Cerebellar Infarct


Article Author:
Kimon Ioannides
Prasanna Tadi


Article Editor:
Imama Naqvi


Editors In Chief:
Donald Kushner
Annabelle Dookie


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
3/24/2019 8:58:42 AM

Introduction

A cerebellar infarct (or cerebellar stroke) is a type of cerebrovascular event involving the posterior cranial fossa, specifically the cerebellum. Impaired perfusion reduces oxygen delivery and causes deficits in motor and balance control. In the case of hemorrhagic events, bleeding can directly damage tissue and worsen these deficits. While comprising a small fraction of strokes, cerebellar strokes are responsible for a disproportionate share of morbidity and mortality due to their sometimes subtle initial presentation and the adverse effects of reactive swelling in the posterior fossa.

Etiology

Like all strokes, cerebellar infarcts are roughly divided into ischemic and hemorrhagic events. Ischemic strokes are caused by arterial obstructions that impair blood and oxygen delivery directly. These can be further subdivided by the source of the obstruction in the blood vessel, either through migration from the heart or directly at the vasculature. The thrombotic phenomenon can occur in large or small vessels, and thromboembolic can travel from large to small vessels. These can be due to atherosclerosis or other vasculopathies, including arterial dissections, typically of the vertebral arteries in cerebellar strokes.[1][2] Emboli that originate from the heart occur due to pump failure, or due to irregular heart rhythm that disrupts smooth blood transit through the heart as in atrial fibrillation or atrial flutter. Emboli can also disseminate from the venous circulation in the presence of a right-to-left shunt such as a patent foramen ovale. Cerebral venous thrombosis can cause obstructed venous outflow resulting in infarction or hemorrhage.

In contrast to ischemic strokes, hemorrhagic strokes are usually caused by arterial bleeding that directly damages brain tissue or obstructs vascular flow through elevated local pressure. These usually occur spontaneously, especially in patients with long-standing hypertension or those taking anticoagulants or antiplatelet agents. Secondary hemorrhagic conversion can also occur from ischemic infarcts, as well as from damaged tissue due to tumor or trauma. Finally, subdural hematomas, which usually stem from tears in bridging veins between the dura and arachnoid mater, can lead to focal neurologic deficits.

Epidemiology

Cerebellar infarcts represent only about 2% of all strokes, but they account for a disproportionate share of resulting morbidity and mortality. In one study of almost 2000 consecutive stroke patients, cerebellar strokes had nearly twice the mortality rate (23%) of more common cerebral strokes (12.5%), with brainstem strokes falling in between (17%).[3]

Pathophysiology

Presenting neurologic deficits are primarily determined by the physiologic function of involved vascular territories (see figure and table). From caudal to rostral, obstruction of the posterior inferior cerebellar artery (PICA, also the most frequent location for a cerebellar infarct) leads to a headache and less commonly vomiting, vertigo, horizontal ipsilateral nystagmus, and truncal ataxia. Anterior inferior cerebellar artery (AICA) territory infarction more often leads to dysmetria, Horner's syndrome, unilateral hearing loss and ipsilateral facial paralysis or anesthesia with contralateral hemibody sensory loss of pain and temperature. Finally, obstruction of the superior cerebellar artery (SCA, located most rostral) tends to produce more ataxia, dysarthria, and nystagmus, with less vertigo, headache, and vomiting.[4] However, presentations can often be atypical or overlap, in particular for hemorrhagic infarcts.

Reactive cerebral edema surrounding the territory of an initial infarct can be especially problematic as it evolves in the case of cerebellar strokes. The cerebellum sits in the relatively tight cranial space of the posterior cranial fossa, between the tentorium cerebelli above it and the occipital bone behind and beside it, with the foramen magnum below and the fourth ventricle and brainstem in front. Swelling can lead to upward transtentorial herniation of the cerebellar vermis to relieve the rising intracranial pressure. Alternatively, edema can also obstruct the fourth ventricle and aqueducts anteriorly, causing direct brainstem compression. Since intracranial pressure builds from the choroid plexus superiorly where cerebrospinal fluid is synthesized and transmitted downwards through the remainder of the brain, obstructing the fourth ventricle can thus also create tremendous downward pressure and lead to disastrous herniation of the cerebellar tonsils into the foramen magnum.

History and Physical

Presenting symptoms of a cerebellar infarction are often nonspecific and overlap with other neurologic, cardiovascular, gastrointestinal, and systemic conditions. Particular attention paid to thoracic, abdominal, and systemic complaints and findings can lessen concern for other immediate life-threatening conditions such as trauma, aortic dissection, acute coronary syndrome, pulmonary embolism, hypovolemia, or sepsis. Other common misdiagnoses include vestibular neuronitis, migraine, syncope (potentially due to orthostasis or arrhythmia), hypertensive emergency, renal failure, hypoglycemia, and ethanol or drug intoxication. As with other strokes, historical features guide risk stratification and treatment planning.

The time of onset and progression of symptoms can be particularly helpful along with provoking and mitigating factors in the determination of cerebellar strokes and differential diagnoses. As a general rule, symptoms starting over seconds to minutes are attributable to benign paroxysmal positional vertigo (BPPV), vasovagal syncope, or arrhythmia. Symptoms starting over minutes to hours are often due to hypoglycemia, migraine, or psychological causes. Finally, symptoms starting over hours to days are attributable to labyrinthitis or medication side effects but are also suspicious for cerebellar infarct. Even longer lasting symptoms can be concerning for a growing posterior fossa mass. Symptoms triggered by loud noises can point towards peripheral inner ear disease, those extinguished by eye closing can point towards an ophthalmologic cause, those arising from changes in body posture (as opposed to head movement) can point towards a cardiovascular condition, but those triggered by walking are most suspicious for a cerebellar infarct. Risk factors for vascular disease such as age, smoking, obesity, diabetes, hyperlipidemia, and hypertension can increase concern for cerebellar infarcts as well.

Commonly, about 75% of patients will report "dizziness" of some form, with a sensation of vertigo or of falling towards one side. Many patients will complain they cannot walk or can do so only with difficulty, either due to ataxia or to focal or systemic "weakness." More than 50% report nausea or vomiting. Most often symptoms are more severe than examination findings. These neurologic findings can include localizing signs such as truncal or limb ataxia, cranial nerve defects such as diplopia or nystagmus (often direction-changing or gaze-evoked, more worrying if vertical or torsional), and dysarthria. In contrast to cerebral strokes, these are usually ipsilesional (occurring on the same side of the patient as the cerebellar stroke). For patients with larger strokes or with advanced features of elevated intracranial pressure or brainstem compression, patients can present simply with lethargy, frank coma, or cardiovascular collapse, each of which portends a poor outcome.

Evaluation

Magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) of the brain represents the gold standard test for cerebellar infarction. This can visualize both poor perfusion and signs of tissue injury. Also, magnetic resonance angiography (MRA) can localize a vascular obstruction and guide endovascular treatment in the presence of large vessel occlusion, which can be particularly helpful in cases of basilar artery occlusion. Unenhanced computed tomography (CT) imaging can be helpful to assess for hemorrhagic lesions and can occasionally demonstrate findings suggestive of infarction. However, it is greatly hampered by the radiopaque temporal and occipital bones that surround the cerebellum, and thus has limited resolution, sensitivity, and specificity compared with other areas of the brain. It is nevertheless usually performed initially, in part to assess for other causes, but also because it is often much more readily available than MRI or MRA. If MRI is not available, enhanced CT angiogram and perfusion imaging can be helpful in its place. Apart from a standard bedside neurological exam, the oculomotor "HINTS" exam (Head Impulse, Nystagmus, and Test of Skew) can be helpful to rule-in peripheral vertigo or suggest cerebellar infarction if the included "alternate eye cover test" shows skew deviation.[5][6] Laboratory, electrocardiographic, echocardiographic, and electroencephalographic evaluation for other systemic conditions can be obtained to assist with management of concurrent medical or surgical management.

Treatment / Management

Cerebellar infarcts are treated largely like other ischemic cerebrovascular accidents. Patients with acute events having a clear time of onset within 4.5 hours may be candidates for thrombolysis with recombinant tissue plasminogen activator (rtPA). However, given the difficulty of diagnosing posterior infarcts, this is often not possible. As with other strokes, thrombectomy can be an option. Since structures in the posterior circulation may have greater white matter content[7] and collateral flow, they are thought to have a stronger tolerance to ischemia and hypoxia than those in the forebrain. Especially in larger basilar artery occlusion, thrombectomy is often considered outside of the usual 6 hour time window, and posterior infarcts are considered amenable to even delayed reperfusion therapy.[8] Brain imaging showing a large difference or “mismatch” between the volume of brain infarcted and the area of decreased perfusion or a high degree of collateral circulation may prompt more emergent thrombectomy. When reperfusion is not an option, aspirin therapy and possibly another antiplatelet agent such as clopidogrel are indicated, with the possible addition of anticoagulation therapy in patients with embolic events. Reactive cerebral edema typically worsens over 3 to 4 days after the initial infarct and if causing worsening neurological symptoms, mandates admission to a neurologic intensive care setting for monitoring. Underlying preventable causes of the infarct are usually investigated during admission. Cardiac monitoring can demonstrate atrial fibrillation or other arrhythmias, echocardiography can reveal a patent foramen ovale or ventricular dysfunction, and blood testing can reveal diabetes mellitus or hyperlipidemia.

Large strokes with significant cerebral edema, especially if intracranial pressure is elevated, often require extraventricular drains, ventriculostomy, or decompressive sub-occipital craniotomy. Neurosurgical removal of infarcted tissue or hematoma is also occasionally necessary. In these cases rapidly reversible agents such as intravenous heparin should be used. In the acute setting, mannitol, hypertonic saline, or hyperventilation can also be helpful to temporarily reduce intracranial pressure.


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    Contributed by B. Petit, CC BY-SA 4.0
Attributed To: Contributed by B. Petit, CC BY-SA 4.0

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Cerebellar Infarct - Questions

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A 67-year-old female with a history of hypertension is brought to the emergency department with a headache, nausea, vomiting, and dizziness. CT is normal. Her examination is normal, but the patient falls to the floor when getting off the stretcher. Select appropriate management.



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A 62-year-old female smoker with a history of hypertension is brought to the emergency department with sudden onset of dizziness, nausea, vomiting, and a bifrontal headache. The basic CT of the brain is negative. What is the most likely diagnosis?



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A 74-year-old male is brought to the emergency department by ambulance after his daughter had not heard from the patient in several days and found him in bed at home unresponsive, with urinary and fecal incontinence. On arrival, he has sonorous respirations at a rate of 16/min, a heart rate of 51 bpm, blood pressure of 193/122 mmHg, and temperature of 98.6F. He has no signs of trauma, withdraws from painful stimuli but will not answer questions or open his eyes. Pupils are 7 mm bilaterally and not reactive, with significant retinal papilledema. What is the most likely underlying cause of this patient’s altered mental status?



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A 53-year-old female with a history of coronary artery disease requiring placement of a drug-eluting sent three years ago presents to a primary care clinic complaining that she cannot feel her left arm and leg for the last few days. On review of systems, she notes that she has been feeling nauseous and dizzy as well. Her neurologic exam is notable for a droopy right eyelid reactive pupils that are 2 mm on the right and 4 mm on the left, and an asymmetric smile. She has complete anesthesia to pain and temperature on the left arm and leg as well as on the right side of her face, and mild left-sided ataxia on finger to nose test. What is the most likely location for the lesion causing her numbness symptoms?



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A 57-year-old male with a history of hypertension and alcoholism in remission presents to the emergency department (ED) at 2 pm, one hour after experiencing sudden severe vertigo with projectile vomiting. His coworkers at a school where he works as history teacher also noted that he was stumbling while at work and had suspected that he was intoxicated earlier in the morning. His symptoms are much improved on ED arrival after getting 500 cc of normal saline from emergency medical services. His case is activated as a “stroke alert” and is taken for emergent computed tomography of the head. You review his scan which appears normal with good grey-white matter differentiation and age-appropriate volume loss, similar to a prior scan from 18 months ago. You go to re-evaluate the patient after he returns from radiology. He states he feels much better and his symptoms are completely resolved. He believes he was dehydrated and is asking when he will be discharged. You assess his NIH stroke scale which is now zero. What is the most reasonable course of action?



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A 45-year-old female lawyer presents one hour after experiencing constant projectile vomiting lasting 10 to 20 minutes just before a court hearing. She had trouble walking out of the bathroom at the courthouse and called 911 using her cell phone for help. On arrival to the emergency department, she is sitting up in the stretcher with her eyes closed but awake, alert, oriented, and appropriate. Her vital signs are heart rate of 82 bpm, blood pressure 122/85 mmHg, respiratory rate of 15/min, temperature of 98.2F, and a point-of-care glucose is 105. She says she still feels nauseous but has not vomited in the last 30 minutes. She also complains that she feels as though she’s spinning constantly, and her voice is slightly slurred but still readily understandable. On exam, she has some dysmetria, and her gait demonstrates mild ataxia. She has intact extraocular movements, no facial weakness, and vertical nystagmus. She complains of discomfort when you palpate her abdomen, worst in the epigastrium, but no guarding or rebound. What is the most appropriate imaging modality to identify the cause of her symptoms?



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A 63-year-old woman presents with a sudden onset of vertigo, nausea, and facial droop with unilateral hearing loss. This is most likely associated with a stroke in which vascular territory?



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A 52-year-old man with a history of migraines, cocaine abuse, schizophrenia, and hypertension is transferred to a tertiary care stroke center from a community hospital with a cerebellar stroke. He received tissue plasminogen activator at the community hospital with improvement in his symptoms while en route. On the third day of admission, he complains of a worsening headache associated with nausea and vomiting. He locates the aching, severe pain in the middle of his head. It is improved when can keep the lights in his hospital room off. He asks for you to give him diphenhydramine and metoclopramide, which he says always relieve his migraines at home. His blood pressure is 151/87 mmHg, and his heart rate is 87 bpm. An admission EKG had a QTc of 416 ms. He has horizontal gaze-evoked nystagmus. What should be done next?



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Cerebellar Infarct - References

References

Clinical and video head impulse test in the diagnosis of posterior circulation stroke presenting as acute vestibular syndrome in the emergency department., Guler A,Karbek Akarca F,Eraslan C,Tarhan C,Bilgen C,Kirazli T,Celebisoy N,, Journal of vestibular research : equilibrium & orientation, 2017     [PubMed]
Isolated Posterior Inferior Cerebellar Artery Dissection., Wada Y,Kitano T,Uemura J,Yagita Y,, Internal medicine (Tokyo, Japan), 2017 Nov 1     [PubMed]
Ataxia and Headache in a Child: A Case of Acute Cerebellar Infarction., Hewett KM,Lorenzetti B,Jackson BF,, Pediatric emergency care, 2017 Aug     [PubMed]
Vertebral Artery Dissection in a Bouncy Castle Injury: Case Report and Literature Review., Ripa V,Urakov TM,Jernigan SC,, Pediatric neurosurgery, 2017     [PubMed]
Kattah JC,Talkad AV,Wang DZ,Hsieh YH,Newman-Toker DE, HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009 Nov;     [PubMed]
Macdonell RA,Kalnins RM,Donnan GA, Cerebellar infarction: natural history, prognosis, and pathology. Stroke. 1987 Sep-Oct;     [PubMed]
Mattle HP,Arnold M,Lindsberg PJ,Schonewille WJ,Schroth G, Basilar artery occlusion. The Lancet. Neurology. 2011 Nov;     [PubMed]
Vergouwen MD,Algra A,Pfefferkorn T,Weimar C,Rueckert CM,Thijs V,Kappelle LJ,Schonewille WJ, Time is brain(stem) in basilar artery occlusion. Stroke. 2012 Nov;     [PubMed]
Kase CS,Norrving B,Levine SR,Babikian VL,Chodosh EH,Wolf PA,Welch KM, Cerebellar infarction. Clinical and anatomic observations in 66 cases. Stroke. 1993 Jan;     [PubMed]
Tohgi H,Takahashi S,Chiba K,Hirata Y, Cerebellar infarction. Clinical and neuroimaging analysis in 293 patients. The Tohoku Cerebellar Infarction Study Group. Stroke. 1993 Nov;     [PubMed]

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