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Show Geotropic Central Paroxysmal Positional Nystagmus in a Patient With Human Immunodeficiency Virus Encephalopathy Tae-Ho Yang, MD, Sun-Young Oh, MD, PhD Abstract: Central vestibular lesions may cause paroxysmal positional nystagmus (PPN) or paroxysmal positional vertigo as a result of lesions involving the brainstem dorsolateral to the fourth ventricle or the cerebellar nodulus/uvular region. PPN usually presents as persistent downbeating nystagmus during head hanging or as apogeotropic horizontal nystag-mus during head turning in the supine position. Geotropic PPN during head turning in the supine position has not been previously reported. We report such a case in a patient with HIV encephalopathy. Journal of Neuro-Ophthalmology 2014;34:159-161 doi: 10.1097/WNO.0000000000000094 © 2013 by North American Neuro-Ophthalmology Society Pathological nystagmus and vertigo during head posi-tioning usually are caused by a peripheral vestibular disorder, such as benign paroxysmal positional vertigo (BPPV) (1). Central lesions, which may cause paroxysmal positional nystagmus (PPN) or paroxysmal positional ver-tigo (PPV), may be the result of a variety of disorders involving the cerebellar nodules/uvula or the region dorso-lateral to the fourth ventricle (1-3). Most often PPV and PPN present as persistent downbeating nystagmus in the head-hanging position or pure torsional or horizontal nys-tagmus (2-4). While apogeotropic PPN has been described (3-5), we are unaware of published reports of geotropic PPN. We present a case of geotropic PPN in a patient with HIV encephalopathy. CASE REPORT A previously healthy 54-year-old man presented with acute vertigo and imbalance, nausea, vomiting, and drowsiness of several weeks in duration. His medical history was unre-markable, except for a recent history of persistent cough and myalgias. Examination showed no spontaneous nystagmus but gaze-evoked nystagmus (GEN) with lateral gaze. Positional tests revealed geotropic horizontal nystagmus during lateral head turning in the supine position. The patient had mild dysmetria and intention tremor bilaterally well as severe ataxia. The remainder of the neurological examination was unremarkable. Video-oculographic recording (0.1° resolution, 60 Hz sampling rate; SMI, Teltow, Germany) showed horizontal GEN (Fig. 1A) and direction-changing, geotropic, horizon-tal nystagmus on lateral head turning in the supine position, with left-beating nystagmus more intense than the right beating (Fig. 1B) (see Video, Supplemental Digital Content, http://links.lww.com/WNO/A92). Subtle down-beat nystagmus also was observed during head hanging and the Dix-Hallpike test in either direction. The patient had saccadic hypometria and impaired smooth pursuit gain in both horizontal directions. Bithermal caloric tests, ocular and cervical vestibular-evoked myogenic potentials, brain-stem auditory-evoked potentials, and subjective visual ver-tical test were normal. Magnetic resonance imaging of the brain showed diffuse periventricular white matter changes without brainstem or cerebellar abnormalities. Cerebrospinal fluid findings were normal. Chest computed tomography revealed right upper and middle lobe consolidation that was proven to be cryptococcal and Pneumocystis carinii pneumonia on biopsy. Serum HIV antibody was positive on enzyme-linked Department of Neurology (T-HY), Chonbuk National University School of Medicine; and Department of Neurology (S-YO), Chonbuk National University, Research Institute of Clinical Medicine, Chonbuk National University Hospital, Jeonju, South 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 Sun-Young Oh, MD, PhD, Department of Neurology, Research Institute of Clinical Medicine, Chonbuk National University, Chonbuk National University Hospital, 20 Geonji-ro, Deokjin-gu, Jeonju 561-712, South Korea; E-mail: ohsun@ jbnu.ac.kr Yang and Oh: J Neuro-Ophthalmol 2014; 34: 159-161 159 Clinical Observation Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. immunosorbent assay and Western blot, and CD4 lympho-cyte count was 25 cells per milliliter with 96,200 HIV-DNA copies per milliliter. Even after repeated repositioning maneuvers, such as barbecue rotation maneuver and forced prolonged position, the positional geotropic nystagmus and vertigo persisted. DISCUSSION Central positional nystagmus usually manifests as down-beating in the head-hanging position (6), or upbeating in the supine position, or torsional nystagmus (7,8). Horizontal positional nystagmus caused by central pathology, such as infarction of the cerebellar nodules usually is apogeotropic (3,5,9,10). Most often, accompanying cerebellar and ocular motor findings allow the clinician to distinguish central from BPPV. However, at times, this may prove difficult because the 2 syndromes may present as isolated positional vertigo and nystagmus without other neurological deficits. In our patient, the acute onset of positional vertigo and direction-changing, persistent, geotropic positional nystagmus with the supine roll test without lying-down or head-bending nystagmus may have led to the diagnosis of geotropic type of horizontal canal (HC)-BPPV. However, the patient also showed horizontal GEN, severe ataxia, and bilateral dysmetria. Moreover, the geotropic positional nystagmus and vertigo persisted even after repeated reposi-tioning maneuvers for geotropic HC-BPPV. GEN is a characteristic sign of impaired gaze-holding and neural integration, and it is usually caused by cerebellar disorders that involve the vestibulocerebellum or by brainstem lesions affecting the nucleus prepositus hypo-glossi and medial vestibular nucleus or their connections (11,12). Apogeotropic central positional nystagmus is caused by lesions involving the cerebellar nodulus (3,4,13), which has connections with the otolith organs and the semi-circular canals and controls otolith-ocular reflexes and oto-lithic modulation of the canal-ocular reflexes. Although the mechanism is unknown, direct or indirect injuries because of HIV infection may damage the otolith, vestibular nuclei, or cerebellum. The change in the graviceptive (otolithic) input induced by positional changes may be the precipitating factor for central PPN, and inactivation or stimulation of these pathways may induce nystagmus that is influenced by the position of the head. HIV/AIDS-associated vestibular dysfunction may be caused by direct effects of the virus on the peripheral and central vestibular system, together with HIV/AIDS- associated opportunistic infections, including otosyphilis, encephalitis, and cochleovestibular neuropathy (14). Previ-ous autopsy findings in HIV patients have revealed subacute encephalitis with diffuse damage to the cortex, cerebellum, and brainstem, with myelinic degeneration (15). Vestibular dysfunctions were evident at all disease stages, even in asymptomatic individuals without reported neurological or vestibular symptoms. Central vestibular involvements were noted in more than 50% of asymptomatic HIV-positive adults (8), and eye movement disorders, including nystag-mus, were present in more than a half of the patients (14). However, to date, there has been no report of geotropic PPN as an early manifestation of HIV-related, central ves-tibular neurological syndrome PPN. REFERENCES 1. Büttner U, Helmchen CH, Brandt TH. Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo: a review. Acta Otolaryngol. 1999;119:1-5. 2. Leigh RJ, Zee DS. The Neurology of Eye Movements, 4th edition. New York, NY: Oxford University Press, 2006:575- 576. 3. Kim HA, Yi HA, Lee H. Apogeotropic central positional nystagmus as a sole sign of nodular infarction. Neurol Sci. 2012;33:1189-1191. 4. Nam J, Kim J, Huh Y. Ageotropic central positional nystagmus in nodular infarction. Neurology. 2009;73:1163. 5. Lee SH, Kim JS. Benign paroxysmal positional vertigo. J Clin Neurol. 2010;6:51-63. 6. Kattah JC, Kolsky MP, Luessenhop AJ. Positional vertigo and the cerebellar vermis. Neurology. 1984;34:527-529. 7. Sakata E, Ohtsu K, Shimura H. Positional nystagmus of benign paroxysmal type (BPPN) due to cerebellar vermis lesions. Pseudo-BPPN. Auris Nasus Larynx. 1987;14:17-21. 8. Barber HO. Positional nystagmus. Otolaryngol Head Neck Surg. 1984;92:649-655. 9. Allen G, Fernandez C. Experimental observations in postural nystagmus: extensive lesions in posterior vermis of the cerebellum. Acta Otolaryngol. 1960;51:2-14. 10. Watson P, Barber HO, Deck J. Positional vertigo and nystagmus of central origin. Can J Neurol Sci. 1981;8:133-137. 11. Zee DS, Yee RD, Cogan DG. Ocular motor abnormalities in hereditary cerebellar ataxia. Brain. 1976;99:207-234. FIG. 1. Video-oculographic recording. A. There is horizontal gaze-evoked nystagmus without spontaneous nystagmus. B. Direction-changing, geotropic, horizontal nystagmus on lateral head turning in the supine position is present. Intensity of left-beating nystagmus during head turning to the left side is greater (upper panel) than the right-beating nystagmus during head turning to the right side (lower panel). LH, horizontal position of the left eye. 160 Yang and Oh: J Neuro-Ophthalmol 2014; 34: 159-161 Clinical Observation Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. 12. Leigh RJ, Zee DS. The Neurology of Eye Movements, 4th edition. New York, NY: Oxford University Press, 2006:160-161. 13. Sheliga BM, Yakushin SB, Silvers A. Control of spatial orientation of the angular vestibulo-ocular reflex by the nodulus and uvula of the vestibulocerebellum. Ann N Y Acad Sci. 1999;871:94-122. 14. Heinze SB, Swanepo DW, Hofmeyr LM. Systematic review of vestibular disorders related to human immunodeficiency virus and acquired immunodeficiency syndrome. J Laryngol Otol. 2011;125:881-890. 15. Tervo T, Elovaara I, Karli H. Abnormal ocular motility as an early sign of CNS involvement in HIV infection. Lancet. 1986;2:512. Ode to Neuro-Ophthalmology Smita Praveen, MBBS, MS Chennai, India Neuroscience is a subject that's first rate Isn't it amazing the way neurons communicate? From crying to laughing And reading to writing It's the brain that rules-no debate! Neuro-ophthalmology is that branch of medical science That deals with problems of our visual appliance It requires eliciting a good history To solve the patient's vision loss mystery Here neurology, radiology and ophthalmology have a holy alliance! Now, the optic nerve could be swollen or pale To decipher the cause I need to go into great detail Is it MS, diabetes or simply a fall That could be the culprit behind it all? It gives me closure when the true reason I can unveil! When there's headache and weight gain and seeing double It could spell major trouble Is the CSF pressure sky high? Is my diet of burgers and fries the bad guy? IIH snaps me out of the fast food bubble! A dysfunctional pupil can result in glare While thyroid disease may leave me with an unsightly stare Tumors and strokes can affect my field of vision Neuro-imaging aids here in making my decision Enabling me to treat the condition with due care. Sometimes when the eyeballs oscillate There are some questions that I must postulate Do the eyes shake up or down or sideways Is it recent or has it been around always To treat nystagmus one must be a doctor consummate! The major challenge for our generation Is to beat the rapid rate of axonal degeneration Tremors and weakness and memory loss Are sufficient to make one quite cross The need of the hour is neuronal regeneration! The last decade was dedicated to studying human genes. But this one is all about brain proteins Neuro-ophthalmology is right up there At the cutting edge of revolutionary healthcare The future belongs to neuroscience and its allied themes! Yang and Oh: J Neuro-Ophthalmol 2014; 34: 159-161 161 Clinical Observation Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
