Diagnosis and Management of Acute Cerebellar Infarction
2014; Lippincott Williams & Wilkins; Volume: 45; Issue: 4 Linguagem: Inglês
10.1161/strokeaha.114.004474
ISSN1524-4628
AutoresJames Wright, Christina Huang, Daniel Strbian, Sophia Sundararajan,
Tópico(s)Traumatic Brain Injury and Neurovascular Disturbances
ResumoHomeStrokeVol. 45, No. 4Diagnosis and Management of Acute Cerebellar Infarction Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBDiagnosis and Management of Acute Cerebellar Infarction James Wright, MD, Christina Huang, MD, Daniel Strbian, MD, PhD and Sophia Sundararajan, MD, PhD James WrightJames Wright From the Neurological Institute, University Hospitals Case Medical Center, Cleveland, OH (J.W., S.S.); Department of Neurological Surgery, University of Southern California Los Angeles County Medical Center, CA (C.H.); and Departments of Neurology and Stroke Units, Helsinki University Central Hospital, Helsinki, Finland (D.S.). , Christina HuangChristina Huang From the Neurological Institute, University Hospitals Case Medical Center, Cleveland, OH (J.W., S.S.); Department of Neurological Surgery, University of Southern California Los Angeles County Medical Center, CA (C.H.); and Departments of Neurology and Stroke Units, Helsinki University Central Hospital, Helsinki, Finland (D.S.). , Daniel StrbianDaniel Strbian From the Neurological Institute, University Hospitals Case Medical Center, Cleveland, OH (J.W., S.S.); Department of Neurological Surgery, University of Southern California Los Angeles County Medical Center, CA (C.H.); and Departments of Neurology and Stroke Units, Helsinki University Central Hospital, Helsinki, Finland (D.S.). and Sophia SundararajanSophia Sundararajan From the Neurological Institute, University Hospitals Case Medical Center, Cleveland, OH (J.W., S.S.); Department of Neurological Surgery, University of Southern California Los Angeles County Medical Center, CA (C.H.); and Departments of Neurology and Stroke Units, Helsinki University Central Hospital, Helsinki, Finland (D.S.). Originally published20 Feb 2014https://doi.org/10.1161/STROKEAHA.114.004474Stroke. 2014;45:e56–e58Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2014: Previous Version 1 IntroductionAn 80-year-old woman was admitted for lethargy and vomiting after diagnostic cardiac catheterization. Initially, her symptoms were attributed to sedation; however, after failing to improve four hours later despite treatment with opioid antagonists, urgent neurological consultation was obtained. Initially, the patient's systolic blood pressure was >180 mm Hg. She was nauseated with continued vomiting. Her examination was significant for lethargy, dysarthria, bilateral upper extremity ataxia, and bilateral inferomedial gaze deviation. Emergent noncontrasted computed tomography (CT) of the head showed questionable bilateral cerebellar infarcts that MRI confirmed (Figure). She was started on low-dose aspirin and clopidogrel and transferred to the Neurological Intensive Care Unit for monitoring. The next morning aspirin and clopidogrel were held in favor of heparin, in case she required neurosurgical intervention. Forty-eight hours after the catheterization, she became obtunded, and CT of the head showed worsening posterior fossa edema and obstructive hydrocephalous (Figure), requiring placement of an external ventricular drain (EVD) followed by urgent suboccipital decompressive. After surgery, her mental status improved. At the time of discharge, she had severe bilateral upper extremity dysmetria and was nonambulatory.Download figureDownload PowerPointFigure. A, Initial computed tomography head showed questionable cerebellar infarcts at 5 hours of symptoms. B, Infarcts were clearly evident on MRI at 6 hours. C, Within 48 hours, cerebral edema effaced the fourth ventricle, enlarged the temporal horns of the lateral ventricles, and compressed the brain stem.This case demonstrates several important points about cerebellar infarcts including the disproportionate number of posterior circulation strokes after cardiac catheterization, the difficulty recognizing cerebellar infarctions and, most importantly, the potential for rapid deterioration requiring urgent neurosurgical intervention.Cerebellar infarcts are relatively uncommon and represent ≈2% of all ischemic strokes.1,2 Potential pathogeneses include cardiac emboli, large-vessel atherosclerosis, vertebral artery dissection, local arterial disease, and less commonly hypercoagulable conditions, vasculitis, venous sinus thrombosis, and drug use.1–4Although 80% to 90% of ischemic infarctions occur in the anterior circulation, >50% of infarcts after cardiac catheterization affect the posterior circulation.3 The reasons for disproportionate embolization to the posterior circulation are unclear, but may, in part, be because of manipulation of the catheter within the subclavian arteries near the vertebral origins while catheterizing the internal mammary arteries.The blood supply of the cerebellum consists of the posterior inferior cerebellar arteries (PICAs), branches of the vertebral artery, and the anterior inferior cerebellar arteries (AICAs) and the superior cerebellar arteries (SCAs), which arise from the basilar artery. PICA supplies the lateral medulla, the inferior cerebellum, and the inferior cerebellar peduncle. AICA supplies the anterior portion of the inferior cerebellum, the middle cerebellar peduncle, and the facial and vestibulocochlear nerves. The superior cerebellar artery supplies most of the cerebellar cortex, the cerebellar nuclei, and the superior cerebellar peduncles.Cerebellar infarcts require special attention because of the danger of cerebral edema within the posterior fossa. The cerebellum and brain stem are tightly constrained by the tentorium cerebelli superiorly, and the occipital bone and foramen magnum posteriorly.5 Within the posterior fossa, cerebral edema can rapidly obstruct the fourth ventricle, causing hydrocephalus. In addition, cerebral edema can compress the brain stem causing potentially fatal transtentorial herniation of the superior vermis through the tentorial notch or downward herniation of the cerebellar tonsils through the foramen magnum.3DiagnosisThe initial symptoms of cerebellar infarction or hemorrhage may be nonspecific such as headache, dizziness, nausea, vomiting, and vertigo; >50% of cerebellar strokes present with nausea and vomiting, and ≈75% of them present with dizziness. Impaired level of consciousness is also common with 26% of patients demonstrating lethargy and 3% presenting with coma.1,6,7 Ninety percentage of patients with cerebellar infarction have localizing signs including truncal and appendicular ataxia, nystagmus, and dysarthria.8 Importantly, 71% of patients with isolated vertigo attributable to cerebellar infarction are unable to walk, and many also have direction-changing or gaze-evoked nystagmus, in which the direction of the nystagmus changes according to the patient's gaze.8 Neuronal tracts between the cerebellum and limbs are either doubly crossed or uncrossed, so that motor deficits are typically ipsilesional.3 Another ominous, but common sign of large cerebellar infarction, is altered mental status, usually lethargy. The German-Austrian Cerebellar Infarction Study, a multicentered prospective study, found that the level of consciousness after onset of clinical deterioration was the greatest predictor of clinical outcome.9Several studies show that symptoms of cerebellar infarction are dependent on the vascular territory affected.1,3,6 Patients with PICA territory infarcts most commonly present with acute vertigo, vomiting, headache, gait disturbances, and horizontal nystagmus ipsilateral to the lesion. Headache is the most common initial symptom, and is 20% to 30% more common in PICA distribution infarcts than AICA or SCA infarcts. Vertigo is also more frequent in PICA strokes as compared with SCA infarcts. In SCA territory infarcts, gait and limb ataxia, dysarthria, and horizontal nystagmus are more pronounced, and fewer patients experience headache and vomiting.1,3,4,6 PICA infarcts are the most common cerebellar infarcts.3,10,11NeuroimagingRapid neuroimaging should be obtained in all patients with acute cerebellar dysfunction to rule out cerebellar hemorrhage. Cerebellar hemorrhage with rapidly expanding hematoma in the posterior fossa is a neurosurgical emergency and may require rapid decompression. Noncontrasted CT is the initial modality of choice to identify hemorrhage or subacute infarction; however, because of bone artifact and white to gray matter ratio, noncontrasted CT has a low sensitivity for detection of posterior fossa infarctions, especially in the acute setting. It is important to note that a normal CT of the head does not rule out cerebellar infarction, either in the acute or in the subacute period. MRI, specifically diffusion-weighted imaging, may be required to make the diagnosis.12,13ManagementManagement of cerebellar infarction is similar to infarcts of other areas of the brain. Thrombolysis is indicated acutely, but few patients receive tissue-type plasminogen activator attributable to the difficulty in recognizing acute cerebellar infarction. Patients should undergo diagnostic testing to determine the cause of the infarct including echocardiogram, testing for stroke risk factors including diabetes mellitus, hypertension, and hyperlipidemia, and treatment with antiplatelet or anticoagulant agents. In addition, because of the potentially fatal consequences of cerebral edema in the posterior fossa, these patients need close neurological monitoring and may require neurosurgical intervention. Clinically significant cerebellar edema, usually manifest by a reduced level of consciousness, typically occurs within 1 to 7 days, with a mean peak of 3 days.9 Medical management with osmotic diuretics such as mannitol or hypertonic saline may help reduce edema and may be sufficient in borderline cases, but surgical treatment is the management of choice.Decompressive SurgeryEmergent decompressive surgery by suboccipital craniectomy, with or without partial removal of infarcted tissue, can be life saving and can preserve quality of life.10,12,14,15 According to the American Stroke Association guidelines, decompressive surgical evacuation of space-occupying cerebellar infarction is effective in preventing and treating herniation and brain stem compression and was given a Class I/Level B evidence recommendation.12 Emerging data indicate that the area of diffusion restriction on MRI may not represent complete permanent damage. These data suggest that resection of necrotic tissue might compromise functional long-term recovery, and tissue resection should be limited to the minimum required to achieve adequate decompression.16,17External Ventricular DrainageThe exact role of EVD placement in cerebellar infarction is still widely debated. Historical studies indicated that EVD placement for cerebellar infarction increased mortality, presumably because of upward herniation or infection. Multiple series have been performed since 2003 indicating that some patients may be managed with EVD placement for symptomatic hydrocephalus, at least as a temporizing measure before surgery.7,9,10,16–18 The American Stroke Association guidelines support operative intervention and decompression compared with EVD placement alone. In the setting of acute hydrocephalus, where transition to the operating room may be delayed, EVD placement and rapid reduction in intracranial pressure may decrease mortality and prove lifesaving.12Take-Home Points:Patients with cerebellar stroke may present with generalized symptoms. A high index of suspicion must be maintained in patients with significant risk factors.CT has low sensitivity for infarctions of the posterior fossa. If suspicion of infarction is high, MRI/diffusion-weighted imaging sequences should be obtained.Emergent placement of an external ventricular drain or posterior fossa decompression may be lifesaving in patients with hydrocephalous or brain stem compression.In cases that may require neurosurgical intervention, rapidly reversible forms of anticoagulation, such as unfractionated heparin infusion, may be preferable to antiplatelet agents.DisclosuresNone.FootnotesCorrespondence to Sophia Sundararajan, MD, Neurological Institute, University Hospitals Case Medical Center, 11100 Euclid Avenue, Cleveland, OH 44106. E-mail [email protected]References1. Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural history, prognosis, and pathology.Stroke. 1987; 18:849–855.LinkGoogle Scholar2. Tohgi H, Takahashi S, Chiba K, Hirata Y. Cerebellar infarction. Clinical and neuroimaging analysis in 293 patients. 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Beyond mismatch: evolving paradigms in imaging the ischemic penumbra with multimodal magnetic resonance imaging.Stroke. 2003; 34:2729–2735.LinkGoogle Scholar18. van Loon J, Van Calenbergh F, Goffin J, Plets C. Controversies in the management of spontaneous cerebellar haemorrhage. A consecutive series of 49 cases and review of the literature.Acta Neurochir (Wien). 1993; 122:187–193.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Soltani Zangbar H, Gorji A and Ghadiri T (2020) A Review on the Neurological Manifestations of COVID-19 Infection: a Mechanistic View, Molecular Neurobiology, 10.1007/s12035-020-02149-0, 58:2, (536-549), Online publication date: 1-Feb-2021. Dusenbury W and Alexandrov A (2020) Clinical Localization of Stroke, Critical Care Nursing Clinics of North America, 10.1016/j.cnc.2019.10.001, 32:1, (1-19), Online publication date: 1-Mar-2020. Costa C, Arneiro G, Branco I, Lucas C, Romão A, Rodrigues C and Proença V (2019) Does vestibular rehabilitation optimize physiotherapy benefits in the early stages of PICA stroke recovery? A case series, Annals of Medicine, 10.1080/07853890.2018.1560738, 51:sup1, (224-224), Online publication date: 29-Mar-2019. Fong J, Gutierrez A and Vohra A (2018) Cerebellar infarction with 4th ventricle compression in a 46 year old man, Visual Journal of Emergency Medicine, 10.1016/j.visj.2018.07.032, 13, (31-32), Online publication date: 1-Oct-2018. April 2014Vol 45, Issue 4 Advertisement Article InformationMetrics © 2014 American Heart Association, Inc.https://doi.org/10.1161/STROKEAHA.114.004474 Manuscript receivedJanuary 7, 2014Manuscript acceptedJanuary 8, 2014Originally publishedFebruary 20, 2014 Keywordsbasal ganglia cerebrovascular diseasestrokePDF download Advertisement SubjectsCardiopulmonary Resuscitation and Emergency Cardiac CareCerebrovascular Disease/Stroke
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