via the computerized traceability of treatments validated by nurses. Among the 31 treatments identified with an anticholinergic score, which represent only 38% of total treatments, the three most frequently given treatments were Lorazepam (47%), Venlafaxine (36%) and Cyamemazine (26%). Delayed recall was the most frequently impaired cognitive function after ECT courses. Using logistic regression, we found no association between the anticholinergic burden and the decrease in cognitive scores after ECT courses, adjusted on MADRS score evolution (p>0.1). Conversely, improvement in MADRS scores were correlated with improvement in attention MoCA subscores. This is a retrospective monocentric study with a moderate sample size using anticholinergic scales to calculate the anticholinergic burden without plasma dosage. Anticholinergic treatments did not seem to explain ECT-related cognitive impairments. This warrants further large prospective investigations including different measures of anticholinergic burden.

Therapeutic effects of stiripentol against ischemia-reperfusion injury in gerbils focusing on cognitive deficit, neuronal death, astrocyte damage and blood brain barrier leakage in the hippocampus.

Stiripentol is an anti-epileptic drug for the treating of refractory status epilepticus. It has been reported that stiripentol can attenuate seizure severity and reduce seizure-induced neuronal damage in animal models of epilepsy. The objective of the present study was to investigate effects of post-treatment with stiripentol on cognitive deficit and neuronal damage in the cornu ammonis 1 (CA1) region of the hippocampus proper following transient ischemia in the forebrain of gerbils. To evaluate ischemia-induced cognitive impairments, passive avoidance test and 8-arm radial maze test were performed. It was found that post-treatment with stiripentol at 20 mg/kg, but not 10 or 15 mg/kg, reduced ischemia-induced memory impairment. Transient ischemia-induced neuronal death in the CA1 region was also significantly attenuated only by 20 mg/kg stiripentol treatment after transient ischemia. In addition, 20 mg/kg stiripentol treatment significantly decreased ischemia-induced astrocyte damage and immunoglobulin G leakage. In brief, stiripentol treatment after transient ischemia ameliorated transient ischemia-induced cognitive impairment in gerbils, showing that pyramidal neurons were protected and astrocyte damage and blood brain barrier leakage were significantly attenuated in the hippocampus. Results of this study suggest stiripentol can be developed as a candidate of therapeutic drug for ischemic stroke.

Meta‐analysis finds medical cannabis has small effect in improving pain

A meta‐analysis encompassing 32 trials has found that non‐inhaled medical cannabis or cannabinoids result in small to very small improvement in symptoms among patients with chronic pain. Use of medical cannabis also results in a small increased risk of adverse effects such as transient cognitive impairment, vomiting, and drowsiness, the researchers reported. Results of the systematic review and meta‐analysis were published online Sept. 8, 2021, in BMJ.