Emergency medical dispatchers’ ability to identify large vessel occlusion stroke during emergency calls

Background In acute ischemic stroke, conjugated eye deviation (CED) is an evident sign of cortical ischemia and large vessel occlusion (LVO). We aimed to determine if an emergency dispatcher can recognise LVO stroke during an emergency call by asking the caller a binary question regarding whether the patient’s head or gaze is away from the side of the hemiparesis or not. Further, we investigated if the paramedics can confirm this sign at the scene. In the group of positive CED answers to the emergency dispatcher, we investigated what diagnoses these patients received at the emergency department (ED). Among all patients brought to ED and subsequently treated with mechanical thrombectomy (MT) we tracked the proportion of patients with a positive CED answer during the emergency call. Methods We collected data on all stroke dispatches in the city of Tampere, Finland, from 13 February 2019 to 31 October 2020. We then reviewed all patient records from cases where the dispatcher had marked ‘yes’ to the question regarding patient CED in the computer-aided emergency response system. We also viewed all emergency department admissions to see how many patients in total were treated with MT during the period studied. Results Out of 1913 dispatches, we found 81 cases (4%) in which the caller had verified CED during the emergency call. Twenty-four of these patients were diagnosed with acute ischemic stroke. Paramedics confirmed CED in only 9 (11%) of these 81 patients. Two patients with positive CED answers during the emergency call and 19 other patients brought to the emergency department were treated with MT. Conclusion A small minority of stroke dispatches include a positive answer to the CED question but paramedics rarely confirm the emergency medical dispatcher’s suspicion of CED as a sign of LVO. Few patients in need of MT can be found this way. Stroke dispatch protocol with a CED question needs intensive implementation.

Association of Cerebral Ischemia With Corneal Nerve Loss and Brain Atrophy in MCI and Dementia

IntroductionThis study assessed the association of cerebral ischemia with neurodegeneration in mild cognitive impairment (MCI) and dementia.MethodsSubjects with MCI, dementia and controls underwent assessment of cognitive function, severity of brain ischemia, MRI brain volumetry and corneal confocal microscopy.ResultsOf 63 subjects with MCI (n = 44) and dementia (n = 19), 11 had no ischemia, 32 had subcortical ischemia and 20 had both subcortical and cortical ischemia. Brain volume and corneal nerve measures were comparable between subjects with subcortical ischemia and no ischemia. However, subjects with subcortical and cortical ischemia had a lower hippocampal volume (P < 0.01), corneal nerve fiber length (P < 0.05) and larger ventricular volume (P < 0.05) compared to those with subcortical ischemia and lower corneal nerve fiber density (P < 0.05) compared to those without ischemia.DiscussionCerebral ischemia was associated with cognitive impairment, brain atrophy and corneal nerve loss in MCI and dementia.

ACUTE STROKE-ELICITED EPILEPSIA PARTIALIS CONTINUA RESPONSIVE TO LEVETIRACETAM

We present an interesting case of epilepsia partialis continua (EPC) responsive to levetiracetam treatment as an acute manifestation of cortical ischemia. A 54 -year-old, right-handed man presented with Epilepsia partialis continua (EPC) ensued as an acute complication of an acute infarct in high parietal region, with clonic jerks of left upper limb, was admitted to our department of general medicine. When the standard treatment with benzodiazepines and phenytoin failed, levetiracetam was started. This completely abolished seizure activity, bringing an improvement of the patient's neurological condition EPC may be an acute complication of cortical ischemic damage and levetiracetam, is an interesting alternative for the treatment of this poorly studied condition.

Taurine Promotes Axonal Sprouting Through Mitochondrial Improvement in Stroke

BackgroundBrain plasticity including axonal sprouting has been recognized in restoring motor function in ischemic stroke. Mitochondrion plays a crucial role in determining axonal sprouting in ischemic injury. Taurine (TAU) could protect brain against experimental stroke as one of the richest amino acids. However, the role of TAU on axonal sprouting and the specific potential mechanism on mitochondria of stroke were unclear. MethodsFocal cerebral cortical ischemia in C57BL/6 mice was preceded. Motor function was assayed by the Rota-Rod test on D7, D14, and D28 after stroke. Axonal sprouting was detected using immunocytochemistry with biotinylated dextran amine (BDA). The expressions of mitochondrial DNA (mtDNA), Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PCG-1a) and Transcription factor A of mitochondria (TFAM) were measured by RT-qPCR. ResultsTAU treatment significantly recovered the motor function of focal cerebral cortical ischemic mice. And TAU promoted axonal sprouting. It was also observed that TAU enhanced mtDNA content, increased the levels of Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PCG-1a) and Transcription factor A of mitochondria (TFAM). ConclusionsCollectively, the data illustrated that TAU exerted a promoting influence on axonal sprouting, through mitochondrial improvement in cerebral ischemic stroke.

Secondary Degeneration of White Matter After Focal Sensorimotor Cortical Ischemic Stroke in Rats

Ischemic lesions could lead to secondary degeneration in remote regions of the brain. However, the spatial distribution of secondary degeneration along with its role in functional deficits is not well understood. In this study, we explored the spatial and connectivity properties of white matter (WM) secondary degeneration in a focal unilateral sensorimotor cortical ischemia rat model, using advanced microstructure imaging on a 14 T MRI system. Significant axonal degeneration was observed in the ipsilateral external capsule and even remote regions including the contralesional external capsule and corpus callosum. Further fiber tractography analysis revealed that only fibers having direct axonal connections with the primary lesion exhibited a significant degeneration. These results suggest that focal ischemic lesions may induce remote WM degeneration, but limited to fibers tied to the primary lesion. These “direct” fibers mainly represent perilesional, interhemispheric, and subcortical axonal connections. At last, we found that primary lesion volume might be the determining factor of motor function deficits.

Electrical stimulation of the lateral cerebellar nucleus promotes neurogenesis in rats after motor cortical ischemia

Deep brain stimulation (DBS) has been tentatively explored to promote motor recovery after stroke. Stroke could transiently activate endogenous self-repair processes, including neurogenesis in the subventricular zone (SVZ). In this regard, it is of considerable clinical interest to study whether DBS of the lateral cerebellar nucleus (LCN) could promote neurogenesis in the SVZ for functional recovery after stroke. In the present study, rats were trained on the pasta matrix reaching task and the ladder rung walking task before surgery. And then an electrode was implanted in the LCN following cortical ischemia induced by endothelin-1 injection. After 1 week of recovery, LCN DBS coupled with motor training for two weeks promoted motor function recovery, and reduced the infarct volumes post-ischemia. LCN DBS augmented poststroke neurogenetic responses, characterized by proliferation of neural progenitor cells (NPCs) and neuroblasts in the SVZ and subsequent differentiation into neurons in the ischemic penumbra at 21 days poststroke. DBS with the same stimulus parameters at 1 month after ischemia could also increase nascent neuroblasts in the SVZ and newly matured neurons in the perilesional cortex at 42 days poststroke. These results suggest that LCN DBS promotes endogenous neurogenesis for neurorestoration after cortical ischemia.

Comparative Enhancement of Motor Function and BDNF Expression Following Different Brain Stimulation Approaches in an Animal Model of Ischemic Stroke

Background Combinatory intervention such as high-frequency (50-100 Hz) excitatory cortical stimulation (ECS) given concurrently with motor rehabilitative training (RT) improves forelimb function, except in severely impaired animals after stroke. Clinical studies suggest that low-frequency (≤1 Hz) inhibitory cortical stimulation (ICS) may provide an alternative approach to enhance recovery. Currently, the molecular mediators of CS-induced behavioral effects are unknown. Brain-derived neurotrophic factor (BDNF) has been associated with improved recovery and neural remodeling after stroke and thus may be involved in CS-induced behavioral recovery. Objective To investigate whether inhibitory stimulation during RT improves functional recovery of severely impaired rats, following focal cortical ischemia and if this recovery alters BDNF expression (study 1) and depends on BDNF binding to TrkB receptors (study 2). Methods Rats underwent ECS + RT, ICS + RT, or noCS + RT treatment daily for 3 weeks following a unilateral ischemic lesion to the motor cortex. Electrode placement for stimulation was either placed ipsilateral (ECS) or contralateral (ICS) to the lesion. After treatment, BDNF expression was measured in cortical tissue samples (study 1). In study 2, the TrkB inhibitor, ANA-12, was injected prior to treatment daily for 21 days. Results ICS + RT treatment significantly improved impaired forelimb recovery compared with ECS + RT and noCS + RT treatment. Conclusion ICS given concurrently with rehabilitation improves motor recovery in severely impaired animals, and alters cortical BDNF expression; nevertheless, ICS-mediated improvements are not dependent on BDNF binding to TrkB. Conversely, inhibition of TrkB receptors does disrupt motor recovery in ECS + RT treated animals.

Prolonged deficit of gamma oscillations in the peri-infarct cortex of mice after stroke

Days and weeks after an ischemic stroke, the peri-infarct area adjacent to the necrotic tissue exhibits very intense synaptic reorganization aimed at regaining lost functions. In order to enhance functional recovery, it is important to understand the mechanisms supporting neural repair and neuroplasticity in the cortex surrounding the lesion. Brain oscillations of the local field potential (LFP) are rhythmic fluctuations of neuronal excitability aimed at synchronizing neuronal activity to organize information processing and plasticity. Although the oscillatory activity of the brain has been probed after stroke in both animals and humans using electroencephalography (EEG), the latter is ineffective to precisely map the oscillatory changes in the peri-infarct zone where synaptic plasticity potential is high. Here, we worked on the hypothesis that brain oscillatory system is altered in the surviving peri-infarct cortex, which may slow down functional repair and reduce the capacity to recovery. In order to document the relevance of this hypothesis, oscillatory power was measured at various distances from the necrotic core at 7 and 21 days after a permanent cortical ischemia induced in mice. Delta and theta oscillations remained at a normal power in the peri-infarct cortex, in contrast to gamma oscillations that displayed a rapid decrease, the closer we get to the lesion core. A broadband increase of power was also observed in the homotopic contralateral sites. Thus, the proximal peri-infarct cortex could become a target of therapeutic interventions aimed at correcting the oscillatory regimen. These results argue for the usefulness of therapeutic intervention aimed at boosting gamma oscillations in order to improve post-stroke functional recovery.