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Show Journal of Clinical Neuro- ophthalmo[ ogy 12( 3): 149- 153, 1992. ' 9 1992 Raven Press, Ltd., New York Sixth Nerve Palsy as the Initial Presenting Sign of Metastatic Prostate Cancer A Case Report and Review of the Literature Joseph E, 0' Boyle, M. D. CPT MC, Thomas A. Gardner, M. D. MAJ MC, Armando Oliva, M. D. MAJ MC, and Robert W. Enzenauer, M. D., M. P. H. LTC MC Cranial nerve palsies secondary to metastatic prostate cancer are uncommon occurrences. Usually appearing late in the course of the disease, they are associated with a poor prognosis. We report a case of a 71- year- old man who initially complained of diplopia and was found to have a right sixth nerve palsy and hyperdeviation caused by a mass in the clivus. Biopsy of the mass and extensive systemic workup revealed metastatic adenocarcinoma of the prostate gland. Key Words: Sixth nerve palsy- HyperdeviationMetastatic prostate carcinoma- Clivus- Initial presentation. From the Ophthalmology ( J. E. O., T. A. G., A. a., R. W. E.) and Neurology ( A. a.) Services, Departments of Surgery and Medicine, Fitzsimons Army Medical Center, Aurora, Colorado, U. S. A. Address correspondence and reprint requests to Dr. Joseph E. O'Boyle, Ophthalmology Service, Departments of Surgery and Medicine, Fitzsimons Army Medical Center, Aurora, CO 80045, U. s. A. The views presented in this article are the expressed views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense. 149 The causes of abducens nerve deficits are numerous. Other than isolated sixth nerve palsies causing lateral rectus dysfunction, pathologic conditions that must be considered in the differential diagnosis include Graves' orbitopathy, myositis, myasthenia gravis, orbital trauma, congenital defects ( e. g., Duane's retraction syndrome or Mobius syndrome) and convergence spasm ( 1), These neuro- ophthalmologic entities are nearly always associated with other symptoms or physical findings. The differential diagnosis of isolated sixth nerve deficits is equally extensive. Nonlocalizing processes include increased intracranial pressure, head trauma, postlumbar puncture, vascular hypertension, diabetes mellitus, parainfectious syndromes ( postviral or otitis media in children), or basilar meningitis ( 1). Localizing mass lesions include pontine syndromes, cerebellopontine angle lesions, clivus lesions, middle fossa disorders, and cavernous sinus or dural arteriovenous fistula ( 1). Again, most of these conditions are associated with additional findings other than the lateral rectus paresis. CASE SUMMARY A 71- year- old man presented to an Australian general practitioner with complaints of sudden onset of diplopia. Images were displaced horizontally and vertically. There were no associated headaches, nausea, or vomiting. The patient also denied photophobia, eye pain, and decreasing central or peripheral vision. Past medical history was remarkable for a myocardial infarction in 1982. Benign prostatic hypertrophy was described on past 150 J. E. O'BOYLE ET AL. physical examinations. His medications included acetominophen, antacids, stool softeners, and flurazepam. Review of systems was significant for an occasional nonproductive cough and blood occasionally seen on toilet tissue after a bowel movement. Upon specific questioning, he did admit to chronic decreased force of urinary stream. Prior to the onset of diplopia, the patient had seen another general practitioner for low back pain that radiated down his left leg. He was injected with an unknown medication, and the pain resolved within 6 days. A computed tomography ( CT) scan was performed in Australia, which reportedly revealed a pituitary tumor. The patient was referred to Fitzsimons Army Medical Center for further evaluation. Ocular examination was requested to evaluate his complaints of diplopia. Visual acuity was 20/ 20 OU. Pupils were equal, round, and briskly reactive OU without a relative afferent pupillary defect. Slit lamp examination was normal. Motility examination revealed decreased abduction 00. A incomitant esotropia of 10 prism diopters in primary position was seen, which increased to 18 prism diopters in right gaze. A constant 2 to 4 PO right hypertropia was present in all fields of gaze. Automated visual field testing was entirely normal. Dilated fundus examination was essentially normal except for scattered drusen in the macula and myelinated nerve fibers along the inferotemporal arcade 00. A flame- shaped hemorrhage was seen along the superonasal arcade OS. Physical examination other than the ocular examination was normal except for diffuse enlargement of the prostate gland. No nodules were appreciated. Neurologic FIG. 1. T1- weighted magnetic resonance image demonstrating an expansile mass of low- to- moderate signal intensity arising from the clivus ( arrow). \:" lir, J''' i, lithalmol, Vol. 12, No. 3, 1992 FIG. 2. T1- weighted mag netic resonance coronal plane enlargement showing the mass's relationship to the internal carotid arteries ( solid arrows) and optic chiasm ( open arrowhead), examination was intact except for presence of the ocular motility disturbance. The patient was admitted to the neurosurgical service with the diagnosis of a primary pituitary tumor. The Endocrinology Service performed an extensive workup, which included hormone assay studies. Screening serum chemistries and blood count were remarkable for hematocrit of 38.2 mV 100 ml and a Wintrobe sedimentation rate of 35 mm/ h. In order to better define the lesion seen on CT scan, magnetic resonance imaging ( MRI) of the head was obtained. This revealed an expansile, low- to- moderate signal intensity lesion, causing bony erosion of the clivus, which was enhanced with gadolinium ( Figs. 1 and 2). The lesion was compressing the sella superiorly and extending into the sphenoid sinus. This tumor was felt to be most consistent with a chordoma, rather than a pituitary adenoma. At this time, the endocrine assays returned and were within normal limits. Lumbosacral spine radiographs were then obtained to evaluate the patient's recurring back pain. These revealed possible metastatic disease in the spine. A bone scan was then obtained, which showed multiple metastatic foci in the ribs, thoracic spine, sternum, pelvis, and right femoral shaft. MRI of the lumbosacral spine confirmed the metastatic appearance of the lesions on the radiographs. Gastroenterologic evaluations, which included colonoscopy and air- contrast barium enema failed to yield the site of the primary tumor. The patient was then seen by the Urology Service SIXTH NERVE PALSY DUE TO PROSTATE CANCER 151 for the evaluation of his enlarged prostate gland. Prostatic acid phosphatase and prostatic specific antigen levels were drawn and returned elevated. A needle biopsy of the prostate gland showed adenocarcinoma of the prostate gland, Gaeta grade III classification ( Fig. 3). A bilateral orchiectomy was performed for androgen ablation therapy. After his recovery, the patient was returned to the operating room where he underwent transsphenoidal subtotal resection of the clivus tumor. Frozen section histopathologic analysis at the time of resection revealed " bone fragments with osteoblastic reaction and tumor cells with microacini cannot rule out metastatic tumor." Permanent section confirmed the diagnosis of metastatic adenocarcinoma ( Fig. 4). The patient was then referred to Radiation Oncology for parasellar region radiotherapy of the metastasis. DISCUSSION This is the first reported case of unrecognized adenocarcinoma of the prostate gland metastatic to the clivus initially presenting as a lateral rectus palsy associated with a hyperdeviation. Isolated sixth nerve palsies are commonly due to ischemic mononeuropathy, for example, diabetes or hypertension ( 1). Vascular inflammation, such as cranial arteritis, would be unusual, but must be considered in an elderly patient ( 1). Aneurysmal dilatation of the posterior inferior cerebellar artery or basilar artery has also been reported to cause abducens deficits usually associated with severe headaches ( 1). Tumors may compress the sixth cranial nerve as it ascends vertically through the subarachnoid space to enter the dura overlying the clivus. Primary tumors include chordoma and other rare tumors of the bones of the skull: osteomas, chondromas, osteochondromas, osteoclastomas, aneurysmal bone cysts, or intraosseous hemangiomas ( 1). Nasopharyngeal carcinoma may extend superiorly into the cavernous sinus to infiltrate or compress the abducens nerve often damaging other structures in the cavernous sinus. It can also cause ipsilateral postganglionic Horner's syndrome, since the oculosympathetic pathways join briefly with the sixth cranial nerve in the cavernous sinus ( 1). Metastatic lesions, most often carcinomas, can spread to the central nervous system, usually via hematogenous dissemination. Lung and breast carcinomas are most common; however, other metastatic tumors include kidney, stomach, prostate, and thyroid ( 2). The frequency of metastatic spread is most closely related to the relative incidence of the tumors themselves. Cranial nerve dysfunction secondary to metastatic prostate carcinoma has been reported previously in 34 patients ( 3- 6). These rare cranial nerve deficits are due to the expansive nature of the bony metastases at the base of the skull, which either compress or infiltrate the affected nerves. In most FIG. 3. Micrograph of prostate gland biopsy showing poorly differentiated adenocarcinoma. ( Hematoxylin and eosin; original magnification x 100.) I Gill Neuro- ophthalmol. Vol. 12. No. 3. 1992 152 B J. E. O'BOYLE ET AL. FIG. 4. Micrographs of the clivus mass showing tumor cells with microacini and bone fragment with osteoblastic reaction consistent with metastatic prostate carcinoma. ( Hematoxylin and eosin; original magnification A: x40, B: x200.) instances, multiple cranial nerves are involved and occur late in the course of the disease process. In all but two of the cases, prostate adenocarcinoma was diagnosed months to years prior to the onset of cranial nerve palsies. Of the cases that initially presented with cranial nerve dysfunction, one patient who complained of right ear pain and headache had imaging studies that showed a lesion involving cranial nerve XII ( 3). In the second case, a ; ," ;."",": · /, II," I", o/. Vol. 12, No. 3, 1992 patient complained of diplopia and exophthalmos, with a lesion involving the 3rd and 6th cranial nerves ( 3). On CT scan, a mass was seen destroying bone in the region of the orbit. Sixth nerve palsies occurred in isolation in only 4 of the 34 patients reported in the literature ( 3- 5). Metastatic spread of adenocarcinoma of the prostate gland is extremely common. At autopsy, the bones most frequently involved, in descending SIXTH NERVE PALSY DUE TO PROSTATE CANCER 153 order, are the spine, femur, pelvis, ribs, sternum, skull, and humerus ( 1,7,8). When the skull becomes involved, metastatic foci are prominent in other bones. Skull metastases, when present, are usually found in the calvaria ( 9). Erosion of the clivus is an exceedingly uncommon event. In a review of the literature of metastatic prostate carcinoma to the skull, only three cases are described as having clivus metastases ( 3). Of these, none had a metastatic clivus lesion as their initial presentation. However, in one patient, the clivus metastasis occurred 14 years after prostate cancer was initially diagnosed, presenting with multiple neurologic manifestations. Hyperdeviations have been described previously in association with isolated unilateral abducens palsies ( 10- 12). Slavin ( 11) found hyperdeviations in a series of 16 patients. The amount of deviation ranged from 4 to 16 prism diopters. In 10 of the cases, the associated hyperdeviation was found in primary gaze as well as peripheral fields of gaze. It was also noted that there was no correlation between degree of abducens deficit and magnitude of the hyperdeviation. In only two of the cases could Slavin ( 11) explain the hyperdeviation in pathologic terms. In one patient with multiple sclerosis, the deviation may have been due to a supranuclear disturbance, that is, skew deviation. In the second case, the subtle hyperdeviation was thought to be due to a right superior oblique palsy. Baker and Buncic ( 12) describe three cases of pseudotumor cerebri in which there was an abducens palsy associated with vertical deviation. In all the cases, the hyperdeviation resolved after intracranial pressure was normalized. Even though this appears to be an isolated case, metastasis to the clivus by prostate carcinoma must be included in the differential diagnosis of 6th nerve palsies in males. REFERENCES I. Miller NR. Walsh alld Hoyt's clillicallleuro- ophthalmology. Vol 2, 4th ed. Baltimore: Williams & Wilkens, 1988: 698- 705. 2. Miller NR. Walsh alld Hoyt's clinicalnel/ ro- ophthalmology. Vol 3, 4th ed. Baltimore: Williams & Wilkens, 1988: 1695- 6. 3. Ransom DT, Dinapoli RP, Richardson RL. Cranial nerve lesions due to base of skull metastases in prostate carcinoma. Callcer 1990; 65: 58&- 9. 4. Svare A. Fossa SD, Heier MS. Cranial nerve dysfunction in metastatic cancer of the prostate. Br I UroI1988; 61: 441- 4. 5. Seymor CH, Peeples WJ. Cranial nerve involvement with carcinoma of the prostate. Urology 1988; 31: 211- 3. 6. Rao KG. Carcinoma of the prostate presenting as intracranial tumor with multiple cranial nerve palsies. Urology 1982; 19: 433- 5. 7. Jacobs Sc. Spread of prostatic cancer to bone. Urology 1983; 21: 337-- 44. 8. Saitoh H, Hida M, Shimbo T, Nakamura K, Yamagata L Satoh T. Metastatic patterns of prostatic cancer: correlation between sites and number of organs involved. Cancer 1984; 54: 3078- 84. 9. Latchaw RE. Metastases. In: Latchaw RE, ed. Compl/ ted tomography of the head, neck alld spine. Chicago: Year Book Medical Publishers, 1985: 271. 10. Kestenbaum A. Clinical methods of nel/ ro- ophthalmologic examination, 2nd ed. New York: Grune & Stratton, 1961: 259- 60, 330 11. Slavin ML. Hyperdeviation associated with isolated unilateral abducens palsy. Ophthalmology 1989; 96: 512- 6. 12. Baker RS, Buncic JR. Vertical ocular motility disturbance in pseudotumor cerebri. I Clin Neuro- ophthalmoI1985; 5: 41- 4. / Gill Neuro- ophthalmol, Vol. 12, No. 3, 1992 |
