Acute Basilar Artery Occlusion Presenting With Convulsive Movements: A Systematic Review

Background and Purpose: Convulsive seizures related to posterior circulation stroke are considered rare. However, some patients with acute basilar artery occlusion (BAO) can present with convulsive movements. Misdiagnosed as seizures may delay the reperfusion therapy for acute BAO. In this study, we have summarized the clinical features and possible mechanisms of BAO presenting with convulsive movements.Methods: We performed an Institutional Review Board-approved institutional database query from 2015 to 2020 and a literature search of the online database PubMed. Clinical data were collected and analyzed.Results: In total, 14 patients with acute BAO presented with convulsions. There were 10 men and 4 women, with a mean age of 53 (range, 23–77) years. All of these patients had different degrees of impaired consciousness (100.0%, 14/14). Convulsive movements were the initial symptoms in 78.6% (11/14) of patients. Further, 64.3% (9/14) of patients presented with paralysis or cranial nerve abnormalities, and 85.7% (12/14) of patients were treated with reperfusion therapy (thrombolysis, 35.7% [5/14]; endovascular thrombectomy, 64.3% [9/14]). The BAO etiology and mechanism were related to embolism, vessel dissections, and severe stenosis of the right vertebral artery in 57.1% (8/14), 21.4% (3/14), and 7.1% (1/14) of patients, respectively; they were undefined in 14.3% (2/14) of patients. Moreover, 42.9% (6/14) of patients had a 90-day modified Rankin Scale score of 0–2, and the mortality rate was 21.4% (3/14).Conclusions: Acute BAO, especially that related to embolism or vessel dissection, may present with convulsive movements. Acute BAO is a devastating, but treatable disease if diagnosed in time. Considering the possibility of BAO is important when dealing with patients presenting with acute-onset convulsive movements. Prompt diagnosis and reperfusion therapy may help achieve a better prognosis.

Antiseizure Effects of Fully Characterized Non-Psychoactive Cannabis sativa L. Extracts in the Repeated 6-Hz Corneal Stimulation Test

Compounds present in Cannabis sativa L. preparations have recently attracted much attention in the treatment of drug-resistant epilepsy. Here, we screened two olive oil extracts from a non-psychoactive C. sativa variety, fully characterized by high-performance liquid chromatography and gas chromatography. Particularly, hemp oils with different concentrations of terpenes were administered at the same dose of cannabidiol (25 mg/kg/day orally), 1 h before the 6-Hz corneal stimulation test (44 mA). Mice were stimulated once a day for 5 days and evaluated by video-electrocorticographic recordings and behavioral analysis. Neuronal activation was assessed by FosB/ΔFosB immunoreactivity. Both oils significantly reduced the percentage of mice experiencing convulsive seizures in comparison to olive oil-treated mice (p < 0.050; Fisher’s exact test), but only the oil enriched with terpenes (K2) significantly accelerated full recovery from the seizure. These effects occurred in the presence of reduced power of delta rhythm, and, instead, increased power of theta rhythm, along with a lower FosB/ΔFosB expression in the subiculum (p < 0.050; Duncan’s method). The overall findings suggest that both cannabinoids and terpenes in oil extracts should be considered as potential therapeutic agents against epileptic seizures and epilepsy.

Dementia with non-convulsive seizures: a case report

Non-convulsive seizures (NCSs) are highly treatable, but appropriate management is usually delayed because of inaccurate diagnoses as a result of variable clinical presentations, including an altered mental state. It is difficult to detect NCSs in patients with dementia. We report a case of NCS superimposed on cognitive decline caused by Alzheimer’s dementia. The patient’s history was carefully recorded. An electroencephalogram was recorded with sphenoidal electrodes, which showed epileptiform discharges in the right mesial temporal lobe and focal, sharply contoured, slow wave activity in the left fronto-temporal area, suggesting an epileptic origin contributing to the patient’s cognitive decline. After treatment with antiepileptic drugs, the patient’s cognitive functioning gradually improved. An accurate diagnosis of NCS relies on performing a detailed inventory of a patient’s history, thorough physical and neurological examinations, and electroencephalogram recordings. In patients with cognitive decline, testing for NCS should always be included in the differential diagnosis of cognitive impairment, even in the case of dementia. Early administration of antiepileptic drug therapy is the mainstay treatment for reversing the condition and for preventing prolonged insults from neurological sequelae.

Cerebral and systemic hemodynamic effect of recurring seizures

The increase in neuronal activity induced by a single seizure is supported by a rise in the cerebral blood flow and tissue oxygenation, a mechanism called neurovascular coupling (NVC). Whether cerebral and systemic hemodynamics are able to match neuronal activity during recurring seizures is unclear, as data from rodent models are at odds with human studies. In order to clarify this issue, we used an invasive brain and systemic monitoring to study the effects of chemically induced non-convulsive seizures in sheep. Despite an increase in neuronal activity as seizures repeat (Spearman’s ρ coefficient 0.31, P < 0.001), ictal variations of cerebral blood flow remained stable while it progressively increased in the inter-ictal intervals (ρ = 0.06, P = 0.44 and ρ = 0.22; P = 0.008). We also observed a progressive reduction in the inter-ictal brain tissue oxygenation (ρ = − 0.18; P = 0.04), suggesting that NVC was unable to compensate for the metabolic demand of these closely repeating seizures. At the systemic level, there was a progressive reduction in blood pressure and a progressive rise in cardiac output (ρ = − 0.22; P = 0.01 and ρ = 0.22; P = 0.01, respectively), suggesting seizure-induced autonomic dysfunction.

Reducing Sudden Unexpected Death in Epilepsy: Considering Risk Factors, Pathophysiology and Strategies

Purpose of Review Sudden Unexpected Death in Epilepsy (SUDEP) is the commonest cause of epilepsy-related premature mortality in people with chronic epilepsy. It is the most devastating epilepsy outcome. We describe and discuss risk factors and possible pathophysiological mechanisms to elucidate possible preventative strategies to avert SUDEP. Recent Findings Sudden death accounts for a significant proportion of premature mortality in people with epilepsy compared to the general population. Unmodifiable risk factors include a history of neurologic insult, younger age of seizure-onset, longer epilepsy duration, a history of convulsions, symptomatic epilepsy, intellectual disability, and non-ambulatory status. Modifiable risk factors include the presence of convulsive seizures, increased seizure frequency, timely and appropriate use of antiseizure medications, polytherapy, alcoholism, and supervision while sleeping. Pathophysiology is unclear, but several possible mechanisms such as direct alteration of cardiorespiratory function, pulmonary impairment, electrocerebral shutdown, adenosine dysfunction, and genetic susceptibility suggested. Summary Methods to prevent SUDEP include increasing awareness of SUDEP, augmenting knowledge of unmodifiable risk factors, obtaining full seizure remission, addressing lifestyle factors such as supervision and prone positioning, and enacting protocols to increase the detection of and intervention for SUDEP. Further studies are required to characterize precisely and comprehensively SUDEP risk factors and pathophysiological drivers and develop evidence-based algorithms to minimize SUDEP in people with epilepsy.

Differential Impact of Severity and Duration of Status Epilepticus, Medical Countermeasures, and a Disease-Modifier, Saracatinib, on Brain Regions in the Rat Diisopropylfluorophosphate Model

Acute organophosphate (OP) toxicity poses a significant threat to both military and civilian personnel as it can lead to a variety of cholinergic symptoms including the development of status epilepticus (SE). Depending on its severity, SE can lead to a spectrum of neurological changes including neuroinflammation and neurodegeneration. In this study, we determined the impact of SE severity and duration on disease promoting parameters such as gliosis and neurodegeneration and the efficacy of a disease modifier, saracatinib (AZD0530), a Src/Fyn tyrosine kinase inhibitor. Animals were exposed to 4 mg/kg diisopropylfluorophosphate (DFP, s.c.) followed by medical countermeasures. We had five experimental groups: controls (no DFP), animals with no continuous convulsive seizures (CS), animals with ∼20-min continuous CS, 31-60-min continuous CS, and &gt; 60-min continuous CS. These groups were then assessed for astrogliosis, microgliosis, and neurodegeneration 8 days after DFP exposure. The 31-60-min and &gt; 60-min groups, but not ∼20-min group, had significantly upregulated gliosis and neurodegeneration in the hippocampus compared to controls. In the piriform cortex and amygdala, however, all three continuous CS groups had significant upregulation in both gliosis and neurodegeneration. In a separate cohort of animals that had ∼20 and &gt; 60-min of continuous CS, we administered saracatinib for 7 days beginning three hours after DFP. There was bodyweight loss and mortality irrespective of the initial SE severity and duration. However, in survived animals, saracatinib prevented spontaneous recurrent seizures (SRS) during the first week in both severity groups. In the ∼20-min CS group, compared to the vehicle, saracatinib significantly reduced neurodegeneration in the piriform cortex and amygdala. There were no significant differences in the measured parameters between the naïve control and saracatinib on its own (without DFP) groups. Overall, this study demonstrates the differential effects of the initial SE severity and duration on the localization of gliosis and neurodegeneration. We have also demonstrated the disease-modifying potential of saracatinib. However, its’ dosing regimen should be optimized based on initial severity and duration of CS during SE to maximize therapeutic effects and minimize toxicity in the DFP model as well as in other OP models such as soman.

The cerebellum initiates severe tonic-clonic seizures by altering neuronal activity in the ventral posteromedial nucleus (VPM) of the thalamus

Thalamo-cortical networks are central to seizures, yet it's unclear how these circuits initiate the seizures. Here, we test the hypothesis that a facial region of the thalamus, the VPM, is a source of convulsive, tonic-clonic seizures. We devised an in vivo optogenetic mouse model to elicit tonic-clonic seizures by driving convergent input to the VPM. With viral tracing, we show dense cerebellar and cerebral cortical afferent input to the VPM. Lidocaine microinfusions into the cerebellar nuclei selectively block seizure initiation. We perform single-unit electrophysiology recordings during awake, convulsive seizures to define the local activity of thalamic neurons before, during, and after seizure onset. We find highly dynamic activity with biphasic properties, raising the possibility that heterogenous activity patterns promote seizures. These data reveal the VPM as a source of tonic-clonic seizures, with cerebellar input providing the predominant signals.