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.

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.

Ceguera cortical transitoria secundaria a angiografía cerebral / Transient cortical blindness after cerebral angiography

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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.

Síndrome de Anton secundario a necrosis occipital por intoxicación aguda con metanol / Anton’s syndrome due to occipital necrosis after methanol poisoning

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Contrast-induced transient cortical blindness.

We present a case of transient cortical blindness secondary to contrast medium toxicity. A 58-year-old man had successful endovascular coiling of a right posterior inferior cerebellar artery aneurysm but became confused and unable to see after the procedure. His visual acuity was no light perception bilaterally. Clinically, there was no new intra-ocular pathology. An urgent non-contrast computed tomography scan of the brain showed cortical hyperdensity in both parieto-occipital cortices, consistent with contrast medium leakage through the blood-brain barrier from the coiling procedure. The man remained completely blind for 72 hours, after which his visual acuity improved gradually back to his baseline level.

Post-anesthetic cortical blindness in cats: twenty cases.

The medical records of 20 cats with post-anesthetic cortical blindness were reviewed. Information collected included signalment and health status, reason for anesthesia, anesthetic protocols and adverse events, post-anesthetic visual and neurological abnormalities, clinical outcome, and risk factors. The vascular anatomy of the cat brain was reviewed by cadaver dissections. Thirteen cats were anaesthetised for dentistry, four for endoscopy, two for neutering procedures and one for urethral obstruction. A mouth gag was used in 16/20 cats. Three cats had had cardiac arrest, whereas in the remaining 17 cases, no specific cause of blindness was identified. Seventeen cats (85%) had neurological deficits in addition to blindness. Fourteen of 20 cats (70%) had documented recovery of vision, whereas four (20%) remained blind. Two cats (10%) were lost to follow up while still blind. Ten of 17 cats (59%) with neurological deficits had full recovery from neurological disease, two (12%) had mild persistent deficits and one (6%) was euthanased as it failed to recover. Four cats (23%) without documented resolution of neurological signs were lost to follow up. Mouth gags were identified as a potential risk factor for cerebral ischemia and blindness in cats.

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.

Methomyl-alphamethrin poisoning presented with cholinergic crisis, cortical blindness, and delayed peripheral neuropathy.

OBJECTIVE: Methomyl-alphamethrin is a mixture of carbamate and pyrethroid insecticides. Carbamate insecticides function as reversible cholinesterase inhibitors, which may produce life-threatening cholinergic syndrome. Cortical blindness and delayed neuropathy were rarely reported complications of carbamate insecticide exposures. Here we reported a case of intentional methomyl-alphamethrin ingestion. CASE REPORT: A 41-year-old woman attempted suicide by drinking 200 mL of methomyl-alphamethrin insecticide and soon presented with unconsciousness, hypothermia, and shock. She developed pulseless electrical activity and regained spontaneous circulation after resuscitation. Diagnosis of carbamate poisoning was made by her clinical features, decreased levels of cholinesterases and the presence of methomyl in her urine. She complained of blurred vision and blindness 4 days post-exposure. Visual evoked potential and brain magnetic resonance imaging study confirmed the diagnosis of cortical blindness. On day 21, she had low limbs numbness, progressive weakness, and right foot drop. Electophysiological tests performed on day 27 revealed neuropathy of bilateral peroneal nerves. CONCLUSION: We reported a patient who manifested severe carbamate insecticide poisoning and developed cortical blindness and delayed neuropathy. Physicians should be aware of these rare toxicities among patients with severe carbamate insecticide poisoning.

[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.