Pearls and Oy-sters: Reversible iatrogenic Balint syndrome
Nicte I. Mejia, MD,
Soojin Park, MD,
MingMing Ning, MD and
Ferdinando S. Buonanno, MD
From the Department of Neurology, Massachusetts General Hospital, Boston.
Address correspondence and reprint requests to Dr. Ferdinando S. Buonanno, Massachusetts General Hospital, Boston, MA 02114 fbuonanno{at}partners.org
The syndrome of ocular apraxia, simultagnosia, and optic ataxiaoriginally described by Balint in 1909 is classically associatedwith bilateral parieto-occipital lesions, but can occur withother combinations of bihemispheric lesions.1,2 This syndromereflects multiple etiologies, most commonly vascular disease,but rarely improves rapidly.3 We describe a patient with cerebralischemia who developed Balint syndrome transiently in the settingof acute hypotension after nitroglycerin use; his presentationexemplifies the importance of blood pressure autoregulationin cerebral ischemia, and elucidates alternative etiologiesof clinical-radiologic mismatch.
A 60-year-old ambidextrous man with uncontrolled hypertension,hyperlipidemia, coronary artery disease, prior myocardial infarction,and a TIA developed difficulty remembering placement of itemson a shelf. This was followed by difficulties with word-findingand comprehension, severe headache, and nausea. Upon initialevaluation at another hospital, he had persistent problems findingwords and answering questions, and a blood pressure (BP) of215/80 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 210/85mm Hg and he showed hesitation and circumlocution of speechwith semantic and phonemic paraphasic errors, as well as difficultieswith naming, concentration, recall, calculation, and executingcomplex commands; he had slight trouble performing rapid alternatingand fine motor movements with his left hand, and decreased sensationto all modalities in his left arm. Otherwise, he had no deficitsin alertness, orientation, word repetition, cranial nerve testing,strength, reflexes, sensation, or gait. Brain MRI with gadolinium,including MR arteriography, demonstrated a diffusion-weightedimage (DWI) bright (figure, A) and apparent diffusion coefficient(ADC) dark lesion in his left posterior temporal area, evidenceof plaque in the distal right common carotid artery, moderatenarrowing of the proximal internal carotid artery, and a severestenosis at the origin of the right vertebral artery (figure, B).He was treated with aspirin; blood pressure was controlled withlabetalol. Six hours later, his systolic BP increased from 140to 170 mm Hg over the course of a few minutes, and he had severesubsternal crushing pain radiating to his left arm, for whichhe received a dose of nitroglycerin 0.4 mg sublingually. TheBP acutely decreased to 90/62 mm Hg. Re-examination at thistime revealed simultagnosia, optic ataxia, optic apraxia, flatteningof the right nasolabial fold, and extinction to double simultaneousstimuli on his right side. Repeat brain MR imaging revealeda stable left posterior temporal infarct, and new small areasof restricted diffusion in both occipital lobes and left thalamus;there was a subtle increase in mean transit time suggestingperfusion-diffusion mismatch (figure, C). Concerns for possiblebasilar thrombosis led to CT angiography, which revealed posteriorcerebral artery stenosis (figure, D). The patient’s systolicBP returned to approximately 150 mm Hg over 2 hours, and visualsymptoms resolved. He received IV heparin, and days later successfullyunderwent left vertebral angioplasty and stenting.
Transient neurologic deficits can occur in patients with cerebralischemia and hypertension as BP is acutely decreased. For example,the literature includes a report of a patient with pre-eclampticposterior reversible encephalopathy syndrome who developed amaurosisafter nitroglycerin-induced BP decrease.4 There is also a descriptionof a patient who underwent renal angioplasty and presented withreversible Balint syndrome with evidence of contrast penetrationin both parieto-occipital cortices, suggesting that disruptionof the blood–brain barrier may lead to transient neurologicsyndromes.5 Our patient developed a reversible Balint syndromeafter acute hypotension following nitroglycerin administration.Although the inability to perceive several items of a visualscene at a time (simultagnosia), shift gaze voluntarily to objectsof interest despite unrestricted eye movements (ocular apraxia),and reach objects under visual guidance despite normal limbstrength (optic ataxia) is usually said to occur as a manifestationof biparietal syndromes, it may be seen in other combinationsof lesions, such as involvement of the left lateral geniculatebody or optic radiation and the right parietal lobe, or evenwith bifrontal or pulvinar damage.1,6
Nitroglycerin, a vasodilator, decreases mean arterial pressure(MAP), and may alter global cerebral blood flow (CBF), reducingcerebral perfusion pressure (CPP).7 In the setting of chronicallyunderperfused parenchyma—as in this patient with preexistingvertebral artery stenosis—dysfunctional cerebrovascularautoregulation would explain why focal CBF could not be adequatelymaintained during the iatrogenic drop in MAP. The co-occurrenceof cardiac and cerebral atherosclerosis has been well-documented.8,9Our patient was treated successfully with vertebral artery stenting.Although there are currently no data that vertebral artery stentingprovides better long-term outcomes than medical therapy (anticoagulationor antiplatelet agents), it is a technically feasible procedurethat offers an alternative to more technically challenging vertebralartery endarterectomies.10,11 This case highlights the possibilityof coexistent intracranial stenoses and cerebral dysautoregulationin patients with coronary disease and the need for caution whenadministering nitroglycerin to such patients.
Hecaen H, de Ajuriaguerra J. Balint’s syndrome (psychic paralysis of visual fixation) and its minor forms. Brain 1954;77:373–400.[Free Full Text]
Rizzo M, Vecera SP. Psychoanatomical substrates of Balint’s syndrome. J Neurol Neurosurg Psychiatry 2002;72:162–178.[Abstract/Free Full Text]
Moreaud O. Balint syndrome. Arch Neurol 2003;60:1329–1331.[Free Full Text]
Finisterer J, Schlager T, Kopsa W, Wild E. Nitroglycerin-aggravated pre-eclamptic posterior reversible encephalopathy syndrome (PRES). Neurology 2003;61:715–716.[Free Full Text]
Merchut MP, Richie B. Transient visuospatial disorder from angiographic contrast. Arch Neurol 2002;59:851–854.[Abstract/Free Full Text]
Valenza N, Murray MM, Ptak R, Vuilleumier P. The space of senses: impaired crossmodal interactions in a patient with Balint syndrome after bilateral parietal damage. Neuropsychologia 2004;42:1737–1748.[Medline]
Weyland A, Grune F, Buhre W, Kazmaier S, Stephan H, Sonntag H. [The effect of nitroglycerin on cerebrovascular circulation, cerebrovascular CO2-reactiity and blood flow rate in basal cerebral arteries]. Anaesthesist 1996;45:1037–1044.[Medline]
Uehara T, Tabuchi M, Mori E. Risk factors for occlusive lesions of intracranial arteries in stroke-free Japanese. Eur J Neurol 2005;12:218–222.[Medline]
Gongora-Rivera F, Labreuche J, Jaramillo A, Steg PG, Hauw JJ, Amarenco P. Autopsy prevalence of coronary atherosclerosis in patients with fatal stroke. Stroke Epub 2007 Mar 1.
Coward LJ, McCabe DJH, Ederle J, Featherstone RL, Clifton A, Brown MM. Long-term outcome after angioplasty and stenting for symptomatic vertebral artery stenosis compared with medical treatment in the carotid and vertebral artery transluminal angioplasty study (CAVATAS). Stroke 2007;38:1526–1530.[Abstract/Free Full Text]
Cloud GC, Crawley F, Clifton A, McCabe DJH, Brown MM, Markus HS. J Neurol Neurosurg Psychiatry 2003;74:586–590.[Abstract/Free Full Text]
This article has been cited by other articles:
K. J. Fullerton, N. I. Mejia, S. Park, M. Ning, and F. S. Buonanno PEARLS AND OY-STERS: REVERSIBLE IATROGENIC BALINT SYNDROME
Neurology,
June 16, 2009;
72(24):
2136 - 2137.
[Full Text][PDF]
Top.
Case report
DISCUSSION
