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Show PHOTO ESSAY Bimedial Rectus Hypermetabolism in Convergence Spasm As Observed on Positron Emission Tomography Seong-Hae Jeong, MD, Young-Mi Oh, MD, Chae-Yong Kim, MD, and Ji Soo Kim, MD FIG. 1. A. The patient has a left head tilt and esotropia in primary gaze position. The right eye is slightly hypertropic, probably due to skew deviation. B. 18F-fluorodeoxyglucose positron emission tomography (PET) in the axial (left) and coronal (right) planes shows mark-edly increasedmetabolism in the medial rectus muscles (arrows). C. For comparison, a normal subject looking straight ahead shows nor-mal PET metabolism in the rectus muscles (arrows). Color bar on right indicates the increasing degrees of metabolism in ascending order. Departments of Neurology (O-HJ, Y-MO, JSK) and Neurosurgery (CYK), Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seoul, Korea. Address correspondence to Ji Soo Kim, MD, Department of Neurology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 300 Gumi-dong, Bundang-gu, Seongnam-si, Gyeonggi-do, 463-707, Korea; E-mail: jisookim@snu.ac.kr J Neuro-Ophthalmol, Vol. 28, No. 3, 2008 217 Abstract: A 52-year-old man developed vertical gaze palsy, convergence spasm, and convergence-retraction nystagmus due to glioblastoma of the right thalamus. 18F-fluorodeoxyglucose positron emission tomography (PET) inadvertently demonstrated mark-edly increased metabolism in the medial rectus muscles. The hypermetabolism indicates active contraction of these extraocular muscles due to excessive convergence drive attributed to inappro-priate activation or disrupted inhibition of conver-gence neurons by the diencephalic lesion. (J Neuro-Ophthalmol 2008;28:217-218) A 52-year-old man presented with a 5-day history of headache, diplopia, and memory loss. He showed leftward head tilt, esotropia, right hypertropia, bilaterally impaired abduction, and upgaze palsy. Vertical saccades and convergence induced convergence-retraction nystag-mus (Fig. 1). Pupillary responses were decreased bilaterally without light-near dissociation. These findings were con-sistent with a dorsal midbrain (pretectal) syndrome (1,2). 18F-fluorodeoxyglucose positron emission tomogra-phy (PET) showed increased metabolism in the mass lesion and in the medial rectus muscles (Fig. 1). MRI dis-closed a mass lesion in the right thalamus with ventric-ulomegaly (Fig. 2). Stereotactic biopsy of the tumor revealed glioblastoma. PET-detected hypermetabolism of the extraocular muscles has been observed during self-generated versional eye movements in the dark (3). During vergence eye movements, PET activation has been documented in the temporo-occipital junction, the inferior parietal lobule, and right fusiform gyrus bilaterally (4). However, there are no PET data on the metabolic changes of the extraocular muscles during vergence. The findings in our patient indi-cate active contraction of the medial recti during conver-gence spasm. As we did not detect hypermetabolism in the cortical areas responsible for vergence eye movements in our patient, disruption of descending inhibition on the convergence neurons or irritation of the convergence neurons due to the diencephalic lesion may have generated an excessive convergence drive (5). REFERENCES 1. Keane JR. The pretectal syndrome: 206 patients. Neurology 1990;40: 684-90. 2. Sharpe JA, Kim JS. Midbrain disorders of vertical gaze: a quantitative re-evaluation. Ann N Y Acad Sci 2002;956:143-54. 3. Law I, Svarer C, Rostrup E, et al. Parieto-occipital cortex activation during self-generated eye movements in the dark. Brain 1998;121: 2189-200. 4. Hasebe H, Oyamada H, Kinomura S, et al. Human cortical areas activated in relation to vergence eye movements-a PET study. Neuroimage 1999;10:200-8. 5. Pullicino P, Lincoff N, Truax BT. Abnormal vergence with upper brainstem infarcts: pseudoabducens palsy. Neurology 2000;55:352-8. FIG. 2. Postcontrast T1 coronal MRI demonstrates a mixed signal intensity enhancing right thalamic lesion that has caused ventriculomegaly and compression of the dorsal midbrain. J Neuro-Ophthalmol, Vol. 28, No. 3, 2008 Jeong et al 218 q 2008 Lippincott Williams & Wilkins |
