CASE REPORT The Journal of TRAUMA威 Injury, Infection, and Critical Care Parietal Contusion and Transient Superior Sagittal Sinus Occlusion Presenting with Cortical Blindness Chung-Ling Liang, MD, Lin-Cheng Yang, MD, Chun-Chung Lui, MD, Michael Hsiao, DVM, PhD, and Kuo-Sheng Hung, MD J Trauma. 2002;53:1006 –1009. C ortical blindness is a consequence of dysfunction or destruction of area 17 in both occipital lobes. The degree of visual loss can vary from subtle visual field deficits to complete visual loss. Permanent destruction of the occipital cortex is most commonly seen in posterior cerebral artery occlusion associated with vertebrobasilar disease. More infrequently, trauma or tumor may cause destruction. To date, here has been no clinical report relating to posterior parietal cortex injury, transient superior sagittal sinus occlusion, and visual field defect. In this report, we presented a patient who suffered from blunt head injury. This patient’s visual field defect was caused by left parietal injury and transient superior sagittal sinus occlusion. CASE REPORT A 27-year-old man experienced blunt head trauma while fighting with others. Physical examination revealed clear consciousness, right raccoon’s eye, left Battle sign, right footdrop, and right visual field defect at confrontation test in the emergency room. The visual field study showed right inferior homonymous quadrantanopia. Computed tomographic (CT) scan of the head showed depressed fracture of the left parietal and left temporal skull, and pneumocephalus. The magnetic resonance (MR) image 2 days posttrauma revealed left parietal injury with depressed bony fracture (left side much more severe than right side area) and mild subarachnoid hemorrhage. A MR venogram (MRV) revealed transient superior sagittal sinus (SSS) compression and obstruction (Fig. 1). An electromyogram (EMG) 5 days posttrauma showed an acute deSubmitted for publication July 19, 2001. Accepted for publication October 23, 2001. Copyright © 2002 by Lippincott Williams & Wilkins, Inc. From the Department of Ophthalmology, Kaohsiung Municipal Ta Tung Hospital (C.-L.L.), Anesthesiology (L.-C.Y.), Diagnostic Radiology (C.-C.L.), and Neurosurgery (K.-S.H.), Chang Gung Memorial Hospital, Kaohsiung Medical Center, Kaohsiung, and Department of Medical Education and Research, Kaohsiung Veterans General Hospital (M.H.), Taiwan, Republic of China. Address for reprints: Kuo-Sheng Hung, MD, Department of Trauma and Neurosurgery, Chang Gung Memorial Hospital, Kaohsiung Medical Center, 123, Ta Pei Road, Niao Sung Hsiang, Kaohsiung Hsien 833, Taiwan, Republic of China; email: kshung25@yahoo.com.tw. DOI: 10.1097/01.TA.0000033754.65011.A9 1006 Fig. 1. Sagittal view of T2-weighted image shows a depression fracture (white arrow) and hyperintensity lesion at the parietal lobe (black arrows). MR venogram shows a focal superior sagittal sinus stenosis (arrowhead). nervation pattern on the right leg. A central lesion such as left parietal contusion was suspected on the EMG study. Visual evoked potentials study 5 days after trauma revealed prolongation of bilateral P100 with decreased amplitude, so bilateral cortical blindness was impressed. Under the diagnosis of parietal depression fracture, left parietal brain contusion, and superior sagittal sinus occlusion with monoplegia of the right leg and right visual field defect, he was admitted to the intensive care unit for close November 2002 SSS Occlusion and Parietal Cortical Blindness Fig. 2. Follow-up MR image 3 months later. Axial view of T2weighted image shows regression of the posterior parietal lobe lesion (arrow). Follow-up MR venogram shows patency of the superior sagittal sinus. observation and medication (dexamethasone 5 mg intravenously every 6 hours for 3 days). Because his right footdrop improved gradually and his consciousness remained clear, we did not perform an operation. He could walk without deficit 2 weeks after trauma. The EMG also revealed marked improvement compared with the previous findings. Meanwhile, the cortical blindness persisted. The MR image 3 months posttrauma showed a left posterior parietal lesion without occipital ischemia and the MRV showed patency of the SSS (Fig. 2). His visual field studies at 1 year posttrauma showed persistent right inferior homonymous quadrantanopia (Fig. 3). The visual field defect was caused by left parietal injury or transient superior sagittal sinus occlusion. DISCUSSION Cortical blindness is a syndrome with a wide variety of clinical presentations and causes, including stroke,1 cardiac arrest,2–5 hemorrhagic shock,6 meningitis,7 uremia,8 vertebral Volume 53 • Number 5 angiography,9,10 cardiac surgery,11 carbon monoxide poisoning,12 and trauma.13 In the young age group, the most frequent causes are head injury, meningitis, and cardiac arrest, whereas in adults, cerebrovascular accidents and episodes of cardiorespiratory arrest predominate.14 The term “cortical blindness” refers only to the condition in which the occipital visual cortex is primarily involved. The visual fibers that terminate in the midbrain are intact and therefore allow the preservation of light reflex. There is full ocular motility and the funduscopic examination is normal. A patient presenting with cortical blindness after a head injury should be given a full neurologic examination, and the case should be discussed with a neurosurgeon and an ophthalmologist. Should clinical findings, such as deteriorating level of consciousness and other neurologic signs, suggest a significant primary brain injury or the development of a treatable secondary complication, an urgent CT scan should be obtained. If brain CT scan does not show intracranial hematoma or other mass lesions and the patient develops permanent cortical blindness, we suggest an MR image study of the brain to see the possible lesions around the occipital lobes. One of the advantages of an MR image study is that the vascular system can be traced easily by MRV or MR angiography. Although our patient did not have lesions at both occipital lobes, he had transient occlusion of the SSS (Fig. 1) and left parietal brain contusion resulting in defect of the right visual field and right footdrop. The reason for his cortical blindness may have been the cascade of the transient occlusion of the SSS, venous hypertension, and occipital cortical dysfunction. We did not obtain an arteriogram for this patient, because the study is invasive. MRV is noninvasive and easier to use for follow-up. However, if the MRV image is ambiguous, an arteriogram is suggested, to confirm the diagnosis. Posttraumatic cortical blindness may be transient or permanent. The incidence of posttraumatic transient cortical blindness (PTTCB) is thought to be as high as 0.4% to 0.6%.15 PTTCB is more common in children, who have a more labile vasculature than adults. The majority of cases of PTTCB resolve within hours, although some prolonged syndromes have been described.16 Our reported case had persistent visual defect for more than a year, although his right footdrop caused by left parietal brain contusion recovered in 2 weeks. We proposed transient occlusion of the SSS, and parietal injury could be one of the reasons for permanent cortical blindness. There is controversy regarding surgery for symptomatic superior sinus occlusions caused by depressed skull fracture. Van den Brink et al.17 suggested that conservative management of depressed cranial fractures overlying such critical areas as the cranial sinus is advocated when there is no vital indication for emergency restoration of venous drainage. When the depressed skull fracture is overlying a cranial venous sinus, the neurosurgical textbooks strongly 1007 The Journal of TRAUMA威 Injury, Infection, and Critical Care Fig. 3. Goldman visual field obtained 12 months posttrauma demonstrating right inferior homonymous quadrantanopia. advise conservative management because of potential mortality caused by uncontrollable bleeding; thus, depressed fractures in these regions are usually left alone. Meltzer et al.18 reported a successful surgical elevation of skull fracture with sagittal sinus occlusion. Because our patient’s right footdrop improved gradually after dexamethasone treatment and his consciousness remained clear, we did not perform an operation. We suggest that in cases of sinus occlusion without life-threatening complications, it is recommended that the patient be managed as if they have intracranial hypertension and to closely observe the course of the diseases. Further studies are needed to investigate the best treatment options for these patients. Sergent et al.19 recently investigated regional cerebral blood flow in normal humans by positron emission tomography. They defined the visual functional anatomy in the superior parietal, occipital, and temporal cortex areas.19 However, no such cortical blindness cases caused by parietal injury were reported. Again, we suggest that the cascade of the transient occlusion of the SSS, venous hypertension, and occipital cortical dysfunction could be the main cause of the cortical blindness in this case. In conclusion, this might be the first reported patient with contralateral inferior homonymous quadrantanopia resulting from parietal cortex injury and transient occlusion of the SSS. Parietal cortex injury and occlusion of the SSS could be one of the reasons for the visual defect. 1008 REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. Symonds C, Mackenzie I. Bilateral loss of vision from cerebral infarction. Brain. 1957;80:415– 454. Hoyt WF, Walsh FB. Cortical blindness with partial recovery following acute cerebral anoxia from cardiac arrest. Arch Ophthalmol. 1958;60:1061–1069. Sabah AH. Blindness after cardiac arrest. Postgrad Med J. 1968; 44:513–516. Weinberger HA, Van De Woude R, Maier HC. Prognosis of cortical blindness following cardiac arrest in children. JAMA. 1962;179:126. McAuley FD. Prolonged visual failure following cardiac arrest due to accidental hypothermia. Br J Ophthalmol. 1964;48:628. Wold A, Leira H. Temporaer cortical blindhet etter blodningssjokk. T Norsk Laegeforen. 1964;84:184 –186. Acers TE, Cooper WC. Cortical blindness secondary to bacterial meningitis. Am J Ophthalmol. 1965;59:226 –229. Tyler HR. Neurologic disorders in renal failure. Am J Med. 1968; 44:734 –738. Silvermann SM, Bergman PS, Bender MB. The dynamics of transient cerebral blindness: report of nine episodes following vertebral angiography. Arch Neurol. 1961;4:333–348. Howland WJ, Curry JL. Transient cerebral blindness: a hazard of vertebral artery catheterization—report of four cases. Radiology. 1964;83:428 – 432. Levedeba RN, Kenevskaya XS. Cortical blindness reported in six cases who had heart and major blood vessel operations, in which the operation in the immediate post-operative period was complicated by a hypoxic state. Klin Med (Moskva). 1965;43:108 –111. Juan J, Prochagha Z. A case of cortical blindness following acute poisoning with CO. Sborn Ved Prac Lek Fak Karlow Univ. 1962; 5:105–111. Rodriguez A, Lozano JA, del Pozo D, Paez JH. Post-traumatic transient cortical blindness. Int Ophthalmol. 1993;17:277–283. November 2002 SSS Occlusion and Parietal Cortical Blindness 14. Drymalski W. Cortical blindness: the changing incidence and shifting etiology. Postgrad Med. 1980;47:149 –156. 15. Greenblatt SH. Post-traumatic transient cerebral blindness. JAMA. 1973;225:1073–1076. 16. Holmes GL. Prolonged cortical blindness after closed head trauma [letter]. South Med J. 1978;71:612– 613. 17. van den Brink WA, Pieterman H, Avezaat CJ. Sagittal sinus occlusion, caused by an overlying depressed cranial fracture, Volume 53 • Number 5 presenting with late signs and symptoms of intracranial hypertension: case report. Neurosurgery. 1996;38:1044 –1046. 18. Meltzer H, LoSasso B, Sobo EJ. Depressed occipital skull fracture with associated sagittal sinus occlusion. J Trauma. 2000; 49:981. 19. Sergent J, Ohta S, Macdonald B. Functional neuroanatomy of face and object processing: a positron emission tomography study. Brain. 1992;115:15–36. 1009