Free
Case Reports  |   August 2003
Cortical Blindness and Neurologic Injury Complicating Cervical Transforaminal Injection for Cervical Radiculopathy
Author Affiliations & Notes
  • Marion R. McMillan, M.D.
    *
  • Cynthia Crumpton, R.N.
  • *Medical Director and †Clinical Nurse Specialist, Foothills Regional Pain Center.
  • Received from the Foothills Regional Pain Center, Seneca, South Carolina.
Article Information
Case Reports
Case Reports   |   August 2003
Cortical Blindness and Neurologic Injury Complicating Cervical Transforaminal Injection for Cervical Radiculopathy
Anesthesiology 8 2003, Vol.99, 509-511. doi:
Anesthesiology 8 2003, Vol.99, 509-511. doi:
SINCE the initial description by Morvan in 1988, cervical transforaminal injection of analgesic solutions and corticosteroids has been a useful diagnostic and therapeutic option for the nonoperative management of cervical radicular pain symptoms. 1,2 Transforaminal cervical epidural injection is technically demanding, and the proximity to vascular and central nervous system structures may increase the risk of complications. Patients with previous cervical spine surgery may be at greater risk for procedural complications because of postsurgical anatomic variations or more advanced pathologic conditions, resulting in the failure of conservative management. Potential complications include nerve root trauma, unintentional dural puncture, unintended spinal anesthesia with respiratory and hemodynamic compromise, vertebral artery injury, and systemic allergic reactions to radiocontrast agents. Transient cortical blindness and brain injury have been infrequently associated with the use of ionic and nonionic radiocontrast agents introduced into the intracranial circulation during angiographic procedures, 3–5 and they may also be embolic in origin. 6 These complications have not been previously reported in association with cervical transforaminal injections for the management of pain. We present a case of acute cortical blindness and prolonged neurologic compromise complicating cervical transforaminal injection with acute disruption of the blood–brain barrier demonstrated by magnetic resonance imaging. Implications for patient management and prevention of complications are discussed.
Case Report
A 54-yr-old man was referred for pain management consultation because of a 14-yr history of neck pain, left cervical radiculopathy, and neuritic left arm pain. He had a 25-pack-year history of cigarette smoking with no known history of vascular disease. Physical examination was remarkable for sensory impairment to cold and light touch without allodynia or hyperalgesia in the left C5and C6dermatomes. Reflex examination documented reduced left biceps and triceps reflexes at 1+, respectively, with the remainder of the reflex and motor examination of the upper extremity demonstrating normal findings. There was distal left cervical spine tenderness, which reproduced neuritic left elbow pain, and the patient complained of left-sided neck pain made worse by right rotation and extension. He had undergone three previous cervical spine operations for circumferential cervical spine stenosis from C3–4to C6–7by magnetic resonance imaging, including decompression from C3to C7, with hardware fusion at C6–74 months before presentation. Postoperative computed tomography with cervical myelography demonstrated mild focal blunting at the left C6nerve root sleeve deemed to be surgically insignificant. He had responded poorly to opioid analgesics, and spinal injections had not been performed. Because of intractable radicular left arm pain, transforaminal cervical epidural steroid injection at the C5–6level was planned.
The left neuroforamen at C 5–6was easily visualized in multiple oblique projections, and after local infiltration analgesia, a 22-gauge, 6-cm needle was advanced under fluoroscopy from an anterior/oblique approach to contact the superior dorsal quadrant of the foramen. On the first pass, bright red blood was aspirated near the opening of the foramen, suggesting left vertebral artery puncture. The needle was retracted, cleared of blood, and repositioned, with negative aspiration test results for blood or cerebrospinal fluid. Loss of resistance to 1 ml of injected air was followed by injection of 2 ml of myelogram-compatible iopamidol nonionic radiocontrast to confirm needle entry into the left lateral recess of the epidural space. The epidurogram was judged to be technically unsatisfactory, and within seconds after injection, the patient developed lateral nystagmus. He remained conscious and verbally responsive, and a final attempt to cannulate the C4–5foramen was aborted because of increasing patient restlessness and agitation. Approximately 45 min after the initial injection of air and radiocontrast and without injection of additional medications, the patient complained of total bilateral blindness, with bedside confirmation of no light perception. Brief bedside neurologic examination demonstrated no focal neurologic abnormalities. Arterial air embolism was suspected, and after consultation with a neurologist, the patient was treated empirically with corticosteroids and intravenous doxycycline. Emergent baseline and gadolinium-enhanced magnetic resonance imaging of the brain was requested. Images acquired 2 h after the initial foraminal injection demonstrated bilateral parenchymal gadolinium enhancement in the occipital lobes and throughout the posterior intracranial circulation, indicating true breakdown of the blood–brain barrier (fig. 1). Unexpectedly, simultaneous diffusion weighted images were normal. The patient remained responsive and alert and was transferred to a tertiary care facility, where he received empiric hyperbaric oxygen treatment within 4 h after the event. During the first 2 h of hyperbaric therapy, he suffered two grand mal seizures, resulting in discontinuation of hyperbaric therapy and transfer to the neurologic acute care unit. Over the next 24 h, he manifested obtundation, confusion, aphasia, swallowing dysfunction, and continued bilateral blindness. A second magnetic resonance scan of the brain on day 4 showed vasogenic and cytotoxic cerebral edema preferentially in the left occipital cortex on T2-weighted images with superimposed abnormalities on diffusion weighted images. Postgadolinium images demonstrated no parenchymal enhancement, and simultaneous magnetic resonance angiography showed patent intracranial arteries. He became more responsive over the next several days, and an ophthalmology consultant documented intact pupillary reflexes, normal funduscopic examination, and globally impaired vision consistent with cortical blindness. He was able to partially track images in a mirror by the seventh hospital day. The patient made continued gradual improvement over the next 3 weeks, noting normalization of cognitive impairment, aphasia, dysphagia, and full return of the left visual field. By day 30, he manifested a mild short-term memory deficit and a persistent partial right homonymous hemianopia, and he was discharged from the hospital.
Fig. 1. Day 1, T1-weighted contrast enhanced magnetic resonance image at 2 h after cervical transforaminal injection demonstrating intense parenchymal uptake in bilateral occipital and temporal lobes compatible with acute disruption of the blood–brain barrier.
Fig. 1. Day 1, T1-weighted contrast enhanced magnetic resonance image at 2 h after cervical transforaminal injection demonstrating intense parenchymal uptake in bilateral occipital and temporal lobes compatible with acute disruption of the blood–brain barrier.
Fig. 1. Day 1, T1-weighted contrast enhanced magnetic resonance image at 2 h after cervical transforaminal injection demonstrating intense parenchymal uptake in bilateral occipital and temporal lobes compatible with acute disruption of the blood–brain barrier.
×
Discussion
Cortical blindness is a rare but recognized complication of the administration of radiocontrast agents into the intracranial vasculature. It has been seen most often in procedures involving the posterior intracranial circulation and is reported to occur during 0.3–1% of vertebral angiograms. 3–5,7 Clinically, visual deficits following administration of radiocontrast agents have been associated with acute cognitive impairment, cranial nerve deficits, oculomotor disturbances, seizures, nausea, and vomiting, and are usually transient with restoration of normal neurologic function after days to weeks, 3–5,8 but they may be permanent. 9 Lantos suggested that the pathognomonic radiographic appearance of direct radiocontrast toxicity is the immediate contrast enhancement of brain parenchyma on computed tomography or magnetic resonance images reflecting true breakdown of the blood–brain barrier. 3 
The primary differential diagnosis in this case includes radiocontrast-induced cerebral injury versus  vertebral artery embolism associated with vertebral artery injury or the use of air for epidural localization. The low sensitivity of negative aspiration tests to detect intravascular injection during caudal 10 and lumbar 11 transforaminal epidural injections has been previously reported. Case reports and published reviews of arterial air embolism indicate that clinical symptoms, time course of recovery, potential long-term sequelae are similar to those reported in association with radiocontrast toxicity. 12–14 In arterial air embolism, hyperbaric oxygen therapy is the treatment of choice, 12 and animal studies also support the use of intravenous lidocaine 15 and doxycycline 16 for the reduction of cerebral injury in experimental cerebral air embolism. Our patient demonstrated acute parenchymal contrast enhancement and normal diffusion weighted images by magnetic resonance on day 1, and no contrast enhancement on day-4 images, when it would usually be expected with cerebral infarction. 17 It is possible that arterial gas embolism may have caused ischemic disruption of the blood–brain barrier and predisposed the patient to subsequent radiocontrast toxicity. Observed neurologic deficits at 4 weeks may have been related to the persistent effects of air or other cerebral embolism, direct cytotoxic effects of the radiocontrast agent itself, or both.
Greater emphasis should be placed on the potential for cortical blindness and brain injury associated with cervical transforaminal injections, the indications for and clinical outcomes of these procedures in patients with persistent cervical radiculopathy after cervical spine surgery, and the risk of vertebral artery injury associated with the classic anterior/oblique approach. Our experience also leads us to suggest that the use of air to identify the cervical periradicular epidural space should be abandoned because of the risk of cerebral air embolism. We believe that the use of radiocontrast agents may be justified after individual assessment of potential benefits and risk of radiocontrast toxicity. Recently, Vallee et al.  reported their results with a lateral periradicular approach for cervical transforaminal injections in 32 patients with cervical radiculopathy without the use of radiocontrast or loss of resistance maneuvers. 18 We believe that additional research comparing the efficacy, safety, and indications for various cervical transforaminal techniques in defined patient populations is warranted.
References
Morvan G, Mompoint D, Bard M, Levi-Valensin G: Direct intra-foraminal injection of corticosteroids in the treatment of cervico-brachial pain, Interventional radiology in bone and joint. Edited by Bard M, Laredo JD. New York, Springer Verlag, 1988, pp 253–7
Bush K, Hillier S: Outcome of cervical radiculopathy treated with periradicular/epidural corticosteroid injections: A prospective study with independent clinical review. Eur Spine J 1996; 5: 319–25Bush, K Hillier, S
Lantos G: Cortical blindness due to osmotic disruption of the blood–brain barrier by angiographic contrast material: CT and MRI studies. Neurology 1989; 39: 567–71Lantos, G
Kermode AG, Chakera T, Mastaglia FL: Low osmolar and non-ionic x-ray contrast media and cortical blindness. Clin Exp Neurol 1992; 29: 272–6Kermode, AG Chakera, T Mastaglia, FL
Lim K, Radford D: Transient cortical blindness related to coronary angiography and graft study. Med J Aust 2002; 177: 43–4Lim, K Radford, D
Sabovic M, Bonac B: An unusual case of cortical blindness associated with aortography: A case report. Angiology 2000; 51: 151–4Sabovic, M Bonac, B
Mani RL, Eisenberg RL: Complications of catheter cerebral arteriography: Analysis of 5000 procedures. III. Assessment of arteries injected, contrast medium used, duration of procedure, and age of patient. Am J Radiol 1978; 131: 871–4Mani, RL Eisenberg, RL
Package insert, Isovue M-200 (Iopamidol injection, 41%) and M-300 (Iopamidol injection, 61%), Braco Diagnostics, Princeton, New Jersey 08543
Package insert, Optiray 160, 240, 300, 320, 350, (Ioversol injection, 34, 51, 64, 68, and 74%), Mallinckrodt, Inc., St. Louis, Missouri 63042
Renfrew DL, Moore T, Kathol M, El-Khoury G, Lemke JH, Walker CW: Correct placement of epidural steroid injections: Fluoroscopic guidance and contrast administration. AJNR Am J Neuroradiol 1991; 12: 1003–7Renfrew, DL Moore, T Kathol, M El-Khoury, G Lemke, JH Walker, CW
Furman M, O'Brien E, Zgleszewski T: Incidence of intravascular penetration in transforaminal lumbosacral epidural steroid injections. Spine 2000; 25: 2628–32Furman, M O'Brien, E Zgleszewski, T
Muth CM, Shank ES: Gas embolism. N Engl J Med 2000; 342: 476–82Muth, CM Shank, ES
Hinkle D, Raizen D, McGarvey M, Liu G: Cerebral air embolism complicating cardiac ablation procedures. Neurology 2001; 56: 792–4Hinkle, D Raizen, D McGarvey, M Liu, G
Akhtar N, Jafri W, Mozaffar T: Cerebral artery air embolism following an esophagogastroscopy: A case report. Neurology 2001; 56: 136–7Akhtar, N Jafri, W Mozaffar, T
Dutka AJ, Mink R, McDermott JJ, Clark JB, Hallenbeck JM: Effect of lidocaine on somatosensory evoked response and cerebral blood flow after canine cerebral air embolism. Stroke 1992; 23: 1515–20Dutka, AJ Mink, R McDermott, JJ Clark, JB Hallenbeck, JM
Reasoner DK, Hindman BJ, Dexter F, Subieta A, Cutkomp J, Smith T: Doxycycline reduces early neurologic impairment after cerebral artery air embolism in the rabbit. A nesthesiology 1997; 87: 569–76Reasoner, DK Hindman, BJ Dexter, F Subieta, A Cutkomp, J Smith, T
Osborn AG, ed: Stroke, Diagnostic neuroradiology. St. Louis, Mosby-Year Book, 1994, pp 347–98
Vallee J-N, Feydy A, Carlier RY, Mutschler C, Mompoint D, Vallee CA: Chronic cervical radiculopathy: Lateral approach periradicular corticosteroid injection. Radiology 2001; 218: 886–92Vallee, J-N Feydy, A Carlier, RY Mutschler, C Mompoint, D Vallee, CA
Fig. 1. Day 1, T1-weighted contrast enhanced magnetic resonance image at 2 h after cervical transforaminal injection demonstrating intense parenchymal uptake in bilateral occipital and temporal lobes compatible with acute disruption of the blood–brain barrier.
Fig. 1. Day 1, T1-weighted contrast enhanced magnetic resonance image at 2 h after cervical transforaminal injection demonstrating intense parenchymal uptake in bilateral occipital and temporal lobes compatible with acute disruption of the blood–brain barrier.
Fig. 1. Day 1, T1-weighted contrast enhanced magnetic resonance image at 2 h after cervical transforaminal injection demonstrating intense parenchymal uptake in bilateral occipital and temporal lobes compatible with acute disruption of the blood–brain barrier.
×