Jerky hemi-seesaw nystagmus and head tilt reaction combined with internuclear ophthalmoplegia from a pontine infarction

Jerky hemi-seesaw nystagmus and head tilt reaction combined with internuclear ophthalmoplegia from a pontine infarction

456 Case Reports / Journal of Clinical Neuroscience 16 (2009) 456–458 differential diagnosis.7 Otherwise a very frequent cystic component (in 10 of ...

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Case Reports / Journal of Clinical Neuroscience 16 (2009) 456–458

differential diagnosis.7 Otherwise a very frequent cystic component (in 10 of 21 cases) is reported for subfrontal schwannoma while it is uncommon for meningiomas.1,2,4 As in our patient, angiography can suggest the preoperative diagnosis if a hypovascular lesion is found without typical signs of a meningioma.1,2,7 4. Conclusions Olfactory groove schwannomas should be kept in mind in the differential diagnosis of anterior cranial fossa neoplasms, especially in young males. However, the pathogenesis still needs to be clarified because of the rarity of the tumour, but immunohistochemical techniques are helpful in obtaining a correct diagnosis and contribute to elucidating the origin of these tumours.

References 1. Yuen A, Trost N, McKelvie P, et al. Subfrontal schwannoma: a case report and literature review. J Clin Neurosci 2004;11:663–5. 2. Murakami M, Tsukahara T, Hatano T, et al. Olfactory groove schwannoma –case report. Neurol Med Chir (Tokyo) 2004;44:191–4. 3. Sabel LH, Teepen JL. The enigmatic origin of olfactory schwannoma. Clin Neurol Neurosurg 1995;97:187–91. 4. Sano H, Hayashi Y, Hasegawa M, et al. Subfrontal schwannoma without hyposmia – case report. Neurol Med Chir (Tokyo) 2004;44:591–4. 5. Yako K, Morita A, Ueki K. Subfrontal schwannoma. Acta Neurochir (Wien) 2005;147:655–7 discussion 657–8. 6. Amador AR, Santonja C, Del Pozo JM, et al. Olfactory schwannoma. Eur Radiol 2002;12:742–4. 7. Yasuda M, Higuchi O, Takano S, et al. Olfactory ensheathing cell tumor: a case report. J Neurooncol 2006;76:111–3.

doi:10.1016/j.jocn.2008.03.016

Jerky hemi-seesaw nystagmus and head tilt reaction combined with internuclear ophthalmoplegia from a pontine infarction Soo-Young Choi, Dae-Hyun Kim *, Ji-Hee Lee, Jei Kim Department of Neurology, Chungnam National University Hospital, 640 Daesa-dong, Joong-gu, Daejeon 301-721, Korea

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Article history: Received 20 December 2007 Accepted 2 March 2008

Keywords: Hemi-seesaw nystagmus Ocular tilt reaction Internuclear ophthalmoplegia

a b s t r a c t Internuclear ophthalmoplegia (INO) is a complex ocular motility disorder caused by damage to the medial longitudinal fasciculus. The occurrence of hemi-seesaw nystagmus in an INO patient has been reported rarely. This nystagmus may be caused by damage to the pathway from the contralateral vertical semicircular canal. The ocular tilt reaction is characterized by ipsilateral head and neck tilt, skew deviation, and ocular torsion. We report a patient who presented with hemi-seesaw nystagmus, ocular tilt reaction, and limb ataxia combined with an INO from a right focal pontine infarction. INO may be accompanied by a variety of ocular findings associated with the disruption of the medial longitudinal fasciculus. Ó 2008 Elsevier Ltd. All rights reserved.

1. Introduction

2. Case report

Internuclear ophthalmoplegia (INO) is characterized by adduction paresis of the ipsilesional eye and dissociated abducting nystagmus of the contralesional eye on attempted gaze to the contralesional side.1 Ocular tilt reaction (OTR) is an eye movement disorder characterized by head tilt, skew deviation, and binocular ocular torsion.2 Hemi-seesaw nystagmus is characterized by mainly torsional movement in one eye and vertical in the contralateral eye.3–5 INO with OTR or with dissociated torsional–vertical nystagmus has been described in a few patients with involvement of the medial longitudinal fasciculus (MLF).6–8 These signs seem to be caused by selective damage to the excitatory fibers originating in the contralateral vertical semicircular canal.3,7,8 We report a patient with INO, hemi-seesaw nystagmus, limb ataxia, and OTR due to a dorsomedial pontine infarction and propose possible mechanisms for hemi-seesaw nystagmus and OTR in patients with INO.

A 46-year-old woman presented with sudden-onset vertigo, diplopia and oscillopsia. She reported horizontal diplopia that improved after closing either eye. Neurological examination on admission revealed that the quick phase of the nystagmus was upbeating and intorsional in the left eye and mainly extorsional in the right eye, resembling half-cycles of seesaw nystagmus. This nystagmus changed to predominantly upbeating on the upward gaze. The patient showed dissociated abduction nystagmus in the left eye and adduction paresis of the right eye on leftward gaze. Her convergent eye movement was unimpaired. Skew deviation with left hypotropia (Fig. 1A) and head tilt to the left (Fig. 1B) were noted (see Video, Supplementary Data). Fundus examination demonstrated 5° intorsion of the right eye and 6° extorsion of the left eye (Fig. 1C). Ataxia was noted in the left upper extremity. All other neurological findings were normal. A T2-weighted and a diffusion-weighted MRI revealed a small lesion in the right dorsomedial pontine tegmentum, with right MLF involvement (Fig. 2). The patient was diagnosed with acute cerebral infarction and treated with an antiplatelet agent. She had no previous history of migraine or connective tissue disease. MR angiography and transesophageal echocardiography were

* Corresponding author. Tel.: +82 42 280 7801; fax: +82 42 252 8654. E-mail address: [email protected] (D.-H. Kim).

Case Reports / Journal of Clinical Neuroscience 16 (2009) 456–458

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Fig. 1. Ocular tilt reaction. (A) Skew deviation with left hypotropia and (B) left head tilt were observed 3 days after symptom onset and resolved 7 days after symptom onset. (C) Fundus photographs taken 3 days after symptom onset show intorsion (5°) of the right eye and extorsion (6°) of the left eye. This figure is available in colour at www.sciencedirect.com.

Fig. 2. (A) Initial T2-weighted axial MRI and (B) diffusion-weighted axial MRI showing a high signal intensity lesion in the right tegmental pons.

normal. Levels of protein C, S, anticardiolipin antibodies and fibrinogen were normal. The patient’s nystagmus, limb ataxia and INO resolved within seven days after onset.

3. Discussion Our patient showed extorsional nystagmus in the ipsilesional eye and upbeat nystagmus in the contralesional eye typical of hemi-seesaw nystagmus. Hemi-seesaw nystagmus is characterized by mainly torsional nystagmus in one eye and vertical nystagmus in the contralateral eye.3–5 Jerky seesaw nystagmus has been attributed to the unilateral inactivation of the torsional eye-velocity integrator, the interstitial nucleus of Cajal (INC), which does not affect the torsional fast-phase generator, the rostral interstitial nucleus of the MLF (riMLF).3,4,6 Although jerky seesaw nystagmus usually occurs with unilateral mesodiencephalic lesions, MLF lesions can cause torsional–vertical nystagmus.6,7 Our findings suggest that a small MLF lesion may cause ipsilateral INC inactivation without affecting the riMLF (Fig. 3). This patient is unique because previous reports of dissociated vertical–torsional nystagmus in unilateral INO were associated with either ipsilateral downbeat nystagmus and contralateral incyclorotatory nystagmus due to selective disruption of the fibers from the

Fig. 3. Hypothetical explanation for the development of hemi-seesaw nystagmus after dorsomedial pontine infarction. Schematic representation of the three-neuron vestibulo-ocular reflex arc between the anterior semicircular canal and the extraocular muscles. The hemi-seesaw nystagmus in our patient may have been caused by the disruption of fibers from the contralateral anterior canal, which innervate the inferior oblique muscle in the right eye and the superior rectus muscle in the left eye. Because the inferior oblique is responsible for the extorsion of the right eye and the superior rectus is mainly a depressor muscle of the left eye, the damage to this excitatory ascending pathway caused by a lesion in the medial longitudinal fasciculus (MLF) would result in tonic intorsion of the right eye and downward deviation of the left eye. The resulting corrective quick phases of nystagmus would be mostly extorsional in the right eye and upbeating in the left eye. AC = anterior semicircular canal, IO = inferior oblique, IR = inferior rectus, LE = left eye, RE = right eye, SO = superior oblique, SR = superior rectus, VN = vestibular nucleus, III = oculomotor nucleus, IV = troclear nucleus.

contralateral posterior semicircular canal, or extorsional downbeat nystagmus in the ipsilesional eye accompanied by intorsional upbeat nystagmus in the contralesional eye caused by simultaneous damage to the fibers from contralateral anterior and posterior canals.6,7 This patient supports the theory that selective damage

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to connections from anterior and posterior semicircular canals, which might occur with MLF lesions, give rise to specific types of jerky seesaw nystagmus. OTR is a sensitive brainstem sign of localizing and lateralizing value. It indicates either a unilateral peripheral vestibular deficit or the involvement of pathways from the vestibular nuclei to the INC in the rostral midbrain.2,5 Ocular skew torsion is always ipsiversive with caudal (pontomedullary) lesions and contraversive with rostral (pontomesencephalic) lesions.2 INO with OTR is reported in patients with MLF involvement.7 We suggest that a unilateral dorsomedial pontine lesion involving the MLF induced contraversive OTR in our patient. Our findings demonstrated that INO can be accompanied by various oculomotor abnormalities, including OTR, abduction nystagmus and hemi-seesaw nystagmus. We suspect that MLF lesions may lead to different types of dissociated torsional–vertical nystagmus, depending on the involvement of fibers from contralateral vertical semicircular canals.

References 1. Leigh RJ, Zee DS. The neurology of eye movement. third ed. New York: Oxford University Press; 1999. pp. 497–511. 2. Brandt T, Dieterich M. Skew deviation with ocular torsion: a vestibular brainstem sign of topographic diagnostic value. Ann Neurol 1993;33:528–34. 3. Choi KD, Jung DS, Park KP, et al. Bowtie and upbeat nystagmus evolving into hemi-seesaw nystagmus in medial medullary infarction: Possible anatomic mechanisms. Neurology 2004;62:663–5. 4. Halmagyi GM, Aw ST, Dehaene I, et al. Jerk-waveform see-saw nystagmus due to unilateral meso-diencephalic lesion. Brain 1994;117:789–803. 5. Helmchen C, Rambold H, Kempermann U, et al. Localizing value of torsional nystagmus in small midbrain lesions. Neurology 2002;59: 1956–64. 6. Oh K, Chang JH, Park KW, et al. Jerky seesaw nystagmus in isolated internuclear ophthalmoplegia from focal pontine lesion. Neurology 2005;64: 1313–4. 7. Marshall RS, Sacco RL, Kreuger R, et al. Dissociated vertical nystagmus and internuclear ophthalmoplegia from a midbrain infarction. Arch Neurol 1991;48:1304–5. 8. Tilikete C, Vighetto A. Internuclear ophthalmoplegia with skew deviation. Two cases with an isolated circumscribed lesion of the medial longitudinal fasciculus. Eur Neurol 2000;44:258–9.

Appendix A. Supplementary data Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.jocn.2008.03.015. doi:10.1016/j.jocn.2008.03.015

Reversible parkinsonism due to chronic bilateral subdural hematomas Sevasti Bostantjopoulou *,1, Zoe Katsarou, Michael Michael, Anastasios Petridis 3rd University Department of Neurology, G. Papanikolaou Hospital, Exohi, Thessaloniki 57010, Greece

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Article history: Received 29 October 2007 Accepted 2 March 2008

Keywords: Parkinsonism Subdural hematoma Head injury

a b s t r a c t Subdural hematoma is a rare cause of secondary parkinsonism. We report a 65-year-old woman with reversible parkinsonism due to bilateral chronic subdural hematomas. Symmetrical parkinsonism evolved acutely 45 days after a trivial head injury. Mild pyramidal signs were also present on her left side. MRI revealed bilateral chronic subdural hematomas. The patient’s parkinsonism was completely abolished one month after successful neurosurgical evacuation of the hematomas. Ó 2008 Elsevier Ltd. All rights reserved.

1. Introduction Acute or subacute onset of parkinsonism is always due to a secondary cause except for the rare form of the dominantly inherited rapid-onset dystonia-parkinsonism linked to chromosome 19.1,2 A variety of etiologies are related to acute secondary parkinsonism including medications, infections, toxins, metabolic disturbances and various structural lesions.1,3 Although chronic subdural hematoma (CSH) is rather common in the elderly, with an incidence of 7.35/100,000 per year for people aged 70–79 years, it rarely causes parkinsonism.4–6 The diagnosis of CSH is not usually suspected at initial presentation.5 Information on head trauma may not be particularly important in the elderly, since in this age group CSH may

* Corresponding author. Tel.: +30 2310 279442; fax: +30 2310 999019. E-mail address: [email protected] (S. Bostantjopoulou). 1 Mailing address: 9 Navarinou Square GR 54622, Thessaloniki, Greece.

result from a trivial and often forgotten head injury.5,7 However, correct diagnosis is paramount because neurosurgical evacuation of CSH offers a good chance of a favorable outcome.5,6 We present a patient with reversible parkinsonism due to bilateral CSH, before surgery (see Video 1, Supplementary data) and in complete remission (see Video 2, Supplementary data) after successful evacuation of the CSH.

2. Case report A 65-year-old woman was admitted because of a dull headache and gait disturbance. Symptoms had started one week before admission and were steadily worsening. She had a history of pulmonary tuberculosis in full remission, but she was still under treatment with rifampicin (600 mg), isoniazid (300 mg) and Vitamin B6 (125 mg). She reported no use of any kind of parkinsonism-inducing medication.