University of Groningen The Posterior Fossa and Foreign Accent Syndrome Keulen, Stefanie; Mariën, Peter; van Dun, Kim; Bastiaanse, Roelien; Manto, Mario; Verhoeven, Jo Published in: Cerebellum DOI: 10.1007/s12311-017-0849-6 IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2017 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Keulen, S., Mariën, P., van Dun, K., Bastiaanse, R., Manto, M., & Verhoeven, J. (2017). The Posterior Fossa and Foreign Accent Syndrome: Report of Two New Cases and Review of the Literature. 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For technical reasons the number of authors shown on this cover page is limited to 10 maximum. Download date: 13-04-2024 Cerebellum (2017) 16:772–785 DOI 10.1007/s12311-017-0849-6 ORIGINAL PAPER The Posterior Fossa and Foreign Accent Syndrome: Report of Two New Cases and Review of the Literature Stefanie Keulen 1,2 & Peter Mariën 1,3 & Kim van Dun 1 & Roelien Bastiaanse 2 & Mario Manto 4 & Jo Verhoeven 5,6 Published online: 23 March 2017 # Springer Science+Business Media New York 2017 Abstract Foreign accent syndrome is a rare motor speech disorder that causes patients to speak their language with a non-native accent. In the neurogenic condition, the disorder develops after lesions in the language dominant hemisphere, often affecting Broca’s area, the insula, the supplementary motor area and the primary motor cortex. Here, we present two new cases of FAS after posterior fossa lesions. The first case is a 44-year-old, right-handed, Dutch-speaking man who suffered motor speech disturbances and a left hemiplegia after a pontine infarction. Quantified SPECT showed a bilateral hypoperfusion in the inferior lateral prefrontal and medial inferior frontal regions as well as a significant left cerebellar hypoperfusion. Further clinical investigations led to an additional diagnosis of brainstem cognitive affective syndrome which closely relates to Schmahmann’s syndrome. The second patient was a 72-year-old right-handed polyglot English man who suffered a stroke in the vascular territory of the left posterior inferior cerebellar artery * Peter Mariën peter.marien5@telenet.be 1 Clinical and Experimental Neurolinguistics, CLIN, Vrije Universiteit Brussel, Brussels, Belgium 2 Center for Language and Cognition Groningen (CLCG), Rijksuniversiteit Groningen, Groningen, The Netherlands 3 Department of Neurology and Memory Clinic, ZNA Middelheim Hospital, Lindendreef 1, B-2020 Antwerp, Belgium 4 Unité d’Étude du Mouvement (UEM), FNRS, ULB Erasme, Brussels, Belgium 5 Department of Language and Communication Science, City University, London, UK 6 Computational Linguistics and Psycholinguistics Research Center (CLIPS), Universiteit Antwerpen, Antwerp, Belgium (PICA) and developed a foreign accent in his mother tongue (English) and in a later learnt language (Dutch). In this paper, we discuss how the occurrence of this peculiar motor speech disorder can be related to a lesion affecting the posterior fossa structures. Keywords Foreign accent syndrome . Posterior fossa . Cerebellum . SPECT Introduction Foreign Accent Syndrome During the last century, more than 170 reports of patients with foreign accent syndrome (FAS) have been published but the disorder is probably much more frequent than currently estimated. Due to speech changes at the segmental (speech segments, e.g., phonemes) and suprasegmental level (contrastive aspects marking speech that are not identified as segments, but rather define the segments, e.g., rhythm, intonation), this rare condition causes the patient with FAS to be perceived by speakers of the same language community as a non-native speaker. FAS has been related to various etiologies including stroke, cerebral trauma, multiple sclerosis, dementia, and psychiatric disorders. In 2010, Verhoeven and Mariën [1] distinguished three different sub-types of FAS: neurogenic FAS [2], including developmental cases [3], but also psychogenic FAS [4] and a mixed-type FAS [5]. Here, we focus on the neurogenic type, which has been the most widely reported variant of FAS. Although most of the patients with this subtype acquired FAS after stroke [e.g., 2; 6, case 2; 7, 8, 9, case 2 ] or brain trauma [e.g., 10; 11, case 2; 12, cases 4 & 5], the lesion sites do not unequivocally point towards a single neuroanatomical substrate. In the majority of the Cerebellum (2017) 16:772–785 vascular cases, the causative lesions were located in the language dominant (left) hemisphere, especially in the frontal [e.g., 13, case 3; 14; 15], fronto-temporal [e.g., 16–18], and frontotemporo-parietal regions [10, 19, 20]. Although handedness was not formally investigated, Bcrossed FAS^ has been reported in three dextral patients after right-hemisphere damage [21, case 3; 13, case 2; 22, 23]. As evidenced by SPECT, the cerebellum was functionally affected (hypoperfusion) in three cases after frontal lesions (mechanism of diaschisis) [2, 9, case 2, 24]. In five other cases, FAS was directly attributed to posterior fossa lesions [6, cases 1 and 2; 23, 25–27]. In this study, we present a survey of the literature and two new cases of FAS after a posterior fossa lesion: the first patient suffered a stroke in the right pons and has been described as an example of brainstem cognitive affective syndrome by Mariën and D’aes [28]. The second patient incurred FAS after a stroke in the left posterior cerebellum. Posterior Fossa and FAS: Two New Cases Case 1 A 44-year-old, right-handed, Dutch-speaking Belgian man with an educational level of 11 years was admitted to the hospital on April 20th, 2012 after an acute loss of consciousness followed by motor speech disturbances and a left hemiplegia. The patient had used Bpoppers;^ alkyl nitrites which, when aspirated, arouse euphoric feelings and relax sphincter muscles to enhance sexual experience. CT and electrocardiography on admission were normal. Five days later, the patient was transferred to the Neurology department of ZNA Middelheim Hospital. Neurological examinations on admission revealed FAS and paralytic dysarthria, a left facial nerve paralysis, tongue protrusion to the left, a left hemiplegia, and a left hypertonia. The patient tested positive for (neurovascular) syphilis (blood and CSF analysis) and was subsequently treated with penicillin for 2 weeks. On admission, the medical staff had the impression that the patient spoke with a Hollandic-like accent. Speech was generally very slow and had a pronounced nasal quality. After he was released from hospital, the patient’s friends also noticed the change in accent. Vowel pronunciation was affected by omissions (especially of schwa) and backing. In addition, diphthongs were often articulated as monophthongs. Consonants were regularly devoiced (esp. fricatives), or omitted (esp. plosives – alveolar and velar). T1-weighted MR imaging of the brain had demonstrated a hypointense lesion at the level of the right pons. T2-weighted axial FLAIR-imaging showed a hyperintense signal in the right pons (Fig. 1). Quantified 99mTc ECD SPECT scan in May 2012 showed a bilateral hypoperfusion in the inferior lateral prefrontal (L: −2.2 SD, R: −2.7 SD) and left medial inferior frontal regions 773 Fig. 1 T2-weighted axial MRI slice of the brain demonstrating an ischemic lesion in the right pons (white arrows) (−2.8 SD). A significant left cerebellar hypoperfusion was also retained (−2.1 SD) (Fig. 2). The EEG recording was mildly impaired over both the left and right hemisphere: polyrhythmic activity on the left showed a fast component whereas on the right a slowing of activities was found. Soon after admission, the patient had a grand mal seizure and treatment with valproic acid was started. A transesophageal echocardiogram disclosed mitral insufficiency and a patent foramen ovale with a clear right to left shunt. Extensive neuropsychological testing was performed in May 2012 (see Table 1). Intelligence, executive and visuospatial functions, memory and frontal behavioural and affective disturbances were investigated. Test results disclosed general cognitive abilities were normal (MMSE: 27/30; −0.5 SD) [29], but the patient had clinically deficient full scale IQ (FSIQ = 73; −1.8 SD) and pathological performance IQ (PIQ = 61, −2.6 SD, with depressed scores for digit symbol substitution (−3 SD), block design (−1.3 SD), matrix reasoning (−1.7 SD), picture completion, (−1.7 SD) and picture arrangement: (−2.7 SD), whereas subtest scores of the verbal IQ were within the normal range (VIQ = 83; −1.1 SD) (Wechsler Adult Intelligence Scale-3rd Edition; [30]). The patient obtained pathological scores on the attention subtests (index 66, −2.3 SD) and delayed recall subtests (index 61, −2.6 SD) of the Wechsler Memory Scale – revised (WMS-R) [31]. Visual memory index amounted to 70 and verbal memory to 80. Index scores on the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) were normal [32]. Scores on the Trail Making Test were depressed (TMT A: < AAT naming - total: −1.46 SD) verbal fluency: weak Infarction Etiology AAT Aachener Aphasie Test [47], Ant. anterior, BDAE Boston Diagnostic Aphasia Examination [44], BNT Boston Naming Test [43], CT computed tomography, ED emergency department, F female, inf. inferior, Judgement of Line Orientation Task [48], L left, m month(s), M male, MCA middle cerebral artery, MMSE Mini-Mental State Examination [29], MRA magnetic resonance angiography, MRI magnetic resonance imaging, NI not indicated, post. posterior, R right, R* right-handed, RCPM Raven Coloured Progressive Matrices [41], ROF Rey-Osterrieth Figure [49], SPECT single photon emission computed tomography, sup. superior, visual form discrimination task [48], WAIS-NL Wechsler Adult Intelligence Scale—Dutch version [45], w weeks(s), WCST Wisconsin Card Sorting Test [34], WMS-R Wechsler Memory Scale-Revised, y year(s) 40/F/R* monolingual Age/gender/ handedness FAS after frontal lesions with related functional involvement of posterior fossa structures (diaschisis) 1 Hwang et al. (2001) [24] Case Table 4 782 Cerebellum (2017) 16:772–785 Cerebellum (2017) 16:772–785 increased muscle tone can be an upper motor neuron sign which characterises patients with (spastic/pseudobulbar) dysarthria. This would constitute an Borganic explanation^ for FAS. However, current patients both presented with dysarthria types associated with muscle tone weakness: paralytic dysarthria and ataxic dysarthria. This explanation does not seem applicable for current patients. Particularly interesting is the neurocomputational viewpoint on FAS. Tomasino et al. [61] argued that the deficits of FAS patients are due to deficient sensory feedback (in the case of primarily subcortical damage) or feedforward (in the case of cortical and perilesional subcortical damage) control mechanisms. They explain deficits in the context of the DIVA-model (i.e., Directions into Velocity of Articulators) [62, 63]. The model describes speech production as relying on two subsystems: a feedforward control system and a feedback control system. Applied to speech development, the model can be explained as follows: the phonemes that were acquired at an early age are stored in speech sound maps in the inferior frontal gyrus and are directly linked to articulator position maps stored in the ventral premotor cortex; together they form the feedforward control loop. Via the feedforward control, one is aware of the phonological results of set of motor programs (predictive component) which are transferred to the articulator position and velocity maps. When the initiation maps in the (bilateral) supplementary motor area (SMA) become active, these commands are released. In these commands, the position of the different articulatory variables (jaw height, tongue height, tongue shape etc.) are encoded, which are translated into movements of the vocal tract. The speech sound maps define the auditory and somatosensory target maps in the feedback control system. When speech is articulated, the somatosensory and auditory-perceptual awareness, mediated by subcortical nuclei, activates the feedback control loop, which allows for an update of the feedforward loop and the correction of the articulatory encoding to achieve targets correctly. If the deficits in FAS are explicable, even partly, in the context of the DIVA model, then a role for the cerebellum— affected in both patients—is not inconceivable. The cerebellum plays an important role in Bthe learning and maintenance of feedforward motor commands^ [63, p. 11]. Since it stands in close connection to the motor areas on the one hand, and on the other hand receives input from the somatosensory cortex and auditory areas [64], it is attributed a cardinal role in feedforward motor control via supposed feedback motor learning in response to a miscalibration of intended movement or execution of targets [64]. These feedforward projections are hypothesised to also include the basal ganglia (axons in the dentate nucleus in the cerebellum project to the contralateral (motor) cortex via the thalamus). This is reconcilable with the theories of Reeves and Norton [65], Blumstein and Kurowski [66], Schiff et al. [67] who claim that FAS is due to a disruption of the corticostriatopallidal-thalamic pathways. Thus, the rhythmic disturbance can be consistent with a defect in the predictions 783 (feedforward control) exerted by the cerebellar circuitry. This could then also serve as an explanation for the semiological resemblances between FAS and AoS, and by inference FAS, AoS, and ataxic dysarthria. The hypothesis of errors in predictions leading to compensatory substitution mechanisms by the unaffected cerebral areas (including the cerebellum itself) could be put forward. From a cognitive perspective, FAS has been viewed as the result of an impairment in distinguishing between a direct and indirect speech encoding route [68]. The results of the SPECT scan for the first patient demonstrated disturbed physiological communication between the cerebellum and frontal regions, which are responsible for speech planning and programming. For the second patient, the left cerebellar hemisphere was damaged. Here, a maladaptive compensation under the form of an aberrant recovery process [69] or an overcompensation mechanism, as reported when the inhibitory signals from the cerebellum are affected, could also be considered [70]. A maladaptive compensation from the part of the contralateral cerebellar hemisphere, exerting distance effects on the frontal cerebral areas (including for instance) the motor cortex, might be hypothesised. The precise roles of (a) the olivo-cerebellar pathway, a second major inflow tract to the cerebellum with a major role in pace-making activity, and (b) the projections from the cerebellar cortex to cerebellar nuclei remain undetermined. However, these explanations are reminiscent of the case described by Cohen et al. [25] who described a 58-year-old woman who developed FAS after an MCA stroke affecting the left frontoparietal lobe. The authors dwell on how the sudden remission after a second cerebellar stroke in the right inferior posterior lobe can be explained. Cerebellar-parietal connections have been argued to underpin phonological storage, although its exact role remains unclear [71, 72]. In conclusion, it seems that a disruption of the cerebrocerebellar circuitry following a right pontine lesion and left cerebellar lesion in the posterior lobe, exerting remote functional effects in the cortical areas subserving planning and organisation, may play a foremost important role in the pathophysiology of FAS following posterior fossa lesions. Several hypotheses have been formulated as to how this damage may be related to the onset of FAS. These explanations were not mutually exclusive. It was argued that FAS can be the consequence of disturbed feedforward and/or feedback speech control mechanisms. The cerebellum has been hypothesised to play an important role in feedforward speech control via projections to the frontal cortex. This is relatable to earlier theories claiming that FAS is the result of a disruption affecting the cortico-striatopallidal-thalamic pathways [66–68]. These theories might explain FAS in the first case: as demonstrated by SPECT, damage to the crossed ponto-cerebellar pathway (inflow tract to the cerebellum) induced (pre)frontal dysfunction. On the other hand, the possibility of maladaptive compensation from the part of, possibly, the contralateral cerebellum could be related to the FAS characteristics in case 2. 784 Cerebellum (2017) 16:772–785 However, this patient was a polyglot. Hence, the impact of the left cerebellar hemisphere lesion on the speech and language in this patient should also be considered in the context of a more bilaterally distributed language network in polyglots. In future studies on FAS, DTI and/or fMRI experiments may be a relevant addition with a view to investigate (possibly disrupted) (bi-hemispheric) network activity, as well as fiber tracts. 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