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Show Isolated Rotational Vertigo Due to Internal Capsular Infarction Kang Min Park, MD, Kyong Jin Shin, MD, Sam Yeol Ha, MD, Jinse Park, MD, Sung Eun Kim, MD, PhD Abstract: Isolated rotational vertigo is most often associ-ated with disorders of the semicircular canals, vestibular nerve, brainstem, or cerebellum but rarely observed follow-ing a supratentorial stroke. A 64-year-old man developed sudden onset of vertigo and horizontal right-beating nystag-mus with a torsional component in primary and eccentric gazes, unsteady gait, and axial lateropulsion to the right side. Magnetic resonance imaging demonstrated an infarc-tion in the posterior limb of left internal capsule, an unusual cause of the patient's signs and symptoms. Journal of Neuro-Ophthalmology 2014;34:61-63 doi: 10.1097/WNO.0000000000000088 © 2013 by North American Neuro-Ophthalmology Society Isolated rotational vertigo is most often associated with abnormalities of the semicircular canals, vestibular nerve, brainstem, or cerebellum (1) but rarely may take place fol-lowing a supratentorial stroke causing ataxic hemiparesis (2). Ataxic hemiparesis is a lacunar syndrome causing hemi-paresis or pyramidal signs and impaired ipsilateral coordi-nation without sensory loss. This may occur following stroke involving the posterior limb of the internal capsule, pons, thalamus, anterior part of the corona radiata, and the basal ganglia (3). We describe a patient who presented with isolated rotational vertigo and imbalance and was found to have internal capsular infarction. His presentation seems unique in that he did not have hemiparesis but did experi-ence axial lateropulsion. CASE REPORT A right-handed 64-year-old man reported acute onset rotational vertigo with unsteady gait. The vertigo was continuous and not affected by changes in position. He complained of nausea and vomiting but denied tinnitus, hearing loss, altered speech, sensory disturbance, or muscle weakness. His medical history was only significant for hypertension requiring medication. Examination revealed spontaneous horizontal right-beating horizontal nystagmus with a torsional component in primary and eccentric positions of gaze, even during visual fixation (See Supplemental Digital Content, Video, http://links.lww.com/WNO/A91). The nystagmus increased in amplitude with right gaze and decreased with left gaze, without a periodic alternating component. It was not mod-ified by vibratory stimulation, hyperventilation, or varying head position. The head impulse test was normal. The range of eye movement was full. The patient could stand unassisted but was unable to stand with the feet together (Rhomberg sign). He also fell to the right when ambulating. He did not demonstrate problems of appendicular coordination, such as dysmetria and dysdiadochokinesia. Motor and sensory examinations were unremarkable and deep tendon reflexes were normal, as was the remainder of the neurological examination. Laboratory studies included complete blood count, elec-trolyte profile, glucose level, urinalysis, renal, liver, and thyroid function tests; all were within normal limits. Magnetic resonance imaging (MRI) performed 2 days after onset of symptoms revealed infarction in the posterior limb of the left internal capsule (Fig. 1). MRA of the intracranial vasculature and major vessels of the neck was unremarkable. Diffusion tensor imaging-fiber tractography showed that the left corti-cospinal tract was not disrupted by the internal capsular stroke Department of Neurology, Haeundae Paik Hospital, Inje University College of Medicine, Busan, Korea. The authors report no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the full text and PDF versions of this article on the journal's Web site (www. jneuro-ophthalmology.com). Address correspondence to Sung Eun Kim, MD, PhD, Department of Neurology, Haeundae Paik Hospital, Inje University College of Medicine, Haeundae-ro 875, Haeundae-gu, Busan 612-896, Korea; E-mail: epidoc@inje.ac.kr Park et al: J Neuro-Ophthalmol 2014; 34: 61-63 61 Clinical Observation Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. (Fig. 2). Video-oculography (VOR) performed 8 days after onset of symptoms documented resolution of spontaneous nystagmus, with only left beating nystagmus observed follow-ing head shaking. Repeat MRI of the brain confirmed a cere-bral infarction restricted to the left internal capsule. The patient was prescribed clopidogrel (75 mg daily) and his ver-tigo and gait gradually improved. He was discharged from the hospital 10 days later without any neurological deficits. FIG. 1. Diffusion-weighted imaging reveals an acute infarction in the posterior limb of the left internal capsule. FIG. 2. Diffusion tensor imaging-fiber tractography. A. Coronal view shows that the left corticospinal tract is similar to the one on the right. B. Axial image demonstrates that the left corticospinal tract is not disrupted by the internal capsular infarction (arrow). 62 Park et al: J Neuro-Ophthalmol 2014; 34: 61-63 Clinical Observation Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. DISCUSSION Rotational vertigo is defined as the perception of spinning or movement of the person or the surrounding environ-ment. It is usually due to an infratentorial abnormality, often involving the vestibular system (2,4) or a disturbance of the posterior cerebral circulation (5,6). Our patient had rotational vertigo and imbalance without hemiparesis. With both clinical testing and neuroimaging studies, we carefully searched for a brainstem or infratentorial lesion, but found none. The normal head impulse test and head-shaking nystagmus in the opposite direction of spon-taneous nystagmus also suggested a central cause (7). Seizure was an unlikely explanation because the patient's symptoms were persistent and not episodic. In a study of 112 patients, Anagnostou et al. (2) reported that leukoaraiosis was associ-ated with dizziness. Although our patient had leukoaraiosis on brain MRI, he did not complain of dizziness but rather rotational vertigo and had spontaneous nystagmus. Thus, leukoaraiosis also was an unlikely cause of his symptoms. Only few cases of isolated rotational vertigo have been described to be caused by a supratentorial cerebral infarc-tion. Most of these cases were caused by lesions in the parieto-insular vestibular cortex (1,8-11), which receives vestibular afferents through thalamic projections and descend to the vestibular nuclei. Any disruption along these pathways can produce vestibular dysfunction (12). Nakajima et al. (13) reported a case of rotational vertigo associated with putaminal infarction similar to the lesion in our case, but the patient also exhibited hemiparesis as a predominant symptom. We are unaware of any reports of infarction of the posterior limb of internal capsular causing isolated rotational vertigo and imbalance without hemiparesis. One possible explanation of the findings in our patient is that internal capsular infarction impaired the pathway between the thalamus and vestibular cortices. Edema from internal capsular infarction may have compressed the thalamus transiently, leading to vestibular dysfunction. Our patient exhibited axial lateropulsion to the right side, most likely due to a disturbance of the spinocerebellar pathway. The spinocerebellar pathway originating from right cerebellum projects through the thalamus to terminate in the left cerebral cortex (14). A left supratentorial lesion, as was the case in our patient, could disturb this pathway and cause truncal ataxia. An alternate explanation for falling to the right may be transient excitation of left vestibulospi-nal pathway by left internal capsular infarction. Acute stroke may cause transient neuronal excitation by enhanced release of glutamate, reduced GABAergic function, mitrochondrial or receptor changes (15). REFERENCES 1. 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