Seesaw nystagmus (SSN) is characterized by conjugate torsional nystagmus with opposite vertical components in the two eyes. The waveform may be pendular or jerk (hemi-seesaw nystagmus, HSSN), in which the slow phase corresponds to one half-cycle and the quick phase to the other. Pendular SSN and HSSN have distinct clinical presentations and underlying causes. The pathophysiology of pendular SSN may be instability of visuovestibular interactions, while the underlying mechanism for HSSN may be related to the ocular tilt reaction or an imbalance in vestibular pathways. We report a patient with HSSN due to unilateral mesodiencephalic infarction that becomes apparent during visual fixation only.
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Midbrain lesion-induced disconjugate gaze: a unifying circuit mechanism of ocular alignment? Maximilian U. Friedrich, Laurin Schappe, Sashank Prasad, Helen Friedrich, Michael D. Fox, Andreas Zwergal, David S. Zee, Klaus Faßbender, Klaus-Ulrich Dillmann Journal of Neurology.2024;[Epub] CrossRef
Facial palsy can be caused by central and peripheral causes, and it can also be caused by brain tumors or infarction. A 59-year-old male, who lost his right hearing 13 years ago due to Ramsay Hunt syndrome, visited our hospital with facial palsy and dizziness. Initial brain diffusion-weighted magnetic resonance imaging (MRI) showed no abnormal findings, and recurrent Ramsay Hunt syndrome or a neoplastic lesion in the internal auditory canal was suspected. After hospitalization, the patient was administered high-dose steroids, and the videonystagmography showed direction-changing gaze-induced nystagmus, so a brain MRI reexamination was scheduled. While waiting for MRI, the patient complained of neurological symptoms such as diplopia, and right lower pontine infarction was diagnosed on MRI. The patient was transferred to the neurologic department and was discharged on the 10th day after conservative treatment. During the 1-year follow-up, pontine infarction did not recur, and neurological symptoms such as facial palsy gradually improved.
Dissociated vertical-torsional nystagmus is a unique form of nystagmus characterized by conjugate torsional but disparate vertical components. It has been mainly reported in internuclear ophthalmoplegia or medial medullary lesion involving the medial longitudinal fasciculus (MLF). The patterns of the nystagmus may be explained by a disruption of vestibulo-ocular reflex pathways from vertical semicircular canal or utriculo-ocular reflex within the MLF, but it is debatable. We described a dissociated upbeat-torsional nystagmus in a patient with vestibular nucleus infarction without involvement of MLF.
The flocculus plays a crucial role in control of eye movements. Based on animal experiment, it is suggested that the flocculus is important for governing vestibuleocular reflexes. In humans, an isolated floccular lesion is extremely rare. We report oculomotor abnormalities in a patient with unilateral infarction of the flocculus, and compare our results with those of previously reported patients with floccular lesion.
Because numerous important nuclei and white matter tracts are concentrated in the narrow midbrain, the tiny lesion can result in various symptoms. The anatomy of the neural network and related structures in the midbrain is complex. The most frequent clinical manifestation of lesions involving the midbrain is an eye movement disorder associated with a nuclear or fascicular origin. We have described patients with acute midbrain stroke, characterized by rare neuro-ophthalmologic manifestations, which neurologists should consider during diagnostic investigations. Case 1 showed internuclear ophthalmoplegia with Horner syndrome. In case 2 showed isolated oculomotor palsy. The third patient presented Parinaud syndrome with an unusual lesion location. Notably, patients with midbrain infarction may present with specific signs and symptoms that are compatible with mesencephalic localization. The isolated or combined neuro-ophthalmologic signs and symptoms should be interpreted in the complex anatomical context described here and investigated by immediate brainstem neuroimaging analyses and careful neurologic examinations.
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A Improved Case of Post Cerebral Infarction Dizziness and Gait Discomfort after Treated with Korean Medicine Treatment and Vestibular Rehabilitation Practice Hongmin Chu, Hyeon-Seo Lim, Kwangho Kim, Young-Ung Lee, Kyungtae Park, Jongwon Jang, Ho-sun Ryu, Su-hak Kim, Cheol-hyun Kim, Sangkwan Lee, Kang-keyng Sung Journal of Korean Medicine Rehabilitation.2020; 30(4): 179. CrossRef
Vertical gaze palsy is usually associated with lesions of the rostral midbrain and thalamo-mesencephalic junction. The rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), the interstitial nucleus of Cajal, and the posterior commissure located in the midbrain are the critical area in supranuclear control of vertical eye movements. We describe a case of vertical one-and-a-half syndrome accompanying contralateral abduction and incomplete depression palsy due to thalamo-mesencephalic infarction. These vertical eye movement abnormalities are presumed to be caused by damage to the ipsilateral riMLF, interstitial nucleus of Cajal, and oculomotor fascicles.
For differential diagnosis between vestibular neuritis and lateral medullary
infarction with similar clinical features, bedside examination of nystagmus is
important. We report a 45-year-old male who presented with acute vertigo for
two days. He showed spontaneous right-beating nystagmus. However, left-beating
nystagmus was evoked during bilateral horizontal gaze and by horizontal head
oscillation. Brain MRI revealed an acute infarction in the left lateral medulla.
Cogan’s syndrome is a rare chronic inflammatory disease Characterized by non-syphilitic keratitis and vestibuloauditory dysfunction. Although the precise pathogenesis of Cogan’s syndrome is unknown, it is thought to develop from vasculitis involving multiple organ system. It can be accompanied with various systemic diseases including arthritis, lymphadenopathy, splenomegaly, and aortitis with insufficiency. We report a case of typical Cogan’s syndrome with multiple cerebral infarctions.
Positional vertigo and nystagmus without focal neurological symptoms and signs are characteristic features of benign paroxysmal positional vertigo (BPPV). And the apogeotropic positional nystagmus can be diagnosed as cupulolithiasis of the horizontal semicircular canal. However, cerebellar lesion involving especially nodulus could be initially presented as positional vertigo like a BPPV without other neurologic signs. In most of the patients with cerebellar involvement, initial presentation shows dysarthria, ataxia, headache, nausea, vomiting and unsteadiness. But in some central lesions, positional nystagmus might be observed in head roll test as if BPPV was presented. It is very important for clinicians of dizziness care unit to differentiate central positional vertigo (CPV) from BPPV. But it is difficult to diagnose CPV at initial visit by history and physical exam only. Therefore, we introduce two cases with cerebellar infarction and hemorrhage initially presenting isolated positional vertigo mimicking BPPV.
A 54-year-old man presented with primary position upbeat nystagmus and wall-eyed bilateral internuclear ophthalmoplegia. He also showed bilateral limb ataxia and impaired horizontal gaze. Upbeat nystagmus obeyed Alexander’s law and attenuated by visual fixation and disappeared by convergence. Brain magnetic resonance imaging showed acute infarction in the bilateral paramedian midbrain involving the crossing of brachium conjunctivum. Multiple mechanisms including the interruption of central vestibulo-ocular projections from anterior canal may be postulated in upbeat nystagmus of this patient.
Sudden hearing loss and vertigo are the typical presentation of anterior inferior cerebellar artery infarction, but may rarely occur in posterior inferior cerebellar artery (PICA) infarction. Here we describe a 65-year-old man who presented with sudden hearing loss in his left ear and severe vertigo. The diffusion-weighted magnetic resonance imaging revealed acute infarction in the territory of PICA and cerebral angiography showed non-visualization of left vertebral artery. Sudden hearing loss and vertigo may be a presentation of PICA infarction.
Background and Objectives: The cerebellar lesion causes an initiation deficit of smooth-pursuit eye movement depending on the location of the lesion. We investigated the initiation of smooth pursuit in patients with cerebellar infarction and in healthy subjects, using step-ramp stimuli. Materials and Methods: Ten patients with cerebellar infarction documented by brain magnetic resonance imaging and fifty healthy subjects are recruited. To estimate the initiation of smooth pursuit, the onset latency and initial acceleration during the first 100ms of the horizontal smooth pursuit were estimated using the step-ramp target stimuli (5°/sec, 10°/sec, and 20°/sec). Results: In healthy subjects, onset latency of pursuit was shortened and initial acceleration was increased as target velocity was increasing. In patients with unilateral cerebellar infarction, the onset latency of ipsilesional smooth pursuit was significantly delayed at the target velocities of 10°/sec and 20°/sec. For the fast target velocity of 20°/sec, there was significant decrease of the initial acceleration of contralesional pursuit. Conclusion: In comparison with the healthy subjects, the patients with unilateral cerebellar lesions showed significant delay of pursuit onset and decrease of initial eye acceleration in the fast target velocity. These results support that the cerebellar lesions affect not only steady-state smooth pursuit gain but also the processing time required to initiate smooth pursuit, i.e., onset latency and initial acceleration. More extensive study is needed to confirm the role of cerebellum for parametric adjustment of each component of smooth pursuit.
Body lateropulsion is a common manifestation of lateral medullary infarction (LMI), and usually associated with vertigo, limb ataxia, sensory disturbance, and Horner’s syndrome. However, isolated body lateropulsion as a presenting symptom of LMI is rare, and the responsible lesion for lateropulsion remains uncertain. We report a 71-year-old woman who showed isolated body lateropulsion as a presenting symptom of LMI. Ipsilateral body lateropulsion in our patient may be ascribed to the involvement of the ascending dorsal spinocerebellar tract rather than the descending lateral vestibulospinal tract, which runs more ventromedially.
Vestibular neuritis (VN) is characterized by the acute onset of vertigo, nausea and vomiting, in the absence of hearing loss or tinnitus. Cerebellar and brain stem infarction represents approximately 2.3% of acute strokes overall. Those can result from occlusion of the superior cerebellar artery, anterior inferior cerebellar artery, or the posterior inferior cerebellar artery. Central vertigo such as cerebellar or brain stem infarction may present with nonspecific symptoms similar to those of VN. Patients with isolated vertigo due to cerebral infarction may pose a significant diagnostic challenge to the neurotologists. It is know n for being frequently misdiagnosed, often with consequent disability. We report 2 cases of cerebral infarction mimicking VN initially with a review of the related literatures.
Background and Objectives Patients with isolated vertigo could have central or peripheral vestibular disorders. Although some differential points exist between the two conditions, sometimes it is not easy to differentiate central vertigo from that of peripheral vestibular origin, especially in patients with isolated vertigo. We performed this study to determine the frequency of acute infarction and predictors of vertigo associated with stroke in isolated spontaneous vertigo.
Materials and Methods We prospectively evaluated 185 consecutive patients who were admitted to neurology department with acute isolated vertigo, after excluding the patients with benign paroxysmal positioning vertigo. Diffusion-weighted MRI (DWI) was obtained in 161 (87.0%) patients. Demographics, stroke risk factors, associated symptoms and signs were reviewed. Also, the locations and vascular territories of the lesions on DWI were investigated.
Results Twenty three (14.3%) patients had acute infarction on DWI. Old age and male sex were the predictors of stroke using multivariate analysis (p=0.03 and 0.02). The lesions were located in the cerebellum in 17 patients, medulla in four, and pons in another four. Cerebellar lesions were in the territory of the posterior inferior cerebellar artery in all patients.
ConclusionIsolated spontaneous vertigo may develop in posterior circulation stroke, especially in men of old age. The possibility of central origin should be considered in patients with isolated vertigo and DWI might be a good diagnostic tool.