Anterior Inferior Cerebellar Artery Territory Research Articles

Evaluation of audiovestibular functions in patients with posterior circulation cerebrovascular stroke

BackgroundIt has been found that 25% of posterior circulation stroke patients experience vertigo. Sudden hearing loss due to a vascular source is typically caused by infarction in the anterior inferior cerebellar artery territory. However, it is uncommon in the posterior inferior cerebellar artery territory infarction.Aim of the workThe objective of the proposed study is to evaluate the function of the auditory and vestibular system in patients with posterior circulation cerebrovascular stroke.MethodsFifty patients with posterior circulation stroke, diagnosed by MRI at least 3 months after onset, were included. The controls consisted of fifty healthy people. The average age in cases was 58.68 ± 8.60 years, while in controls, it was 55.44 ± 11.72. The Health Stroke Scale (NIHSS) was used to conduct clinical assessments. All study groups were investigated using pure tone audiometry, auditory brain stem-evoked potential (ABR), videonystagmography (VNG), and vestibular-evoked myogenic potential (VEMP).ResultsMRI findings revealed that pontine infarction was the most frequent lesion in 36 (72%) patients. The latencies of ABR waves I, III, V, 1–III, I–V, and III–V were all considerably longer in cases than controls. Cervical VEMP P1 latency was considerably delayed in cases compared to controls, as the amplitude was lower. VNG data found abnormalities in all test parameters, indicating central disease.ConclusionPosterior circulation stroke causes acute sensorineural hearing loss with varying degrees. Videonystagmography is an accurate assessment of oculomotor function that can be combined with vestibular-evoked myogenic potential to objectively assess posterior circulation stroke patients.

Vascular vertigo and dizziness: Diagnostic criteria.

This paper presents diagnostic criteria for vascular vertigo and dizziness as formulated by the Committee for the Classification of Vestibular Disorders of the Bárány Society. The classification includes vertigo/dizziness due to stroke or transient ischemic attack as well as isolated labyrinthine infarction/hemorrhage, and vertebral artery compression syndrome. Vertigo and dizziness are among the most common symptoms of posterior circulation strokes. Vascular vertigo/dizziness may be acute and prolonged (≥24 hours) or transient (minutes to < 24 hours). Vascular vertigo/dizziness should be considered in patients who present with acute vestibular symptoms and additional central neurological symptoms and signs, including central HINTS signs (normal head-impulse test, direction-changing gaze-evoked nystagmus, or pronounced skew deviation), particularly in the presence of vascular risk factors. Isolated labyrinthine infarction does not have a confirmatory test, but should be considered in individuals at increased risk of stroke and can be presumed in cases of acute unilateral vestibular loss if accompanied or followed within 30 days by an ischemic stroke in the anterior inferior cerebellar artery territory. For diagnosis of vertebral artery compression syndrome, typical symptoms and signs in combination with imaging or sonographic documentation of vascular compromise are required.

Anterior Inferior Cerebellar Artery Infarct Presenting as Unilateral Deafness in a Young Patient

Acute ischemic stroke in the supply of the anterior inferior cerebellar artery is known to be connected with facial weakness, nystagmus, hearing loss, hypalgesia, and ataxia. This is a case of a young man with unilateral deafness caused due to infarction of anterior inferior cerebellar artery. Clinical findings and audiometry showed evidence suggestive of cochlear localization for deafness. MRI (Magnetic resonance imaging) Brain shows involvement of pons with infarct is seen in the right Anterior inferior cerebellar artery (AICA) territory. The inclusion of labyrinthine auditory artery suggests sensorineural hearing loss.

Case report: the etiology of anterior inferior cerebellar artery infarction: what does basi-parallel anatomic scanning magnetic resonance imaging tell us?

BackgroundThe precise etiology of anterior inferior cerebellar artery (AICA) infarction is difficult to identify because of the high anatomic variability of vertebrobasilar arteries and the limitations of conventional vascular examinations. Basi-parallel anatomic scanning magnetic resonance imaging (BPAS-MRI) can reveal the outer contour of the intracranial vertebrobasilar arteries, which may be helpful to distinguish the arteriosclerosis from congenital dysplasia and dissection.Case presentationIn this study, we reported 3 cases of AICA infarction and discussed the diagnostic value of BPAS-MRI in the evaluation of vascular etiology.ConclusionsThe BPAS-MRI could be considered as an important supplementary in the diagnosis of vascular etiology of infarction in AICA territory.

Where in the Brain do Strokes Occur? A Pilot Study and Call for Data.

Background: Every year, more than 795,000 people in the United States have a stroke, and each year about 140,000 Americans die from strokes. Although there is abundant information on the epidemiology, risk factors, pathophysiology, and many clinical features of strokes, there is a lack of specific numerical quantitation on the neuroanatomical distribution of strokes.Methods: This retrospective study utilized de-identified reports of radiologic imaging to determine the neurovascular anatomical location of acute ischemic cerebral infarcts in a 637-bed regional hospital in a rural area during the one-year interval from October 1, 2018 through September 30, 2019.Results: During the one-year study period, there were 418 acute ischemic strokes, and 54.6% (228/418) were in the territory of a single large vessel. Of the single large vessel strokes, 62.3% (142/228) were in a middle cerebral artery (MCA) territory, 12.1% (29/228) in a posterior cerebral artery (PCA) territory, 8.8% (20/228) in a basilar artery distribution, 7.5% (17/228) in a posterior inferior cerebellar artery (PICA) distribution, 6.6% (15/228) in an anterior cerebral artery (ACA) distribution, 1.8% (4/228) in a superior cerebellar artery (SCA) distribution, and 0.4% (1/228) in an anterior inferior cerebellar artery (AICA) territory. Internal capsule lacunar strokes accounted for 17.7% (74/418) of the total, brainstem lacunar strokes for 8.1% (34/418) and thalamic lacunar strokes for 5% (21/418) of the infarctions. Watershed infarctions accounted for 2.9% (12/418) of the strokes, 9 in the MCA/PCA watershed area and 3 in the MCA/ACA watershed area.Conclusions: This pilot study illustrates a methodology for collecting data to substitute specific numerical quantitation for vague generalities about the neuroanatomical distribution of strokes. Such quantification can enable evidence-based data-driven improvements in the care of stroke patients.

Posterior Petrous Meningioma Fed by a Branch of the Persistent Trigeminal Artery Terminating in the Anterior Inferior Cerebellar Artery

Persistent trigeminal artery (PTA) is the most common persistent carotid-basilar fetal anastomosis and terminates extremely rarely directly in the dominant hemispheric branch of the anterior inferior cerebellar artery (AICA). We present a case of a branch of this PTA variant (Saltzman type 3b) demonstrated as the feeding artery of a large posterior petrous meningioma, which was confirmed under direct vision during surgery through the extended retrosigmoid approach. Meticulous dissection from the tumor surface provided early identification of the feeding branch from the PTA and its bifurcation at the attachment of the posterior petrous surface adjacent to the jugular foramen enabled preservation of the terminal cortical branch of the cerebellar hemisphere. Meningioma in the posterior cranial fossa may recruit substantial supply from branches of the PTA terminating in the AICA. This PTA variant should be recognized during surgical resection of posterior fossa neoplasms to prevent ischemic complication of the AICA territory.

Brainstem vertigo: A brainstorming clinical entity for a clinician

Stroke at the brain stem and cerebellum may cause sudden vestibular syndromem and isolated audiovestibular loss can herald impeding for infarction at the anterior inferior cerebellar artery territory. Patients complaining sudden isolated dizziness or vertigo are higher chance for the stroke than the general population. Proper bedside assessment of the patient is superior to the imaging such as magnetic resonance imaging for detecting the central cause. Misdiagnosis of the stroke in patient of brain stem vertigo leads to significant morbidity and mortality. The overdiagnosis of this clinical entity will cause unnecessary costly workups and medical treatment. It is important for a clinician to differentiate brain stem vertigo with isolated dizziness or vertigo from the benign disorders of the labyrinth as the treatment strategy and prognosis are different in these two situations. Bedside clinical indicators are often helpful to identify the central pathology, and so neuroimaging should be advised accordingly. This review article focuses on the epidemiology, pathophysiology, clinical presentations, and current management of the brain stem vertigo. This article will surely increase awareness among the clinicians for accurate diagnosis and treatment of the brain stem vertigo.

Double adjacent basilar artery fenestration with cerebellar infarct: Case report and new classification of double basilar fenestrations

Basilar artery (BA) fenestration is an uncommon congenital variant associated with aneurysms and posterior circulation infarcts. We present a 42-year-old male, smoker and hypertensive who came with acute onset vertigo and gait ataxia. Cerebellar signs were positive on the left side. Diffusion-weighted brain magnetic resonance imaging showed acute infarct in the left anterior inferior cerebellar artery (AICA) territory. Computed tomography angiography showed BA double adjacent fenestration of proximal segment of BA, without thrombus, dissection/aneurysm. To the best of our knowledge, only three cases of double adjacent BA fenestration have been described so far. The association between vertebro-BA fenestrations and posterior circulation stroke is controversial. It has been suggested that turbulent flow at the site of fenestration predisposes to thrombus formation, which may be cause of stroke. This rare anatomic variant of the posterior circulation is important to recognize and may have associated neurologic consequences (double BA fenestrations are rare yet known congenital variants associated with aneurysms and associated neurological implications) (double adjacent BA fenestration presenting with AICA infarct are still rarer with only three cases reported across the world).

Anterior Inferior Cerebellar Artery Bypasses: The 7-Bypass Framework Applied to Ischemia and Aneurysms in the Cerebellopontine Angle.

Aneurysms of the anterior inferior cerebellar artery (AICA) are rare. Primary clip reconstruction of these lesions is a challenge because of the limited surgical exposure and frequent nonsaccular aneurysm morphology. Endovascular treatment options exist, but outcomes are equivalent to those for open surgery. Historically, AICA aneurysms not amenable to clipping or primary coiling have been treated with parent vessel sacrifice. To determine whether an AICA revascularization strategy would afford for the safe treatment of AICA aneurysms and other posterior circulation pathologies without compromising perfusion of the AICA territories. We describe a series of AICA bypasses to treat 4 AICA aneurysms and 3 vertebral artery/AICA occlusions. We used 7 types of bypasses to revascularize the AICA territory. Bypass types included extracranial-to-intracranial (EC-IC) bypass without an interpositional graft, EC-IC with an interpositional graft, in situ bypass, reanastomosis, reimplantation, intracranial-to-intracranial bypass with interpositional graft, and combination bypasses. In particular, we performed the following 7 bypasses: OA-a3 AICA, OA-RAG-a3 AICA, p3 PICA-a3 AICA, a2 AICA reanastomosis, V4 VA-a3 AICA, V3 VA-SVG-a3 AICA, and a combined OA-a3 AICA bypass and p3 PICA reanastomosis. AICA revascularization allows for the safe treatment of AICA aneurysms and other posterior circulation pathologies without compromising perfusion of the AICA territories. All 7 AICA bypasses are feasible for application to AICA aneurysms and ischemic disease. Our experience with the 7-bypass framework demonstrates the utility of the framework as a decision-making tool and the breadth of bypass innovation possible in this anatomically challenging region.

Feasibility of magnetic resonance imaging in the differential diagnosis of isolated acute audiovestibular loss.

Isolated acute audiovestibular loss is characterized by the sudden onset of unilateral hearing loss and prolonged vertigo. The purpose of this study is aimed to identify the value of magnetic resonance imaging (MRI) for the evaluation of isolated acute audiovestibular loss. We retrospectively enrolled 31 patients with isolated acute audiovestibular loss from March 2007 to December 2017. Specific medical records including initial and final pure tone audiometry (PTA), and canal paresis value were reviewed. Abbreviated MRI was performed in all patients. Fifteen patients showed increased signal of labyrinth on FLAIR images and eleven revealed negative findings on MRI. Two patients showed an infarction in the anterior inferior cerebellar artery (AICA) territory and three exhibited vestibular schwannoma in the internal auditory canal. There were no significant differences in initial, final PTA, and hearing recovery between negative and labyrinthine abnormality groups on MRI. Our results show that isolated acute audiovestibular loss due to labyrinthitis is more common than other secondary causes including vestibular schwannoma or AICA infarction. However, MRI with a tailored, abbreviated protocol is strongly recommended in patients with isolated acute audiovestibular loss to identify the exact etiologies.

Postcardiac injury syndrome and stroke following permanent pacemaker insertion

An 80-year-old woman initially presented with an episode of pleuritic chest pain 10 days after implantation of a dual chamber permanent pacemaker. She returned to hospital a day later with...

Recent Advances in Understanding Audiovestibular Loss of a Vascular Cause.

Acute audiovestibular loss is characterized by abrupt onset of prolonged (lasting days) vertigo and hearing loss. Acute ischemic stroke in the distribution of the anterior inferior cerebellar artery (AICA) is known to be the leading cause of acute audiovestibular loss. So far, eight subgroups of AICA territory infarction have been identified according to the patterns of audiovestibular dysfunctions, among which the most common pattern is the combined loss of auditory and vestibular functions. Unlike inner ear dysfunction of a viral cause, which can commonly present as an isolated vestibular (i.e., vestibular neuritis) or cochlear loss (i.e., sudden deafness), labyrinthine dysfunction of a vascular cause rarely results in isolated loss of vestibular or auditory function. As audiovestibular loss may precede the central symptoms or signs of an ischemic stroke in the posterior circulation, early diagnosis and proper management of audiovestiubular loss may provide a window to prevent the progression of infarction to larger areas of the posterior circulation. A clinician should consider the possibility that acute audiovestibular loss may herald impending AICA territory infarction, especially when patients have basilar artery occlusive disease close to the origin of the AICA on brain MRA. This review aims to highlight the recent advances in understanding audiovestibular loss of a vascular cause and to address its clinical significance.

The Diagnostic Accuracy of Truncal Ataxia and HINTS as Cardinal Signs for Acute Vestibular Syndrome.

The head impulse, nystagmus type, test of skew (HINTS) protocol set a new paradigm to differentiate peripheral vestibular disease from stroke in patients with acute vestibular syndrome (AVS). The relationship between degree of truncal ataxia and stroke has not been systematically studied in patients with AVS. We studied a group of 114 patients who were admitted to a General Hospital due to AVS, 72 of them with vestibular neuritis (based on positive head impulse, abnormal caloric tests, and negative MRI) and the rest with stroke: 32 in the posterior inferior cerebellar artery (PICA) territory (positive HINTS findings, positive MRI) and 10 in the anterior inferior cerebellar artery (AICA) territory (variable findings and grade 3 ataxia, positive MRI). Truncal ataxia was measured by independent observers as grade 1, mild to moderate imbalance with walking independently; grade 2, severe imbalance with standing, but cannot walk without support; and grade 3, falling at upright posture. When we applied the HINTS protocol to our sample, we obtained 100% sensitivity and 94.4% specificity, similar to previously published findings. Only those patients with stroke presented with grade 3 ataxia. Of those with grade 2 ataxia (n = 38), 11 had cerebellar stroke and 28 had vestibular neuritis, not related to the patient’s age. Grade 2–3 ataxia was 92.9% sensitive and 61.1% specific to detect AICA/PICA stroke in patients with AVS, with 100% sensitivity to detect AICA stroke. In turn, two signs (nystagmus of central origin and grade 2–3 Ataxia) had 100% sensitivity and 61.1% specificity. Ataxia is less sensitive than HINTS but much easier to evaluate.

A case of dorsolateral pontine infarct: Description of a new vascular alternating syndrome

IntroductionInferolateral pontine infarcts are well-described lesions of the anterior inferior cerebellar artery territory with a wide variety of clinical presentations. We report the case of isolated unilateral hearing loss and contralateral sensation of coldness due to a dorsolateral lower pontine infarct. Case descriptionWe describe the case of a 48-year-old female patient who developed isolated selective high-frequency hearing loss on the left side, and contralateral hemibody sensation of coldness. MRI showed a left-sided dorsolateral lower pontine ischemic lesion. A subsequent angiogram revealed the lesion to result from the spontaneous dissection of a long circumferential branch of the basilar artery. ConclusionTo our knowledge, this is the first reported case of a vascular alternating syndrome consisting of isolated ipsilateral hearing loss and contralateral thermal dysesthesia from a dorsolateral lower pontine infarct. Occlusion of a long perforating branch of the basilar artery and consequent posterolateral lower pontine infarct may result in an alternating syndrome with subtle clinical symptoms. Knowledge of this type of syndrome may direct physicians towards the diagnosis of a dorsolateral lower pontine infarct, despite vague clinical complaints.

Recent Advances in Cerebellar Ischemic Stroke Syndromes Causing Vertigo and Hearing Loss.

Cerebellar ischemic stroke is one of the common causes of vascular vertigo. It usually accompanies other neurological symptoms or signs, but a small infarct in the cerebellum can present with vertigo without other localizing symptoms. Approximately 11% of the patients with isolated cerebellar infarction simulated acute peripheral vestibulopathy, and most patients had an infarct in the territory of the medial branch of the posterior inferior cerebellar artery (PICA). A head impulse test can differentiate acute isolated vertigo associated with PICA territory cerebellar infarction from more benign disorders involving the inner ear. Acute hearing loss (AHL) of a vascular cause is mostly associated with cerebellar infarction in the territory of the anterior inferior cerebellar artery (AICA), but PICA territory cerebellar infarction rarely causes AHL. To date, at least eight subgroups of AICA territory infarction have been identified according to the pattern of neurotological presentations, among which the most common pattern of audiovestibular dysfunction is the combined loss of auditory and vestibular functions. Sometimes acute isolated audiovestibular loss can be the initial symptom of impending posterior circulation ischemic stroke (particularly within the territory of the AICA). Audiovestibular loss from cerebellar infarction has a good long-term outcome than previously thought. Approximately half of patients with superior cerebellar artery territory (SCA) cerebellar infarction experienced true vertigo, suggesting that the vertigo and nystagmus in the SCA territory cerebellar infarctions are more common than previously thought. In this article, recent findings on clinical features of vertigo and hearing loss from cerebellar ischemic stroke syndrome are summarized.

Failure of Fixation Suppression of Spontaneous Nystagmus in Cerebellar Infarction: Frequency, Pattern, and a Possible Structure.

To investigate the frequency and pattern of failure of the fixation suppression (FFS) of spontaneous nystagmus (SN) in unilateral cerebellar infarction, and to identify the structure responsible for FFS, 29 patients with acute, mainly unilateral, isolated cerebellar infarction who had SN with a predominantly horizontal component were enrolled in this study. The ocular fixation index (OFI) was defined as the mean slow phase velocity (SPV) of the horizontal component of SN with fixation divided by the mean SPV of the horizontal component of SN without fixation. The OFI from age- and sex-matched patients with vestibular neuritis was calculated and used as the control data. The FFS of SN was only found in less than half (41%, 12/29) of the patients. Approximately 65% (n = 7) of the patients with isolated anterior inferior cerebellar artery territory cerebellar infarction showed FFS, whereas only a quarter (n = 3) of the patients with isolated posterior inferior cerebellar artery (PICA) territory cerebellar infarction showed FFS. The proportion of gaze-evoked nystagmus (6/12 [50%] vs. 2/17 [12%], p = 0.04) and deficient gain of ipsilesional pursuit (10/12 [83%] vs. 6/17 [35%], p = 0.05) was more frequent in the FFS group than in the group without FFS. Lesion subtraction analysis in isolated PICA territory cerebellar infarction revealed that the nodulus was commonly damaged in patients with FFS, compared to that of patients without FFS. Our study shows that FFS of SN due to acute cerebellar infarction is less common than previously thought and the nodulus may be an important structure for the suppression of SN in humans.

Trial of ORG 10172 in Acute Stroke Treatment (TOAST) classification and vascular territory of ischemic stroke lesions diagnosed by diffusion-weighted imaging.

BackgroundThe association between the location and the mechanism of a stroke lesion remains unclear. A diffusion‐weighted imaging study may help resolve this lack of clarity.Methods and ResultsWe studied a consecutive series of 2702 acute ischemic stroke patients whose stroke lesions were confirmed by diffusion‐weighted imaging and who underwent a thorough etiological investigation. The vascular territory in which an ischemic lesion was situated was identified using standard anatomic maps of the dominant arterial territories. Stroke subtype was based on the Trial of ORG 10172 in Acute Stroke Treatment, or TOAST, classification. Large‐artery atherosclerosis (37.3%) was the most common stroke subtype, and middle cerebral artery (49.6%) was the most frequently involved territory. Large‐artery atherosclerosis was the most common subtype for anterior cerebral, middle cerebral, vertebral, and anterior and posterior inferior cerebellar artery territory infarctions. Small vessel occlusion was the leading subtype in basilar and posterior cerebral artery territories. Cardioembolism was the leading cause in superior cerebellar artery territory. Compared with carotid territory stroke, vertebrobasilar territory stroke was more likely to be caused by small vessel occlusion (21.4% versus 30.1%, P<0.001) and less likely to be caused by cardioembolism (23.2% versus 13.8%, P<0.001). Multiple‐vascular‐territory infarction was frequently caused by cardioembolism (44.2%) in carotid territory and by large‐artery atherosclerosis (52.1%) in vertebrobasilar territory.ConclusionsInformation on vascular territory of a stroke lesion may be helpful in timely investigation and accurate diagnosis of stroke etiology.

Cerebellar Infarctions Mimicking Acute Peripheral Vertigo

To determine the prevalence of cases of missed cerebellar stroke mimicking acute peripheral vertigo (APV), the so-called pseudo-APV, and to identify the clinical indicators useful for differentiating APV from cerebellar infarction that presents as isolated vertigo. Case series with chart review. Tertiary referral center. We conducted a retrospective chart review of cases of missed cerebellar infarction over the past 5 years. All patients had first undergone an otoneurological evaluation and computed tomography brain scan in the emergency department before a complete bedside examination was performed in our otoneurological unit. We identified 11 patients with pseudo-APV (2.8% of all the cases presenting to our unit complaining of acute vertigo). Spontaneous nystagmus (of central type in 2 cases) was recorded in all patients. The Head Impulse Test was clearly negative in 9 cases. The duration of vertigo lasted more than 72 hours in 7 patients. In 4 patients, delayed neurological signs followed acute vertigo 2 to 3 days after the onset. Magnetic resonance imaging showed 8 cases of infarction in the posterior-inferior cerebellar artery territory; in 1 patient, an involvement of the anterior-inferior cerebellar artery territory was recorded; 2 patients showed a hemispheric ischemic cerebellar involvement. Pseudo-APV is not an uncommon diagnosis in otoneurological practice. The presence of moderate-severe imbalance and the persistence of vertigo for more than 72 h from the onset, together with the results of bedside examination tests (spontaneous nystagmus and Head Impulse Test), are useful indicators for recognizing a cerebellar ischemic origin in cases of acute vertigo.

Sensorineural Hearing Loss Due to Vertebrobasilar Artery Ischemia-Illustrative Case and Literature Review

Acute sensorineural hearing loss is commonly caused by peripheral vestibulocochlear disorders such as sudden deafness, Meniere’s disease, and Ramsay Hunt syndrome, but is rarely due to infarction of the vertebrobasilar artery. In this report, a case of right anterior inferior cerebellar artery syndrome presenting with sudden deafness and vertigo is described in order to feature acute sensorineural hearing loss due to vertebrobasilar artery ischemia, and sensorineural hearing loss due to vertebrobasilar artery ischemia is reviewed and discussed. A 79-year-old man presented with right acute sensorineural hearing loss preceded by occasional, minute-long periods of dizziness without cranial neural symptoms other than vestibulocochlear symptoms. Magnetic resonance imaging (MRI) revealed infarction of the right anterior inferior cerebellar artery territory. The vertebrobasilar artery supplies the vestibulocochlear organ, brainstem, and cerebellum, whose abnormalities are related to vestibulocochlear symptoms. Vertigo is a major symptom associated with vertebrobasilar artery ischemia. Further, acute sensorineural hearing loss is caused by hypoperfusion of the vertebrobasilar artery. Vertigo and/or acute sensorineural hearing loss could be a prodrome of subsequent infarction of the vertebrobasilar artery territory. The artery most often responsible for acute sensorineural hearing loss is the anterior inferior cerebellar artery, whereas ischemia of the basilar artery, the posterior inferior cerebellar artery, and the superior cerebellar artery rarely cause acute sensorineural hearing loss. Patients with acute sensorineural hearing loss who are at a high risk of cerebrovascular disease must be examined with imaging tools such as MRI.

Sudden vertigo in a 49-year-old man

The diffusion-weighted MRI (DWI) showed a small, subacute right middle cerebellar peduncle infarct in the territory of the anterior inferior cerebellar artery (AICA) without brainstem infarction (Fig. 1). Audiometry showed a total right hearing loss with normal hearing on the left; caloric testing showed absent responses from the right. CT angiography revealed only right vertebral artery hypoplasia. He was given anti-hypertensive treatment and aspirin. One year later he still had a total right hearing loss, positive rightward Head Impulse Test, a positive Romberg test standing on foam and absent caloric responses from the right. Sudden unilateral vestibular loss (SVL) produces a stereotyped syndrome of vertigo, vomiting, nystagmus beating away from the affected side, ipsiversive lateropulsion and ocular tilt reaction. The Head Impulse Test is invariably positive towards the affected side. Whereas the SVL syndrome invariably resolves within 1 week, the Head Impulse Test will, if the ear does not recover, remain positive forever. When the SVL is spontaneous and isolated, the cause is usually presumed to be due to herpes simplex virus infection and since the cochlea is spared, it is called ‘‘acute vestibular neuritis’’. When there is simultaneous sudden unilateral hearing loss (SHL) the cause is presumed to be herpes zoster virus infection – ‘‘herpes zoster oticus’’ or the ‘‘Ramsay Hunt syndrome’’, affecting the labyrinth as well as in the vestibulo-cochlear nerve, and such cases are called ‘‘acute viral labyrinthitis’’ or ‘‘neuro-labyrinthitis’’. However, labyrinthine infarction can also cause combined SVL+SHL, although this diagnosis is as hard to verify as that of viral labyrinthitis, since MRI of the inner ear is usually normal in both. The internal auditory artery, usually a branch of the AICA, supplies the inner ear. With AICA occlusion there can be infarction in the cerebellum or the brainstem, or both, as well as the inner ear. The hearing loss with AICA infarction is mostly cochlear and can improve in time, as can the canal paresis. A cerebellar or even brainstem component of an AICA territory infarct, evident on DWI, can be clinically asymptomatic so that the patient will present with isolated SHL+SVL and if a DWI is not requested (in time), the patient will be assumed to have viral