Motor cortex stimulation for the treatment of trigeminal neuralgia after brainstem infarction: A case report. / 运动皮层电刺激治疗脑干梗死后三叉神经痛1例.

Secondary trigeminal neuralgia after brainstem infarction is rare and rarely reported. A patient with secondary trigeminal neuralgia after brainstem infarction was admitted to the Department of Neurosurgery, Xiangya Hospital, Central South University. The patient was a 44 years old male who underwent motor cortex stimulation treatment after admission. The effect was satisfactory in the first week after surgery, but the effect was not satisfactory after one week. This disease is relatively rare and the choice of clinical treatment still requires long-term observation.

[A case of bilateral middle cerebellar peduncle infarction with hot cross bun sign].

A 71-year-old man with hypertension and diabetes mellitus presented to our hospital because he felt lightheaded. Diffusion-weighted images (DWI) on brain MRI showed high signal lesions in the left cerebellar hemisphere and the right pons. The diagnosis of cerebellar infarction was made, but he refused treatment. One month later, he came to our hospital because his body leaned to the left. Neurological examination revealed dysarthria and cerebellar truncal ataxia. An electrocardiogram showed atrial fibrillation. DWI on brain MRI showed high signal lesions in the bilateral cerebellar hemispheres and middle cerebellar peduncles (MCP). Dabigatran 300 |mg/day was administered for cardiogenic cerebral embolism. On the 12th day of onset, he was transferred to a rehabilitation hospital. At 72 years old, T2*-weighted images on brain MRI showed hot cross bun sign (HCBs) in the pons. We considered that HCBs were caused by antegrade or retrograde degeneration (or both) of pontine infarcts and bilateral MCP infarcts in the pontine cerebellar tract. It seemed preferable to use T2*-weighted images or proton density-weighted images rather than T2-weighted images to detect HCBs. When HCBs is detected, it should be noted that HCBs can be caused by bilateral MCP infarcts in addition to multiple system atrophy.

Hemodynamic signal changes during volitional swallowing in dysphagia patients with different unilateral hemispheric stroke and brainstem stroke: A near-infrared spectroscopy study.

BACKGROUND AND OBJECTIVES: Strokes will result in decreased in cortical excitability and changed in the balance between the affected and unaffected hemispheres. Previous studies have focused on cortical changes in healthy subjects during swallowing, while they remain unknown in patients with stroke at different locations. Thus, the purpose of this study was to research cortical activation patterns of swallowing in patients with dysphagia and healthy subjects by the functional near-infrared spectroscopy (fNIRS). We also focus on the comparability of brain activation areas associated with swallowing between patients with different stroke locations and healthy subjects. METHODS: total of 104 participants were invited to our study, involving 86 patients with dysphagic unilateral hemispheric stroke and 18 age and sex matched healthy controls. The stroke patients were categorized into patients with left unilateral stroke lesions (n = 30), patients with right unilateral stroke lesions (n = 32) and patients with brainstem injury (n = 24) according to different stroke sites. All patients underwent a series of clinical swallowing function assessments, such as the Fiberoptic endoscopic dysphagia severity scale (FEDSS), penetration-aspiration scale (PAS) of Rosenbek, the gugging swallowing screen (GUSS) and the functional oral Intake scale (FOIS) after informed consent has been signed. All participants received the fNIRS system assessment. RESULTS: The results showed that extensive areas of the cerebral cortex activated during the swallowing tasks in healthy participants (P < FDR 0.05). For patients with left unilateral stroke lesions, the HbO concentration were strongest over the right hemisphere (P < FDR 0.05). In addition, a less severe activation was also observed in the left hemisphere. Comparable to patients with left unilateral stroke lesions, the strongest activation during swallowing task were found in the left hemisphere in patients with right unilateral stroke lesions (P < FDR 0.05). Similarly, the right hemisphere also has activated less. In contrast, patients with brain stem injury showed more bilaterally activation patterns. CONCLUSION: Our finding states that cortical activation areas differ between patients with different stroke locations and healthy subjects during swallowing. There was a more bilateral activation in healthy participants and patients with lesions in the brainstem while more cortical activation in unaffected hemisphere in patients with unilateral hemispheric stroke. It also provides a basis for the future treatment of dysphagia after stroke.

Endoscopic botulinum toxin injection combined with balloon dilatation for treatment of cricopharyngeal achalasia in patient with brainstem stroke. / æ¶ˆåŒ–å† é•œå¼•å¯¼ä¸‹è‚‰æ¯’æ¯’ç´ æ³¨å°„è”åˆçƒå›Šæ‰©å¼ æ²»ç–—è„‘å¹²æ¢—æ­»åŽçŽ¯å’½è‚Œå¤±å¼›ç¼“çš„æ•ˆæžœ.

OBJECTIVES: At present, there are many reports about the treatment of cricopharyngeal achalasia by injecting botulinum toxin type A (BTX-A) into cricopharyngeal muscle guided by ultrasound, electromyography or CT in China, but there is no report about injecting BTX-A into cricopharyngeal muscle guided by endoscope. This study aims to evaluate the efficacy of endoscopic BTX-A injection combined with balloon dilatation in the treatment of cricopharyngeal achalasia after brainstem stroke, and to provide a better method for the treatment of dysphagia after brainstem stroke. METHODS: From June to December 2022, 30 patients with cricopharyngeal achalasia due to brainstem stroke were selected from the Department of Rehabilitation Medicine, the First Hospital of Changsha. They were randomly assigned into a control group and a combined group, 15 patients in each group. Patients in both groups were treated with routine rehabilitation therapy, while patients in the control group were treated with balloon dilatation, and patients in the combined group were treated with balloon dilatation and BTX-A injection. Before treatment and after 2 weeks of treatment, the patients were examined by video fluoroscopic swallowing study, Penetration-aspiration Scale (PAS), Dysphagia Outcome Severity Scale (DOSS), and Functional Oral Intake Scale (FOIS) were used to assess the swallowing function. RESULTS: In the combined group, 1 patient withdrew from the treatment because of personal reasons. Two weeks after treatment, the scores of DOSS, PAS, and FOIS in both groups were better than those before treatment (all P<0.01), and the combined group was better than the control group (all P<0.001). The effective rate was 85.7% in the combined group and 66.7% in the control group, with no significant difference between the 2 groups (P>0.05). CONCLUSIONS: BTX-A injection combined with balloon dilatation is more effective than balloon dilatation alone in improving swallowing function and is worthy of clinical application.

A New Neurological Screening Approach for Diagnosing Brainstem Infarction Using the Calling Method and Familiar Voices.

This report proposes a new approach to assess dysarthria in patients with brainstem infarction by involving familiar individuals. Collaboration provides valuable insights compared to subjective traditional methods. A man in his 70s presented with resolved positional vertigo. Standard neurological tests showed no abnormalities, and inquiries with the patient's friend did not reveal voice changes. While inquiring about voice changes with family, friends, and acquaintances is a common practice in clinical settings, our approach involved the patient calling out to his friend from a distance. Despite the physician detecting no abnormalities, the friend noticed a lower voice. Subsequent magnetic resonance imaging (MRI) confirmed brainstem infarction. Early and subtle symptoms of brainstem infarction pose a detection challenge and can lead to serious outcomes if overlooked. This report provides the first evidence that distance calling can detect subtle voice changes associated with brainstem infarction potentially overlooked by conventional neurological examinations, including inquiries with individuals familiar with the patient's voice. Detecting brainstem infarction in emergency department cases is often missed, but conducting MRIs on every patient is not feasible. This simple method may identify patients overlooked by conventional screening who should undergo neuroimaging such as MRI. Further research is needed, and involving non-professionals in assessments could significantly advance the diagnostic process.

Brainstem Infarction in Immunodeficiency Identified as Adenosine Deaminase 2 Deficiency: Case Report.

PURPOSE: We present the case of a 24-year-old male with CNS granulomatosis due to an immunodeficiency syndrome which was identified as deficiency of adenosine deaminase 2 (DADA2) as a cause of brainstem infarction. METHODS: Case report and detailed description of the clinical course of diagnosis and treatment. CASE: The patient's medical history consisted of an unknown immunodeficiency syndrome. Based on former findings, common variable immunodeficiency (CVID) was diagnosed. The patient suffered from three consecutive brainstem strokes of unknown etiology within 3 years. An MRI scan detected gadolinium-enhancing, granulomatous-suspect lesions in the interpeduncular cistern, temporal lobe, and tegmentum. Laboratory analysis was compatible with CVID, with leukopenia and immunoglobulin deficiency. Because granulomatous CNS inflammation was suspected, the patient received methylprednisolone immunosuppressive therapy, which led to partially regressive MRI lesions. However, in contrast to imaging, the patient showed a progressive cerebellar syndrome, indicating plasma exchange therapy and immunoglobulin treatment, which led to rapid symptom amelioration. After a relapse and a further stroke, expanded analysis confirmed DADA2 (and not CVID) as the inflammatory cause for recurrent stroke. After starting the therapy with immunoglobulins and adalimumab, no further strokes occurred. CONCLUSION: We present the case of a young adult with diagnosis of DADA2 as a cause for recurrent strokes due to vasculitis. This stroke etiology is rare but should be considered as a cause of recurrent stroke of unknown origin in young patients to avoid a disabling disease course by disease-specific treatment options.

Intraoperative venous congestion and brainstem venous hemorrhagic infarction during retrosigmoid for acoustic neuroma.

Venous hemorrhagic infarction is rare but can occur during acoustic neuroma resection [1-5]. We present the case of a 27-year-old male with 1.5 years of progressive headaches, tinnitus, imbalance and hearing loss. Imaging revealed a left Koos 4 acoustic neuroma. The patient underwent a retrosigmoid approach for resection. During surgery, a vein of significant size within the capsule of the tumor was encountered and was necessary to take to proceed with resection. After coagulation of the vein, intraoperative venous congestion with cerebellar edema and hemorrhagic infarction ensued, requiring resection of a portion of the cerebellum. Given the hemorrhagic nature of the tumor, continuing tumor resection was necessary to prevent postoperative hemorrhage. This was carried out until hemostasis was achieved. 85 % resection was achieved, leaving a residual against the brainstem and cisternal course of the facial nerve. Postoperatively, the patient required 5 weeks hospitalization followed by 1 month of rehabilitation. At discharge to rehabilitation, patient had trach, PEG, left House-Brackmann 5 facial weakness, left sided deafness, and right upper extremity hemiparesis (1/5). At 7 months follow up, he continued to have left House-Brackmann 5 facial weakness and left sided deafness but trach and PEG had been removed and strength had improved to 5/5. We demonstrate in this video the unfortunate and rare occurrence of intraoperative venous hemorrhagic infarction during acoustic neuroma resection - particularly for large tumors in young patients - and discuss its etiology and surgical steps that are necessary to partially remedy its devastating impact on the patient. The patient consented to the procedure and participating in this surgical video.

[Preliminary exploration of clinical prediction model of severe swallowing disorder after acute ischemic stroke based on nomogram model].

OBJECTIVE: To establish a predictive model for severe swallowing disorder after acute ischemic stroke based on nomogram model, and evaluate its effectiveness. METHODS: A prospective study was conducted. The patients with acute ischemic stroke admitted to Mianyang Central Hospital from October 2018 to October 2021 were enrolled. Patients were divided into severe swallowing disorder group and non-severe swallowing disorder group according to whether severe swallowing disorder occurred within 72 hours after admission. The differences in general information, personal history, past medical history, and clinical characteristics of patients between the two groups were compared. The risk factors of severe swallowing disorder were analyzed by multivariate Logistic regression analysis, and the relevant nomogram model was established. The bootstrap method was used to perform self-sampling internal validation on the model, and consistency index, calibration curve, receiver operator characteristic curve (ROC curve), and decision curve were used to evaluate the predictive performance of the model. RESULTS: A total of 264 patients with acute ischemic stroke were enrolled, and the incidence of severe swallowing disorder within 72 hours after admission was 19.3% (51/264). Compared with the non-severe swallowing disorder group, the severe swallowing disorder group had a higher proportion of patients aged of ≥ 60 years old, with severe neurological deficits [National Institutes of Health stroke scale (NIHSS) score ≥ 7], severe functional impairments [Barthel index, an activity of daily living functional status assessment index, < 40], brainstem infarction and lesions ≥ 40 mm (78.43% vs. 56.81%, 52.94% vs. 28.64%, 39.22% vs. 12.21%, 31.37% vs. 13.62%, 54.90% vs. 24.41%), and the differences were statistically significant (all P < 0.01). Multivariate Logistic regression analysis showed that age ≥ 60 years old [odds ratio (OR) = 3.542, 95% confidence interval (95%CI) was 1.527-8.215], NIHSS score ≥ 7 (OR = 2.741, 95%CI was 1.337-5.619), Barthel index < 40 (OR = 4.517, 95%CI was 2.013-10.136), brain stem infarction (OR = 2.498, 95%CI was 1.078-5.790) and lesion ≥ 40 mm (OR = 2.283, 95%CI was 1.485-3.508) were independent risk factors for severe swallowing disorder after acute ischemic stroke (all P < 0.05). The results of model validation showed that the consistency index was 0.805, and the trend of the calibration curve was basically consistent with the ideal curve, indicating that the model had good prediction accuracy. ROC curve analysis showed that the area under the ROC curve (AUC) predicted by nomogram model for severe swallowing disorder after acute ischemic stroke was 0.817 (95%CI was 0.788-0.852), indicating that the model had good discrimination. The decision curve showed that within the range of 5% to 90%, the nomogram model had a higher net benefit value for predicting the risk of severe swallowing disorder after acute ischemic stroke, indicating that the model had good clinical predictive performance. CONCLUSIONS: The independent risk factors of severe swallowing disorder after acute ischemic stroke include age ≥ 60 years old, NIHSS score ≥ 7, Barthel index < 40, brainstem infarction and lesion size ≥ 40 mm. The nomogram model established based on these factors can effectively predict the occurrence of severe swallowing disorder after acute ischemic stroke.

Immediate effects of electroacupuncture in oculomotor nerve palsy following brainstem infarction: A case report.

INTRODUCTION: Research has demonstrated that electroacupuncture (EA) stimulation of paralyzed muscles significantly improves nerve regeneration and functional recovery. DESCRIPTION: An 81-year-old man with no history of diabetes mellitus or hypertension presented with a history of brainstem infarction. Initially, the patient had medial rectus palsy in the left eye and diplopia to the right in both eyes, which almost returned to normal after six sessions of EA. METHODS: The CARE guidelines informed the case study report. The patient was diagnosed with oculomotor nerve palsy (ONP) and photographed to document ONP recovery after treatment. The selected acupuncture points and surgical methods are listed in the table. DISCUSSION: Pharmacological treatment of oculomotor palsy is not ideal, and its long-term use has side effects. Although acupuncture is a promising treatment for ONP, existing treatments involve many acupuncture points and long cycles, resulting in poor patient compliance. We chose an innovative modality, electrical stimulation of paralyzed muscles, which may be an effective and safe complementary alternative therapy for ONP.

Cerebellar and brainstem stroke possibly associated with booster dose of BNT162b2 (Pfizer-BioNTech) COVID-19 vaccine.

As COVID-19 vaccination becomes widely available and administered globally, there have been several reports of side effects attributed to the vaccine. This report highlights a patient who developed stroke 2 days following the administration of the COVID-19 vaccine, although its association remains uncertain. A man in his late 30s developed acute neurological symptoms 2 days after receiving the booster dose of the BNT162b2 (Pfizer-BioNTech) mRNA COVID-19 vaccine. History and neurological examination suggested a posterior circulation stroke, which was confirmed by MRI, as a right-sided posterior inferior cerebellar artery stroke. Full workup did not suggest other causes of the stroke. Due to the patient's age and well-controlled risk factors, it was presumed to be a rare adverse effect of the vaccine. Medical management with aspirin, statin therapy and rehabilitation led to the improvement of symptoms and enabled ongoing restoration of function. Further cases of stroke following administration of COVID-19 vaccine have been documented in the literature, but the association is yet to be established.

Neuroimaging markers of early neurological deterioration in acute isolated pontine infarction.

BACKGROUND: Imaging indicators of early neurological deterioration (END) in patients with acute isolated pontine infarctions (AIPI) remained ambiguous. We aimed to find more specific neuroimaging markers for the development of END in patients with AIPI. METHODS: Patients with AIPI within 72 h of stroke onset were screened from a stroke database from January 2018 to July 2021 in the First Affiliated Hospital of Zhengzhou University. Clinical characteristics, laboratory tests, and imaging parameters were collected. The layers having the largest infarct area on diffusion-weighted imaging (DWI) and T2 sequences were chosen. On the transverse plane of DWI and sagittal plane of T2-Flair images, the maximum length (a, m) and maximum width (b, n) vertical to the length of the infarcted lesions were measured respectively. On the sagittal plane of T2-Flair image, the maximum ventrodorsal length (f) and rostrocaudal thickness (h) were measured. On the sagittal plane, lesions were evenly split into upper, middle, and lower types based on the lesion's location in the pons. The ventral and dorsal types of location were separated based on whether the ventral borders of the pons were involved on transvers plane. END was defined as a ≥2 point increase in the National Institutes of Health Stroke Scale (NIHSS) total score or a ≥1 point increase in the motor items within 72 h after admission. Multivariate logistic regression analyses were used to explore risk factors associated with END. The receiver operating characteristic (ROC) curve analysis and the area under the curve (AUC) was performed to estimate the discriminative power and determine the optimal cut-off points of imaging parameters on the prediction of END. RESULTS: A total of 218 patients with AIPI were included in the final analysis. END occurred in 61 cases (28.0%). Multivariate logistic regression analysis showed that the ventral type of lesion location was associated with END in all models adjusted. In addition, in Model 1, b (odds ratio (OR) 1.145, 95% confidence interval (95% CI), 1.007-1.301) and n (OR 1.163, 95% CI 1.012-1.336); in Model 2, b*n (OR 1.010, 95% CI 1.002-1.018); in Model 3, n (OR 1.179, 95% CI, 1.028-1.353); and in Model 4, b (OR 1.143, 95% CI 1.006-1.298) and n (OR 1.167, 95% CI 1.016-1.341) were found to be associated with END respectively after different adjustments. ROC curve analysis with END showed that the AUC, the optimal cut-off value, and its sensitivity and specificity were 0.743 (0.671-0.815), 9.850 mm, and 68.9% and 79.0% for b; 0.724 (0.648-0.801), 10.800 mm, and 57.4% and 80.9% for n; and 0.772 (0.701-0.842), 108.274 mm2, and 62.3% and 85.4% for b*n, respectively (b*n vs b: P =0.213; b*n vs n: P =0.037; b vs n: P =0.645). CONCLUSIONS: Our study revealed that besides the ventral type of lesion location, the maximum width of lesion on the transverse plane of DWI and sagittal plane of T2 image (b, n) may be imaging markers for the development of END in AIPI patients, and the product of the two (b*n) showed a better prediction value on the risks of END.

"Uncrossed Central Facial Paralysis" Caused by Pontine Infarction: A Case Report.

INTRODUCTION: We report a patient with extraordinary pontine infarction-induced contralateral central facial palsy and weakened limb strength. CASE REPORT: This is a 66-year-old man with left arm movement difficulty for 10 days and worsening over the last 1 day. His left nasolabial fold flattening and left arm strength and sensory were decreased. He could not complete the finger-nose test well with his right hand. Magnetic resonance and magnetic resonance angiography tests confirmed his right pontine acute infarction but without large vessel stenosis or occlusion. CONCLUSION: "Uncrossed paralysis" patients may present with contralateral face and body weakness with pontine infarcts, if the infarct occurs above the level of the facial nucleus head, and may be simmilar with the higher level pontine lesions or cerebrum semisphere infarction, which need particular attention during clinical practice.

Rapidly progressive cerebral atrophy following a posterior cranial fossa stroke: Assessment with semiautomatic CT volumetry.

BACKGROUND: The effect of posterior cranial fossa stroke on changes in cerebral volume is not known. We assessed cerebral volume changes in patients with acute posterior fossa stroke using CT scans, and looked for risk factors for cerebral atrophy. METHODS: Patients with cerebellar or brainstem hemorrhage/infarction admitted to the ICU, and who underwent at least two subsequent inpatient head CT scans during hospitalization were included (n = 60). The cerebral volume was estimated using an automatic segmentation method. Patients with cerebral volume reduction > 0% from the first to the last scan were defined as the "cerebral atrophy group (n = 47)," and those with ≤ 0% were defined as the "no cerebral atrophy group (n = 13)." RESULTS: The cerebral atrophy group showed a significant decrease in cerebral volume (first CT scan: 0.974 ± 0.109 L vs. last CT scan: 0.927 ± 0.104 L, P < 0.001). The mean percentage change in cerebral volume between CT scans in the cerebral atrophy group was -4.7%, equivalent to a cerebral volume of 46.8 cm3, over a median of 17 days. The proportions of cases with a history of hypertension, diabetes mellitus, and median time on mechanical ventilation were significantly higher in the cerebral atrophy group than in the no cerebral atrophy group. CONCLUSIONS: Many ICU patients with posterior cranial fossa stroke showed signs of cerebral atrophy. Those with rapidly progressive cerebral atrophy were more likely to have a history of hypertension or diabetes mellitus and required prolonged ventilation.

Morphological predictors of neurological deterioration in patients with acute isolated pontine infarct.

OBJECTIVE: To investigate morphological predictors of neurological deterioration (ND) in patients with acute isolated pontine infarct. METHODS: Acute isolated pontine infarct patients within 7 days after onset of stroke symptoms were included retrospectively and classified into ND and non-ND groups. Morphological phenotypes (paramedian pontine infarct [PPI], atypical PPI, small deep infarct, and other types), topographical location, and lesion size were evaluated on axial diffusion-weighted imaging. RESULTS: There were 210 eligible patients, of whom 62 patients had ND (29.5%). The proportion of PPI was significantly higher in ND than that in non-ND (62.9% vs 39.6%). ND occurred more frequently in PPI patients than non-PPI patients (39.8% vs 20.5%). PPI located more frequently in lower pontine (20.4% vs 8.0%) and less in upper pontine (17.3% vs 30.4%, P = 0.028), and had larger ventro-dorsal length (13.8 ± 3.8 vs 9.9 ± 3.1) and width (8.3 ± 2.3 vs 6.2 ± 1.8) than non-PPI patients. The morphological phenotype of PPI was an independent risk factor for ND (OR 4.81, 95%CI 1.54-15.07, P = 0.007) in patients with isolated pontine infarct. The ventro-dorsal length of pontine infarct lesion was associated with ND (OR 1.18, 95%CI 1.01, 1.37, P = 0.034) in PPI patients. CONCLUSIONS: The morphological phenotype of PPI was a potential predictor for ND in patients with acute isolated pontine infarct. The ventro-dorsal length of pontine infarct lesion was possibly associated with ND in PPI patients.

A Case of Sudden Cardiac Arrest After Brainstem Infarction.

Research on the causes of sudden cardiac arrest (CA) after ischemic stroke, especially disruption of the autonomic nervous system's central control, has recently focused more on the widespread cortical and subcortical network than on autonomic circuits at the spinal and brainstem level. However, no clinical case of sudden CA requiring cardiopulmonary resuscitation (CPR) after brainstem infarction has been reported. We report a case of a 78-year-old woman who died suddenly from a brainstem infarction. Her husband heard a falling sound and found her unresponsive and lying with agonal breathing. The initial cardiac rhythm was pulseless electrical activity confirmed by emergency medical technicians. Recovery of spontaneous circulation was achieved after CPR. Basilar artery occlusion was shown on computed tomography, but no other findings that could have caused CA were found. Targeted temperature management was initiated, but she died on hospital day 22. Brainstem infarction may cause sudden CA; therefore, definitive treatment may achieve better outcomes.

Acute truncal ataxia without nystagmus in patients with acute vertigo.

BACKGROUND AND PURPOSE: Differentiating between peripheral and central aetiologies can be challenging in patients with acute vertigo, given substantial symptom overlap. A detailed clinical history and focused physical eye movement examination such as the HINTS eye examination appear to be the most reliable approach to identify acute cerebellar/brainstem stroke, outperforming even acute brain imaging. We have observed, however, that isolated vertigo of central cause may be accompanied by acute truncal ataxia, in the absence of nystagmus. METHODS: We explored the frequency of ataxia without concurrent nystagmus in a cross section of patients with acute vertigo who presented to the emergency department at two centres in Argentina (Group A) and the UK (Group B). Patients underwent detailed clinical neuro-otological assessments (Groups A and B), which included instrumented head impulse testing and oculography (Group B). RESULTS: A total of 71 patients in Group A and 24 patients in Group B were included in this study. We found acute truncal ataxia-without nystagmus-in 15% (n = 14) of our overall cohort. Lesions involved stroke syndromes affecting the posterior inferior cerebellar artery, anterior inferior cerebellar artery, and superior cerebellar artery, thalamic stroke, cerebral hemisphere stroke, multiple sclerosis, and a cerebellar tumour. Additional oculomotor deficits did not reliably identify a central cause in these individuals, even with oculography. CONCLUSIONS: We have identified a significant subpopulation of patients with acute vertigo in whom the current standard approaches such as the HINTS examination that focus on oculomotor assessment may not be applicable, highlighting the need for a formal assessment of gait in this setting.