Bilateral Cerebellar Infarcts Research Articles

Dynamic vertebral artery occlusion aka bow hunter syndrome causing posterior fossa stroke in a young adult: a case report

BackgroundBow Hunter syndrome (BHS) is a rare, but important cause of posterior circulation stroke. It is also known as Rotational vertebral artery syndrome and is caused by transient dynamic vertebro-basilar insufficiency on movement of the neck in the presence of certain soft tissue or bone anomalies in the cranio-vertebral region.Case presentationWe present a case of Bow hunter syndrome in an 18-year-old adult male who presented with vomiting, occipital headache and loss of balance, with findings of posterior circulation stroke on imaging. Medical causes of young stroke, including vasculitis and clotting disorders were ruled out, following which a diagnostic conventional angiography and CT angiography was performed. The cause of vascular compromise in our case was the presence of vertebral anomalies, in particular, the presence of a partial ponticulus posticus with formation of an incomplete arcuate foramen. He was treated with cervical spine immobilisation and C1–C2 fixation. In addition, our patient had a single posterior inferior cerebellar artery (PICA) on the side of the dynamic insufficiency, which lead to bilateral cerebellar infarcts. Our case is unique because it demonstrates a combination of osseous and vascular developmental anomalies resulting in posterior circulation stroke.ConclusionsThough uncommon, BHS should be considered in the list of differentials in otherwise unexplained cases of posterior circulation stroke. Conventional angiography with dynamic manoeuvres is the modality of choice for documenting the rotational vertebral artery occlusion.

Fatal Vertebral Artery Dissection Following Self-Manipulation of the Cervical Spine.

Cervical spine manipulation is a known risk factor for vertebral artery dissection. In this report, we present a case of fatal vertebral artery dissection that occurred as the result of self-manipulation of the cervical spine. The decedent was a 40-year-old man with no significant past medical history. He was observed to "crack his neck" while at work. Soon after, he began experiencing neck pain, then developed strokelike symptoms and became unresponsive. He was transported to a local medical center, where imaging showed bilateral vertebral artery dissection. His neurological status continued to decline, and brain death was pronounced several days later. An autopsy examination showed evidence of cerebellar and brainstem infarcts, herniation, and diffuse hypoxic-ischemic injury. A posterior neck dissection was performed to expose the vertebral arteries, which showed grossly visible hemorrhage and dilation. There was no evidence of traumatic injury to the bone or soft tissue of the head or neck. Bilateral dissection tracts were readily appreciated on microscopic examination. Death was attributed to self-manipulation of the neck, which in turn led to bilateral vertebral artery dissection, cerebellar and brainstem infarcts, herniation, hypoxic-ischemic injury, and ultimately brain death.

Patient with Recurrent Acute Ischemic Strokes Found to have Cryptococcal Meningitis: A Case Report (P12-5.023)

<h3>Objective:</h3> n/a <h3>Background:</h3> Cryptococcal meningitis is a rare cause of ischemic stroke. Infections most often present in immunocompromised patients, classically AIDS or transplant patients. We present a case of a seemingly immunocompetent patient who presented with recurrent strokes found to have cryptococcal meningitis. <h3>Design/Methods:</h3> n/a <h3>Results:</h3> The patient was a 55-year-old male construction worker with hypertension. A year prior to admission, he was hospitalized for a week with mild SARS-COVID-19 infection. He had received two doses of the mRNA Covid vaccines. One month prior to admission, he developed headaches initially treated as sinus infection with oral antibiotics and steroids. Two weeks later, there was concern for acute-onset aphasia. He was afebrile with mild leukocytosis (13.6 B/L). MRI brain showed multiple, bilateral, scattered lacunar infarcts and left cerebellar infarcts. Transthoracic and transesophageal echocardiography were unremarkable. A loop recorder was placed. He was started on dual antiplatelet and statin therapy. A week later, he was encephalopathic and lethargic. Repeat MRI brain showed new acute lacunar and bilateral cerebellar infarcts. The loop recorder was negative for arrhythmias. A lumbar puncture (LP) was deferred for unclear reasons. Patient was transferred to our stroke service, where he was febrile (102.3°F) with leukocytosis (17.4 B/L). He was encephalopathic and had nuchal rigidity. LP showed elevated opening pressure (55 cm H2O) and tested positive for Cryptococcal antigen. Liposomal amphotericin B and flucytosine were initiated. Diagnostic angiogram was negative for vasculitis. His CD4 count was 332 (normal 410–1,590), however HIV testing was negative and pan-CT scan showed no signs of underlying malignancy. His prolonged hospital course was complicated by elevated intracranial pressure, further strokes, and poor mental status requiring placement of tracheostomy and enteral tube access. <h3>Conclusions:</h3> It is important to keep infection, including cryptococcal meningitis, in the differential for the cause of recurrent strokes even in seemingly immunocompetent patients. <b>Disclosure:</b> Lauren Thaete has nothing to disclose. Dr. Azuma has nothing to disclose.

Hot Cross Bun Sign in Bilateral Middle Cerebellar Peduncle Infarction.

HomeStrokeVol. 54, No. 4Hot Cross Bun Sign in Bilateral Middle Cerebellar Peduncle Infarction No AccessCase ReportRequest AccessFull TextAboutView Full TextView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessCase ReportRequest AccessFull TextHot Cross Bun Sign in Bilateral Middle Cerebellar Peduncle Infarction Katsuya Nishida and Naonobu Futamura Katsuya NishidaKatsuya Nishida Correspondence to: Katsuya Nishida, MD, National Hospital Organization Hyogo-Chuo National Hospital, 1314 Ohara, Sanda, Hyogo 669-1592, Japan. Email E-mail Address: [email protected] https://orcid.org/0000-0003-4978-5382 Department of Neurology, National Hospital Organization Hyogo-Chuo National Hospital, Sanda, Japan. Department of Neurology, Yoka Hospital, Hyogo, Japan. Search for more papers by this author and Naonobu FutamuraNaonobu Futamura Department of Neurology, National Hospital Organization Hyogo-Chuo National Hospital, Sanda, Japan. Department of Neurology, Yoka Hospital, Hyogo, Japan. Search for more papers by this author Originally published21 Feb 2023https://doi.org/10.1161/STROKEAHA.122.042453Stroke. 2023;54:e163–e164"Hot Cross Bun Sign in Bilateral Middle Cerebellar Peduncle Infarction." Stroke, 54(4), pp. e163–e164FootnotesFor Sources of Funding and Disclosures, see page e163.Correspondence to: Katsuya Nishida, MD, National Hospital Organization Hyogo-Chuo National Hospital, 1314 Ohara, Sanda, Hyogo 669-1592, Japan. Email nishida.katsuya.[email protected]hosp.go.jp

Influence of Bilateral Cerebellar Infarction on Functional Outcome After Endovascular Treatment for Basilar Artery Occlusion

To measure the magnitude of the effect of the infarct location measured using the posterior circulation Alberta Stroke Program Early Computed Tomographic Score (pc-ASPECTS) on the functional outcome at 90days in patients with basilar artery (BA) occlusion undergoing endovascular therapy (EVT). Of the acute ischemic stroke patients undergoing EVT for acute posterior circulation large vessel occlusion enrolled in the multicenter observational registry from December 2013 to February 2021, patients with BA occlusion were included. A favorable outcome was defined as achieving a modified Rankin Scale score of 0-3 at 90days. The effect of pc-ASPECTS including the distribution on favorable outcomes was evaluated. One hundred patients were analyzed. Fifty-one patients (51%) achieved favorable outcome. Patients achieving a favorable outcome were younger, had a lower National Institutes of Health Stroke Scale score before EVT, and had a higher pc-ASPECTS before EVT than those not achieving a favorable outcome. Multivariable logistic analysis showed a significant association between higher pc-ASPECTS and a favorable outcome (odds ratio [OR] 1.24; 95% confidence interval [CI] 1.02-1.52; P=0.028). Considering the infarct location, bilateral cerebellar infarction was significantly associated with a lower frequency of favorable outcomes than those without cerebellar infarction (OR 0.16; 95% CI 0.04-0.51; P=0.002). A higher pc-ASPECTS before EVT could be a predictor of a favorable outcome after EVT for BA occlusion. In particular, the presence of bilateral cerebellar infarction before EVT was significantly associated with a lower likelihood of a favorable outcome.

A rare case of neurosyphilis presenting as generalized dystonia with bilateral cerebellar infarctions.

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Abstract 15654: Mitral Valve Strands in a Patient With Cerebellar Infarcts

Case Description: A 56-year-old man with a history of hypertension, diabetes, hyperlipidemia, and ischemic stroke 2 years ago presented with left-sided weakness, unsteady gait, and vomiting for 12 hours. The patient was vitally stable, and examination revealed dysarthria, left ataxic hemiparesis, and chronic right facial droop. Magnetic Resonance Imaging (MRI) brain showed an evolving acute infarct in the left superior cerebellum with trace petechial hemorrhage, chronic small right posterior inferior cerebellar infarct, and chronic bilateral cerebellar lacunar infarcts. The patient had an implantable loop recorder placed after his previous stroke, which did not show any arrhythmias on interrogation. MRI Angiography of the head/neck did not show large vessel occlusions. Transesophageal echocardiography (TEE) ruled out a patent foramen ovale but did reveal multiple filamentous structures (&lt;5mm in size) on the atrial side of the posterior mitral valve leaflet (figure 1); these were consistent with fibrin valve strands, or Lambl’s excrescences (LE). Anticoagulation therapy was started, and surgical excision was recommended. Discussion: LE are rare fibrous/filamentous valvular strands caused by wear and tear at the closure lines of left-sided heart valves. LE can be associated with thromboembolic strokes and acute coronary syndromes; however, it can also be found incidentally. TEE is the gold standard in diagnosis. This is a middle-aged man without a clear cause of ischemic strokes, subsequently found to have LE on the mitral valve. There is a paucity of evidence on the management of LE due to its rarity. Prior case reports suggest the use of antiplatelets/anticoagulants in symptomatic patients and surgery in cases of recurrent thromboembolic episodes refractory to conservative treatment. Given multiple strokes, this patient was started on anticoagulation and will be evaluated for surgery. Further high-powered studies are needed to guide management.

Large vessel occlusions requiring repeated mechanical thrombectomy caused by silent myocardial infarction in a young adult

ObjectivesSilent myocardial ischemia, defined as objective evidence of myocardial ischemia without symptoms, is associated with ischemic stroke. Nevertheless, silent myocardial infarction is a rare cause of ischemic stroke, especially in young adults with no medical history. Materials and methodsHerein, we report a young adult patient with acute ischemic stroke treated with repeated mechanical thrombectomy for recurrent large vessel occlusions caused by left ventricular thrombus following a silent myocardial infarction. ResultsA 40-year-old man was transferred by ambulance to our hospital because of a generalized seizure. He was diagnosed with cerebral infarction and left middle cerebral artery occlusion. We performed intravenous thrombolysis and mechanical thrombectomy. Recanalization was achieved and his symptoms gradually improved. However, the day after treatment he developed bilateral cerebellar infarction and basilar artery occlusion. We performed a second mechanical thrombectomy and recanalization was achieved. Transthoracic echocardiography revealed a mobile left ventricular thrombus. Although he had no previous chest symptomatic episodes, cardiac examination confirmed myocardial infarction of unknown onset. He was diagnosed with acute ischemic stroke with large vessel occlusions caused by left ventricular thrombus following a silent myocardial infarction. Anticoagulation therapy reduced the amount of thrombus. At 1-year follow-up, he had not experienced any recurrences or symptoms. ConclusionsSilent myocardial infarction should be considered a cause of ischemic stroke in young adults, even without any vascular risk factors. Recurrent large vessel occlusion may occur in patients with left ventricular thrombus, and repeated mechanical thrombectomy should be considered for treatment.

A 54-year-old with dysarthria.

A 54-year-old male with a history of intravenous heroin abuse presented to the emergency department for dysarthria. The patient was initially found down with an unknown last known well time. The patient had a blood pressure of 237/101 mmHg. He was alert with a left-sided gaze preference and right-sided Romberg drift. Labs were remarkable for white blood cell count (WBC) 25.7 103/μl and creatine kinase (CK) 5776. Drug screen was positive for opiates. Computed tomography brain and angiography imaging showed bilateral cerebellar hemispheric ischemia, lateral ventricle dilatation, and a right proximal vertebral artery with non-occlusive diminutive distal flow (Figure 1). Several hours later, the patient subsequently experienced a rapid neurological decline from Glasgow Coma Scale (GCS) 11 (E4V2M5) to GCS7 (E2V1M4), prompting intubation for airway protection. Mannitol and 2% hypertonic saline were administered. External ventricular drain was prepared for potential deterioration. Subsequent magnetic resonance imaging showed stable, bilateral subacute cerebellar infarcts with hydrocephalus (Figure 2) and the patient was ultimately extubated and required prolonged rehabilitation. Bilateral ischemic cerebellar strokes are rare cerebrovascular accidents (CVAs).1 Large volume infarcts have a high risk of developing space-occupying brain edema in the compact posterior fossa—risk of rapid, life-threatening herniation through compression of the brain stem and the fourth ventricle with resultant hydrocephalus.2 Opiate abuse has been described as a rare cause of cerebral ischemia though mechanisms including vasospasm and severe hypoperfusion, rhabdomyolysis via muscle compression, and direct toxicity.3, 4 In our case, stable repeat imaging and an elevated CK suggested a subacute presentation and prompted holding off suboccipital craniectomy given the high likelihood of being outside of the acute edema window for effective surgical intervention.5 A positive drug screen with a known history of intravenous drug abuse point to a rare drug-associated ischemia as a potential etiology. Timing of pathology, repeat imaging and clinical assessment, and maintaining a wide differential, including drug-induced ischemia, in relatively young patients without typical CVA risk factors are essential in management of severe cerebellar strokes with unknown onset.

A Case of Bilateral Cerebellar Infarction Treated with Suboccipital Decompressive Craniectomy after Thrombectomy for Acute Basilar Artery Occlusion

A Case of Bilateral Cerebellar Infarction Treated with Suboccipital Decompressive Craniectomy after Thrombectomy for Acute Basilar Artery Occlusion

Osteogenesis Imperfecta With Cerebral Atherosclerosis: A Family Report

Background: Osteogenesis imperfecta (OI) is a rare hereditary connective tissue disease. It is mainly associated with pathogenic variants in COL1A1 or COL1A2. Patients with OI usually have repeated history of bone fractures. Besides, osteogenesis imperfecta is associated with some cardiovascular complications, such as aortic and mitral valve dysfunction, aneurysm and aortic dissection. But the relationship between these diseases has not been well studied. Case Presentation: A 55-year-old man was admitted to our hospital mainly due to “dizziness for 2 hours”. He had a 4-month history of hypertension and a history of smoking for more than 20 years. He had no history of drinking alcohol. He had hunchback and O-type legs. Besides, the patient and some of his relatives had a history of repeated brittle fractures,which was considered as “osteogenesis imperfecta”. The clinical manifestation of OI in this family varies to a certain extent, from simple tooth disintegration to severe fracture deformity. The most serious patient of his family was unable to walk. CT and MRI revealed multiple systemic arteriosclerosis, including vertebral artery, posterior inferior cerebellar artery, cervical artery, and bilateral cerebellar multiple lacunar cerebral infarction. The blood sample of the patient was tested by whole exome sequencing, and the saliva samples of the patient’s family members were tested by Sanger sequencing. A mutation c.3159 + 2T > A was detected in COL1A2 gene associated with OI, also found in the other affected family members, which had not been reported before. It was a segregating mutation in the family. The clinical severity of the family members was heterogeneous.Discussion: This case is worth learning from the following aspects: 1. A pathogenic heterozygous mutation, c.3159 + 2T > A was detected in COL1A2 gene in the patient with OI, which is not reported in previous cases of OI. 2. The clinical manifestation of OI in this family varies to a certain extent, from simple tooth disintegration to severe fracture deformity. The most serious patient of his family was unable to walk. It presented the clinical heterogeneity of OI. Further basic researh on the mutation site of related gene of OI are needed. 3. We found the possibility of developing cerebral atherosclerosis in patients with OI. Therefore, patients with OI should give up smooking, exercise properly and keep on a low fat diet. They should pay attention to control blood pressure and blood lipid so as to reduce the risk of atherosclerosis. Conclusion: A c.3159 + 2T>A mutation in COL1A2 gene detected by whole exome sequencing was the causing reason of OI, the discovery enriched the gene mutation spectrum of OI. We also found that OI may have relationship with premature atherosclerosis, and the abnormal bones of the cervical spine may lead to vertebrobasilar ischemia.

Recurrent cerebellar infarction due to vertebral artery dissection in an athetotic patient

AbstractA 42‐year‐old man with longstanding athetotic‐type cerebral palsy and history of cervical spine fusion surgery was affected by multiple episodes of vertebral artery dissections, resulting in bilateral cerebellar infarction. Continuous involuntary movements noted in the upper limbs and neck, as well as a limited cervical range of motion due to the operation might have precipitated the dissecting events.

From Cerebellar Apoplexy in 1849 to Cerebellar Stroke in the 2020s: Robert Dunn's Contribution.

Stroke of the cerebellum represents about 10% of strokes of the brain. Both infarction and hemorrhage manifest with symptoms related to the location and extent of the lesion(s). Bilateral cerebellar infarcts constitute up to one third of all cerebellar infarctions. The leading cause of cerebellar infarcts is emboli of cardiac origin or from intra-arterial sources. Potential complications include brainstem compression and hydrocephalus. Malignant cerebellar edema is a life-threatening complication of ischemic posterior circulation stroke requiring urgent management. The advent of MRI has revolutionized the early diagnosis in vivo, showing small and large territorial infarcts, hemorrhages, and venous infarcts. Endovascular procedures are growingly applied and are impacting on the prognosis of stroke, although cerebellar stroke from occlusion of small cerebellar arteries is currently not accessible to thrombectomy. Surgical procedures of space-occupying stroke include external ventricular drainage, suboccipital craniotomy, or combined procedures. In 1849, Robert Dunn (1799-1877), an English surgeon, reported the details of a case of apoplexy of the cerebellum in a 52-year-old man, pointing to the importance of post-mortem studies of patients followed meticulously during lifetime. Dunn discussed inflammation surrounding hemorrhage as a source of cerebral degeneration, linking for the first time cerebellar stroke, neuroinflammation, and atherosclerosis.

Evaluation of Clinical Features and Stroke Etiology in Patients with Bilateral Middle Cerebellar Peduncle Infarction

Objective: The aim of this study was to characterize clinical features, etiologies, and mechanisms of strokes due to bilateral middle cerebellar peduncle infarction (BMCPI). Methods: Cases diagnosed as BMCPI in our hospital were retrieved, and a literature review was performed. Data on clinical features and brain MRI were obtained. Extracranial and intracranial segments of the vertebrobasilar artery were assessed by using digital subtraction angiography, magnetic resonance angiography, or computed tomography angiography. Results: Thirteen cases (11 men and 2 women) of BMCPI were identified. A high-intensity signal of diffusion-weighted imaging sequence involving the bilateral middle cerebellar peduncle was observed in all patients. Most patients experienced vertigo, dysarthria, ataxia, and hearing disorders. Eleven of these cases were classified as large artery atherosclerosis, one as traumatic vertebral artery (VA) dissection, and one as giant cell arteritis. Conclusion: BMCPI is a rare cerebrovascular disease characterized by vertigo, ataxia, and dysarthria, which may also be accompanied by a hearing deficit or clinical signs of brainstem damage. BMCPI may be associated with hypoperfusion secondary to occlusive disease of the bilateral VA or proximal basilar artery.

Multiple Cerebral and Cerebellar Infarctions following Russell's Viper (Daboia Russelii) Envenomation - A Case Report

Ischemic stroke is a rare neurological complication following SriLankan Russell's viper envenomation. We report a case of a 44-year-old person, who developed multiple cerebral and cerebellar infarctions following SriLankan Russell's viper envenomation. The patient developed both local and systemic envenomation and was treated with Snake Venom Anti-Serum I.P. (VinsBioproducts Ltd). On day six, this patient developed left-sided hemiparesis. CT scan of the brain showed bilateral cerebellar, bilateral occipital, and right-sideparietal lobe infarctions.

46. GCA: Diagnosed with a heavy heart

IntroductionGiant cell arteritis (GCA) represents a common cause of uncertainty for physicians. GCA can present as an indolent or aggressive process with a wide spectrum of symptoms and signs. The key to diagnosis is good clinical acumen and awareness of both common and rare associated conditions. Here we describe a rare and atypical presentation of a patient with GCA and chest pain.Case descriptionAn 83-year old male was admitted to the medical take with 3 hours of crushing chest pain associated with diaphoresis and nausea. He had been started on 60mg prednisolone by his GP 3 days preceding this for suspected GCA (scalp tenderness, jaw claudication, polymyalgia). Past medical history included: hypertension, recent strokes (bilateral cerebellar infarcts 3 months prior), previous DVTs and COPD. Examination revealed no abnormalities. Admission ECGs showed sinus rhythm with fixed T-wave inversion in aVL and V3. Chest radiograph was normal. Bloods tests revealed mildly raised inflammatory markers (CRP, ESR 24) and a dynamic troponin (324 – 1241 – 1431 ng/L). He was diagnosed with a non-ST elevation myocardial infarction (NSTEMI) and was referred to Cardiology for an angiogram. He was started on dual antiplatelets and high dose atorvastatin. On review by Rheumatology, his recent history of bilateral posterior circulation strokes was investigated further. Multi-level bilateral vertebral artery stenosis was seen on CT angiogram at the regional hyper-acute stroke unit and diagnosed as atheromatous in origin due to: a negative right-sided temporal artery biopsy, no GCA symptoms and modest inflammatory markers (CRP in the 30s and ESR in the 20s). Due to the onset of clear and acute GCA symptoms a left-sided temporal artery biopsy and PET scan was scheduled. Prednisolone was reduced to 40mg OD due to concern over its atherogenicity during a suspected NSTEMI. Coronary angiogram went on to show clear arteries and a subsequent cardiac MRI confirmed acute myocarditis. The left temporal artery biopsy revealed chronic inflammation with scattered giant cells. The patient was diagnosed with: GCA, extra-cranial vasculitis and myocarditis. He was treated with intravenous methylprednisolone, a weaning course of prednisolone and started on methotrexate (15mg weekly). The patient’s chest pain settled soon after admission and his troponin and inflammatory markers fell with prednisolone. DiscussionGCA seldom presents with myocarditis and can lead to significant morbidity and mortality. This remains an important differential in a patient with clear GCA features and chest pain. This case report adds to the growing body of evidence that myocarditis is a recognised feature of GCA. A literature review revealed 8 articles and a total of 9 patients with GCA who presented with or developed myocarditis.The initial diagnosis of an NSTEMI was reasonable in this case and the most probable cause of the patient’s symptoms, signs and blood results at the time. To this end, starting dual anti-platelets was justified. His prednisolone was reduced to 40mg due to concerns over accelerated atherosclerosis with high dose glucocorticoids in an already high-risk male with smoking history, hypertension and a stroke history. In retrospect, this was an unnecessary step, but arguably reasonable when weighing the risks and benefits of one treatment against a simultaneous acute illness (NSTEMI).Each subsequent investigation helped to diagnose and exclude certain conditions: the angiogram was necessary to exclude an acute coronary syndrome; cardiac MRI then went on to provide evidence of myocarditis; temporal artery biopsy confirmed GCA and a PET scan excluded any significant large vessel involvement. Interestingly, the first right-sided temporal artery biopsy 3 months prior was negative but the second left-sided biopsy was diagnostic. The BSR states that “contralateral biopsy is usually unnecessary”; however, a few studies have found discordant results when carrying out simultaneous bilateral biopsies with an increased diagnostic yield (Boyev et al., 1999; Breuer et al., 2009 and Durling et al., 2014), suggesting bilateral temporal artery biopsies could lead to less treatment delays and more accurate diagnoses.Key learning pointsMyocarditis is a recognised complication of giant cell arteritis.The key to diagnosis here was a thorough history and an open mind with regards to his background, particularly the bilateral strokes. Investigations initially did not support GCA-associated myocarditis. But the preceding typical GCA symptoms and recent strokes raised the suspicion of a more systemic vasculitis.Working off others’ diagnosis can be misleading. The very recent bilateral posterior circulation strokes and vertebral artery abnormalities were overlooked on admission due to being thoroughly worked up and disregarded as vasculitic by a tertiary stroke centre.Conflicts of interestThe authors have declared no conflicts of interest.

Long-term functional outcome after decompressive suboccipital craniectomy for space-occupying cerebellar infarction

ObjectivesSuboccipital decompressive craniectomy (SDC) is considered the best treatment option in patients with space-occupying cerebellar infarction and clinical signs of deterioration. The primary purpose of this study was to evaluate long-term functional outcome in patients one year after SDC for space-occupying cerebellar infarction, and secondly, to determine factors associated with outcome. Patients and methodsAll patients treated with SDC due to space-occupying cerebellar infarction between January 2009 and October 2015 were included in the study. Data was retrospectively collected from patient records, CT/MRI scans and surgical protocols. Long-term functional outcome was determined by the modified Rankin Scale (mRS) and mRS ≥ 4 was defined as unfavorable outcome. ResultsTwenty-two patients (16 male, 6 female) were included in the study. Median age was 53 years. Nine patients were treated with external ventricular drainage as an initial treatment attempt prior to SDC. Median time from symptom onset (stroke ictus) to initiation of the SDC surgery was 48 h (IQR 28–99 hours) and median GCS before SDC was 8 (IQR 5–10). At follow up, median mRS was 3 (IQR 2–6). Outcome was favorable (mRS 0–3) in 12 patients and unfavorable in 10 (3 with major disability, 7 dead). Brainstem infarction and bilateral cerebellar infarction were associated with unfavorable outcome. ConclusionsIn this small study, functional long-term outcome in patients with space-occupying cerebellar infarction treated by SDC was acceptable and comparable to previously published results (favorable outcome in 54% of patients). Brainstem infarction and bilateral cerebellar infarction were associated with unfavorable outcome.

Therapeutic Effect of Steroids in Osmotic Demyelination of Infancy

An 11-month-old male presented with acute gastroenteritis, seizures, and altered mental status. Laboratory workup revealed serum sodium of 177 mmol/L. Magnetic resonance imaging of the brain showed reduced diffusion in the supratentorial white matter, T2 hyperintensities in the left central pons and midbrain, subacute stroke in the right occipital lobe, and bilateral cerebellar hemorrhagic infarcts. The child was presumed to have hypernatremia-induced central pontine and extrapontine myelinolysis. He received 5 days of high-dose methylprednisolone for persistent encephalopathy and spastic quadriparesis with rapid recovery of his cognitive function and neurological examination. The child remained seizure-free and achieved normal development at 3-month and 2-year follow-ups. Osmotic demyelination of infancy may leave children with a significant neurological deficit. For favorable neurological outcome, early steroids should be considered.

Post traumatic vertebro basilar dissection: case report and review of literature

Abstract Posterior circulation territory stroke following mild head injury is a known entity although rarely seen. Numerous case reports appear in literature from time to time highlighting this complication. Blunt trauma to the head and neck possibly causes injury to the vertebrobasilar system in the form of angiorrhexis, subintimal, intramural and perivascular hemorrhage which causes secondary narrowing of the injured vessel. These processes can be complicated by progressive thrombosis &amp; vascular occlusion. Here we are reporting a case of post traumatic vertebra-basilar dissection causing bilateral cerebellar and brainstem infarct.

Cryptococcal meningitis presenting as acute onset bilateral cerebellar infarct.

Cryptococcal meningitis presenting as acute onset bilateral cerebellar infarct.