Cerebellar Stroke Research Articles

Epidemiology and pathogenesis of stroke in preterm infants: A systematic review.

BACKGROUND:Perinatal stroke is one of the principal causes of cerebral palsy (CP) in preterm infants. Stroke in preterm infants is different from stroke in term infants, given the differences in brain maturation and the mechanisms of injury exclusive to the immature brain. We conducted a systematic review to explore the epidemiology and pathogenesis of periventricular hemorrhagic infarction (PVHI), perinatal arterial ischemic stroke (PAIS) and cerebral sinovenous thrombosis (CSVT) in preterm infants.METHODS:Studies were identified based on predefined study criteria from MEDLINE, EMBASE, SCOPUS and WEB OF SCIENCE electronic databases from 2000 –2019. Results were combined using descriptive statistics.RESULTS:Fourteen studies encompassed 546 stroke cases in preterm infants between 23 –36 weeks gestational ages and birth weights between 450 –3500 grams. Eighty percent (436/546) of the stroke cases were PVHI, 17%(93/546) were PAIS and 3%(17/546) were CSVT. Parietal PVHI was more common than temporal and frontal lobe PVHI. For PAIS, left middle cerebral artery (MCA) was more common than right MCA or cerebellar stroke. For CSVT partial or complete thrombosis in the transverse sinus was universal. All cases included multiple possible risk factors, but the data were discordant precluding aggregation within a meta-analysis.CONCLUSION:This systematic review confirms paucity of data regarding the etiology and the precise causal pathway of stroke in preterm infants. Moreover, the preterm infants unlike the term infants do not typically present with seizures. Hence high index of clinical suspicion and routine cUS will assist in the timely diagnosis and understanding of stroke in this population.

Posterior Circulation Alberta Stroke Program Early Computed Tomography Score (pc-ASPECT) for the Evaluation of Cerebellar Infarcts.

Patients with cerebellar ischemic stroke may be misdiagnosed and may exhibit a delayed time to acute stroke treatment compared with patients with anterior circulation ischemic stroke. The posterior circulation Alberta stroke program early computed tomography score (pc-ASPECT) score has been used to evaluate hyperacute stroke, much as the ASPECT in anterior circulation stroke recently. Our main objective was to evaluate the associations of the clinical and etiological characteristics of ischemic cerebellar infarction patients on admission with their pc-ASPECT scores, as well as the correlations of the pc-ASPECT score with morbidity and mortality rates. We include 114 patients with cerebellar infarction who underwent 1 year of follow-up into the study. Patients with a pc-ASPECT score <7 were more likely to present with impaired consciousness ( P <0.001), multiple posterior circulation infarcts ( P <0.001), hydrocephalus ( P <0.001), lesions of the vermis ( P =0.028), and peduncle ( P =0.024), perfusion deficits in the total of posterior inferior cerebellar artery, anterior inferior cerebellar artery, superior cerebellar artery ( P <0.05), and basilar artery stenosis ( P =0.005), ischemia in additional anatomical structures in the posterior circulation ( P <0.001) compared with those with a score ≥7. Although the pc-ASPECT score alone is insufficient in some cases like vertebral artery dissection, using it together with the National Institutes of Health Stroke Scale (NIHSS) score and clinical findings may be beneficial during the hyperacute period of cerebellar ischemia. Presentation with impaired consciousness, basilar artery pathologies, vermian ischemia, and ischemia in additional anatomical structures in the posterior circulation other than the cerebellum appeared as important clinical and radiologic parameters predicting long-term prognosis.

Predictors of Neurological Deterioration during Admission for Patients with Cerebellar Strokes

Objective: Despite less common, cerebellar stroke frequently results in unfavorable outcomes, especially after deterioration. Therefore, this study was aimedto identify the significant predictors of neurological deterioration during admission (NDDA) in ischemic and hemorrhagic cerebellar strokes.Material and Methods: We retrospectively reviewed all medical records of patients diagnosed with ischemic and hemorrhagic cerebellar strokes; during 2002-2018, in Songklanagarind Hospital. Comparison of patients’ demographic data, initial clinical presentations, neuroradiological results, timing and signs of NDDA, and outcomes between cerebellar strokes were descriptively analyzed. Logistic regression model was applied for determining the significant predictors of NDDA from initial clinical presentations.Results: From this, 74 of 100 patients were eligible. They comprised of 42 (57.0%) cerebellar ischemia (CI) and 32 (43.0%) cerebellar hemorrhage (CH). Elevated diastolic blood pressure (DBP) and neuro-radiological evidences suggesting increased posterior cranial fossa pressure were significantly prevalent in neurological deterioration patients. NDDA was found in 31 patients (42.0%), without significant difference between CI and CH. 42 (56.8%), patients had poor neurological outcomes. The independent predictors for NDDA were DBP 120 mmHg (adjusted odds ratio [adj. OR] 15.39, 95% CI 1.58- 149.59; p-value=0.004), time from onset to arrival (adj. OR 0.98, 95% CI 0.97-1.00; p-value=0.044), and hemispheric cerebellar signs at presentation (adj. OR 0.22, 95% CI 0.06-0.75; p-value=0.012).Conclusion: CH was not an independent predictor of NDDA in overall cerebellar strokes. Only high DBP predicted NDDA; whereas, time from onset to arrival, and hemispheric cerebellar signs at presentation showed protective impact.

Rate of Infarct–Edema Growth on CT Predicts Need for Surgical Intervention and Clinical Outcome in Patients with Cerebellar Infarction

BackgroundUp to 20% of patients with cerebellar infarcts will develop malignant edema and deteriorate clinically. Radiologic measures, such as initial infarct size, aid in identifying individuals at risk. Studies of anterior circulation stroke suggest that mapping early edema formation improves the ability to predict deterioration; however, the kinetics of edema in the posterior fossa have not been well characterized. We hypothesized that faster edema growth within the first hours after acute cerebellar stroke would be an indicator for individuals requiring surgical intervention and those with worse neurological outcomes.MethodsConsecutive patients admitted to the neurological intensive care unit with acute cerebellar infarction were retrospectively identified. Hypodense regions of infarct and associated edema, “infarct–edema”, were delineated by using ABC/2 for all computed tomography (CT) scans up to 14 days from last known well. To examine how rate of infarct–edema growth varied across clinical variables and surgical intervention status, nonlinear and linear mixed-effect models were performed over 2 weeks and 2 days, respectively. In patients with at least two CT scans, multivariable logistic regression examined clinical and radiological predictors of surgical intervention (defined as extraventricular drainage and/or posterior fossa decompression) and poor clinical outcome (discharge to skilled nursing facility, long-term acute care facility, hospice, or morgue).ResultsOf 150 patients with acute cerebellar infarction, 38 (25%) received surgical intervention and 45 (30%) had poor clinical outcome. Age, admission National Institutes of Health Stroke Scale (NIHSS) score, and baseline infarct–edema volume did not differ, but bilateral/multiple vascular territory involvement was more frequent (87% vs. 50%, p < 0.001) in the surgical group than that in the medical intervention group. On 410 serial CTs, infarct–edema volume progressed rapidly over the first 2 days, followed by a subsequent plateau. Of 112 patients who presented within two days, infarct–edema growth rate was greater in the surgical group (20.1 ml/day vs. 8.01 ml/day, p = 0.002). Of 67 patients with at least two scans, after adjusting for baseline infarct–edema volume, vascular territory, and NIHSS, infarct–edema growth rate over the first 2 days (odds ratio 2.55; 95% confidence interval 1.40–4.65) was an independent, and the strongest, predictor of surgical intervention. Further, early infarct–edema growth rate predicted poor clinical outcome (odds ratio 2.20; 95% confidence interval 1.30–3.71), independent of baseline infarct–edema volume, brainstem infarct, and NIHSS.ConclusionsEarly infarct–edema growth rate, measured via ABC/2, is a promising biomarker for identifying the need for surgical intervention in patients with acute cerebellar infarction. Additionally, it may be used to facilitate discussions regarding patient prognosis.

Comparison of the Agreement and Accuracy Between Paramedic and Hospital Diagnosis

ObjectiveMaking an accurate clinical diagnosis in the field of prehospital is of great challenge in medical services. This study aimed to determine agreement between prehospital and in-hospital diagnoses. MethodsThe diagnostic agreement was determined by a comparison of the discharge diagnosis with the prehospital emergency technicians in a period of 6 months at the emergency medical services in northwest Azerbaijan. The diagnostic agreement of discharge diagnoses was compared with the fist diagnosis by the paramedics. The results were analyzed using the kappa agreement coefficient and the chi-square test. ResultsThe overall agreement between the diagnosis made by the emergency medical technicians and the hospital's first diagnosis was 67% (95% confidence interval [CI], 61%-77%; k = 0.61; 95% CI, 0.56-0.67), whereas the agreement between the first diagnosis made by the emergency medical technicians and the hospital discharge diagnosis was 58% (95% CI, 49%-65%; k = 0.42; 95% CI, 0.37-0.48).There was a high proportion of diagnostic agreement for pregnancy (100%), poisoning by drugs (88%), essential (primary) hypertension (86%), and ischemic heart diseases (72%). There was a low proportion of diagnostic agreement for weakness (39%), mixed anxiety and depressive disorder (43%), and cerebellar stroke syndrome (59%). ConclusionOur attention in practice and emergency medical courses should be directed to diseases that have a subjective history, such as weakness and anxiety, due to the high proportion of incorrect diagnoses by the prehospital emergency technician. It should be noted that most of the incorrectly diagnosed cases were overestimated with another coronary syndrome.

Spinal Cord Injury, Vertebral Artery Dissection, and Cerebellar Strokes After Chiropractic Manipulation.

Spinal Cord Injury, Vertebral Artery Dissection, and Cerebellar Strokes After Chiropractic Manipulation.

Teaching NeuroImage: Bilateral Middle Cerebellar Peduncle Stroke in Giant Cell Arteritis.

Teaching NeuroImage: Bilateral Middle Cerebellar Peduncle Stroke in Giant Cell Arteritis.

Delayed cerebral atrophy after cerebellar stroke: topographical relation and clinical impact.

Remote dysconnectivity following cerebellar ischaemic stroke may have a negative impact on supratentorial brain tissue. Since the cerebellum is connected to the individual cerebral lobes via contralateral tracts, cerebellar lesion topography might determine the distribution of contralateral supratentorial brain tissue changes. We investigated (i) the occurrence of delayed cerebral atrophy after cerebellar ischaemic stroke and its relationship to infarct volume; (ii) whether cerebellar stroke topography determines supratentorial atrophy location; and (iii) how cortical atrophy after cerebellar stroke impacts clinical outcome. We performed longitudinal volumetric MRI analysis of patients with isolated cerebellar stroke from the Swiss Stroke Registry database. Stroke location and volume were determined at baseline MRI. Delayed cerebral atrophy was measured as supratentorial cortical volumetric change at follow-up, in contralateral target as compared to ipsilateral reference-areas. In patients with bilateral stroke, both hemispheres were analysed separately. We obtained maps of how cerebellar lesion topography, determines the probability of delayed atrophy per distinct cerebral lobe. Clinical performance was measured with the National Institutes of Health Stroke Scale and modified Rankin Scale. In 29 patients (age 58 ± 18; 9 females; median follow-up: 6.2 months), with 36 datasets (7 patients with bilateral cerebellar stroke), delayed cerebral atrophy occurred in 28 (78%) datasets. A multivariable generalized linear model for a Poisson distribution showed that infarct volume (milliliter) in bilateral stroke patients was positively associated with the number of atrophic target areas (Rate ratio = 1.08; P = 0.01). Lobe-specific cerebral atrophy related to distinct topographical cerebellar stroke patterns. By ordinal logistic regression (shift analysis), more atrophic areas predicted higher 3-month mRS scores in patients with low baseline scores (baseline score 3–5: Odds ratio = 1.34; P = 0.02; baseline score 0–2: OR = 0.71; P = 0.19). Our results indicate that (i) isolated cerebellar ischaemic stroke commonly results in delayed cerebral atrophy and stroke volume determines the severity of cerebral atrophy in patients with bilateral stroke; (ii) cerebellar stroke topography affects the location of delayed cerebral atrophy; and (iii) delayed cerebral atrophy negatively impacts clinical outcome.

Acute vestibular disorders: Stroke or not?

Acute vestibular syndrome of severe vertigo, nausea/vomiting, spontaneous nystagmus and postural imbalance is commonly due to viral or post-viral inflammation of the vestibular nerve or labyrinth. However, similar symptoms and signs may occur in cerebellar or brainstem strokes in which vertigo may be an isolated or the initial symptom without other focal neurologic deficits. Since cerebellar or brainstem strokes may be fatal, it is important to recognize acute vestibular syndrome of vascular etiologies.

A RARE CAUSE OF PARAPLEGIA: DISTRIBUTIVE SHOCK CAUSING BORDER ZONE STROKES

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Simultaneous bilateral cerebrovascular infarction is relatively uncommon and is an entity seen rarely in watershed cerebral infarctions which occur at the border between cerebral vascular territories in the setting of severe hypotension. CASE PRESENTATION: 84-year-old male with history of CAD, cerebellar stroke, peripheral arterial disease was admitted to the ICU with distributive shock and intubated for toxic metabolic encephalopathy. Initial CT head on admission was unremarkable. On day 2 of hospitalization his neuro assessment was notable for bilateral lower extremity paresis with preservation of sensation, proprioception and temperature but had sluggish reflexes and loss of motor strength. Repeat CT head did not show a bleed and subsequently, MRI brain with MRA head and neck revealed bilateral acute anterior cerebral artery strokes. Given the location and duration of symptoms he was not a TPA candidate and was treated with medical management with aspirin and statin. Echocardiogram and carotid ultrasounds were done that were unremarkable for embolic cause of stroke. DISCUSSION: The anterior cerebral artery is a major vessel supplying blood to the interhemispheric region. ACA territory infarction accounts for only 0.3% to 4.4% of cerebral infarctions. Bilateral ACA infarction is even rarer. Twenty-seven cases of ACA territory infarction were reported among 1490 cases of cerebral infarction in the Lausanne Stroke Registry; among them, only two cases had bilateral ACA territory infarction. Bilateral ACA infarction can occur due to vasospasm in the setting of subarachnoid hemorrhage caused by a rupture of aneurysms of the anterior communicating arteries or distal ACAs, thrombosis or embolism in case of anomaly of circle of Willis or bilateral anaplastic ACAs. In our patient the area of infarction was in a watershed zone bilaterally, unfortunately affected by hypotension which is rare in the absence of any of the above-mentioned anomalies as predisposing factors. The true incidence of bilateral ACA infarction is unknown, with few cases reported in the literature. CONCLUSIONS: This case report highlights the possibility of developing simultaneous bilateral cerebral infarctions in the setting of profound systemic hypotension and shock, especially if the patient has baseline chronic small vessel changes. REFERENCE #1: Orlandi G, Moretti P, Fioretti C, Puglioli M, Collavoli P, Murri L. Bilateral medial frontal infarction in a case of azygous anterior cerebral artery stenosis. Ital J Neurol Sci. 1998;19:106–108. doi: 10.1007/BF02427567. [PubMed] [CrossRef] [Google Scholar] REFERENCE #2: Gacs G, Fox AF, Barnett HJ, Vinuela F. Occurrence and mechanisms of occlusion of the anterior cerebral artery. Stroke. 1983;14:952–959. [PubMed] [Google Scholar] REFERENCE #3: Bogousslavsky J, Regli F. Anterior cerebral artery territory infarction in the Lausanne Stroke Registry. Clinical and etiologic patterns. Arch Neurol. 1990;47:144–150. [PubMed] [Google Scholar] DISCLOSURES: No relevant relationships by Imama Ahmad, source=Web Response No relevant relationships by Christine Blaski, source=Web Response No relevant relationships by Sneha Lakshman, source=Web Response

In Reply to the Letter to the Editor Regarding “Association of Early White Blood Cell Trend with Outcomes in Aneurysmal Subarachnoid Hemorrhage”

Giant aneurysms of the intracranial vertebral artery and posterior inferior cerebellar artery are challenging to treat as they often necessitate direct sacrifice of the diseased segment, which is thought to carry high morbidity due to brainstem and cerebellar stroke. Here, we report images of twin giant aneurysms of the left posterior inferior cerebellar artery at the brainstem and cerebellopontine angle region in a young child.

A Cerebrovascular Accident Presenting With Bilateral Vocal Cord Paresis

Diagnosing a stroke requires careful attention to clinical indicators on physical exam, especially the more subtle manifestations of cerebellar lesions. An 85-year-old male with vascular risk factors and new-onset atrial fibrillation was admitted for left upper extremity weakness, headaches, and tremors. The patient developed stridor during hospitalization and was found to have a new cerebellar infarct with hemorrhagic transformation on computed tomography (CT) of the head, with laryngoscopy showing bilateral vocal cord paresis. While strokes outside of the cerebellum are a known cause of unilateral vocal cord paresis, cerebellar strokes are a rare culprit and rarely cause bilateral cord paresis. Consideration beyond the more common pulmonary and iatrogenic causes of vocal cord paresis should be considered, with particular attention to stroke.

Acute Vestibular Syndrome in Cerebellar Infarction: A Case Report

Introduction: Acute vestibular syndrome (AVS) is characterized by rapid onset of vertigo, nausea and vomiting, and gait unsteadiness in association with head motion intolerance and nystagmus, lasting days to weeks. Although the majority of AVS patients have acute peripheral vestibulopathy, some may also have brainstem or cerebellar strokes. Cerebellar infarctions sometimes only cause vertigo. The Head Impulse Test, skew deviation, and nystagmus testing provide for great sensitivity and specificity in distinguishing between peripheral vestibular impairment and stroke. Case: A 41-year-old male patient suffered from acute-onset vertigo and dizziness about 5 hours before admission, which started when he started doing his morning routine. Patients also feel gait unsteadiness and almost fall to the left side. There was no weakness in extremities, skew face or slurred speech. Patient's neurological status showed the cerebellar examination was positive left dysmetria, left dysdiadochokinesia, the Romberg test open eye fell to the left, normal Head Impulse Test (HIT), with horizontal bidirectional nystagmus and negative skew deviation test. Cerebellum infarction was discovered using computed tomography imaging. After passing through the acute stroke period, patients are offered symptomatic therapy in the form of betahistine, antiplatelet medication, and vestibular rehabilitation planning. On the tenth day after the onset, the patient's symptoms began to improve. Conclusion: Proper diagnosis of acute vestibular syndrome will guide the necessary tests. The HINTS oculomotor test at the bedside can detect acute vestibular stroke. Keywords: acute vestibular syndrome, vertigo, cerebellum, HINTS

Precipitated Withdrawal, Delirium, and Cerebellar Stroke: The Pharmacology of Buprenorphine Induction in Non-pharmaceutical Fentanyl and the Neuropsychiatric Manifestations of Cerebellar Stroke

Precipitated Withdrawal, Delirium, and Cerebellar Stroke: The Pharmacology of Buprenorphine Induction in Non-pharmaceutical Fentanyl and the Neuropsychiatric Manifestations of Cerebellar Stroke

Celiac disease with acute cerebellar stroke as first presentation: A case report

Celiac disease is an immune disorder occurring in response to ingestion of gluten in genetically predisposed individuals. It is a complex multiorgan disease with possible neurological involvement. Thrombotic events can occur but rarely as presenting symptom. We describe the case of a young man admitted to the Stroke Unit for worsening headache, nausea, vomiting, unsteadiness, dysarthria, and dysmetria. Brain CT scan showed an ischemic hypodense lesion of the right cerebellar hemisphere with compression of the adjacent IV ventricle. Studies to determine the etiology of stroke showed positive serology for celiac disease. On follow up he has completely recovered clinically. He is on gluten-free diet and the serology is now negative. Our case demonstrated that in young stroke, even without gastrointestinal symptoms, celiac disease should be considered a possible differential diagnosis and the appropriate serology test performed.

Engaging Medical Students in Neurointervention: Rationale and Recruitment

Giant aneurysms of the intracranial vertebral artery and posterior inferior cerebellar artery are challenging to treat as they often necessitate direct sacrifice of the diseased segment, which is thought to carry high morbidity due to brainstem and cerebellar stroke. Here, we report images of twin giant aneurysms of the left posterior inferior cerebellar artery at the brainstem and cerebellopontine angle region in a young child.

Twin Giant Intracranial Aneurysms

Giant aneurysms of the intracranial vertebral artery and posterior inferior cerebellar artery are challenging to treat as they often necessitate direct sacrifice of the diseased segment, which is thought to carry high morbidity due to brainstem and cerebellar stroke. Here, we report images of twin giant aneurysms of the left posterior inferior cerebellar artery at the brainstem and cerebellopontine angle region in a young child.

Acute brain stem vertigo without neurological deficits

An infarct at the brain stem or cerebellum is rarely associated with vertigo without any other localizing clinical features. Stroke at the posterior circulation of the brain may cause spontaneous vertigo and imbalance. In some cases, isolated posterior inferior cerebellar artery infraction presents isolated vertigo and nystagmus. The diagnosis of the brain stem vertigo can be done easily when associated with other neurological symptoms along with vertigo, whereas, when the vertigo occurs in isolation, it may be difficult to differentiate it from the other benign disorders affecting the inner ear. A head impulse test may differentiate the acute isolated vertigo with cerebellar stroke from more benign disorders associated with labyrinth. Appropriate evaluation of the patient is better than imaging for diagnosis of the brain stem vertigo. Here, we are presenting a case of isolated acute onset of the vertigo due to brain stem infarct which mimics to the peripheral vestibular pathology.

Mapping the Cerebellar Cognitive Affective Syndrome in Patients with Chronic Cerebellar Strokes.

The cerebellar cognitive affective syndrome (CCAS) has been consistently described in patients with acute/subacute cerebellar injuries. However, studies with chronic patients have had controversial findings that have not been explored with new cerebellar-target tests, such as the CCAS scale (CCAS-S). The objective of this research is to prove and contrast the usefulness of the CCAS-S and the Montreal Cognitive Assessment (MoCA) test to evaluate cognitive/affective impairments in patients with chronic acquired cerebellar lesions, and to map the cerebellar areas whose lesions correlated with dysfunctions in these tests. CCAS-S and MoCA were administrated to 22 patients with isolated chronic cerebellar strokes and a matched comparison group. The neural bases underpinning both tests were explored with multivariate lesion-symptom mapping (LSM) methods. MoCA and CCAS-S had an adequate test performance with efficient discrimination between patients and healthy volunteers. However, only impairments determined by the CCAS-S resulted in significant regional localization within the cerebellum. Specifically, patients with chronic cerebellar lesions in right-lateralized posterolateral regions manifested cognitive impairments inherent to CCAS. These findings concurred with the anterior-sensorimotor/posterior-cognitive dichotomy in the human cerebellum and revealed clinically intra- and cross-lobular significant regions (portions of right lobule VI, VII, Crus I-II) for verbal tasks that overlap with the "language" functional boundaries in the cerebellum. Our findings prove the usefulness of MoCA and CCAS-S to reveal cognitive impairments in patients with chronic acquired cerebellar lesions. This study extends the understanding of long-term CCAS and introduces multivariate LSM methods to identify clinically intra- and cross-lobular significant regions underpinning chronic CCAS.

Disequilibrium double-whammy: A case of concurrent BPPV and cerebellar stroke

Disequilibrium double-whammy: A case of concurrent BPPV and cerebellar stroke