Crossed Aphasia in a Dextral Patient With Logopenic/ Phonological Variant of Primary Progressive Aphasia Asli Demirtas-Tatlidede, MD,*w Hakan Gurvit, MD,* Oget Oktem-Tanor, PhD,* and Murat Emre, MD* Background: Crossed aphasia is a rare phenomenon, with a prevalence of 1% to 2% among all right-handed patients. Two crossed aphasic patients with a nonfluent variant of primary progressive aphasia (PPA) have been reported previously. This report aims to document for the first time the occurrence of crossed logopenic progressive aphasia in a dextral patient. Case Report: A 57-year-old monolingual housewife presented with word-finding difficulties. She was strongly right handed, had no clinical history for brain damage to the left hemisphere, and no left handers in her family history. Her language comprised simple, grammatically correct sentences with a fluctuating speech rate and intermittent word-finding pauses. Rare phonological errors were noted. Sentence repetition tasks showed impairments with gram- matically complex sentences. Comprehension was intact as were writing and reading. The language disability remained isolated for 3 years. Cranial magnetic resonance imaging depicted somewhat asymmetrical atrophy of the parietal lobes (R>L), whereas single- photon-emitted computed tomographic imaging demonstrated hypoperfusion in the right parietal cortex, indicating right hemi- sphere dominance for language. Conclusions: This case report provides evidence that crossed PPA can present with a logopenic variant in addition to the nonfluent type demonstrated by others. Functional neuroimaging showed unexpected right-sided hypoperfusion in this case with only subtle structural brain asymmetry, implicating a reverse pattern of language dominance. Key Words: primary progressive aphasia, PPA, logopenic/phono- logical progressive aphasia, LPA, logopenic variant of primary progressive aphasia, crossed aphasia, dementia, SPECT, Alzheimer disease. (Alzheimer Dis Assoc Disord 2012;26:282–284) T he term “crossed aphasia in dextrals” denotes any aphasic syndrome resulting from cerebral damage “ipsilateral” to the dominant right hand. 1 This is a rare phenomenon, with a prevalence of 1% to 2% among all right-handed patients. Although the vast majority of cases reported in the literature are caused by cerebrovascular disorders, 2 patients with a nonfluent variant of primary progressive aphasia (PPA) have been described. 2,3 Logopenic progressive aphasia (LPA) is a recently defined third variant of PPA, which clinically, anatomically and probably pathogenetically differs from the other variants, that is progressive non-fluent aphasia and semantic dementia. 4–7 LPA is clinically distinguished by impaired confrontation naming but intact single-word comprehension, spared syntax, and impaired sentence repetition. The brunt of pathology lies in the left posterior temporal and inferior parietal regions with distinctive peak atrophy in Broadmann area 37, as revealed by the neuro- imaging findings. 8 It is currently under debate whether Alzheimer disease may be the underlying pathology in most cases. 5,6 CASE REPORT Patient Description A 57-year-old monolingual housewife with eight-grade education presented with word-finding difficulties. She was strongly right handed (100% dexterity, modified Edinburgh questionnaire 9 ), had no clinical history for brain damage to the left hemisphere, and no left handers in her family history. Her mother reportedly died with an unspecified dementia at the age of 82. The first clinical examination was conducted approximately 6 months after symptom onset. Her spontaneous speech, elicited by a thorough clinical interview with open-ended questions, was remarkable for grammatically correct sentences and frequent word-finding pauses; phonemic paraphasias were noted. She was able to name the first 12 items of the 31-item Boston Naming Test 10 Turkish version and phonemic cues were needed for the rest. The Cookie Theft picture from the Boston Diagnostic Aphasia Examination 11 comprised simple, grammatically correct sentences summing up to 75 syllables (33 words) overall. The picture description task from the Promoting Aphasics’ Communicative Effectiveness, 12 which requires the construction of regular sen- tences comprising subject, object, and the predicate (eg, the man is eating an orange), showed no grammatical errors. The auditory verbal comprehension for single words, as assessed by confronta- tion naming involving objects, object parts, body parts, and colors, was found to be normal. Sentence comprehension, which was tested by (1) yes/no questions, 13 (2) performance on simple commands (1- step, 2-step, and 3-step commands including pointing instructions), and (3) performance on complex commands (Token Test with commands including a syntactic element and/or grammatical complexity), was intact. Reading comprehension examination was carried out using written instructions and pairing a written word with a corresponding picture, which revealed a normal performance. Sentence repetition showed impairments with grammatically complex sentences. Reading aloud and writing were fully preserved, as were all daily living activities and hobbies. Neurological examination was normal. Within 3 years after the first clinical examination, the patient’s anomia showed progression. She needed phonemic cues starting from the first item of the Boston Naming Test and phonological errors were much more frequent. The Boston Diagnostic Aphasia Examination performance was slightly lower, Received for publication January 4, 2011; accepted July 23, 2011. From the *Department of Neurology, Behavioral Neurology and Movement Disorders Unit, Istanbul Faculty of Medicine, Istanbul University; and wDepartment of Neurology, Bakirkoy Sadi Konuk Research and Training Hospital, Istanbul, Turkey. The authors declare no conflicts of interest. Reprints: Asli Demirtas-Tatlidede, MD, Department of Neurology, Behavioral Neurology and Movement Disorders Unit, Istanbul University, Istanbul, Turkey (e-mail: aslidemirtas@yahoo.com). Copyright r 2012 by Lippincott Williams & Wilkins BRIEF REPORT 282 | www.alzheimerjournal.com Alzheimer Dis Assoc Disord  Volume 26, Number 3, July–September 2012