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In longitudinal event data, a crude rate is a simple quantification of the event rate, defined as the number of events during an evaluation window, divided by the at-risk population size at the beginning or mid-time point of that window. The crude rate recently received revitalizing interest from medical researchers who aimed to improve measurement of misdiagnosis-related harms using administrative or billing data by tracking unexpected adverse events following a "benign" diagnosis. The simplicity of these measures makes them attractive for implementation and routine operational monitoring at hospital or health system level. However, relevant statistical inference procedures have not been systematically summarized. Moreover, it is unclear to what extent the temporal changes of the at-risk population size would bias analyses and affect important conclusions concerning misdiagnosis-related harms. In this article, we present statistical inference tools for using crude-rate based harm measures, as well as formulas and simulation results that quantify the deviation of such measures from those based on the more sophisticated Nelson-Aalen estimator. Moreover, we present results for a generalized multibin version of the crude rate, for which the usual crude rate is a single-bin special case. The generalized multibin crude rate is more straightforward to compute than the Nelson-Aalen estimator and can reduce potential biases of the single-bin crude rate. For studies that seek to use multibin measures, we provide simulations to guide the choice regarding number of bins. We further bolster these results using a worked example of stroke after "benign" dizziness from a large data set.

To verify the accuracy of automated nystagmus detection algorithms.Video-oculography (VOG) plots were analyzed from consecutive patients with dizziness presenting to a neurology clinic. Data were recorded for 30 s in upright position with fixation block. For automated nystagmus detection, slow-phase algorithm parameters included mean and median slow-phase velocity (SPV), and slow-phase duration ratio. Quick-phase algorithm parameters included saccadic difference and saccadic ratio. For verification, two independent blinded assessors reviewed VOG traces and videos and coded presence or absence of nystagmus. Assessor consensus was used as reference standard. Accuracy of slow-phase and quick-phase algorithm parameters were compared, and ROC analysis was performed.Among 524 analyzed VOG traces, 99 were verified as nystagmus present and 425 were verified as nystagmus absent. Prevalence of nystagmus in the sample population was 18.9%. In ROC analysis, areas under the curve of individual algorithm parameters were 0.791-0.896. With optimal thresholds for determining presence or absence of nystagmus, algorithm sensitivity (70.7-87.9%), specificity (71.8-84.0%), and negative predictive value (91.7-96.4%) were ideal, but positive predictive value (38.8-53.4%) was not ideal. Combining algorithm parameters using logistic regression models mildly improved detection accuracy.Both slow-phase and fast-phase algorithms were accurate for detecting nystagmus. Due to low positive predictive value, the utility of independent automated nystagmus detection systems is limited in clinical settings with low prevalence of nystagmus. Combining parameters using logistic regression models appears to improve detection accuracy, indicating that machine learning may potentially optimize the accuracy of future automated nystagmus detection systems.

Background and purpose Convergence of the eyes during head rotation increases the gain (eye velocity/head velocity) of the vestibulo-ocular reflex (VOR). We sought to know whether convergence would increase the VOR gain (mean + SD) in unilateral vestibular hypofunction (UVH). Methods Vestibulo-ocular reflex gain during ipsi- and contralesional horizontal head rotation at near (15 cm) and far (150 cm) targets was measured in 22 subjects with UVH and 12 healthy controls. Retinal slip was estimated (retinal slip index [RSI]) as the difference between ideal VOR gain (no retinal slip) and the actual VOR gain. Results Convergence did not significantly enhance VOR gain for ipsilesional rotation (mean difference, 0.04; 95% confidence interval [CI], -0.01 to 0.09), near viewing (0.77 ± 0.34) versus far viewing (0.72 ± 0.29), yet the VOR gain during contralesional rotation was greater for near viewing (1.20 ± 0.23) than for far viewing (0.97 ± 0.21; mean difference, 0.23; 95% CI, 0.13-0.32). In the 36% of subjects with recovery of their ipsilesional VOR gain, the vergence effect trended to recover (far VOR gain: 1.06 ± 0.17 vs near VOR gain 1.16 ± 0.21; mean difference, 0.10; 95% CI, -0.02 to 0.22). Ipsilesional head rotation induced greater retinal slip for near (RSI = 0.90 ± 0.34) targets than for far targets (RSI = 0.35 ± 0.29; mean difference, 0.56; 95% CI, 0.51-0.61). Discussion and conclusions The convergence-mediated VOR gain enhancement is preserved during contralesional but impaired during ipsilesional head rotation. Recovery of ipsilesional passive VOR gain does not equate to restored convergence enhancement, although it did increase ∼10%. These data suggest head motion viewing near targets will increase retinal slip, which warrants consideration as a gaze stability exercise for subjects with UVH.Video Abstract available for more insights from the authors (see Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A325).

Most prior studies of the subjective visual vertical (SVV) focus on inaccuracy of subjects' SVV responses with the head in an upright position. Here we investigated SVV imprecision during lateral head tilt in patients with chronic dizziness compared to healthy controls. Forty-five dizzy patients and 45 healthy controls underwent SVV testing wearing virtual reality (VR) goggles, sitting upright (0°) and during head tilt in the roll plane (± 30°). Ten trials were completed in each of three static head positions. The SVV inaccuracy and SVV imprecision were analyzed and compared between groups, along with systematic errors during head tilt, i.e., A-effect and E-effect (E-effect is a typical SVV response during head tilts of ± 30°). The SVV imprecision was found to be affected by head position (upright/right head tilt/left head tilt, p 0.001) and underlying dizziness (dizzy patients/healthy controls, p = 0.005). The SVV imprecision during left head tilt was greater in dizzy patients compared to healthy controls (p = 0.04). With right head tilt, there was a trend towards greater SVV imprecision in dizzy patients (p = 0.08). Dizzy patients were more likely to have bilateral (6.7%) or unilateral (22.2%) A-effect during lateral head tilt than healthy controls (bilateral (0%) or unilateral (6.7%) A-effect, p 0.01). Greater SVV imprecision in chronically dizzy patients during head tilts may be attributable to increased noise of vestibular sensory afferents or disturbances of multisensory integration. Our findings suggest that SVV imprecision may be a useful clinical parameter of underlying dizziness measurable with bedside SVV testing in VR.

Identifying dangerous causes of dizziness is a challenging task for neurologists, as it requires interpretation of subtle bedside exam findings, which become even more subtle with time. Nystagmus can be instrumental in differentiating peripheral from central vestibular disorders. Conventional teaching is that peripheral vestibular nystagmus is accentuated by removal of visual fixation. We sought to systematically test the hypothesis that, in some cases, vertical nystagmus due to central vestibular disorders may also be easier to identify when fixation is removed.To identify patients with vertical nystagmus, we retrospectively reviewed clinical, MRI, and VNG data of consecutive patients undergoing VNG in our vestibular clinic over a 9-month period. We analyzed clinical features, bedside neuro-otological examination, MRI results, and VNG findings in fixation as well as those with fixation removed.Two hundred and fourteen charts were reviewed. Twenty-six patients had vertical nystagmus with fixation removed on VNG. Only three (11.5%) of these patients had vertical nystagmus apparent with fixation (and only two had nystagmus observed clearly at the bedside with the unaided eye). Thirteen (50%) of the patients had posterior fossa lesions on MRI and eight of the rest (30.8%) were diagnosed with central vestibular disorders. Of the 13 patients with MRI-confirmed lesions, 3 patients (23.1%) had no neurological signs or conventional bedside oculomotor signs; in these cases, vertical nystagmus without fixation was the only sign of a central lesion.Our findings go against conventional teaching and show that removing fixation can uncover subtle vertical nystagmus due to central vestibular disease, particularly from focal or chronic lesions.

Objectives Isolated dizziness is a challenging stroke presentation in the emergency department, but little is known about this problem in other clinical settings. We sought to compare stroke hospitalizations after treat-and-release clinic visits for purportedly “benign dizziness” between general and specialty care settings. Methods This was a population-based retrospective cohort study from a national database. We included clinic patients with a first incident treat-and-release visit diagnosis of non-specific dizziness/vertigo or a peripheral vestibular disorder (ICD-9-CM 780.4 or 386.x [not 386.2]). We compared general care (internal medicine, family medicine) vs. specialty care (neurology, otolaryngology) providers. We used propensity scores to control for baseline stroke risk differences unrelated to dizziness diagnosis. We measured excess (observed>expected) stroke hospitalizations in the first 30 d (i.e., missed strokes associated with an adverse event). Results We analyzed 144,355 patients discharged with “benign dizziness” (n=117,117 diagnosed in general care; n=27,238 in specialty care). After propensity score matching, patients in both groups were at higher risk of stroke in the first 30 d (rate difference per 10,000 treat-and-release visits for “benign dizziness” 24.9 [95% CI 18.6–31.2] in general care and 10.6 [95% CI 6.3–14.9] in specialty care). Short-term stroke risk was higher in general care than specialty care (relative risk, RR 2.2, 95% CI 1.5–3.2) while the long-term risk was not significantly different (RR 1.3, 95% CI 0.9–1.9), indicating higher misdiagnosis-related harms among dizzy patients who initially presented to generalists after adequate propensity matching. Conclusions Missed stroke-related harms in general care were roughly twice that in specialty care. Solutions are needed to address this care gap.

A 65-year-old woman with right-sided Meniere disease experienced one of her usual and frequent acute vertigo attacks during eye movement recording (video 1). The attacks were associated with right-sided tinnitus, hearing loss, and vomiting. She initially demonstrated right-beating nystagmus, but after 2 minutes, the nystagmus gradually reversed and became left-beating (video 1). During the reversal, downbeat nystagmus was present temporarily. The left-beating nystagmus then persisted for 2 hours.

The pathophysiology of acute, vertical spontaneous eye movements following pontine hemorrhage is not well understood. Here, we present and discuss the video-oculography findings of a patient with acute pontine hemorrhage who developed vertical pendular oscillation and ocular bobbing while comatose. The amplitudes, peak velocities, frequency distribution, and phase planes (velocity versus position) of the eye movements were analyzed. The vertical pendular oscillation was rhythmic with a peak frequency of 1.7 Hz, but amplitudes (mean 1.9°, range 0.2-8.2°) and peak velocities (mean 20.6°/s; range 5.9-60.6°/sec) fluctuated. Overall, their peak velocities were asymmetric, faster with downward than upward. Higher peak velocities were seen with larger amplitudes (downward phase r = 0.95, p < 0.001; upward phase r = 0.91, p < 0.001) and with movements beginning at eye positions lower in the orbit (downward phase r = - 0.64, p < 0.001; upward phase r = - 0.86, p < 0.001). Interspersed were typical ocular bobbing waveforms with a fast (peak velocity 128.8°/s), large-amplitude (17.5°) downward movement, sometimes followed by a flat interphase interval (0.5 s) when the eye was nearly stationary, and then a slow return to mid-position with a decaying velocity waveform. To account for the presence and co-existence of pendular oscillations and bobbing, we present and discuss three hypothetical models, not necessarily mutually exclusive: (1) oscillations originating in the inferior olives due to disruption of the central tegmental tract(s); (2) unstable neural integrator function due to pontine cell group damage involving neurons involved in gaze-holding; (3) low-frequency saccadic intrusions following omnipause neuron damage.

Background Amongst the most challenging diagnostic dilemmas managing patients with vestibular symptoms (i.e. vertigo, nausea, imbalance) is differentiating dangerous central vestibular disorders from benign causes. Migraine has long been recognized as one of the most common causes of vestibular symptoms, but the clinical hallmarks of vestibular migraine are notoriously inconsistent and thus the diagnosis is difficult to confirm. Here we conducted a prospective study investigating the sensitivity and specificity of combining standard vestibular and neurological examinations to determine how well central vestibular disorders (CVD) were distinguishable from vestibular migraine (VM). Method Twenty-seven symptomatic patients diagnosed with CVD and 36 symptomatic patients with VM underwent brain imaging and clinical assessments including; 1) SVV bucket test, 2) ABCD2, 3) headache/vertigo history, 4) presence of focal neurological signs, 5) nystagmus, and 6) clinical head impulse testing. Results Mean absolute SVV deviations measured by bucket testing in CVD and VM were 4.8 ± 4.1° and 0.7 ± 1.0°, respectively. The abnormal rate of SVV deviations (> 2.3°) in CVD was significantly higher than VM (p

A nationwide, population-based, retrospective cohort study.To investigate whether benign paroxysmal positional vertigo (BPPV) is associated with an increased risk of fracture.Benign paroxysmal positional vertigo is a brief rotational vertigo induced by head position change that may increase the risk of falls and, therefore, fracture.Data from the Taiwan National Health Insurance Research Database were used for this study. We selected a case cohort comprising 3796 patients aged over 20 years who were newly diagnosed with BPPV between 2000 and 2006. In addition, we randomly selected a control cohort of 15 184 individuals without BPPV. Patients with BPPV were matched to individuals in the control group according to sex, age, and index year. A Cox proportional hazard regression was performed to compute the hazard ratio of fracture, after adjusting for demographic characteristics and comorbidities.The prevalence of comorbidities was higher among patients with BPPV. After adjusting for age, sex, and comorbidities, patients with BPPV exhibited a 1.14-fold (95% confidence interval [CI]: 1.04, 1.25; P.01) higher risk of fracture than those without BPPV. Trunk fracture (vertebra, rib, and pelvis) was the fracture type with the highest adjusted hazard ratio (1.24; 95% CI: 1.06, 1.45; P.01) in patients with BPPV relative to those without BPPV. An analysis stratified according to demographic factors revealed that men with BPPV exhibited a 1.43-fold (95% CI: 1.22, 1.66; P.001) higher risk of fracture. Patients with BPPV aged over 65 years exhibited a significantly higher risk of fracture (adjusted hazard ratio = 1.17; 95% CI: 1.03, 1.33; P.05) than did those without BPPV.Patients with BPPV exhibited a higher risk of fracture than did those without BPPV.Prognosis, level 2b.

Background Because it is unknown whether sudden hearing loss (SHL) in acute vertigo is a “benign” sign (reflecting ear disease) or a “dangerous” sign (reflecting stroke), we sought to compare long-term stroke risk among patients with (1) “SHL with vertigo,” (2) “SHL alone,” and (3) “vertigo alone” using a large national health-care database. Methods Patients with first-incident SHL (International Classification of Diseases, Ninth Edition, Clinical Modification [ICD-9-CM] 388.2) or vertigo (ICD-9-CM 386.x, 780.4) were identified from the National Health Insurance Research Database of Taiwan (2002-2009). We defined SHL with vertigo as a vertigo-related diagnosis ±30 days from the index SHL event. SHL without a temporally proximate vertigo diagnosis was considered SHL alone. The vertigo-alone group had no SHL diagnosis. All the patients were followed up until stroke, death, withdrawal from the database, or current end of the database (December 31, 2012) for a minimum period of 3 years. The hazards of stroke were compared across groups. Results We studied 218,656 patients (678 SHL with vertigo, 1998 with SHL alone, and 215,980 with vertigo alone). Stroke rates at study end were 5.5% (SHL with vertigo), 3.0% (SHL alone), and 3.9% (vertigo alone). Stroke hazards were higher in SHL with vertigo than in SHL alone (hazard ratio [HR], 1.93; 95% confidence interval [CI], 1.28-2.91) and in vertigo alone (HR, 1.63; 95% CI, 1.18-2.25). Defining a narrower window between SHL and vertigo (±3 days) increased the hazards. Conclusions The combination of SHL plus vertigo in close temporal proximity is associated with increased subsequent stroke risk over SHL alone and vertigo alone. This suggests that SHL in patients with vertigo is not necessarily a benign peripheral vestibular sign.

Importance It is important to know whether recovery of the vestibuloocular reflex (VOR) as measured by the video head impulse test (vHIT) is associated with the recovery of dynamic balance. It is also critical to know how much change in VOR gain is clinically relevant for establishing the recovery of dynamic balance. Objectives To investigate the association between improved VOR gain as measured by the vHIT and improved dynamic balance (reduced fall risk) as measured by the dynamic gait index (DGI) and to calculate the minimal clinically important difference of VOR gain. Design, Setting, and Participants This retrospective case series study was performed at a tertiary referral center at the Johns Hopkins University School of Medicine. Thirty-eight consecutive patients with subacute or chronic dizziness from January 1, 2014, through May 31, 2017, who visited the vestibular physical therapy clinic were included in the study. Interventions Each patient was evaluated with room light and video-infrared oculomotor examination, vHIT, and balance testing before and after vestibular physical therapy. Main Outcomes and Measures Gain of the lesioned VOR and score on the DGI. Results Among the 38 patients (25 women [66%]; mean [SD] age, 65 [14] years), the mean (SD) initial lesioned VOR gain was 0.66 (0.23) and initial DGI score was 16 (3). No correlation was found between initial VOR gain and initial DGI score (r = −0.04; 95% CI, −0.35 to 0.28). At follow-up, 15 patients (39%) had an improved VOR gain and 30 (79%) had an improved DGI score, which was correlated (r = 0.49; 95% CI, 0.20-0.69). In those 15 patients with improved VOR gain, 14 (93%) had improvement of DGI score. In the 23 patients without improvement of VOR gain, 16 (70%) still showed improvement in their DGI score. When using VOR gain to estimate improvement of DGI, the minimal clinically important difference of VOR gain was −0.06. Conclusions and Relevance The change of VOR gain in the vHIT was moderately associated with the change of DGI score. Improved VOR gain was associated with a high probability of improved dynamic balance. However, in most of the patients whose VOR gains did not improve, balance improvement occurred putatively through sensory reweighting strategies.

Background Benign paroxysmal positional vertigo (BPPV), the most common type of vertigo in the general population, is thought to be caused by dislodgement of otoliths from otolithic organs into the semicircular canals. In most cases, however, the cause behind the otolith dislodgement is unknown. Dental procedures, one of the most common medical treatments, are considered to be a possible cause of BPPV, although this has yet to be proven. This study is the first nationwide population-based case-control study conducted to investigate the correlation between BPPV and dental manipulation. Methods Patients diagnosed with BPPV between January 1, 2007 and December 31, 2012 were recruited from the National Health Insurance Research Database in Taiwan. We further identified those who had undergone dental procedures within 1 month and within 3 months before the first diagnosis date of BPPV. We also identified the comorbidities of the patients with BPPV, including head trauma, osteoporosis, migraine, hypertension, diabetes, hyperlipidemia and stroke. These variables were then compared to those in age- and gender-matched controls. Results In total, 768 patients with BPPV and 1536 age- and gender-matched controls were recruited. In the BPPV group, 9.2% of the patients had undergone dental procedures within 1 month before the diagnosis of BPPV. In contrast, only 5.5% of the controls had undergone dental treatment within 1 month before the date at which they were identified (P = 0.001). After adjustments for demographic factors and comorbidities, recent exposure to dental procedures was positively associated with BPPV (adjusted odds ratio 1.77; 95% confidence interval 1.27–2.47). This association was still significant if we expanded the time period from 1 month to 3 months (adjusted odds ratio 1.77; 95% confidence interval 1.39–2.26). Conclusions Our results demonstrated a correlation between dental procedures and BPPV. The specialists who treat patients with BPPV should consider dental procedures to be a risk factor, and dentists should recognize BPPV as a possible complication of dental treatment.

The reported prevalence of cavum septum pellucidum (CSP) and cavum Vergae (CV) in brain computed tomography (CT) is 5.5% in Great Britain and 1.24% in China but unknown in Taiwan. Moreover, CSP and/or CV has generally been thought to decrease as age progresses, but the evidence of actual prevalence at different age levels is still limited in the literature.A total of 19,031 patients with brain CT at a regional hospital in northern Taiwan from July 2008 to August 2010 were included in this study. Their radiological official reports were retrospectively reviewed to check for CSP and/or CV. An X2 test was used for statistical analysis (α = .05).The prevalence of CSP and/or CV in all brain CT was 0.93% (n = 177), which was lower. than that in the Chinese and British studies. Among them, 2.8% (n = 5) had only CSP, 1.7% (n = 3) had only CV, and 95.5% (n = 169) had coexistent CSP and CV. There is a significant difference in prevalence between the age groups (p = .009), and the prevalence is the highest in the group aged 20-29 years (1.56%) and lowest in the group aged above 80. After age 20-29, the prevalence tends to decrease with increasing age.This is not only the first study of CSP and CV in the Taiwanese population but the study population is also larger than those in the literature. The prevalence was found to approximately decrease as age progresses, but would reach the peak in the young adult group rather than the children or adolescent group.

To investigate whether patients with vestibular migraine (VM) are more susceptible to carsickness than patients with non-vestibular migraine (NVM) or Meniere's disease (MD).Consecutive patients with a diagnosis of definite VM, probable VM, NVM, or MD at our Headache and Dizziness clinics were interviewed using the same three questions to investigate the history of carsickness. The patients who had experienced carsickness in their lifetime and those who had still experienced carsickness in the past ten years were identified. The rates of carsickness were compared between groups.78.4% of the VM patients had experienced carsickness in their lifetime, which was significantly higher than the patients with NVM (43.6%) and MD (18.2%). Both the lifetime rate of carsickness and the rate in the past ten years were highest in the patients with definite VM, followed by probable VM, NVM, and MD (p less than 0.05, chi-square test). The odds ratio of lifetime carsickness for VM versus MD was high (8.7).Both patients with definite VM and probable VM were more susceptible to carsickness than the patients with NVM or MD. This reinforces the theory of vestibular hypersensitivity in VM. We suggest that a past history of carsickness may help in the diagnosis of VM, and especially in distinguishing VM from MD.

Vestibular paroxysmia is defined as paroxysmal, brief, and carbamazepine-responsive vertigo. Although neurovascular cross-compression (NVCC) of the vestibulocochlear nerve is believed to be the cause of vestibular paroxysmia, the mechanism remains controversial. Herein, we describe the case of a man with NVCC who presented with paroxysmal vertigo associated with paroxysmal pulsatile tinnitus.A 68-year-old man presented with paroxysmal vertigo for one month. Paroxysmal pulsatile tinnitus in the right ear occurred simultaneously with the vertigo. Magnetic resonance imaging demonstrated that the right anterior inferior cerebellar artery was compressing the right vestibulocochlear nerve. The vertigo and tinnitus completely disappeared within one week after treatment with carbamazepine.The pulsatile nature of the patient's tinnitus implied that the auditory nerve was being compressed by a pulsating artery and was found to consolidate the causal relationship between NVCC and vestibular paroxysmia.

A 68-year-old man developed vertigo with a lateral medullary syndrome (figure). Right-beating nystagmus, seen under Frenzel lenses, reversed when a vibrator (60 Hz) was applied on either sternocleidomastoid muscle or either mastoid. When the vibrator was turned off, the nystagmus returned to right-beating (video on the Neurology ® Web site at [www.neurology.org][1]). The authors thank Prof. David Zee for critically reviewing the manuscript. [1]: http://www.neurology.org

A 60-yr-old man presented with chronic vestibulopathy induced by Ramsay Hunt syndrome for 1 yr. Prolonged dizziness and postural imbalance affected his quality-of-life. He was treated using a 2-mo protocol of customized vestibular rehabilitation therapy consisting of 16 treatment sessions in a rehabilitation clinic and daily home exercises. Significant improvements in the subjective perception of dizziness and objective balance function were found. The results suggest that vestibular rehabilitation therapy may be an effective therapeutic method for chronic vestibulopathy of Ramsay Hunt syndrome.

We report a case of a tiny infarct on the left dorsolateral pons in a 50-year-old man who presented with prolonged and isolated vertigo. The clinical features mimic vestibular neuritis and can easily lead to misdiagnosis. Selective involvement of the left superior vestibular nucleus might explain the resemblance to acute peripheral vestibulopathy.

Since the outbreak of novel influenza A (H1N1) in 2009, various neurological complications have been cited. We described a male patient with H1N1-associated encephalopathy/encephalitis presenting with severe neurological symptoms and signs. Residual neurological sequelae were dominant. This is the first report of extensive cortical-subcortical necroses over the bilateral frontal-parietal areas based on an MRI study.

We describe a patient who presented with unilateral paresthesia after acute isolated infarct of the splenium.A 74-year-old woman presented with acute onset of right sided numbness and tingling. MR imaging of the brain showed hypointensity on T1-weighted images and on apparent diffusion coefficient maps, and hyperintensity on T2-weighted and on diffusion-weighted images in the splenium, suggestive of acute infarction. MR angiography showed narrowing of left posterior cerebral artery with decreased branches. On detailed high cortical function assessment, she did not have frontal lobe dysfunction, alien hand syndrome, apraxia, optic ataxia, cortical sensation dysfunction, alexia, agraphia, visual field defect, nor color agnosia.Infarcts of the splenium are not common. Splenial lesion may be associated with altered mental status, ataxia, recent seizure, hemispheric disconnection, and dysarthria. The presentation of isolated unilateral paresthesia makes the patient different from those previously described. The paresthesia could be caused by selective lacunar infarcts in the diencephalic and mesencephalic regions or could be caused by the diaschisis in the parietal cortex. Single photon emission CT may be indicated to provide further information of central nervous system dysfunction in splenial lesion.

Hypertensive encephalopathy (HE) is one of the acknowledged hypertensive emergencies. Isolated hypertensive brainstem encephalopathy (HBE) without concomitant typical parietooccipital lesion is unusual. Patients with HBE may or may not present with symptoms attributable to brainstem and the diagnosis is challenging in an emergency setting. The most important differential diagnosis in HBE is brainstem infarction, because the goals of blood pressure treatment are different. Evidence of vasogenic edema on magnetic resonance image, i.e. absence of high signal lesions on diffusion weighted images and increased value of apparent diffusion coefficient are diagnostic indicators of HBE, but not brainstem infarction. Prompt recognition of HBE and adequately lowering blood pressure offer the best outcomes.