Progressive Supranuclear Palsy: Subcortical Tau Depositions Are Associated with Cortical Perfusion in Frontal and Limbic Regions.

 In progressive supranuclear palsy (PSP), subcortical tau and cortical perfusion can be assessed using the tracer [18F]PI-2620. We investigated if subcortical tau (globus pallidus internus, dentate nucleus) and frontal/limbic perfusion correlate in a cohort of 32 PSP patients. Tau in subcortical regions showed significant negative correlation with perfusion in limbic cortex. Perfusion in frontal regions was negatively associated with tau in both subcortical regions, but the significance threshold was only passed for the dentate nucleus. A reason could be a diaschisis-like phenomenon; that is, subcortical tau could lead to reduced connectivity to frontal regions and, thereby, to decreased perfusion.

In a study of 32 patients with progressive supranuclear palsy (PSP), we used a molecular imaging tracer called [18F]PI-2620 to measure two things: the presence of a protein called tau in deep brain areas (specifically, the globus pallidus internus and dentate nucleus) and the function of the brain's cortex by assessing blood flow (perfusion). We found that higher amounts of tau in these deep brain areas were associated with reduced blood flow in the limbic cortex, which is involved in emotion regulation. Also, the frontal areas of the brain showed reduced blood flow related to tau in these deep brain regions. However, this connection was statistically significant only for the dentate nucleus. This study suggests that the buildup of tau protein in deeper brain areas can disrupt function in parts of the brain's cortex, highlighting the damaging role of tau in PSP.

Global Aphasia Secondary to Bilateral Thalamic Hyperintensities Post-cardiac Arrest.

Thalamic aphasia is thought to occur secondary to disruptions in the cortico-subcortical connections. Although rare, thalamic aphasia is a well-known phenomenon that usually presents with primarily lexical-semantic deficits with preservation of comprehension and repetition. Global aphasia secondary to thalamic injury is extremely rare, with only a few case reports of patients with left thalamic hemorrhages. The prognosis for thalamic aphasia is generally good, with most patients showing little to no symptoms after days or weeks. However, global thalamic aphasia carries a more guarded prognosis with limited recovery months after injury. Here, we report a case of global thalamic aphasia secondary to bilateral thalamic damage post-cardiac arrest.

Crossed cerebellar Diaschisis in mesial temporal sclerosis: a rare clinical entity.

Crossed cerebellar diaschisis (CCD) is a phenomenon of functional diaschisis that occurs after damage to the cerebral hemisphere and results in decreased activity of the cerebellum outside the primary focus. In this case report, we present the case of a patient admitted for seizures who was diagnosed with CCD due to Mesial temporal sclerosis (MTS). This event is generally observed in ischemic stroke cases and can occur epileptic seizure disorders. However, association of CCD with MTS is very rare. This article provides a comprehensive overview of CCD and related MRI findings to better understand their pathophysiology, clinical implications, and potential therapeutic approaches. The article highlights the importance of MRI in CCD detection and monitoring and discusses its usefulness in different clinical scenarios.

Metabolic Diaschisis in Mild Traumatic Brain Injury.

Neurophysiological diaschisis presents in traumatic brain injury (TBI) as functional impairment distant to the lesion site caused by axonal neuroexcitation and deafferentation. Diaschisis studies in TBI models have evaluated acute phase functional and microstructural changes. Here, in vivo biochemical changes and cerebral blood flow (CBF) dynamics following TBI are studied with magnetic resonance. Behavioral assessments, magnetic resonance spectroscopy (MRS), and CBF measurements on rats followed cortical impact TBI. Data were acquired pre-TBI and 1-3 h, 2-days, 7-days, and 14-days post-TBI. MRS was performed on the ipsilateral and contralateral sides in the cortex, striatum, and thalamus. Metabolites measured by MRS included N-acetyl aspartate (NAA), aspartate (Asp), lactate (Lac), glutathione (GSH), and glutamate (Glu). Lesion volume expanded for 2 days post-TBI and then decreased. Ipsilateral CBF dropped acutely versus baseline on both sides (-62% ipsilateral, -48% contralateral, p < 0.05) but then recovered in cortex, with similar changes in ipsilateral striatum. Metabolic changes versus baseline included increased Asp (+640% by Day 7 post-TBI, p < 0.05) and Lac (+140% on Day 2 post-TBI, p < 0.05) in ipsilateral cortex, while GSH (-67% acutely, p < 0.05) and NAA decreased (-50% on Day 2, p < 0.05). In contralateral cortex Lac decreased (-73% acutely, p < 0.05). Analysis of variance showed significance for Side (p < 0.05), Time after TBI (p < 0.05), and interactions (p < 0.005) for Asp, GSH, Lac, and NAA. Transient decreases of GSH (-30%, p < 0.05, acutely) and NAA (-23% on Day 2, p < 0.05) occurred in ipsilateral striatum with reduced GSH (-42%, p < 0.005, acutely) in the contralateral striatum. GSH was decreased in ipsilateral thalamus (-59% ipsilateral on Day 2, p < 0.05). Delayed increases of total choline were seen in the contralateral thalamus were noted as well (+21% on Day 7 post-TBI, p < 0.05). Both CBF and neurometabolite concentration changes occurred remotely from the TBI site, both ipsilaterally and contralaterally. Decreased Lac levels on the contralateral cortex following TBI may be indicative of reduced anaerobic metabolism during the acute phase. The timing and locations of the changes suggest excitatory and inhibitory signaling processes are affecting post-TBI metabolic fluctuations.

Fronto-Cerebellar Diaschisis and Cognitive Dysfunction after Pontine Stroke: A Case Series and Systematic Review.

It is well known that cortical damage may affect cognitive functions, whereas subcortical damage, especially brainstem stroke, would be far less likely to cause cognitive decline, resulting in this condition being overlooked. Few studies have focused on cognitive dysfunction after a pontine stroke. Here, we begin with describing our nine new case reports of in-depth neuropsychological findings from patients with pontine stroke. The dominant domain of cognitive dysfunction was commonly characterized by executive dysfunction, almost in line with previous studies. The severity was relatively mild. We give an overview of the available literature on cognitive decline following a pontine stroke. This is followed by discussions regarding the prognosis of the cognitive disabilities. Based on previous neuroimaging findings, we would like to get to the core of the neuropathology underlying the cognitive declines in the context of "diaschisis", a phenomenon of a broad range of brain dysfunctions remote from the local lesions. Specifically, our unique paper, with two modalities of neuroimaging techniques, may help us better understand the pathology. SPECT scans yield evidence of frontal and thalamic hyper-perfusion and cerebellar hypo-perfusion in patients with pontine stroke. Functional near-infrared spectroscopy, when focusing on the supplementary motor area (SMA) as one of the hyper-perfusion areas, exhibits that SMA responses may be subject to the severity of cognitive decline due to a pontine stroke and would also be related to the recovery. Finally, we posit that cognitive decline due to pontine stroke could be explained by the failure of hierarchical cognitive processing in the fronto-ponto-cerebellar-thalamic loop.

Reduced cerebral blood flow and cognitive dysfunction following isolated cerebellar infarction: two case reports.

Cognitive impairment in focal cerebellar disorders has been widely recognized and is described as cerebellar cognitive affective syndrome (CCAS). However, the relationship between CCAS and crossed cerebello-cerebral diaschisis (CCD) has rarely been discussed. The present report describes the uncommon phenomenon of CCD in two cases with isolated cerebellar infarction, and discuss its contribution to cognitive impairment. Cognitive performance was examined using the CCAS scale and a battery of neuropsychological assessments. Moreover, the relative distribution of cerebral and cerebellar blood flow was measured using three-dimensional arterial spin labeling imaging. Case 1 showed deficits in general cognition and had impaired language, episodic memory, and executive function. Case 2 showed deficits in general cognition at baseline, and cognitive deterioration of visuospatial abilities, language, episodic memory, and executive function was observed at the 3-month follow-up. Both cases met the diagnosis criteria of CCAS. Reduced cerebral blood flow was observed in the cerebral hemisphere contralateral to the cerebellar infarction at baseline in Case 1, and at the 3-month follow-up in Case 2. The present report describes cognitive decline after isolated cerebellar infarction in combination with contralateral cerebral hypoperfusion, as measured using quantitative arterial spin labeling. One possible mechanism involves the functional depression of cerebello-cerebral pathways.

Effects of brain atrophy and altered functional connectivity on poststroke cognitive impairment.

BACKGROUND AND PURPOSE: Brain atrophy and disrupted functional connectivity are often present in patients with poststroke cognitive impairment (PSCI). This study aimed to explore the relationship between remote brain atrophy, connectional diaschisis and cognitive impairment in ischemic stroke patients to provide valuable information about the mechanisms underlying cognitive function recovery. METHODS: Forty first-time stroke patients with basal ganglia infarcts and twenty-nine age-matched healthy people were enrolled. All participants underwent T1-weighted and functional MRI scans, comprehensive cognitive function assessments at baseline, and 3-month follow-up. Brain volumes were calculated, and the atrophic regions were regarded as regions of interest in seed-based functional connectivity analyses. Pearson correlation analysis was used to explore the relationships among cognitive performance, brain atrophy, and functional connectivity alterations. RESULTS: Compared with healthy participants, stroke patients had worse cognitive performance at baseline and the 3-month follow-up. Worse cognitive performance was associated with smaller bilateral thalamus, left hippocampus, and left amygdala volumes, as well as lower functional connectivity between the left thalamus and the left medial superior frontal gyrus, between the right thalamus and the left median cingulate and paracingulate gyri, between the right hippocampus and the left medial superior frontal gyrus, and between the left amygdala and the right dorsolateral superior frontal gyrus. CONCLUSIONS: In patients with basal ganglia infarction, connectional diaschisis between remote brain atrophy and the prefrontal lobe plays a significant role in PSCI. This finding provides new scientific evidence for understanding the mechanisms of PSCI and indicates that the prefrontal lobe may be a target to improve cognitive function after stroke.

Ataxic hemiparesis: a narrative review for clinical practice in rehabilitation.

BACKGROUND: Ataxic hemiparesis (AH) is a well-recognized clinical lacunar stroke syndrome, characterized by paresis with ataxia on the same side of the body. It affects patients with stroke involving the basal ganglia, pons, internal capsule, corona radiata, and thalamus. In the past, lacunar syndrome denotes good functional recovery with low mortality and morbidity rate. However, recent evidence suggests AH has an association with more debilitating outcomes in the long term. OBJECTIVE: To provide a comprehensive narrative review of published literatures on the topics related with AH and update clinical practice including rehabilitation. METHODS: Literature review was performed by using the keywords "Subcortical Ataxia," "Lacunar Stroke," "Diaschisis", and "Ataxic Hemiparesis" on PubMed and Google Scholar Engines from 1978 to 2022. All papers published in English were reviewed and manual search of references from retrieved literature was performed for other relevant articles. RESULTS: A comprehensive review was carried out on the following topics: neuroanatomical localization, pathogenesis, clinical features and clinical assessment scales, pharmacological and non-pharmacological modalities for ataxia treatment, prognosis, and outcome. CONCLUSION: AH imposes significant challenges on stroke survivors when it comes to remediation of balance and coordination. It is associated with increased risk of mortality, stroke recurrence, and dementia. Though application of the concept of neuroplasticity and the utilization of repetitive transcranial magnetic stimulation have shown early promising results, further research is needed to establish the practice guidelines for rehabilitation of patients with AH.

Functional ultrasound imaging of stroke in awake rats.

Anesthesia is a major confounding factor in preclinical stroke research as stroke rarely occurs in sedated patients. Moreover, anesthesia affects both brain functions and the stroke outcome acting as neurotoxic or protective agents. So far, no approaches were well suited to induce stroke while imaging hemodynamics along with simultaneous large-scale recording of brain functions in awake animals. For this reason, the first critical hours following the stroke insult and associated functional alteration remain poorly understood. Here, we present a strategy to investigate both stroke hemodynamics and stroke-induced functional alterations without the confounding effect of anesthesia, i.e., under awake condition. Functional ultrasound (fUS) imaging was used to continuously monitor variations in cerebral blood volume (CBV) in +65 brain regions/hemispheres for up to 3 hr after stroke onset. The focal cortical ischemia was induced using a chemo-thrombotic agent suited for permanent middle cerebral artery occlusion in awake rats and followed by ipsi- and contralesional whiskers stimulation to investigate on the dynamic of the thalamocortical functions. Early (0-3 hr) and delayed (day 5) fUS recording enabled to characterize the features of the ischemia (location, CBV loss), spreading depolarizations (occurrence, amplitude) and functional alteration of the somatosensory thalamocortical circuits. Post-stroke thalamocortical functions were affected at both early and later time points (0-3 hr and 5 days) after stroke. Overall, our procedure facilitates early, continuous, and chronic assessments of hemodynamics and cerebral functions. When integrated with stroke studies or other pathological analyses, this approach seeks to enhance our comprehension of physiopathologies towards the development of pertinent therapeutic interventions.

Associations of lesion location, structural disconnection, and functional diaschisis with depressive symptoms post stroke.

Introduction: Post-stroke depressive symptoms (PSDS) are common and relevant for patient outcome, but their complex pathophysiology is ill understood. It likely involves social, psychological and biological factors. Lesion location is a readily available information in stroke patients, but it is unclear if the neurobiological substrates of PSDS are spatially localized. Building on previous analyses, we sought to determine if PSDS are associated with specific lesion locations, structural disconnection and/or localized functional diaschisis. Methods: In a prospective observational study, we examined 270 patients with first-ever stroke with the Hospital Anxiety and Depression Scale (HADS) around 6 months post-stroke. Based on individual lesion locations and the depression subscale of the HADS we performed support vector regression lesion-symptom mapping, structural-disconnection-symptom mapping and functional lesion network-symptom-mapping, in a reanalysis of this previously published cohort to infer structure-function relationships. Results: We found that depressive symptoms were associated with (i) lesions in the right insula, right putamen, inferior frontal gyrus and right amygdala and (ii) structural disconnection in the right temporal lobe. In contrast, we found no association with localized functional diaschisis. In addition, we were unable to confirm a previously described association between depressive symptom load and a network damage score derived from functional disconnection maps. Discussion: Based on our results, and other recent lesion studies, we see growing evidence for a prominent role of right frontostriatal brain circuits in PSDS.

Application study of DTI combined with ASL in the crossed cerebellar diaschisis after subacute cerebral hemorrhage.

PURPOSE: To study the value of 3.0T magnetic resonance imaging with diffusion tensor imaging (DTI) and 3D-arterial spin labeling (ASL) perfusion imaging in the diagnosis of the crossed cerebellar diaschisis (CCD) after the unilateral supratentorial subacute cerebral hemorrhage. METHODS: Fifty-eight patients with the unilateral supratentorial subacute cerebral hemorrhage who underwent diffusion tensor imaging (DTI), 3D-arterial spin labeling (ASL), and conventional magnetic resonance imaging (MRI) scanning were enrolled. Cerebral blood flow (CBF) values of the perihematomal edema (PHE) and bilateral cerebellar hemisphere were measured on ASL mapping, and the fractional anisotropy (FA) and mean diffusivity (MD) values of the bilateral cortical, pontine, and middle cerebellar peduncle (MCP) were measured on DTI mapping. RESULTS: In the CCD(+) group, FA values of the cerebral cortex and pontine ipsilateral to the lesion were statistically reduced compared to the contralateral side (P < 0.05), and the FA and MD values of the middle cerebellar peduncle (MCP) contralateral to the lesion were statistically reduced compared to the ipsilateral side (P < 0.05). Positive correlation was detected between the CBF values of the perihematomal edema (PHE) and the CBF values of cerebellar hemispheres (r = 0.642, P < 0.05), whereas the CBF values of PHE had a significantly high positive correlation with the FA in the contralateral MCP (r = 0.854, P < 0.05). CBF values in the contralateral cerebellar hemisphere correlated with FA (r = 0.466, P < 0.05) and MD values (r = 0.718, P < 0.05) in the contralateral MCP. CONCLUSION: Hemodynamic alterations of PHE and cortical-ponts-cerebellum (CPC) fibrous pathway damage are associated with the development of CCD; DTI technique can assess the degree of CPC fiber pathway injury at an early stage.

Cortical Ribbon and Crossed Cerebellar Diaschisis in Subclinical Status Epilepticus: A Case Report.

Cortical ribbon is an uncommon finding that is characteristic of Creutzfeldt-Jakob disease but has a broad differential diagnosis. On the other hand, crossed cerebellar diaschisis is also an uncommon finding in brain magnetic resonance imaging (MRI). Herein, we are describing an 88-year-old male patient with dementia, ambulatory dysfunction, and frequent falls who presented with acute on chronic right-sided subdural hemorrhage that was discovered after an episode of seizure. Although the subdural hemorrhage was associated with mild midline shift and lateral ventricle compression, no surgical drainage was attempted, and only middle meningeal artery embolization was pursued. Lack of further evidence of seizure and clinical stability prompted discharge. However, he was soon re-admitted for left-sided focal seizure that failed multiple antiepileptic medications and evolved into status epilepticus. MRI brain showed evidence of both cortical ribbon as well as crossed cerebellar diaschisis. No evidence of infection or autoimmune inflammation was found with continuous mental status deterioration. Code status was changed by his family, and comfort care was pursued. This case is not only interesting because of the rarity of both cortical ribbon and crossed cerebellar diaschisis, but this case helps to remind clinicians of the relationship between these findings and seizure/status epilepticus.

Syntactic Impairment Associated with Hypoperfusion in the Left Middle and Inferior Frontal Gyri after Right Cerebellar Hemorrhage.

Cerebellar injuries can cause syntax impairments. Cortical dysfunction due to cerebello-cerebral diaschisis is assumed to play a role in this phenomenon. Functional magnetic resonance imaging studies have repeatedly shown the activation of Broca's area in response to syntactic tasks. However, there have been no reports of selective syntax impairment and hypoperfusion restricted to this area after cerebellar injury. We herein report a patient with right cerebellar hemorrhage that led to marked syntax impairment along with severe hypoperfusion confined to the Brodmann area (BA) 45 (anterior part of Broca's area) and BA46.

Rapidly progressive cerebral atrophy following a posterior cranial fossa stroke: Assessment with semiautomatic CT volumetry.

BACKGROUND: The effect of posterior cranial fossa stroke on changes in cerebral volume is not known. We assessed cerebral volume changes in patients with acute posterior fossa stroke using CT scans, and looked for risk factors for cerebral atrophy. METHODS: Patients with cerebellar or brainstem hemorrhage/infarction admitted to the ICU, and who underwent at least two subsequent inpatient head CT scans during hospitalization were included (n = 60). The cerebral volume was estimated using an automatic segmentation method. Patients with cerebral volume reduction > 0% from the first to the last scan were defined as the "cerebral atrophy group (n = 47)," and those with ≤ 0% were defined as the "no cerebral atrophy group (n = 13)." RESULTS: The cerebral atrophy group showed a significant decrease in cerebral volume (first CT scan: 0.974 ± 0.109 L vs. last CT scan: 0.927 ± 0.104 L, P < 0.001). The mean percentage change in cerebral volume between CT scans in the cerebral atrophy group was -4.7%, equivalent to a cerebral volume of 46.8 cm3, over a median of 17 days. The proportions of cases with a history of hypertension, diabetes mellitus, and median time on mechanical ventilation were significantly higher in the cerebral atrophy group than in the no cerebral atrophy group. CONCLUSIONS: Many ICU patients with posterior cranial fossa stroke showed signs of cerebral atrophy. Those with rapidly progressive cerebral atrophy were more likely to have a history of hypertension or diabetes mellitus and required prolonged ventilation.

Effects of intravascular photobiomodulation on cognitive impairment and crossed cerebellar diaschisis in patients with traumatic brain injury: a longitudinal study.

The association between intravascular photobiomodulation (iPBM) and crossed cerebellar diaschisis (CCD) and cognitive dysfunction in patients with traumatic brain injury (TBI) remains unknown. We postulate that iPBM might enable greater neurologic improvements. The objective of this study was to evaluate the clinical impact of iPBM on the prognosis of patients with TBI. In this longitudinal study, patients who were diagnosed with TBI were recruited. CCD was identified from brain perfusion images when the uptake difference of both cerebella was > 20%. Thus, two groups were identified: CCD( +) and CCD( -). All patients received general traditional physical therapy and three courses of iPBM (helium-neon laser illuminator, 632.8 nm). Treatment assemblies were conducted on weekdays for 2 consecutive weeks as a solitary treatment course. Three courses of iPBM were performed over 2-3 months, with 1-3 weeks of rest between each course. The outcomes were measured using the Rancho Los Amigos Levels of Cognitive Functioning (LCF) tool. The chi-square test was used to compare categorical variables. Generalized estimating equations were used to verify the associations of various effects between the two groups. p < 0.05 indicated a statistically significant difference. Thirty patients were included and classified into the CCD( +) and CCD( -) groups (n = 15, each group). Statistics showed that before iPBM, CCD in the CCD( +) group was 2.74 (exp 1.0081) times higher than that of CCD( -) group (p = 0.1632). After iPBM, the CCD was 0.64 (exp-0.4436) times lower in the CCD( +) group than in the CCD( -) group (p < 0.0001). Cognitive assessment revealed that, before iPBM, the CCD( +) group had a non-significantly 0.1030 lower LCF score than that of CCD( -) group (p = 0.1632). Similarly, the CCD( +) group had a non-significantly 0.0013 higher score than that of CCD( -) after iPBM treatment (p = 0.7041), indicating no significant differences between the CCD( +) or CCD( -) following iPBM and general physical therapy. CCD was less likely to appear in iPBM-treated patients. Additionally, iPBM was not associated with LCF score. Administration of iPBM could be applied in TBI patients to reduce the occurrence of CCD. The study failed to show differences in cognitive function after iPBM, which still serves as an alternative non-pharmacological intervention.

Thalamocortical disconnection involved in pusher syndrome.

The presence of both isolated thalamic and isolated cortical lesions have been reported in the context of pusher syndrome-a disorder characterized by a disturbed perception of one's own upright body posture, following unilateral left- or right-sided stroke. In recent times, indirect quantification of functional and structural disconnection increases the knowledge derived from focal brain lesions by inferring subsequent brain network damage from the respective lesion. We applied both measures to a sample of 124 stroke patients to investigate brain disconnection in pusher syndrome. Our results suggest a hub-like function of the posterior and lateral portions of the thalamus in the perception of one's own postural upright. Lesion network symptom mapping investigating functional disconnection indicated cortical diaschisis in cerebellar, frontal, parietal and temporal areas in patients with thalamic lesions suffering from pusher syndrome, but there was no evidence for functional diaschisis in pusher patients with cortical stroke and no evidence for the convergence of thalamic and cortical lesions onto a common functional network. Structural disconnection mapping identified posterior thalamic disconnection to temporal, pre-, post- and paracentral regions. Fibre tracking between the thalamic and cortical pusher lesion hotspots indicated that in cortical lesions of patients with pusher syndrome, it is disconnectivity to the posterior thalamus caused by accompanying white matter damage, rather than the direct cortical lesions themselves, that lead to the emergence of pusher syndrome. Our analyses thus offer the first evidence for a direct thalamo-cortical (or cortico-thalamic) interconnection and, more importantly, shed light on the location of the respective thalamo-cortical disconnections. Pusher syndrome seems to be a consequence of direct damage or of disconnection of the posterior thalamus.

Diaschisis Profiles in the Cerebellar Response to Hemodynamic Stimuli: Insights From Dynamic Measurement of Cerebrovascular Reactivity to Identify Occult and Transient Maxima.

BACKGROUND: Crossed cerebellar diaschisis (CCD) refers to depressions in perfusion and metabolism within the cerebellar hemisphere contralateral to supratentorial disease. Prior investigation into CCD in cerebrovascular reactivity (CVR) has been limited to terminal CVR estimations (CVRend ). We recently have demonstrated the presence of unsustained CVR maxima (CVRmax ) using dynamic CVR analysis, offering a fully dynamic characterization of CVR to hemodynamic stimuli. PURPOSE: To investigate CCD in CVRmax from dynamic blood oxygen level-dependent (BOLD) MRI, by comparison with conventional CVRend estimation. STUDY TYPE: Retrospective. POPULATION: A total of 23 patients (median age: 51 years, 10 females) with unilateral chronic steno-occlusive cerebrovascular disease, without prior knowledge of CCD status. FIELD STRENGTH/SEQUENCE: A 3-T, T1-weighted magnetization-prepared rapid gradient-echo (MPRAGE) and acetazolamide-augmented BOLD imaging performed with a gradient-echo echo-planar imaging (EPI) sequence. ASSESSMENT: A custom denoising pipeline was used to generate BOLD-CVR time signals. CVRend was established using the last minute of the BOLD response relative to the first-minute baseline. Following classification of healthy versus diseased cerebral hemispheres, CVRmax and CVRend were calculated for bilateral cerebral and cerebellar hemispheres. Three independent observers evaluated all data for the presence of CCD. STATISTICAL TESTS: Pearson correlations for comparing CVR across hemispheres, two-proportion Z-tests for comparing CCD prevalence, and Wilcoxon signed-rank tests for comparing median CVR. The level of statistical significance was set at P ≤ 0.05. RESULTS: CCD-related changes were observed on both CVRend and CVRmax maps, with all CCD+ cases identifiable by inspection of either map. Diseased cerebral and contralateral cerebellar hemispheric CVR correlations in CCD+ patients were stronger when using CVRend (r = 0.728) as compared to CVRmax (r = 0.676). CVR correlations between healthy cerebral hemispheres and contralateral cerebellar hemispheres were stronger for CVRmax (r = 0.739) than for CVRend (r = 0.705). DATA CONCLUSION: CCD-related alterations could be observed in CVR examinations. Conventional CVRend may underestimate CVR and could exaggerate CCD. EVIDENCE LEVEL: 4. TECHNICAL EFFICACY: Stage 3.

Crossed Cerebellar Diaschisis in Thalamic Lymphoma on 18 F-FDG PET/CT.

Primary central nervous system lymphomas (PCNSLs) are extranodal variant forms of non-Hodgkin lymphoma arising within the brain parenchyma, leptomeninges, or spinal cord. PCNSL can present with varied neurological symptoms and imaging findings, making diagnosis without biopsy difficult. PCNSLs are highly aggressive, causing rapid deterioration, but are responsive to chemotherapy and radiotherapy making early diagnosis important. Crossed cerebellar diaschisis (CCD) is mostly seen with cerebral cortex vascular insults and is rarely reported with thalamic lesions and even rarer with thalamic lymphoma. However, CCD has also been described in other brain tumors (including primary glioma), chronic subdural hematoma, congenital insults, intracranial infections, and various dementia subtypes. We present a rare case of thalamic lymphoma evaluated with positron emission tomography/computed tomography that showed hypermetabolism of thalamus and associated hypometabolism in ipsilateral cerebral cortex and contralateral cerebellum representing CCD.

Crossed Cerebellar Diaschisis Worsens the Clinical Presentation in Acute Large Vessel Occlusion.

INTRODUCTION: Initial NIHSS in anterior large vessel occlusion (LVO) correlates partially with the hypoperfusion volume. We aimed at assessing the contribution of crossed cerebellar diaschisis (CCD) from the hypoperfused territory on LVO initial clinical deficit. METHODS: CCD was retrospectively identified by brain CT perfusion imaging (CTP) in patients with anterior LVO treated by mechanical thrombectomy from January 2017 to July 2021. CCD was defined by CTP parameter alteration in the contralateral cerebellar hemisphere to the LVO. NIHSS, clinical/perfusion variables, and CCD were included in regression models to assess their interrelationships. RESULTS: 206 patients were included. CCD was present in 90 patients (69%). NIHSS scores were higher on admission and at stroke discharge among patients with CCD (17.90 ± 6.1 vs. 11.4 ± 8.4, p < 0.001; 9.6 ± 7.7 vs. 6.6 ± 7.9, p = 0.049; respectively). Patients with a CCD had higher stroke volumes (118.2 ± 60.3 vs. 69.3 ± 59.7, p < 0.001) and lower rate of known atrial fibrillation (22% vs. 41%, p = 0.021). On multivariable logistic regression, CCD independently worsened the initial NIHSS (OR 4.85 [2.37-7.33]; p < 0.001). CONCLUSION: CCD is found in 69% of LVO on admission CTP, correlates with stroke volumes, and independently worsens initial NIHSS.

A Measure of Neural Function Provides Unique Insights into Behavioral Deficits in Acute Stroke.

BACKGROUND: Clinical and neuroimaging measures incompletely explain behavioral deficits in the acute stroke setting. We hypothesized that electroencephalography (EEG)-based measures of neural function would significantly improve prediction of acute stroke deficits. METHODS: Patients with acute stroke (n=50) seen in the emergency department of a university hospital from 2017 to 2018 underwent standard evaluation followed by a 3-minute recording of EEG at rest using a wireless, 17-electrode, dry-lead system. Artifacts in EEG recordings were removed offline and then spectral power was calculated for each lead pair. A primary EEG metric was DTABR, which is calculated as a ratio of spectral power: [(Delta*Theta)/(Alpha*Beta)]. Bivariate analyses and least absolute shrinkage and selection operator (LASSO) regression identified clinical and neuroimaging measures that best predicted initial National Institutes of Health Stroke Scale (NIHSS) score. Multivariable linear regression was then performed before versus after adding EEG findings to these measures, using initial NIHSS score as the dependent measure. RESULTS: Age, diabetes status, and infarct volume were the best predictors of initial NIHSS score in bivariate analyses, confirmed using LASSO regression. Combined in a multivariate model, these 3 explained initial NIHSS score (adjusted r2=0.47). Adding any of several different EEG measures to this clinical model significantly improved prediction; the greatest amount of additional variance was explained by adding contralesional DTABR (adjusted r2=0.60, P<0.001). CONCLUSIONS: EEG measures of neural function significantly add to clinical and neuroimaging for explaining initial NIHSS score in the acute stroke emergency department setting. A dry-lead EEG system can be rapidly and easily implemented. EEG contains information that may be useful early after stroke.