Case report: Bitter vertigo.

Background: There are many causes of episodes of vertigo and very few causes of episodes of changes in taste, and the combination of the two is very rare. Here, we describe a patient with recurrent short episodes of vertigo in combination with simultaneous episodes of recurrent paroxysmal dysgeusia and altered feeling on the left side of face. The symptoms were caused by compression of the vestibulocochlear nerve and the facial nerve due to dolichoectasia of the basilar artery. Methods: The patient was diagnosed in our routine clinical practice and underwent a complete neurological and neuro-otological examination, including video head impulse test, caloric irrigation, ocular and cervical vestibular evoked myogenic potentials, acoustic-evoked potentials, neuro-orthoptic examination, cranial MRI, and MR angiography. The patient was seen twice for follow-up. Case: A 71-year-old patient primarily presented with a 2-year history of recurrent short episodes of spinning vertigo. Each of the episodes began with an altered feeling on the left side of the face, followed by a bitter taste on the left half of the tongue, and subsequently vertigo lasting for up to 15 s. The frequency of the attacks was high: up to 80 times per day. Laboratory tests revealed signs of a peripheral vestibular deficit on the left side. There were no signs of sensory or motor deficits or of altered taste between the episodes. An MRI of the brain showed an elongated basilar artery leading to an indentation of the facial and vestibulocochlear nerves on the left side. Conclusion: We propose a neurovascular compression in the proximal part of two cranial nerves because of pulsatile compression by the elongated basilar artery with ephatic discharges as the cause of the recurrent episodes. Consistent with the theory of ephatic discharges, treatment with the sodium channel blocker lacosamide for over six months with a final dosage of 200 mg per day p.o. led to a significant reduction of the attack frequency and intensity. This treatment option with a sodium channel blocker should therefore not only be considered in vestibular paroxysmia but also in cases of paroxysmal dysgeusia.

Uncrossed corticospinal tract in health and genetic disorders: Review, case report, and clinical implications.

BACKGROUND AND PURPOSE: Crossing pathologies of the corticospinal tract (CST) are rare and often associated with genetic disorders. However, they can be present in healthy humans and lead to ipsilateral motor deficits when a lesion to motor areas occurs. Here, we review historical and current literature of CST crossing pathologies and present a rare case of asymmetric crossing of the CST. METHODS: Description of the case and systematic review of the literature were based on the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. The PubMed database was searched for peer-reviewed articles in English since 1950. All articles on ipsilateral stroke, uncrossed CST, and associated neurologic disorders were screened. Furthermore, a literature review between the years 1850 and 1980 including articles in other languages, books, opinions, and case studies was conducted. RESULTS: Only a few descriptions of CST crossing pathologies exist in healthy humans, whereas they seem to be more common in genetic disorders such as horizontal gaze palsy with progressive scoliosis or congenital mirror movements. Our patient presented with aphasia and left-sided hemiparesis. Computed tomographic (CT) scan revealed a perfusion deficit in the left middle cerebral artery territory, which was confirmed by diffusion-weighted magnetic resonance imaging (MRI), so that thrombolysis was administered. Diffusion tensor imaging with fibre tracking revealed an asymmetric CST crossing. CONCLUSIONS: The knowledge of CST crossing pathologies is essential if a motor deficit occurs ipsilateral to the lesion side. An ipsilateral deficit should not lead to exclusion or delay of therapeutic options in patients with suspected stroke. Here, a combined evaluation of CT perfusion imaging and MRI diffusion imaging may be of advantage.

Acute binocular diplopia: peripheral or central?

OBJECTIVES: Acute diplopia is a diagnostic challenge for clinicians, in particular in the emergency department. The most common cause of acute diplopia are ocular motor nerve palsies (OMP). In this prospective study, we focused on identifying the most crucial signs and symptoms for differentiating between peripheral and central OMP. METHODS: We prospectively evaluated 56 non-consecutive patients who presented at our emergency department with acute binocular diplopia (≤ 10 days). The patient history was taken using a standardized questionnaire and patients underwent a neurological, neuro-ophthalmological and neuro-otological examination, including measurement of the subjective visual vertical (SVV), Harms tangent screen test, and cranial MRI. RESULTS: Forty-six out of 56 patients were diagnosed with an ocular motor cranial nerve palsy (OMP), 21 of peripheral and 23 of central origin; in two patients, the etiology remained unknown. The following features were different in peripheral and central OMP: (1) the presence of vertigo/dizziness was more frequent in central (43.5%) than in peripheral (9.5%) OMP. (2) Central ocular motor signs, such as saccadic smooth pursuit, additional internuclear ophthalmoplegia, skew deviation, and saccade palsies, were also found more frequently in the central than in the peripheral group (86.7% vs. 33.3%). (3) Further, a pathological SVV deviation by monocular testing of the non-affected eye was also more common in central (77.3%) than in peripheral OMP (38.9%). The presence of all three factors has a positive predictive value of 100% (CI 50-100%) for the presence of a central lesion. CONCLUSIONS: In acute diplopia due to central OMP, the most important accompanying symptom is vertigo/dizziness, and the most important clinical signs are central ocular motor disorders (which require examination of the non-paretic eye) and an SVV deviation in the non-paretic eye.

Changes of brain DTI in healthy human subjects after 520 days isolation and confinement on a simulated mission to Mars.

INTRODUCTION: Long-term confinement is known to be a stressful experience with multiple psycho-physiological effects. In the MARS500 project, a real-time simulation of a space-flight to Mars conducted in a hermetically isolated habitat, effects of long-term confinement could be investigated in a unique manner. The aim of this study was to evaluate effects of long-term-confinement on brain cytoarchitecture. MATERIAL & METHODS: The participants of the MARS500 project underwent 3T-MR imaging including a dedicated DTI-sequence before the isolation, right after ending of confinement and 6 months after the experiment. Voxelwise statistical analysis of the DTI data was carried out using tract-based-spatial statistics, comparing an age-matched control group. RESULTS: At all three sessions, significant lower fractional anisotropy (FA) than in controls was found in the anterior parts of the callosal body of the participants. Furthermore, after ending of confinement a wide-spread FA reduction could be seen in the right hemisphere culminating in the temporo-parietal-junction-zone. All these areas with decreased FA predominantly showed an elevated radial diffusivity and mean diffusivity while axial diffusivity was less correlated. DISCUSSION: Long-term confinement does have measurable effects on the microstructure of the brain white matter. We assume effects of sensory deprivation to account for the regional FA reductions seen in the right TPJ. The differences in the Corpus callosum were interpreted as due to preliminary conditions, e.g. personality traits or training effects. FA and radial diffusivity were the predominant DTI parameters with significant changes, suggesting underlying processes of myelin plasticity.

Diffusion Tensor Imaging for Surgical Planning in Patients with Cervical Spondylotic Myelopathy.

BACKGROUND AND STUDY AIMS/OBJECTIVE: Despite its invasiveness, computed tomography myelography (CTM) is still considered an important supplement to conventional magnetic resonance imaging (MRI) for preoperative evaluation of multilevel cervical spondylotic myelopathy (CSM). We analyzed if diffusion tensor imaging (DTI) could be a less invasive alternative for this purpose. MATERIAL AND METHODS: In 20 patients with CSM and an indication for decompression of at least one level, CTM was performed preoperatively to determine the extent of spinal canal/cerebrospinal fluid (CSF) space and cord compression (Naganawa score) for a decision on the number of levels to be decompressed. Fractional anisotropy (FA) and apparent diffusion coefficient (ADC) were correlated with these parameters and with MRI-based increased signal intensity (ISI). Receiver operating characteristic analysis was performed to determine the sensitivity to discriminate levels requiring decompression surgery. European Myelopathy Score (EMS) and neck/radicular visual analog scale (VAS-N/R) were used for clinical evaluation. RESULTS: According to preoperative CTM, 20 levels of maximum and 16 levels of relevant additional stenosis were defined and decompressed. Preoperative FA and particularly ADC showed a significant correlation with the CTM Naganawa score but also with the ISI grade. Furthermore, both FA and ADC facilitated a good discrimination between stenotic and nonstenotic levels with cutoff values < 0.49 for FA and > 1.15 × 10-9 m2/s for ADC. FA and especially ADC revealed a considerably higher sensitivity (79% and 82%, respectively) in discriminating levels requiring decompression surgery compared with ISI (55%). EMS and VAS-N/R were significantly improved at 14 months compared with preoperative values. CONCLUSION: DTI parameters are highly sensitive at distinguishing surgical from nonsurgical levels in CSM patients and might therefore represent a less invasive alternative to CTM for surgical planning.

Ruptured basilar artery perforator aneurysms--treatment regimen and long-term follow-up in eight cases.

INTRODUCTION: Basilar artery (BA) perforator aneurysms may lead to severe subarachnoid hemorrhage (SAH). The acute management is uncertain. The anatomic approach is challenging both for coiling and clipping, and flow diverter stenting may be dangerous due to the required antiplatelet therapy. We report on our experiences in eight patients. METHODS: We retrospectively analyzed eight patients with ruptured BA perforator aneurysm, including clinical characteristics, imaging data, treatment regimen, clinical course, and long-term outcome. RESULTS: Patients presented with major SAH and World Federation of Neurosurgical Societies (WFNS) scores of I in three, II in two, and V in three cases. In four patients, the aneurysm was detected in the initial angiography, in four only in follow-up angiography. Five patients were treated conservatively and three patients had endovascular therapy. In the conservative group, the aneurysm spontaneously thrombosed in three cases. One patient suffered from a re-SAH and stayed permanently dependent due to an associated perforator stroke (modified Rankin Scale (mRS) 5). The remaining four patients recovered well (mRS 0 and 1 in two cases, each) including three patients also exhibiting perforator strokes. Regarding the endovascular group, one parent vessel was an angioma feeder and embolized with Onyx. The second aneurysm spontaneously thrombosed periinterventionally. The third patient underwent coiling. Two parent vessels were occluded postinterventionally, resulting in perforator strokes. Final mRS scores were 0, 2, and 2, respectively. CONCLUSION: Conservative management of ruptured BA aneurysms might be a first-line treatment option with common spontaneous aneurysm occlusion, low rate of re-SAH, and promising clinical outcome.

Arginine vasopressin V1a receptor-deficient mice have reduced brain edema and secondary brain damage following traumatic brain injury.

The formation of brain edema and subsequent intracranial hypertension are major predictors of unfavorable outcome following traumatic brain injury (TBI). Previously, we reported that arginine vasopressin (AVP) receptor antagonists reduce post-traumatic and post-ischemic brain edema in mice. The aim of the current study was to investigate further the contribution of arginine vasopressin V1a receptors to TBI-induced secondary brain damage in V1a receptor knock-out mice. V1a receptor knock-out (V1a -/-) and wild-type mice were subjected to controlled cortical impact (CCI), and edema (brain water content measured before and 24 h after CCI), primary and secondary contusion volume (15 min and 24 h after CCI), neurological function (one day before and seven days after CCI), body weight (before and seven days after CCI) and mortality were measured. Twenty-four h after CCI, V1a receptor knock-out mice had significantly less brain water content than wild-type mice (mean±standard error of the mean: 79.8%±0.3 vs. 80.6%±0.2, respectively), and secondary contusion volume was significantly smaller (38.2±1.7 mm(3) vs. 45.1±1.5 mm(3) in wild-type mice). Furthermore, the V1a receptor knock-out mice had less neurological dysfunction (3.2±0.8 vs. 7.0±1.4 in wild-type mice) and weight loss (1.0±1.0% vs. 4.9±1.8% in wild-type mice) seven days after CCI. Our data show that mice lacking V1a receptors have less secondary brain damage following experimental traumatic brain injury. We therefore conclude that V1a receptors may represent a novel drug target for preventing post-traumatic brain edema.