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Show PHOTO ESSAY Magnetic Resonance Imaging of Third Cranial Nerve Palsy and Trigeminal Sensory Loss Caused by Herpes Zoster Susannah V. Quisling, MD, Vinay A. Shah, MD, Ho K. Lee, MD, PhD, Bruno Policeni, MD, Wendy R. K. Smoker, MD, FACR, Coleman Martin, MD, and Andrew G. Lee, MD FIG. 1. A. Post- contrast axial T1 - weighted MRI shows enhancement and thickening of the cisternal and cavernous portions of the right third cranial nerve ( arrow). B. Axial FLAIR MRI shows high signal at the right lateral aspect of the medulla corresponding to the location of the trigeminal nucleus and tract ( arrow). Abstract: A 44- year- old man with right- sided herpes zoster ophthalmicus ( HZO) developed ipsilateral third and sixth cranial nerve palsies and first- division trigeminal ( fifth cranial nerve) sensory loss. MRI revealed contrast enhancement of the cisternal and cavernous portions of the third cranial nerve and high signal on a FLAIR sequence within the ipsilateral medulla at the presumed location of the trigeminal nucleus and tract. To our knowledge, this is the first report of the combination of these imaging findings in HZO. ( J Neuro- Ophthalmol 2006; 26: 47- 48) Departments of Ophthalmology ( SVQ, VAS, AGL), Neurology ( CM, AGL), Neurosurgery ( AGL), and Radiology- Neuroradiology ( HKL, BP, WRKS), University of Iowa Hospitals and Clinics, Iowa City, Iowa. Address correspondence to Andrew G. Lee, MD, Department of Ophthalmology, PFP 200 Hawkins Drive, Iowa City, IA 52246; E- mail: Andrew- Lee ( Sluiowa. edu A 44- year- old man developed right- sided ptosis and diplopia. Four weeks earlier, he had noted a painful vesicular rash over the right forehead and received a diagnosis of herpes zoster ophthalmicus ( HZO). He developed a keratitis and uveitis OD and he was treated with topical steroids. Two weeks later, he noted that his right upper lid was swollen and droopy. Four weeks after onset of the rash, he noted an ipsilateral dilated pupil, complete ptosis, and ophthalmoplegia. Past medical history was negative for intravenous drug use or immunodeficiency Visual acuity was 20/ 30 OD and 20/ 20 OS. The right ophthalmic division of the trigeminal nerve ( Vi) had decreased sensation to pinprick testing. There was a healing vesicular eruption in the right Vx distribution. The pupil OD measured 8.5 mm and was unreactive to direct light. The pupil OS measured 6 mm and constricted normally to direct light. There was no relative afferent pupillary defect. Confrontation visual fields were full OU. The OD had reduced supraduction and abduction and a 50 prism- diopter esotropia in primary position. He had complete right ptosis. Slit- lamp J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 47 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 Quisling et al examination showed a few punctuate epithelial erosions but no active uveitis OD. Intraocular pressure measurements were 10 mm Hg OD and 13 mm Hg OS. Other aspects of the ophthalmic and neurologic examinations were normal. Brain MRI revealed enhancement and thickening of the cisternal and cavernous portions of the right third cranial nerve ( Fig. 1 A). FLAIR MRI demonstrated high signal intensity in the right posterolateral medulla consistent with presumed involvement of the trigeminal nucleus and tract ( Fig. IB). The clinical and imaging findings were attributed to herpes zoster. Cerebrospinal fluid ( CSF) analysis demonstrated 30 white blood cells/ mm3, a protein 56 mg/ dl, and glucose 107 mg/ dl. The patient was treated with intravenous acyclovir 660 mg TID for ten days and intravenous methylprednisolone 1 gm/ d for three days. He was then treated with oral acyclovir 500 mg 8X per day for two months and oral prednisone in a tapering dose over several weeks. The MRI was not repeated but at last follow- up examination three months after onset, he had no uveitis, a 9 prism- diopter right hypertropia, and only 2 mm of right upper lid ptosis. HZO- related ophthalmoplegia is uncommon but can affect cranial nerves III, i y or Vi ( 1,2). Most patients are over the age of 50 years. The ophthalmoplegia usually occurs one to two weeks after the rash. The reported cases of HZO ophthalmoplegia have demonstrated abnormal enhancement of the orbit, cranial nerves, optic nerve, and pons ( 3,4). To our knowledge, this is the first case of HZO-associated ophthalmoplegia with enhancement of the third cranial nerve and FLAIR MRI abnormalities involving the trigeminal nucleus in the medulla. Other authors, however, have reported the T2 signal abnormality in the medulla with or without enhancement of the trigeminal nerve. Kondo et al ( 9) reported a 64- year- old woman with herpes zoster meningo- encephalitis followed by involvement of cranial nerves IX, X, XL On the T2- weighted MRI, there was a high- signal lesion in the left dorsal part of the medulla. Haanpaa et al ( 10) reviewed brainstem MRI findings of 16 cases of uncomplicated herpes zoster ( 12 trigeminal and four cervical) and reported a focal T2- weighted hyperintensity in nine patients, most often within the trigeminal nuclear complex, including the spinal trigeminal nucleus in four cases. Three cases had trigeminal nerve enhancement. Nagane et al ( 11) reported a case of right second- division trigeminal zoster with right upper cervical neuralgia and facial palsy from zoster sine herpete. The brainstem MRI revealed T2- weighted hyperintensity in the right spinal trigeminal nucleus from the lower pons to C2. The spread of the HZV to the spinal trigeminal nucleus and tract has been hypothesized to be due to centripetal migration from the gasserian ganglion ( 5). There are no high- quality data to support treatment of HZO- associated ophthalmoplegia. Systemic antiviral medication and corticosteroids have been recommended, however. The ophthalmoplegia typically shows significant improvement or resolution within several months ( 6). Rarely, patients may have severe neurologic complications of HZO, including delayed contralateral hemiplegia ( 7,8). Our patient experienced gradual improvement over three months after treatment with intravenous and oral acyclovir and corticosteroids. REFERENCES 1. March RJ, Dulley B, Kelly V External ocular motor palsies in ophthalmic zoster: a review. Br J Ophthalmol 1977; 61: 677- 82. 2. Marsh RJ, Cooper M. Ophthalmic herpes zoster. Eye 1993; 7: 350- 70. 3. Krasnianski M, Sievert M, Bau Y Zierz S. External ophthalmoplegia due to ocular myositis in a patient with ophthalmic herpes zoster. Neuromuscul Disord 2004; 14: 438^ U. 4. Lexa FJ, Galetta SL, Yousem DM, Farber M, Oberholtzer JC, Atlas SW. Herpes zoster ophthalmicus with orbital pseudotumor syndrome complicated by optic nerve infarction and cerebral granulomatous angiitis: MR- pathologic corrrelation. AJNRAm JNeuroradiol 1993; 14: 185- 90. 5. Nogueira RG, Seeley WW. Ramsay Hunt syndrome associated with spinal trigeminal nucleus and tract involvement on MRI. Neurology 2003; 61: 1306- 7. 6. Chang- Godinich A, Lee AG, Brazis PW, Liesegang TJ, Jones DB. Complete ophthalmoplegia after zoster ophthalmicus. J Neuro-ophthalmol 1997; 17: 262- 5. 7. Laws HW Herpes zoster ophthalmicus complicated by contralateral hemiplegia. Arch Ophth 1960; 63: 273- 80. 8. Acers TE. Herpes zoster ophthalmicus with contralateral hemiplegia. Arch Ophthalmol 1964; 71: 371- 6. 9. Kondo M, Hokezu Y, Nagai M, Mori T, Nagamatsu K. A case of herpes zoster meningoencephalitis followed by involvement of cranial nerves IX, X, XI. Rinsho Shinkeigaku 1994; 34: 720- 3. 10. Haanpaa M, Dastidar P, Weinberg A, et al. CSF and MRI findings in patients with acute herpes zoster. Neurology 1998; 51: 1405- 11. 11. Nagane Y, Utsugisawa K, Yonezawa H, Tohgi H. [ A case with trigeminal herpes zoster manifesting a long lesion of the spinal trigeminal nucleus and tract on MR T2- weighted image.]. Rinsho Shinkeigaku 2001; 41: 56- 9. 48 © 2006 Lippincott Williams & Wilkins Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. |
