Ocular Ipsipulsion Caused by Posterior Inferior Cerebellar Artery Stroke
2022; Lippincott Williams & Wilkins; Volume: 53; Issue: 3 Linguagem: Inglês
10.1161/strokeaha.121.037510
ISSN1524-4628
Autores Tópico(s)Ophthalmology and Eye Disorders
ResumoHomeStrokeVol. 53, No. 3Ocular Ipsipulsion Caused by Posterior Inferior Cerebellar Artery Stroke Free AccessCase ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessCase ReportPDF/EPUBOcular Ipsipulsion Caused by Posterior Inferior Cerebellar Artery Stroke Zelie Britton, MBBS, BSc and Gregory Scott, MBBS, PhD Zelie BrittonZelie Britton National Hospital for Neurology and Neurosurgery, London, United Kingdom (Z.B., G.S.). and Gregory ScottGregory Scott Correspondence to: Gregory Scott, MBBS, PhD, Honorary Clinical Lecturer, Department of Brain Sciences, Imperial College London, London, W12 0NN, United Kingdom. Email E-mail Address: [email protected] https://orcid.org/0000-0001-8063-5871 National Hospital for Neurology and Neurosurgery, London, United Kingdom (Z.B., G.S.). Department of Brain Sciences, Imperial College London, United Kingdom (G.S.). Originally published9 Feb 2022https://doi.org/10.1161/STROKEAHA.121.037510Stroke. 2022;53:e122–e125Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: February 9, 2022: Ahead of Print A 65-year-old right-handed woman presented to our hyperacute stroke service with sudden onset rotatory vertigo, vomiting, inability to walk or stand unaided, and left hand numbness. She had a history of Grave disease, hypertension, and atrial fibrillation secondary to mitral valve disease, for which she had undergone a mitral valve repair 3 months previously. Her anticoagulation had been stopped 2 weeks before presentation after the finding of sinus rhythm on a routine ECG.On examination, she was alert and orientated with a blood pressure of 148/76 mm Hg. An ECG showed atrial fibrillation. There was a tonic conjugate deviation of the eyes towards the left, apparent when the eyes opened after a period of closure, which was overcome by fixation (Video, from 00 m:00 s). There was a full range of eye movements, but right-beating nystagmus, most pronounced on rightward gaze (00:16). Horizontal saccades were hypermetric when directed towards the left and hypometric towards the right (00:16). Vertical saccades were deviated to the left. Pursuit movements were jerky bilaterally, worse when directed leftwards. There was no Horner syndrome. There was subtle left upper and lower limb ataxia (01:09) with upper limb dysmetria. Pinprick and temperature sensation were reduced on the left side of the face (00:53) but on the right side of the trunk and extremities. The gait was severely ataxic. The remaining neurological examination was normal.Urgent CT head and CT angiography demonstrated subtle hypodensity within the left cerebellar hemisphere in the posterior inferior cerebellar artery (PICA) territory with corresponding occlusion of the left PICA and a free-floating thrombus in the left vertebral artery (V4; Figure [A]). There was no associated atheroma, suggesting a cardio-embolic cause. Leftward conjugate ocular deviation was noted on these scans (Figure [B]).Download figureDownload PowerPointFigure. Acute imaging.A, Acute CT head and angiography demonstrated subtle hypodensity within the left cerebellar hemisphere (red star) in the posterior inferior cerebellar artery (PICA). Just distal to the origin of the left PICA, there was a filling defect within the V4 segment, representing a floating thrombus (red arrow). B, Leftward conjugate gaze deviation is evident on the acute CT scan. C and D, Restricted diffusion (shown on diffusion weighted imaging and apparent diffusion coefficient sequences, respectively) in the left cerebellum and posterior left medulla, consistent with a left PICA infarction.The patient had arrived outside the window for intravenous thrombolysis and mechanical thrombectomy. Given the vertebral artery thrombus, she was treated with low molecular weight heparin. She was admitted to the hyperacute stroke unit. The next day, a magnetic resonance imaging scan demonstrated restricted diffusion and swelling in the left cerebellum and posterior left medulla consistent with a subacute left PICA infarction (Figure [C] and [D]). Transthoracic echocardiography showed normal biventricular function, borderline left atrial enlargement, and evidence of recent mitral valve repair. There was no intracardiac thrombus or valvular vegetations.After one week, her vertigo and nausea had improved. The eye signs had largely resolved but she remained ataxic, and the ipsilateral face and contralateral trunk and limb sensory signs persisted. The thrombus resolved on repeat angiography. She was discharged to neurorehabilitation.DiscussionAcute vertigo is a common presentation to the emergency department, and ≈5% of cases are caused by stroke.1 Examination of ocular movements is helpful in differentiating central from peripheral causes of acute vertigo, as in this case of lateral medullary syndrome, but the features may be subtle.Localization of Conjugate Eye DeviationHorizontal conjugate eye deviation (CED) provides valuable localizing information and occurs in about 20% of acute stroke presentations.2,3 The causes of CED are summarized in the Table. In our case, the patient's eyes were at times tonically deviated to the left, which became apparent when fixation was removed, with eyes closed and in the scanner. Traditional teaching is that the gaze deviation is generally directed towards the side of the lesion in the well-recognized case of supratentorial strokes which disrupt the cortical frontal eye fields and associated pathways. More rarely, CED can be directed contralaterally, as in a pontine lesion, resulting from disruption to the paramedian pontine reticular formation, or horizontal gaze center. Lateral medullary lesions, here associated with PICA occlusion, are therefore unusual for an infratentorial lesion in that gaze is deviated towards the side of the lesion. In lateral medullary syndrome, CED is not uncommon, but it may go unnoticed unless actively sought: in one study of 14 cases, CED was found in 12 patients with eyes closed but only 4 with eyes open.4Table 1. Localization of Horizontal Conjugate Eye DeviationLocalizationDirection relative to side of lesionNotesSupratentorial (FEF, others*)Ipsilateral (common)≈30% of acute supratentorial stroke, more common in right hemisphere lesions.3Contralateral (very rare)Can be contralateral ("wrong-way deviation") in extensive hemispheric stroke (secondary damage to midbrain)Pontine (PPRF)Contralateral (rare)Associated with internuclear ophthalmoplegia, contralateral hemiparesis and hemisensory loss, and ipsilateral lower motor neuron facial nerve palsyLateral medullaIpsilateral (common)Associated with other features of lateral medullary syndromeSeizureFEFContralateral to side of seizure activitySeizures involving the frontal lobe may also show contralateral head version.Postictally, with subsequent FEF hypoactivity, eyes may deviate ipsilaterally (relative hyperactivity in unaffected opposite FEF).OthersThalamicContralateral (rare)"Wrong-way deviation," typically associated with hemorrhage.Thalamic and midbrain lesions are more commonly associated with vertical gaze abnormalities.FEF indicates frontal eye fields; and PPRF, paramedian pontine reticular formation.* Includes both the FEF and other pathways involved directly in eye movements, and structures implicated in hemi-spatial neglect.Ocular IpsipulsionIn lateral medullary syndrome, CED is the result of tonic ocular drift towards the side of the lesion: ocular ipsipulsion. This drift is faster when fixation is removed and when looking away from the lesion.5 Ocular ipsipulsion is accompanied by saccadic lateropulsion (hypometric saccades away from the lesion and hypermetric saccades towards the lesion). Vertical saccades, particularly when directed upwards, are deflected towards the lesion. The fast phase of optokinetic and vestibular nystagmus are also affected, with reduced amplitudes directed away from the lesion.5 Smooth pursuit is impaired, with pursuit away from the lesion slowed and requiring catch-up saccades, and relatively normal, or too fast, pursuit towards the lesion.5 The cause of ocular ipsipulsion in lateral medullary syndrome is believed to be functional impairment of the ipsilesional vestibular nucleus, leading to an asymmetry in resting vestibular tone, driving the eyes away from the intact vestibular nucleus and thus towards the side of the lesion. In our case, with a lesioned left vestibular nucleus, the patient had slow phase eye movement towards the left as a result of a relative right-sided vestibular hyperactivity, with additional right-beating nystagmus.The PICA supplies the lateral medulla and the inferior cerebellar surface. The cerebellar flocculus is supplied by the anterior inferior cerebellar artery. Most commonly, PICA infarcts affect the lateral medulla dorsally up to the inferior olive, an area that is traversed by crossed, inhibitory olivocerebellar fibers. These fibers project via the ipsilateral cerebellar peduncle to Purkinje fibres, whose inhibitory inputs on the ipsilateral vestibular nuclei increase, thus leading to an asymmetry of vestibular nuclear tone with relatively more tone from the contralateral vestibular nucleus, driving the eyes away from itself—and towards the side of the lesion. In animal studies, lesions of the inferior olive and of climbing fibres result in an increase in the firing rate of Purkinje cells, with subsequent reduced activity of vestibular nuclei neurons, that returns to normal over 2 to 4 weeks.6 Interestingly, in a study examining the eye movements of patients with MR-confirmed PICA-territory infarctions, ocular drift and the accompanying nystagmus was not seen in those patients who had exclusively cerebellar (and not lateral medullary) infarctions.5Neural Control of Eye MovementsWe briefly review the control of the relevant eye movements. Eye movements can be classified into 7 categories: fixation, smooth pursuit, quick-phase nystagmus, saccades, vergence, optokinetic, and vestibular movements.SaccadesVoluntary saccades are largely generated by the frontal eye field, while involuntary saccades are triggered by the superior colliculus. Both connect to the paramedian pontine reticular formation from where burst neurons project to the ipsilateral abducens nucleus and via the medial longitudinal fasciculus to the contralateral oculomotor nucleus. Saccadic accuracy is maintained by the cerebellar dorsal vermis, whose inhibitory Purkinjie fibres discharge just before and at the end of saccades. The dorsal vermis also controls initiation and maintenance of smooth pursuit. Lesions in the dorsal vermis cause an ipsilateral hypometria with subtle contralateral hypermetria, tonic contralateral gaze deviation, and disrupted smooth pursuit towards the lesion.7 Experimental lesions in the fastigial nucleus causes ipsilateral saccadic hypermetria, contralateral hypometria, gaze deviation towards the lesion, and disrupted smooth pursuit away from the lesion.8PursuitInitiation (and termination) of smooth pursuit is generated in the visual cortex, middle temporal/medial superior temporal region, the supplementary eye fields and frontal eye field, which project via the pons to the dorsal vermis and fastigial nucleus of the cerebellum. Pursuit is maintained by the cerebellar flocculus and paraflocculus, nucleus prepositus hypoglossi in the pons/medulla oblongata, and the vestibular nuclei.Gaze-HoldingGaze-holding relies on common neural integrators that provide information about velocity and position. The medial vestibular nuclei and nucleus prepositus hypoglossi are the horizontal neural integrators, and receive inputs from the vestibular nuclei, cerebellar fastigial nuclei, flocculus and ipsilateral paramedian pontine reticular formation, and project to the nuclei of the extraocular muscles (and to the vestibular nuclei, vestibulo-cerebellum and posterior vermis). The vertical integrator is the interstitial nucleus of Cajal, receiving inputs from the rostral interstitial nucleus of medial longitudinal fasciculus and vestibular nuclei.Subregions of cerebellum and brain stem play important roles in both gaze and gaze-holding. Lesions of the cerebellar flocculus and paraflocculus cause impaired smooth pursuit, gaze-evoked and downbeat nystagmus, and impaired vestibulo-ocular reflex suppression. The nodulus and ventral uvula integrate signals to distinguish tilt from translation, with lesions resulting in skew deviation.ConclusionsClose examination of the eye movements, including observing the resting eye position (at the bedside and in the scanner), pursuit and saccadic movements, can yield important localizing information in patients with acute vertigo.Take Home PointsOcular ipsipulsion is a manifestation of lateral medullary lesions, commonly posterior inferior cerebellar artery stroke, with horizontal conjugate gaze deviation towards the side of the lesion.Knowledge of the causes of horizonal gaze deviation and other eye movement abnormalities can facilitate the localization of brain lesions.Article InformationAcknowledgmentsDr Scott saw the patient and had the idea for the article. Z. Britton examined the patient for video. Dr Scott and Z. Britton wrote the article. Dr Scott made the figure and video. We thank the patient and Dr Bernadette Monaghan.Sources of FundingNone.DisclosuresNone.Supplemental MaterialVideoNonstandard Abbreviations and AcronymsCEDconjugate eye deviationPICAposterior inferior cerebellar arteryFootnotesSupplemental Material is available at: https://www.ahajournals.org/doi/suppl/10.1161/STROKEAHA.121.037510.For Sources of Funding and Disclosures, see page e125.Correspondence to: Gregory Scott, MBBS, PhD, Honorary Clinical Lecturer, Department of Brain Sciences, Imperial College London, London, W12 0NN, United Kingdom. Email gregory.[email protected]ac.ukReferences1. Tehrani ASS, Kattah JC, Kerber KA, Gold DR, Zee DS, Urrutia VC, Newman-Toker DE. Diagnosing stroke in acute dizziness and vertigo: pitfalls and pearls.Stroke. 2018; 49:788–795. doi: 10.1161/STROKEAHA.117.016979LinkGoogle Scholar2. Shah NH, Bhatt N, Tipirneni A, Condes D, Khandelwal P, Romano JG. 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Wang H, Shi T, Shang Y, Chen X, Xu J and Geng Y (2023) Case report: Spiller syndrome initially mimicking vestibular neuritis, Frontiers in Neurology, 10.3389/fneur.2022.1072220, 13 March 2022Vol 53, Issue 3 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/STROKEAHA.121.037510PMID: 35135321 Originally publishedFebruary 9, 2022 Keywordsbrain stemneurological examinationstrokeeye movementsvertigoPDF download Advertisement SubjectsImagingIschemic Stroke
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