Transient Loss of Vision after Coronary Angiogram - A Case Report.

A 50-year old, diabetic, hypertensive patient with post-CABG status developed complete loss of vision about one hour after coronary angiogram (CAG). Thorough ophthalmological and neurological examination as well as magnetic resonance imaging of brain especially of the occipital region revealed no abnormality. The patient had complete recovery of vision about 48 hours later. We could not document any specific cause or mechanism for the visual loss, although the selective vulnerability of occipital lobes to contrast agent toxicity (Cortical blindness) was the most likely underlying mechanism.

First description of posterior reversible encephalopathy syndrome as a complication of glycerolnitrate patch following open cardiac surgery.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) affects predominantly the parietal and occipital lobes. Frequent clinical features are epileptic seizure, altered mental status and visual disturbances. CLINICAL PRESENTATION: We present the first case of a patient with pericarditis and mitral valve insufficiency, who developed PRES after application of a glycerolnitrate patch day three post-operatively and whose neurological deficits improved within 2 days after withdrawal of patch therapy. CONCLUSION: The precise pathomechanism of PRES is unknown. The lower sympathetic innervation of the posterior circulation may be one explanation for its particular vulnerability to vasodilatation caused by glycerolnitrate.

Transient cortical blindness post angiography--a case report.

A 56-year old female reported having had a fall two weeks prior to presentation. Computed Tomography (CT) scan showed an acute right-sided convexity subdural haematoma. A computed tomography angiogram revealed no vascular anomaly. One hour post procedure she had bilateral cortical blindness. Her vision subsequently was fully restored. A diagnosis of transient cortical blindness was made. Transient cortical blindness is a rare but recognized complication ofintra-arterial injection of iodinated contrast agents.

Persistent cortical blindness after a thoracic epidural test dose of bupivacaine.

Thoracic epidural anesthesia is considered as an essential component of the perioperative care for patients undergoing lung resection. Although neurologic adverse events have been associated with this technique, permanent injury is rare. These events primarily involve the peripheral nervous system; for example, nerve root injury. We present a case of persistent cortical blindness after a test dose of bupivacaine was administered into an uneventfully placed thoracic epidural catheter.

[Cerebral complications induced by neurotoxity of nonionic contrast medium after embolization of unruptured cerebral aneurysms: report of 2 cases].

We successfully performed endovascular coil embolization for 2 patients with unruptured saccular aneurysms. However, transient cortical blindness and generalized seizure associated with CNS neurotoxity of contrast medium were noted for each patient after the procedure. In the first case of a 62-year-old woman with a right BA-SCA aneurysm, she complained of blindness with restlessness one day after the intervention but no evidence of embolism on MRA. Abnormal EEG with slow, large amplitudes and 99mTc-HMPAO SPECT-evidenced hyperperfusion were observed in the occipital area. Accompanied by resolution of the edematous changes on MRI in conjunction with normalization of EEG and rCBF by anticonvulsant administration, her visual acuity completely recovered 8 days after the onset. According to these findings, we considered this case as transient cortical blindness. In the second case of a 68-year-old man with a left MCA aneurysm, he exhibited generalized seizure 8 hours after the procedure. CT scan revealed retention of the contrast medium over the left hemisphere. Postictal EEG one day after the seizure showed left frontal slowing but had no evidence of contrast medium retention or hyperperfusion. He recovered well with corticosteroid, anticonvulsant, and intravenous hydration. His follow-up DSA 2 years after the coiling was performed without trouble by reducing the amount/concentration of the contrast medium and by prophylactic steroid and hydration. Non-ionic contrast medium-related neurotoxity as represented by transient cortical blindness or generalized seizure should be recognized as a possible complication of endovascular surgery where patients' brain areas are locally vulnerable to contrast medium exposure.

[Recurrent cortical blindness after LSD-intake]. / Rezidivierende kortikale Blindheit nach LSD-Einnahme.

Recurrent disturbances of vision associated with headaches are typical signs of a migraine. A 15-year-old girl suffered from common migraine. The patient had a headache and nausea five days after a first and proved intake of LSD. Shortly later, a complete blindness of both eyes developed within seconds. These symptoms continued for 48 hours. As the pupillar reactions were intact the findings were consistent with cortical blindness. MRI and MR-angiography of the brain, analysis of the cerebrospinal fluid and blood investigations for thrombophilia were normal. The EEG showed a bilateral symmetrical delta wave slowing over the occipital areas. Within the following three months the girl had three more episodes with complete blindness over a period of 12-36 hours. There have never been any visual disturbances in between the episodes and afterwards. Extended diagnosis with long term blood pressure measurement, Doppler sonography and visual evoked potentials were normal. The occipital slowing in the EEG persisted for 18 months. As the symptoms were unusually long and severe for a complicated migraine it is possible that the temporary blindness was the correlate of flash backs caused by the LSD. LSD intake could trigger additional, local cortical dysfunction (e. g. in the occipital areas) in preexisting migraine.

[Visual cortes--is it a concern?]. / Le cortex visuel est-il concerné?

The visual cortex may be involved in adverse drug reactions, leading to three different clinical presentations: cortical blindness, visual hallucinations and visual aura without headache. The drugs with potential visual cortex toxicity are described.

Contrast-associated transient cortical blindness: three cases with MRI and electrophysiology findings.

Transient cortical blindness (TCB) is a rare but striking complication following contrast agent injection. TCB might be secondary to a direct toxicity of the contrast agent, leading to an osmotic disruption of the blood-brain barrier (BBB), with a preferential involvement of the posterior circulation and occipital cortex. We report a series of three patients with contrast medium-associated TCB (intra-arterial injection of non-ionic contrast agent during diagnostic cerebral angiography for two of them and coronary angioplasty for the other one). In two patients, the magnetic resonance imaging (MRI) was unremarkable; in the other patient, typical MRI findings were observed, with FLAIR hyperintensities in the right occipital cortex and decreased apparent diffusions coefficient (ADC). Interestingly, this patient also presented posterior rhythmic epileptiform activities on electroencephalogram during the first 36 h. Visual evoked potentials (VEPs) showed normal retinal potential, but a massive destructuration of the later potentials of the cortical origin. To our knowledge, this is the first time that VEPs acquired during TCB are reported. We discuss these findings with respect to the pathophysiology of TCB.

Case report and literature review on contrast-induced encephalopathy.

Contrast-induced encephalopathy (CIE) is a rare neurological complication following the administration of injectable intravascular contrast media. Patients with CIE present a wide spectrum of symptoms such as headache, transient cortical blindness, seizure and focal neurological deficits. The diagnosis of CIE requires a high index of suspicion. Its early recognition is of paramount importance in instituting the appropriate supportive treatment in the form of intravenous fluids and also in avoiding unnecessary potentially harmful treatment such as intravenous thrombolysis for suspected ischemic stroke. Here, we report the case of a 62-year-old male patient with a typical presentation of CIE immediately following coronary angiography. We then continue to briefly review the relevant literature on CIE to date.

Reversible posterior leukoencephalopathy syndrome after bevacizumab/FOLFIRI regimen for metastatic colon cancer.

OBJECTIVE: To describe a patient with reversible posterior leukoencephalopathy syndrome following the administration of bevacizumab (Avastin), a monoclonal antibody against vascular endothelial growth factor. DESIGN: Case report/literature review. SETTING: University hospital. PATIENT: A 52-year-old man receiving chemotherapy for stage IV rectal carcinoma. RESULTS: Clinical and radiographic evidence consistent with reversible posterior leukoencephalopathy syndrome was found following the administration of irinotecan hydrochloride, leucovorin calcium, and fluorouracil (FOLFIRI) regimen chemotherapy and bevacizumab. CONCLUSIONS: Reversible posterior leukoencephalopathy syndrome following treatment with angiogenesis modulators can occur. In addition to raising clinical suspicion in appropriate patients, this report may yield clues to the pathophysiologic underpinnings of reversible posterior leukoencephalopathy syndrome.

Transient cortical blindness during chemotherapy (PVB) for ovarian germ cell tumor.

A 17 year-old female with stage IIIc endodermal sinus tumor of the ovary developed transient cortical blindness and severe hypertension after 5 cycles of PVB regimen consisting of cisplatin, vinblastine and bleomycin. Clinical and radiological findings were compatible with Posterior LeukoEncephalopathy (PLE). Her visual acuity and blood pressure completely recovered within a few days after supportive treatment with antihypertensive drug. This condition is unpredictable but it can be reversible without long term sequelae. Most reports suggested that this rare toxicity was from cisplatin therapy. However, the exact pathophysiogenesis of this condition was not known precisely. Prompt reduction in blood pressure and withdrawal of immunosuppressive agents might lead to rapid reversal of this syndrome and prevent permanent brain damage.

Reversible cortical blindness and convulsions with cyclosporin A toxicity in a patient undergoing allogeneic peripheral stem cell transplantation.

A 40-year-old woman underwent allogeneic peripheral blood stem cell transplantation for relapsed AML-M6. She developed graft-versus-host disease on day +15 post-transplant, for which she was treated with cyclosporin A and methyl prednisolone. On day +19 she developed cortical blindness, headache and convulsions which were associated with white matter changes on MRI scanning of the head and elevated cyclosporin A levels. A diagnosis of cyclosporin A encephalopathy was made and cyclosporin A was discontinued. Her vision recovered completely after 48 h and the other symptoms resolved. This is the first case of cyclosporin A encephalopathy to be reported in an allogeneic PBSC recipient.

Cortical blindness and seizures in a patient receiving FK506 after bone marrow transplantation.

A 54-year-old woman with a myelodysplastic syndrome treated with high-dose chemotherapy and an allogenic bone marrow transplant developed acute cortical blindness while receiving tacrolimus (FK506). MRI showed white matter abnormalities. After discontinuation of FK506, the patient's vision returned within 8 days. FK506 neurotoxicity is similar to cyclosporine neurotoxicity and can occur in allogenic bone marrow transplant patients treated with FK506.

Late onset cyclosporine-induced cerebral blindness with abnormal SPECT imagings in a patient undergoing unrelated bone marrow transplantation.

A 23-year-old woman underwent HLA-matched unrelated BMT for CML. She developed cerebral blindness on day 81. Brain magnetic resonance imaging revealed hyperintensity on a T2-weighted image in the white and gray matter of the right frontal and both occipital lobes. Single-photon emission computed tomography (SPECT) was consistent with a decrease in radionuclide uptake in these areas, suggesting a vasoconstrictive mechanism. A diagnosis of CsA-induced encephalopathy was made and CsA was discontinued. Her vision recovered completely after 24 h and abnormal imaging resolved within 2 weeks. This case demonstrates late onset CsA-induced cerebral blindness with the previously unreported abnormalities on SPECT.

Cortical blindness after contrast-enhanced CT: complication in a patient with diabetes insipidus.

Transient cortical blindness is an uncommon but well-known complication following cerebral angiography. One possible cause of this complication is an adverse reaction to contrast agent, resulting in an osmotic disruption of the blood-brain barrier that seems to be selective for the occipital cortex. We report the case of a 16-year-old male patient with cortical blindness after intravenous application of nonionic contrast agent during CT angiography performed because of seizure that was attributed to thrombosis of the basilar artery on the basis of clinical findings. To our knowledge, the development of cortical blindness after CT angiography has not been described in the literature. The patient's symptoms were triggered by hyponatriemia and diabetes insipidus.

MR findings of cortical blindness following cerebral angiography: is this entity related to posterior reversible leukoencephalopathy?

We describe MR findings in three patients who experienced transient cortical blindness following cerebral angiograms. All angiograms were performed by using the same nonionic contrast medium. On the basis of similar clinical and radiologic findings, we believe that this entity is closely related to and probably has the same pathophysiology as posterior reversible leukoencephalopathy.

Cortical blindness following coronary angiography.

A 53-year-old man developed transient cortical blindness after coronary angiography, which appears to be an adverse reaction to contrast agent. A possible mechanism of this complication is contrast penetration of the blood-brain barrier with direct neurotoxicity to the occipital cortex.