Pearls &amp; Oy-sters: Isolated prosopagnosia as the presenting complaint in glioblastoma

Das, Saurav; Burton, Eric

doi:10.1212/wnl.0000000000008204

Cited by 3 publications

(4 citation statements)

References 7 publications

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“…Prosopagnosia is typically accompanied by additional neurological symptoms and is rarely caused by an isolated structural lesion [ 14 ]. A variety of medical conditions, including posterior cerebral artery strokes, hematomas, tumors, traumatic brain injuries, neurodegenerative disorders, and others, that occur primarily in the occipitotemporal cortex are known to be referred to as AP [ 2 ].…”

Section: Discussionmentioning

confidence: 99%

Prosopagnosia Due to Metastatic Brain Tumor: A Case-Based Review

Ivanova,

Kyuchukova,

Tsalta-Mladenov

et al. 2024

Cureus

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Prosopagnosia, also referred to as “face blindness,” is a type of visual agnosia characterized by a decreased capacity to recognize familiar faces with a preserved ability to identify individuals based on non-facial visual traits or voice. Prosopagnosia can be categorized as developmental (DP) or acquired (AP) owing to a variety of underlying conditions, including trauma, neurodegenerative diseases, stroke, neuroinfections, and, less frequently, malignancies. Facial recognition is a complex process in which different neuronal networks are involved. The infrequent but notable higher visual-processing abnormalities can be caused by lesions of the inferior longitudinal fasciculus (ILF) in the non-dominant temporal lobe. We report a rare case of AP in a 69-year-old patient who is right-hand dominant with rectal carcinoma cerebral metastases. The patient complained of dizziness, vertigo, falls, and trouble recognizing her family members’ faces. The CT scan of the head with contrast revealed two metastatic brain lesions with vasogenic edema, as one of them was in the right cerebellar hemisphere, causing dislocation and compression of the ILF. Corticosteroids and osmotherapy were utilized as a conservative treatment approach, which resulted in the prosopagnosia being completely withdrawn. In conclusion, patients with primary brain tumors or metastatic disease rarely present with an isolated cognitive deficit such as prosopagnosia. Based on the anatomical features and the personalized approach, a conservative or surgical approach may be useful to improve higher cortical functioning.

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Section: Discussionmentioning

confidence: 99%

Prosopagnosia Due to Metastatic Brain Tumor: A Case-Based Review

Ivanova,

Kyuchukova,

Tsalta-Mladenov

et al. 2024

Cureus

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“…Prosopagnosia as a presentation of a seizure disorder or as a post-ictal phenomenon has been reported. 70-72 Similar to infarcts, 23-27 published case reports have linked brain tumours with prosopagnosia 73 as well as prosopagnosia arising after resection of a primary brain tumour 74 , 75 or resection for seizure treatment. One of our patients developed prosopagnosia after gamma knife surgery for resection of an arteriovenous malformation in the right basal ganglia suggesting that surgical procedures targeting lesions in the right temporal–occipital area can cause collateral damage resulting in prosopagnosia.…”

Section: Discussionmentioning

confidence: 99%

Prosopagnosia: face blindness and its association with neurological disorders

Josephs,

Josephs

2023

Brain Communications

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Loss of facial recognition or prosopagnosia has been well-recognized for over a century. It has been categorized as developmental or acquired depending on whether the onset is in early childhood or beyond, and acquired cases can have degenerative or non-degenerative etiologies. Prosopagnosia has been linked to involvement of the fusiform gyri, mainly in the right hemisphere. The literature on prosopagnosia comprises case reports and small case series. We aim to assess demographic, clinical, and imaging characteristics, and neurological and neuropathological disorders associated with a diagnosis of prosopagnosia in a large cohort. Patients were categorized as developmental versus acquired; those with acquired prosopagnosia were further subdivided into degenerative versus non-degenerative, based on neurological etiology. We assessed regional involvement on 18F-fluorodeoxyglucose PET and MRI of the right and left frontal, temporal, parietal, and occipital lobes. The Intake and Referral Center at the Mayo Clinic identified 487 patients with possible prosopagnosia, of which 336 met study criteria for probable or definite prosopagnosia. Ten patients, 80.0% male, had developmental prosopagnosia including one with Niemann-Pick type C, and another with a Forkhead-box G1 gene mutation. Of the 326 with acquired prosopagnosia, 235 (72.1%) were categorised as degenerative, 91 (27.9%) as non-degenerative. The most common degenerative diagnoses were posterior cortical atrophy, primary prosopagnosia syndrome, Alzheimer’s disease dementia, and semantic dementia, with each diagnosis accounting for >10% of this group. The most common non-degenerative diagnoses were infarcts (ischemic and hemorrhagic), epilepsy-related, and primary brain tumours, each accounting for >10%. We identified a group of patients with non-degenerative transient prosopagnosia in which facial-recognition loss improved or resolved over time. These patients had migraine-related prosopagnosia, posterior reversible encephalopathy syndrome, delirium, hypoxic encephalopathy, and ischemic infarcts. On 18F-fluorodeoxyglucose PET, the temporal lobes proved to be the most frequently affected regions in 117 patients with degenerative prosopagnosia, while in 82 patients with non-degenerative prosopagnosia MRI revealed the right temporal and right occipital lobes as most affected by a focal lesion. The most common pathological findings in those with degenerative prosopagnosia were frontotemporal lobar degeneration with hippocampal sclerosis, and mixed Alzheimer’s and Lewy body disease pathology. In this large case series of patients diagnosed with prosopagnosia, we observed that facial-recognition loss occurs across a wide range of acquired degenerative and non-degenerative neurological disorders, most commonly in males with developmental prosopagnosia. The right temporal and occipital lobes, and connecting fusiform gyrus, are key areas. Multiple different pathologies cause degenerative prosopagnosia.

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“…[3] Cerebrovascular disease, epilepsy, trauma, brain tumor, encephalitis, and carbon monoxide poisoning have been reported as the causes of acquired prosopagnosia. [1,2,[4][5][6][7]9,11] With regard to brain tumors, lesions in the right lingual and fusiform gyrus are generally considered to be responsible for prosopagnosia. [8] For lung adenocarcinoma with epidermal growth factor receptor (EGFR) mutation, tyrosine kinase inhibitors (TKIs) have become the first-line drugs of choice.…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Treatment of transient prosopagnosia with a tyrosine kinase inhibitor in a case of brain metastasis from EGFR-mutated lung adenocarcinoma

Soyama

Matsuda

Hontsu

et al. 2022

Surgical Neurology International

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Background: Prosopagnosia is a rare form of apraxia, in which a person has normal memory and vision, but has impaired cognition of human faces that are manifested through symptoms such as not being able to recognize the face of a familiar person, one has known or not being able to remember the face of a person. Here, we report the case of a patient with transient prosopagnosia associated with brain metastasis from epidermal growth factor receptor (EGFR)-mutated lung adenocarcinoma who was treated with tyrosine kinase inhibitors (TKIs). Case Description: A 52-year-old right-handed man with lung adenocarcinoma was introduced to our department because brain metastasis. On admission, he complained that he could not recognize his wife’s face, but he could recall her face based on her voice. MRI revealed a right temporo-occipital enhancing lesion with perifocal edema and dissemination that were indicative of brain metastasis from lung adenocarcinoma. Two weeks after open biopsy, he was started on TKI therapy with osimertinib at a dosage of 80 mg/day. An MRI scan taken 1 month later revealed shrinkage of the metastasis. In addition, he had recovered from transient prosopagnosia and returned to normal life. Conclusion: In this study, the TKI osimertinib was administered to a patient with brain metastasis of EGFR-mutated lung adenocarcinoma who presented with prosopagnosia, and the patient’s lesion shrunk and his symptoms were reversed with this treatment.

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Pearls & Oy-sters: Isolated prosopagnosia as the presenting complaint in glioblastoma

Cited by 3 publications

References 7 publications

Prosopagnosia Due to Metastatic Brain Tumor: A Case-Based Review

Prosopagnosia Due to Metastatic Brain Tumor: A Case-Based Review

Prosopagnosia: face blindness and its association with neurological disorders

Treatment of transient prosopagnosia with a tyrosine kinase inhibitor in a case of brain metastasis from EGFR-mutated lung adenocarcinoma

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