Bilingual Aphasia in a Trilingual Patient With Juxtaposed Homonymous Hemianopia

Clinical Correspondence Section Editors: Robert Avery, DO Karl C. Golnik, MD Caroline Froment, MD, PhD An-Guor Wang, MD Bilingual Aphasia in a Trilingual Patient With Juxtaposed Homonymous Hemianopia John Placide, MD, MPH, Peter W. Mortensen, MD, Subahari Raviskanthan, MBBS, Virginia A. Lee, Andrew G. Lee, MD B ilingual aphasia is characterized by the inability to understand or express speech due to brain damage in an individual who speaks 2 or more languages (1,2). The degree of language impairment varies considerably and is dependent on the location and extent of the brain injury. In addition, language deficits may be limited to only some of the languages spoken by the individual (2). Depending on the location of the cerebral insult, individuals with bilingual aphasia often present with other neurologic impairments such as visual field deficits. Hence, ophthalmologists should be aware of the clinical manifestations of bilingual aphasia because ophthalmic manifestations can accompany aphasia, and prompt neurorehabilitation can aid in the recovery of the patient. To the best of our knowledge, based on our review of the English language ophthalmic literature, this case of bilingual aphasia in a trilingual patient with juxtaposed homonymous hemianopsia is unique. A 58-year-old woman with multiple vasculopathic risk factors (type 2 diabetes, hypertension, and hyperlipidemia) and multiple prior ischemic infarcts presented with bilateral visual deficits and language impairment after infarction of the left middle cerebral artery (MCA) region. This patient had an extensive history of prior ischemic infarcts involving the left basal ganglia, right posterior cerebral artery (PCA), and the brainstem. She was managed with left carotid endarterectomy, aspirin, and physical therapy. This patient was raised in India and had previously learned to speak Gujarati (L1) as her primary language. In elementary and middle school, she later learned to speak a second language, English (L2), for which she was fluent. She then learned a third McGovern Medical School at The University of Texas Health Science Center (JP), Houston, Texas; Department of Ophthalmology (PWM, SR, AGL), Blanton Eye Institute, Houston Methodist Hospital, Houston, Texas; Summer Research Intern Program (VAL), Houston Methodist Hospital Academic Institute, Houston, Texas; Departments of Ophthalmology, Neurology, and Neurosurgery (AGL), Weill Cornell Medicine, New York, New York; Department of Ophthalmology (AGL), University of Texas Medical Branch, Galveston, Texas; University of Texas MD Anderson Cancer Center (AGL), Houston, Texas; Texas A and M College of Medicine (AGL), Bryan, Texas; and Department of Ophthalmology (AGL), The University of Iowa Hospitals and Clinics, Iowa City, Iowa. The authors report no conflicts of interest. Address correspondence to Andrew G. Lee, MD, Department of Ophthalmology, Blanton Eye Institute, Houston Methodist Hospital, 6560 Fannin Street, Suite 450, Houston, TX 77030; E-mail: aglee@ houstonmethodist.org Placide et al: J Neuro-Ophthalmol 2024; 44: e167-e169 language, Hindi (L3) in early adulthood although she was less proficient in Hindi than either English or Gujarati. After her left MCA infarction, the patient lost her ability to speak 2 of her 3 languages (Gujarati and English) but retained comprehension of these languages. She could still speak and comprehend her third language, Hindi. On neuro-ophthalmic examination, the visual acuity was count fingers in both eyes (OU). The pupils were isochoric without a relative afferent pupillary defect. Slit-lamp examination showed mild nuclear sclerotic cataracts in both eyes. Fundus examination was unremarkable in both eyes. Automated perimetry (Automated visual field stimulus V) showed bilateral juxtaposed homonymous hemianopsias, and optical coherence tomography of the retinal nerve fiber layer showed diffuse atrophy in both eyes (Fig. 1). MRI of the brain showed bilateral acute (left MCA stroke) and chronic (prior right PCA stroke) lesions consistent with her aphasia and juxtaposed homonymous hemianopic visual loss and cerebral blindness (Fig. 2). The patient was diagnosed with bilingual expressive aphasia with bilateral juxtaposed homonymous hemianopia and was managed with neurorehabilitation and vision therapy. Our patient presented with expressive aphasia of both English and Gujarati yet retained the ability to both speak and understand her third language, Hindi (which she learned later in life than English and Gujarati). She was also found to have bilateral juxtaposed homonymous hemianopsias secondary to bilateral sequential, ischemic MCA and PCA cerebral lesions. Similar to general aphasia, the leading cause of bilingual aphasia is cerebral infarction (1). Other causes of bilingual aphasia include toxic metabolites, seizures, and cerebral insults such as trauma (1). The cause of language and visual deficits in our patient is multiple cerebral infarcts, given her history of multiple prior infarctions and MRI brain showing multiple cerebral lesions. Aphasia results from a lesion in the language pathway. The Broca–Wernicke–Lichtheim–Geschwind model describes the language pathway and consists of the auditory cortex, visual cortex, Wernicke area, Broca area, motor cortex, and Geschwind territory. Insults along this pathway result in variable presentations of aphasia, including expressive and receptive aphasia. Speakers of multiple languages can develop aphasia affecting one or multiple languages (e.g., bilingual or trilingual aphasia). The global incidence of bilingual aphasia is estimated to be 45,000 cases per year, and this incidence is increasing as a e167 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Clinical Correspondence FIG. 1. Optical coherence tomography (OCT) of the retinal nerve fiber layer (left) and automated visual fields of the left and right eyes. FIG. 2. Magnetic resonance image of the brain shows hyperintense T2 lesions indicating ischemic infarction in multiple cerebral regions including the left basal ganglia, right occipital lobe, and left middle cerebral artery territory. result of globalization and an increase in the number of multilingual speakers (2). The pathophysiology of bilingual aphasia is closely linked to the cerebral representation of language. Language in multilingual individuals is represented by both specific and shared sites (3). Notably, the cerebral representations of primary and secondary languages differ in anatomical distribution (4). Although exceptions exist, the anterior motor region usually contains the largest percentage of shared sites for both primary and secondary languages while the posterior receptive region contains the largest percentage of specific sites for secondary languages (4). This indicates that lesions in the anterior expressive region are likely to cause language impairment in both primary and secondary languages while lesions in the posterior expressive region are likely to cause deficits in secondary languages. Our patient lost e168 the ability to speak both a primary language (Gujarati) and a secondary language (English). Therefore, this suggests that her language deficits are due to a lesion in the shared sites in the anterior expressive region. Although the management of bilingual aphasia is comparable with that of monolingual aphasia, the treatments are not interchangeable. Bilingual aphasia management is centered on a multidisciplinary approach that incorporates neurorehabilitation in all languages that are impaired (5). Owing to the scarcity of multilingual therapy, cross-linguistic therapies have been generated that leverage the interlinkage of language because therapy in one language can alleviate deficits in another language (5). Because patients with bilingual aphasia can present with visual impairments, vision therapy can be considered to optimize recovery. Overall, clinicians should be aware that aphasia can Placide et al: J Neuro-Ophthalmol 2024; 44: e167-e169 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Clinical Correspondence occur concomitantly with visual impairments after episodes of cerebral infarction, and prompt therapy is critical in recovery. STATEMENT OF AUTHORSHIP Conception and design: J. Placide, S. Raviskanthan, P. W. Mortensen, A. G. Lee; Acquisition of data: J. Placide, V. A. Lee, S. Raviskanthan, P. W. Mortensen, A. G. Lee; Analysis and interpretation of data: J. Placide, S. Raviskanthan, P. W. Mortensen, A. G. Lee. Drafting the manuscript: J. Placide, V. A. Lee, S. Raviskanthan, P. W. Mortensen, A. G. Lee; Revising the manuscript for intellectual content: J. Placide, V. A. Lee, S. Raviskanthan, P. W. Mortensen, A. G. Lee. Final approval of the completed manuscript: J. Placide, V. A. Lee, S. Raviskanthan, P. W. Mortensen, A. G. Lee. Placide et al: J Neuro-Ophthalmol 2024; 44: e167-e169 REFERENCES 1. Wu C, Qin Y, Lin Z, Yi X, Wei X, Ruan Y, He J. Prevalence and impact of aphasia among patients admitted with acute ischemic stroke. J Stroke Cerebrovasc Dis. 2020;29:104764. 2. Blumenfeld HK, Kaushanskaya M. Bilingual Aphasia. Encyclopedia of Clin. Neuropsychol. 2018;01:569–576. 3. Lorenzen B, Murray LL. Bilingual aphasia: a theoretical and clinical review. Am J Speech Lang Pathol. 2008;17:299–317. 4. Lucas TH, McKhann GM, Ojemann GA. 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