Pearls and Oy-sters: Reversible iatrogenic Balint syndrome

Abstract

The syndrome of ocular apraxia, simultagnosia, and optic ataxia originally described by Balint in 1909 is classically associated with bilateral parieto-occipital lesions, but can occur with other combinations of bihemispheric lesions.1,2 This syndrome reflects multiple etiologies, most commonly vascular disease, but rarely improves rapidly. 3 We describe a patient with cerebral ischemia who developed Balint syndrome transiently in the setting of acute hypotension after nitroglycerin use; his presentation exemplifies the importance of blood pressure autoregulation in cerebral ischemia, and elucidates alternative etiologies of clinical-radiologic mismatch.CASE REPORT A 60-year-old ambidextrous man with uncontrolled hypertension, hyperlipidemia, coronary artery disease, prior myocardial infarction, and a TIA developed difficulty remembering placement of items on a shelf. This was followed by difficulties with word-finding and comprehension, severe headache, and nausea. Upon initial evaluation at another hospital, he had persistent problems finding words and answering questions, and a blood pressure (BP) of 215/80 mm Hg but without other apparent neurologic deficits; cranial noncontrast computerized tomography (CT) was unremarkable. He was transferred to our institution, where his BP was 210/85 mm Hg and he showed hesitation and circumlocution of speech with semantic and phonemic paraphasic errors, as well as difficulties with naming, concentration, recall, calculation, and executing complex commands; he had slight trouble performing rapid alternating and fine motor movements with his left hand, and decreased sensation to all modalities in his left arm. Otherwise, he had no deficits in alertness, orientation, word repetition, cranial nerve testing, strength, reflexes, sensation, or gait. Brain MRI with gadolinium, including MR arteriography, demonstrated a diffusion-weighted image (DWI) bright (figure, A) and apparent diffusion coefficient (ADC) dark lesion in his left posterior temporal area, evidence of plaque in the distal right common carotid artery, moderate narrowing of the proximal internal carotid artery, and a severe stenosis at the origin of the right vertebral artery (figure, B). He was treated with aspirin; blood pressure was controlled with labetalol. Six hours later, his systolic BP increased from 140 to 170 mm Hg over the course of a few minutes, and he had severe substernal crushing pain radiating to his left arm, for which he received a dose of nitroglycerin 0.4 mg sublingually. The BP acutely decreased to 90/62 mm Hg. Reexamination at this time revealed simultagnosia, optic ataxia, optic apraxia, flattening of the right nasolabial fold, and extinction to double simultaneous stimuli on his right side. Repeat brain MR imaging revealed a stable left posterior temporal infarct, and new small areas of restricted diffusion in both occipital lobes and left thalamus; there was a subtle increase in mean transit time suggesting perfusion-diffusion mismatch (figure, C). Concerns for possible basilar thrombosi...

Optic Ataxia: From Balint’s Syndrome to the Parietal Reach Region

“…Infectious processes have been reported to cause optic ataxia in Balint’s syndrome including cerebral toxoplasmosis and progressive multifocal leukoencephalopathy secondary to the JC Virus in immunocompromised patients with HIV (Ayuso-Peralta et al, 1994; Garcia Guijo et al, 1990), and in herpes encephalitis in an infant (Amin et al, 2012). Iatrogenic causes reported include administration of nitroglycerin leading to hypotension and watershed infarcts and secondary to angiography contrast prior to CT (Mejia et al, 2008; Rafal, 2001; Merchut and Richie, 2002). Finally, Balint’s syndrome has been reported in a case of status epilepticus due to an uncontrolled seizure disorder (Ristic et al, 2012).…”

Ocular Dysfunctions Presenting in Tacrolimus‐Induced Posterior Reversible Encephalopathy Syndrome: A Case Presentation

“…Rudolph Balint first described simultanagosia, optic ataxia, and ocular apraxia in 1907 [1,5,6]; the combination of these deficits is known as Balint syndrome. The most common causes of Balint syndrome are arterial occlusive disease and acute hypertension resulting in bilateral parieto‐occipital ischemia [7,8].…”

A Rare Syndrome: Balint Syndrome

“…Arteriel okluzif hastalık [20,21] veya akut hipotansiyon [22] Balint sendromunun en sık nedenidir. Alzheimer hastalığı, kortikobazal dejenerasyon, posterior kortikal atrofi, Creutzfeldt_Jakob hastalığı, Progresif multifokal lökoensefalopati, kafa travması, subakut HIV ensefaliti, serebral tokoplazmozis ve serebral metastazlar gibi durumları içeren multiple etyolojiler tanımlanmıştır [15,23].…”