Management of Acute Cerebellar Stroke

7/25/2019 Management of Acute Cerebellar Stroke

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NEUROLOGICAL REVIEW

SECTION EDITOR: DAVID E. PLEASURE, MD

Management of Acute Cerebellar Stroke

Matt B. Jensen, MD; Erik K. St. Louis, MD

Acute cerebellar infarction or hemorrhage may initially manifest in a clinically indo-

lent manner only to later deteriorate into a life-threatening neurologic catastrophe.

At the other end of the spectrum, some patients with cerebellar stroke may present in

a moribund comatose state. In both patient groups, it is often unclear at what point

surgical intervention should be considered either to prevent further neurologic deterioration or to

try to salvage a meaningful neurologic recovery. In this review, we present clinical cases that il-lustrate decision points in the management of patients with acute cerebellar stroke, with emphasis

on clinical and imaging characteristics. We conclude with an analysis of clinical decision making

in the management of patients with space-occupying cerebellar stroke. The management of acute

cerebellar infarction or hemorrhage often requires difficult and prompt decisions by treating neu-

rologists, and certain easily identifiable clinical and imaging findings may assist in appropriate pa-

tient triage and timely neurosurgical intervention. Arch Neurol. 2005;62:537-544

Acute cerebellar infarction and hemor-rhage require constant vigilance by phy-siciansowing to often unpredictable clini-

cal behavior. Cerebellar stroke maymanifest with ataxia, vertigo, dysarthria,nausea, vomiting, and often a prominentheadache. Rapid deterioration in these pa-tients is particularly vexing because of thedifficulty in mobilizing neurosurgical in-tervention and the uncertainty regardingthe mechanism of deterioration. It is alsodifficult to determine whether ensuingcoma results from potentially reversiblecauses, such as evolving hydrocephalus,brainstem compression by mass effect, orirreversible brainstem infarction.

Data to aid clinical decision making are

limited and largely focus on the final pa-tient prognosis rather than on predictionof neurologic deterioration or the effect ofintervention on outcome. A few recentlarge retrospectiveand prospective casese-ries have attempted to address these is-sues, and they are reviewed herein in thecontext of illustrative cases. In this ar-

ticle, we present actual patient cases thatshow the clinical spectrum of cerebellarstroke, ranging from clinically stable pa-

tients to moribund patients who are co-matose at presentation. The effects of clini-cal signs and imaging results on practicalmanagement are reviewed, and conclu-sions based on a review of the literaturefor guiding decision making are pre-sented.

PREDICTING NEUROLOGICDETERIORATION IN

INITIALLY STABLE PATIENTS

Clinical Case 1: Cerebellar Infarction

A 47-year-old man with hypertension, hy-perlipidemia, and diabetes mellitus devel-oped vertigo, nausea, and vomiting. Thiscontinued to a mild extent and then wors-ened 10 days later, with a brief episode ofright hemi-numbness, right ear tinnitus,poor balance, and incoordination of theright hand that persisted. Magnetic reso-nance imaging showed bilateral cerebellarinfarcts, right larger than left (Figure 1).Magnetic resonance angiography showed

Author Affiliations:Department of Neurology, University of Iowa Hospitals andClinics and University of Iowa Carver College of Medicine, Iowa City.

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a small left vertebral artery and a high-grade stenosis inthe right vertebral artery before the origin of the poste-rior inferior cerebellar artery. The patient was admittedto the hospital and was observed closely but had no clini-cal change. His symptoms resolved, except for clumsi-ness of the right hand, which gradually improved withphysical therapy. He was given antiplatelet agents, and heachieved better risk factor control and was scheduled for

a conventional angiogram with the possibility of endo-vascular intervention of his stenosis.This case illustrates the value of serial clinical follow-

up, which is best performed in a neurologic intensive careunit. Patients with cerebellar stroke should ideally be ad-mitted to a neurologicintensive care unit for 72 to 96hoursafter first being seen to permit continuous neurosciencenursing staffobservation and frequent physician reexami-nation. If the patient remains stable through the first fewdays, when infarct swelling is expected, further deteriora-tion from cerebellar infarction is unlikely. A similar fore-

castis not always possible with cerebellar hemorrhage; theliterature is replete with cases of neurologic deteriorationdays and even weeks afterthe clinical ictusof symptom on-set.1-4 However, most patients with a cerebellar hematomawho remain stable during the first 5 hospital days are un-likely to deteriorate, and they may be safely transferred toa ward setting with continued close observation.

Clinical Case 2:Cerebellar Hemorrhage

An 81-year-old woman with a history of hypertension, dia-betes mellitus, hyperlipidemia, myocardial infarction, is-chemic stroke, and atrial fibrillation treated with warfa-rin sodium developed nausea and vomiting, followed byvertigo, left-handed clumsiness, and difficulty walking.Head computed tomography (HCT) showed a 1- to 2-cmhematoma in the cerebellum just lateralto the vermis, witha small amount of intraventricular extension (Figure 2).

Figure 1.Magnetic resonance image showing a bilateral cerebellar infarction (right left). Note the lack of compression on the brainstem and fourth ventricle.





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Her anticoagulation was reversed. On transfer to the Uni-versity of Iowa Hospitals and Clinics, she was fully alert(Glasgow Coma Scale [GCS] score of 15), andthe exami-nationfindings were normal except for mild gait, left arm,and left leg ataxia and diminished sensation in a bilateralstocking distribution, with loss of ankle jerks. The nextday the patient became progressively drowsy, with a newHCT showing hydrocephalus; ventriculostomy was per-formed. Shereturned to full alertness, andduring the nextfew weeks her ataxia improved. She was discharged from

the hospital in good condition.Most data generated on cerebellar stoke have at-tempted to predict outcome. However, on hospital ad-mission, physicians are most concerned about the po-tential for a patients condition to deteriorate. In a largeretrospective study1 regarding the prediction of neuro-logic deterioration in cerebellar hemorrhage, 46% of ini-tially alert patients (GCS score of 13-15) experienced de-terioration, with a decreasing level of consciousness,evolution of newbrainstem signs, or worsened motor re-sponse on the GCS. Statistically significant clinical andimaging features that predicted neurologic deteriora-tion included a hospital admission systolic blood pres-sure greater than 200 mm Hg, pinpoint pupils, abnor-

mal corneal or oculocephalic reflexes, extension ofhemorrhage into the cerebellar vermis, a hematoma of 3cm or greater, visible brainstem distortion on CT,thepres-ence of intraventricular hemorrhage, upward hernia-tion, and acutehydrocephalus. Multivariate analysis dem-onstrated that hemorrhage in the vermis and acutehydrocephalus independently predicted deterioration.Ourpatient had a small hemorrhage; however, it involved thevermis, with extension into the fourth ventricle.

The main differential diagnostic possibilities with de-teriorating cerebellar stroke are brainstem compression

by direct mass effect, evolution of obstructive hydro-cephalus from compression of the fourth ventricle, andocclusion of the cerebral aqueduct as a secondary phe-nomenon accompanying upward herniation of vermiancerebellar tissue through the tentorial notch.

The existing literature regarding the best approach tosuch deteriorating cerebellar stroke is relatively sparseand inconclusive. When the primary mechanism of neu-rologic deterioration seems to result from direct brain-stem compression, the literature suggests that definitive

surgical management requires a suboccipital craniec-tomy with evacuation of the hematoma or resection ofinfarcted cerebellar tissue to relieve the directly offend-ing mass effect on the brainstem.2 In addition, when de-terioration seems to result from obstructive hydrocepha-lus alone and there is no obvious evidence of directbrainstem compression by clinical examination or im-aging findings, it remains unclear whether ventriculos-tomy alone may be adequate for the prevention of fur-ther deterioration or whether definitive resection shouldstill be performed to relieve ventricular obstruction andbrainstem compression. Some experts have advocated astagedapproach, in which patients with deteriorating lev-els of consciousness, gaze palsy, or a herniation syn-

drome have emergency HCT to determine whether themechanism seems to primarily be evolving obstructivehydrocephalus, direct brainstem compression, or up-ward herniation.

If hydrocephalus seems to be the main mechanism re-sponsible for deterioration, a temporizing ventriculos-tomy can be considered. If the patient improves, no fur-ther surgical therapy may be needed. If the patient doesnot improve, then a definitive posterior fossa decom-pressive suboccipital craniectomy should be urgently un-dertaken.5,6 Because craniotomy carries an attendant el-

Figure 2.Head computed tomographic scan showing vermis involvement and minimal hemorrhage into the fourth ventricle, with little mass effect.





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evated risk of morbidity and mortality, when the patientsclinical course of deterioration is relatively slow for sev-eral hours, a strategy of staged procedures with initial ven-triculostomy followed by craniectomy if necessary is rea-

sonable. However, with more catastrophic and rapidlyevolving neurologic deterioration, for less than an arbi-trary 8-hour limit, and when theriskof craniectomy isrela-tively low, such as in younger individuals, then primarycraniectomy should probably be the treatment of choice.

Clinical Case 3:Cerebellar Infarction

A 48-year-old aerobics instructor, on traversing a step tothe right while teaching a class, developed abrupt vertigo

and continued walking to the right until she reached thewall,whichsheleaned on for support. Her symptoms sub-sided, and she finished the class. That night she vomitedtwice. For the next 2 days she had a severe headache, mildvertigo, and a tendency to veer to the right while walk-ing. She was seen for the continued headache. Her neu-rologic examination findings were normal, except for fall-ing to the right with tandem gait. After CT, the patientunderwent magnetic resonance imaging, which showedan infarct of the medial left lobe of the cerebellum

(Figure 3). Magnetic resonance angiography showed oc-clusion of the left vertebral artery, with otherwise normalcerebrovasculature. Her headache improved, and she wasdischarged from the hospital.

This case demonstrates the potential discrepancy be-tween the size of a cerebellar infarct on imaging and theseverity of the clinical course. The extent and locationof the infarct made the possibility of hydrocephalus fromobstruction of the fourth ventricle concerning enoughto warrant hospital admission for close observation in ad-dition to evaluation for the etiology of her stroke. As itturned out, had she tolerated her headache for 1 moreday, it is likely that no one would have ever known aboutthe stroke. Many cases of mild cerebellar infarction prob-

ably never reach medical attention.7

Clinical Case 4:Subdural Hemorrhagein the Posterior Fossa

A 57-year-old woman with mechanical aortic and mi-tral valves was admitted to the hospital for ischemic co-litis. She underwent hemicolectomy, before which war-farin sodium therapy was changed to heparin therapy.After a week of uneventful recovery she became progres-sively drowsy in a 24-hour period to the point of obtun-dation. Head CT showed bilateral subdural hematomasin the posterior fossa, with mass effect obliterating the

fourth ventricle and basal cisterns, and hydrocephalus(Figure 4). Anticoagulant therapy was stopped. Poste-rior fossa craniectomy with evacuation of the hema-toma and ventriculostomy were performed (Figure 5).The patient returned to full alertness and did well neu-rologically,although she developedmultiple medical com-plications that kept her in the intensive care unit.

This is an unusual case ofa vascular eventcausing acutemass effect in the posterior fossa. It demonstrates manyof the same clinical and imaging features as cerebellarstroke. The small volume of the posterior fossa allows

Figure 3.Magnetic resonance image showing an infarct of the left cerebellum with narrowing of the fourth ventricle but no hydrocephalus.

Figure 4.Head computed tomographic scan showing bilateral subduralhematomas in the posterior fossa with hydrocephalus.





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even less room for a subdural hematoma than the supra-tentorial compartment. The ominous features of thiscasewere progressive deterioration in the level of alertness,obliteration of the fourth ventricle and basal cisterns, andacute hydrocephalus. Surgical evacuation and ventricu-lar drainage prevented a likely fatal event in this patient.

CLINICALLY MORIBUNDOR COMATOSE PATIENTS

AT INITIAL EXAMINATION

The following cases demonstrate the opposite end of theclinical spectrum, when patients with a cerebellar strokeare in a comatose state on initial examination. The over-riding issue in such patients is determining neurologicsalvageability and avoiding futile surgical intervention.


A 56-year-old man began to feel unwell at a fair and wastaken to a local emergency department. During the courseof several hours he became comatose and was intu-

bated. A noncontrast HCT showed a 5-cm hematoma inthe right cerebellar hemisphere, with extension into thevermis and the fourth ventricle, acutehydrocephalus withblood present in all 4 ventricles, and effacement of thebasal cisterns (Figure 6). He was given mannitol andwas transferred to the University of Iowa Hospitals andClinics. On initial examination, the patient was coma-tose (GCS score of 4) and intubated; his pupils were 3mm and nonreactive, and corneal reflexes were absent.He had spontaneous cough. There was no motor re-sponse except decerebrate posturing of the right arm. Aright frontal ventriculostomy and a suboccipital crani-otomy with posterior fossa clot evacuation were per-formed. After surgery, there was lability of blood pres-

sure and heart rate and increasing pupillary size withoutreaction. A new HCT showed a large fourth ventricle fullof blood and upward transtentorial herniation (Figure 7).He was taken back to the operating room for reevacua-tion and decompression. After the second operation therewas no cough, gag, or brainstem reflexes or motor re-sponses. The family decided to withdraw life support, andthe patient died.


A 66-year-old man experienced the worst headache ofhis life and became unresponsive within hours. He was

intubated and then defibrillated and resuscitatedafter ven-tricular tachycardia. An HCT showed a 4-cm hematomain the left cerebellar hemisphere, with compression ofthe fourth ventricle, blood in the third and lateral ven-tricles, perihematoma hypodensity, a suggestion of up-ward herniation, and obliteration of the basal cisterns(Figure 8). His GCS score was 3, and his blood pres-sure was 67/50 mm Hg. He was administered vasopres-sors and was transferred to the University of Iowa Hos-pitals and Clinics. On arrival, the patient was comatoseand intubated, with pupils mid-position and fixed and

bilateral vitreal hemorrhages. There were no corneal, gag,oculocephalic, or motor responses. There were no spon-taneous respirations. His family decided to withdraw lifesupport, and the patient died.

CASE DISCUSSION

These cases are included in our discussion of space-occupying cerebellar stroke to point out that not all pa-

tients with deterioration have a reversible mechanism.Taneda et al8 described 3 patient groups with acute cer-ebellar stroke causing coma that vary by their clinical pre-sentation, course, and neuroradiologic appearance:

1. Alert at onset, with paroxysmal cerebellar symp-toms and signs and subsequent stabilization for 10 to 36hours, and then rapid and progressive deterioration ofconsciousness in 2 to 18 hours. This group was usuallyfound to have a syndrome of progressive direct brain-stem compression by the expanding hematoma or edema.

2. Sudden cerebellar symptoms with rapid deterio-ration of consciousness, representing hemorrhage intoa cerebellar infarct. These patients present with a cer-

ebellar hematoma, with a subsequent diagnosis of ische-mic infarction as the pathogenic mechanism made onlyat the time of surgery or autopsy.

3. Sudden unresponsiveness and coma within hoursof symptom onset, without substantial further deterio-ration. This was found to almost universally result fromextensive concurrent brainstem infarction at the time ofcerebellar hermorrhage or infarction, as was likely seenin our case 6 described previously. Amarenco9 also foundthat in patients with a hemiplegia or a tetraplegia, oftena massive comorbid paramedianpontine infarction rather

Figure 5.Head computed tomographic scan of the same patient shown inFigure 4 after craniectomy, evacuation, and ventriculostomy.





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Figure 6.A noncontrast head computed tomographic scan showing a large hematoma with vermis involvement, blood in all of the ventricles, hydrocephalus, andloss of the prepontine and quadrigeminal cisterns.

Figure 7.Despite hematoma evacuation, another computed tomographic scan of the patient in Figure 6 shows the persistence of basal cistern effacement,hydrocephalus, and upward herniation.

Figure 8.A head computed tomographic scan showing a large hematoma that obliterates the fourth ventricle, with loss of the basal cisterns, hydrocephalus, andupward herniation.





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than brainstem compression was responsible for theirdeterioration.

Several retrospective studies3,10-14 have analyzedclinical and imaging features that are predictive of pooroutcome in cerebellar hemorrhage. Clinical features onhospital admission in patients with cerebellar hemor-rhage previously correlated with a poor outcome haveincluded systolic blood pressure greater than 200mm Hg (presumed to be part of the Cushing response),4

gaze paresis,4,15,16 and a decreased level of conscious-ness,11,12,15-18 which are all indications of compression atthe pontine level. The CT scan features indicative of apoor prognosis are a midline location,13,15,19-21 an oblit-erated fourth ventricle and basal cisterns,1,13,19,22 up-ward herniation,8,23 intraventricular hemorrhage,24 andhydrocephalus.2,4,18,23 A widely accepted neurosurgicaladage is to evacuate a cerebellar hemorrhage that ismore than 3 cm in cross-sectional diameter by CT scan,but, as seen in our patient, the outcome remains poor inmany patients, and clinical criteria must enter into thedecision making.

One retrospective study25 of patient outcomes in cer-ebellar hemorrhage identified clinical and imaging fea-

tures predictive of poor outcome. Predictors of disabil-ity included a hospital admission systolic blood pressuregreater than 200 mm Hg, a hematoma size greater than3 cm in diameter, visible brainstem distortion, and acutehydrocephalus on hospital admission CT. Significant pre-dictors of death were abnormal corneal and oculoce-phalic reflexes, a GCS score less than 8, motor responseless than localization to pain, acute hydrocephalus, andintraventricular hemorrhage on CT. An absent cornealreflex on hospital admission was found to be highly pre-dictive of poor outcome. The best outcomes were in pa-tients younger than 70 years with normal corneal re-flexes. After adjustment for confounding factors, comaon hospital admission (GCS score 8) and intraven-

tricular hemorrhage were independently predictive ofdeath. Although retrospective dataare subject to bias, theclinical and imaging features identified may help curtailthe generation of unrealistic hope and may affect discus-sions regarding prognosis and intervention with familymembers.

SUGGESTIONS FOR CLINICALDECISION MAKING IN PATIENTS

WITH CEREBELLAR STROKE

These cases illustrate the range of clinical presentationsand courses in patients with cerebellar stroke. There are

many retrospective studies and a few prospective obser-vational trials that are helpful in guiding clinical deci-sion making. In the absence of data from a randomizedcontrolled trial, a reasonable framework for patient carehas been suggested by Kirolloset al,24 who treated 50 con-secutive patients using a protocol based on the appear-ance of thefourth ventricle and theGCS score. If thefourthventricle was completely effaced, the patient underwentsurgical evacuation and ventricular drainage. If the fourthventricle appeared normal, the patient was treated con-servatively, unless the GCS score deteriorated, in which

case the patient underwent ventricular drainage. If thefourth ventricle was compressed (but not completely ef-faced), the patient wastreated conservatively if fully alert,shunted if the GCS score deteriorated and hydrocepha-lus was present, or evacuated if there was no hydrocepha-lus (or if the GCS score did not improve with shunting).Mortality at 3 months was 40% (a sizeable proportionfrom medical issues). Of the survivors, 80% had a goodoutcome (independent in activities of daily living, with

a Glasgow Outcome Scale score of 4 or 5). None of thepatients with a completely effaced fourth ventricle andcoma (GCS score8) survived with a good outcome. Inthis analysis by Kirollos et al,24 outcome correlated bestwith fourth ventricular grade (P.002) and preopera-tive GCS score (P.003). Their data suggested thatpatients did better if they underwent surgery before de-terioration.

CONCLUSIONS

The clinical and imaging features of patients with cer-ebellar stroke can be helpful in clinical decision mak-ing. No single clinical or imaging finding can be used in

isolation when deciding whether to use aggressive sur-gical management or to withhold such therapy; the over-all clinical gestalt of the patient with cerebellar stroke re-mains paramount.

During the patients first week in the hospital, obser-vation in a neurologic intensive care unit may facilitatethe timely recognition of neurologic deterioration andpermit immediate repeated imaging to guide an appro-priate and tailored surgical approach. Ventriculostomymay be an adequate temporizing measure in the patientwith deterioration predominantly resulting from obstruc-tive hydrocephalus, whereas definitive treatment of pro-gressive brainstem compression most often requires cra-niectomy for decompression of the posterior fossa.

Patients with declining levels of consciousness, newbrainstem signs (particularly loss of corneal reflexes),evolving hydrocephalus, and midline cerebellar strokeare at increased risk for deterioration and poor out-come. Whether prophylactic ventriculostomy or decom-pression prevents neurologic deterioration is not clear,and this issue should be addressed in a randomized con-trolled trial; perhaps diffusion-perfusion magnetic reso-nance imaging could contribute to a better understand-ing of the importance of infarct volume or ischemicpenumbra on the risk of subsequent deterioration andpoor outcome.

Accepted for Publication:April 20, 2004.

Correspondence:Erik K. St Louis, MD, Department ofNeurology, University of Iowa Hospitals and Clinics, 200Hawkins Dr, Iowa City, IA 52242 ([email protected]).Author Contributions:Study concept and design: Jensenand St Louis. Acquisition of data: Jensen and St Louis.Analysis and interpretation of data:Jensen and St Louis.Drafting of the manuscript:Jensen and St Louis. Criticalrevision of the manuscript for important intellectual con-tent: Jensen and St Louis. Administrative, technical, andmaterial support:Jensen.Study supervision:St Louis.





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Management of Acute Cerebellar Stroke