Buccofacial Apraxia Research Articles

Buccofacial apraxia in primary progressive aphasia.

Buccofacial apraxia (BFA) is associated with nonfluent/agrammatic variant primary progressive aphasia (nfvPPA) as well as with the severity of apraxia of speech (AOS), a core symptom of nfvPPA. However, an association with agrammatism has not been established. The aim of this study was to examine the association between BFA and agrammatism in nfvPPA and to determine differences in atrophic regions in primary progressive aphasia (PPA) with and without BFA. Seventy-four patients with PPA were recruited, including 34, 15, 10, and 15 patients with nfvPPA, semantic variant PPA, logopenic variant PPA, and unclassified PPA, respectively. All patients underwent language examination and BFA evaluations. Voxel-based morphometry (VBM) was performed to determine whether atrophy of a specific lesion correlated with the presence of BFA. BFA was observed in 20 and 3 patients with nfvPPA and unclassified PPA, respectively. In a comparison of patients with nfvPPA with and without BFA, the BFA group showed significantly worse spontaneous speech and writing in the Western Aphasia Battery. The agrammatism ratio or the ratio of agrammatic errors to the total number of particles was higher in the BFA group; however, the severity of prosodic and phonetic components of AOS did not differ between the two groups. VBM showed that the severity of BFA correlated with atrophy of the opercular and triangular areas of the inferior frontal gyrus to a part of the left middle frontal gyrus. BFA has a different anatomical basis from AOS in patients with nfvPPA and that BFA is characterized by more anterior degeneration compared to that of AOS.

Language profile in different kinds of apraxia in post-stroke patients

BackgroundStroke affects all aspects of communication of patients by causing disorders of motor control (dysarthria or apraxia) or language (dysphasia) or both. The aim of this study is to evaluate language skills in patients post-stroke presented with comorbidity with different types of apraxia.MethodsAn analytical cross-sectional study was carried out, and a number of 58 stroke adults with comorbid apraxic manifestations of various types were included after assessing them using the protocol of motor programming skills that was extracted from thesis titled “Assessment protocol of motor programming skills after cerebrovascular insults” from October 2016 to July 2018. They were subjected to the interview and personal history taking, and a modified comprehensive aphasia test to determine their language profile.ResultsPatients with verbal apraxia showed difficulty with tasks tapping verbal fluency, repetition, and picture description. The language deficits in ideational apraxia patients included cognition tasks, verbal fluency, sentence comprehension, and naming. Constructional apraxia patients showed language deficits in word comprehension, complex word repetition, and naming. Limb apraxia showed greater deficits on tasks tapping working memory and processing speed while buccofacial apraxia was accompanied by fewer language deficits in reading and repeating complex words.ConclusionHeterogeneous language profile was found in different types of apraxia.

Evaluation of the Dementia Apraxia Test in Parkinson’s Disease Patients

Introduction: Ideomotor apraxia, a disorder of skilled movements affecting limbs and/or face, can be seen in patients with Parkinson’s disease (PD), yet tests of apraxia in PD are rare. The aim of this project was to evaluate the psychometric properties and validity of the Dementia Apraxia Test (DATE) in a PD sample. Methods: 118 PD patients were included. Besides DATE performance, motor and non-motor burden, cognition, and activity of daily living (ADL) function were assessed. Patients were classified as cognitively impaired (n = 41) or non-cognitively impaired (n = 77). Results: Interrater reliability of the DATE (sub-)scores between video ratings and on-site ratings by the investigator was good (0.81 ≤ r_k ≤ 0.87). Items were mostly easy to perform, especially the buccofacial apraxia items, which had also low discriminatory power. DATE scores were associated with cognition and ADL function. DATE performance was confounded by motor impairment and patients’ age; however, when analysed for both cognitive groups separately, the correlation between DATE and motor performance was not significant. Discussion/Conclusion: The DATE seems to be an objective and predominantly valid apraxia screening tool for PD patients, with a few items needing revision. Due to the potential effect of motor impairment and age, standardized scores adjusting for these confounders are needed.

Gesture errors in left and right hemisphere damaged patients: A behavioural and anatomical study

ObjectiveErroneous gesture execution is at the core of motor cognition difficulties in apraxia. While a taxonomy of errors may provide important information about the nature of the disorder, classifications are currently often inconsistent. This study aims to identify the error categories which distinguish apraxic from non-apraxic patients. Method. Two groups of mixed (bucco-facial and limb) and bucco-facial apraxic patients suffering from stroke were compared to non-apraxic, left and right hemisphere damaged patients in tasks tapping the ability to perform limb and bucco-facial actions. The errors were analysed and classified into 6 categories relating to content, configuration or movement, spatial or temporal parameters and unrecognisable actions. Furthermore, an anatomical investigation (VLMS) was conducted in the whole group of left hemisphere damaged patients to investigate potential correlates of the various error categories. Results. Although all the above error typologies may be observed, the most indicative of mixed apraxia is the content-related one in all the typologies of actions (transitive and intransitive), and configuration errors in transitive ones. Configuration and content errors in mouth actions seem to be typical of bucco-facial apraxia. Spatial errors are similar in both apraxic and right brain damaged, non-apraxic patients. A lesion mapping analysis of left-brain damaged patients demonstrates that all but the spatial error category are associated with the fronto-parietal network. Moreover, content errors are also associated with fronto-insular lesions and movement errors with damage to the paracentral territory (precentral and postcentral gyri). Spatial errors are often associated to ventral frontal lesions. Conclusions. Bucco-facial and mixed apraxic patients make different types of errors in different types of actions. Not all errors are equally indicative of apraxia. In addition, the various error categories are associated with at least partially different neural correlates.

Neurocognitive assessment and DNA sequencing expand the phenotype and genotype spectrum of Alström syndrome.

Alström syndrome (OMIM#203800) is an ultra-rare autosomal recessive monogenic disease presenting pathogenic variants in ALMS1 (chromosome 2p13). It is characterized by early onset of blindness, hearing loss and systemic comorbidities, with delayed development without cognitive impairment. We aimed to investigate the cognitive functions and describe new pathogenic variants in Alström syndrome patients. Nineteen patients (13 adults, 6 children) underwent a thorough clinical, genetic, laboratory, instrumental, and neurocognitive assessment. Six new pathogenic variants in ALMS1 including the first described in exon 6 were identified. Four patients displayed a "mild phenotype" characterized by slow disease onset or absence of complications, including childhood obesity and association with at least one pathogenic variant in exon 5 or 6. At neurocognitive testing, a significant proportion of patients had deficits in three neurocognitive domains: similarities, phonological memory, and apraxia. In particular, 53% of patients showed difficulties in the auditory working memory test. We found ideomotor and buccofacial apraxia in 74% of patients. "Mild phenotype" patients performed better on auditory working memory and ideomotor apraxia test than "typical phenotype" ones (91.9 + 16.3% vs. 41.7 + 34.5% of correct answers, Z = 64.5, p < .01 and 92.5 + 9.6 vs. 61.7 + 26.3, Z = 61, p < .05, respectively). Deficits in auditory working memory, ideomotor, and buccofacial apraxia were found in these patients and fewer neuropsychological deficits were found in the "mild" phenotype group. Furthermore, in the "mild" phenotype group, it was found that all pathogenic variants are localized before exon 8.

Buccofacial Apraxia, Oropharyngeal Dysphagia, and Dementia Severity in Community-Dwelling Elderly Patients.

Apraxia occurs frequently in patients with dementia. Buccofacial apraxia (BFA) characteristics have been less investigated than limb or speech apraxia. An association between BFA and oropharyngeal dysphagia (OD) in old patients with dementia has not yet been explored. We aimed to assess the prevalence of BFA in patients with dementia and evaluate the relationship between BFA, OD, and dementia. We have prospectively included 117 outpatients with dementia referred to a geriatric consultation. Oropharyngeal dysphagia was diagnosed using the volume viscosity swallowing test (V-VST). Buccofacial apraxia was evaluated by miming 7 meaningless gestures. A complementary geriatric assessment of 6-domains completed the evaluation. Buccofacial apraxia was present in 54 (48.6%) patients. Proxies reported OD more frequently in the group of patients with BFA compared to the group without (P = .04). Prevalence of OD assessed with the V-VST was similar between patients with and without apraxia (P = .9). Patients with BFA had a significant lower Mini-Mental State Examination suggesting a more severe cognitive decline (18.1 ± 4.5 vs 15.8 ± 5, P = .01), a lower activities of daily living relative to disabilities (5 ± 0.8 vs 4.3 ± 1.3, P = .001), and had a lower gait speed that indicated frailty (P = .03).In conclusion, our results indicate a relationship between BFA and severity of dementia, disability, and frailty with no significant association between BFA and OD.

Recovery from apraxic deficits and its neural correlate.

Apraxia is a deficit of motor cognition leading to difficulties in actual tool use, imitation of gestures, and pantomiming object use. To date, little data exist regarding the recovery from apraxic deficits after stroke, and no statistical lesion mapping study investigated the neural correlate of recovery from apraxia. Accordingly, we here examined recovery from apraxic deficits, differential associations of apraxia task (imitation vs. pantomime) and effector (bucco-facial vs. limb apraxia) with recovery, and the underlying neural correlates. We assessed apraxia in 39 patients with left hemisphere (LH) stroke both at admission and approximately 11 days later. Furthermore, we collected clinical imaging data to identify brain regions associated with recovery from apraxic deficits using voxel-based lesion-symptom mapping (VLSM). Between the two assessments, a significant recovery from apraxic deficits was observed with a tendency of enhanced recovery of limb compared to bucco-facial apraxia. VLSM analyses revealed that within the lesion pattern initially associated with apraxia, lesions of the left insula were associated with remission of apraxic deficits, whereas lesions to the (inferior) parietal lobe (IPL; supramarginal and angular gyrus) and the superior longitudinal fasciculus (SLF) were associated with persistent apraxic deficits. Data suggest that lesions affecting the core regions (and white matter) of the fronto-parietal praxis network cause more persistent apraxic deficits than lesions affecting other regions (here: the left insula) that also contribute to motor cognition and apraxic deficits.

Reduced awareness for apraxic deficits in left hemisphere stroke.

Reduced awareness for motor or cognitive impairments has mainly been studied in relation to right-hemispheric deficits such as left-sided hemiparesis. However, recent studies suggest that also left hemisphere (LH) stroke can lead to reduced awareness for neurological/neuropsychological deficits, for example, aphasia. The aim of the current study was to characterize reduced awareness for apraxic as well as aphasic deficits in patients suffering from LH stroke. After the assessment of apraxia and aphasia, patients (n = 32) were asked to rate their performance on a 1- to 5-point rating scale. An unawareness score (UAS) was computed as the difference between the examiners' ratings and self-ratings, resulting in negative scores for patients who overestimated their performance in a given assessment, that is, exhibited reduced awareness for their stroke-related deficits. Patients with apraxia (n = 14) and aphasia (n = 16) significantly overestimated their performance in the respective assessment. However, the level of awareness was not generally related to the severity of apraxia, and there were no group differences in other variables between patients with full (n = 7) and reduced awareness (n = 7) for apraxic deficits. The reduction of awareness for apraxic deficits did not differ significantly for buccofacial versus limb gestures. Data show that LH stroke can lead to reduced awareness not only for aphasic deficits but also for buccofacial and limb apraxia. (PsycINFO Database Record

Progressive dysphasic dementia with bucco-facial apraxia: a case report.

A patient with progressive dementia, prominent non-fluent aphasia and signs of frontal lobe involvement, was evaluated by neuropsychological testing, magnetic resonance imaging (MRI) and high resolution single photon emission tomography (SPET). The presence of severe bucco-facial apraxia, associated with spared imitation of limb movements, correlated well with a marked reduction of cerebral perfusion in the left fronto-temporal cortex. This case emphasizes the usefulness of SPET as a valuable alternative to PET for the diagnosis of conditions, such as progressive neuropsychological syndromes, where a coupled reduction of metabolism and blood flow can be expected.

Dementia Apraxia Test (DATE): A Brief Tool to Differentiate Behavioral Variant Frontotemporal Dementia from Alzheimer's Dementia Based on Apraxia Profiles.

Standardized praxis assessments with modern, empirically validated screening tests have substantially improved clinical evaluation of apraxia in patients with stroke. Although apraxia may contribute to early differential diagnosis of Alzheimer's dementia (AD) and behavioral variant frontotemporal dementia (bvFTD), no comparable test is readily available to clinicians for this purpose to date. To design a clinically useful apraxia test for the differentiation of AD and bvFTD. 84 test items pertaining to twelve praxis subdomains were evaluated for their efficacy to discriminate between patients with bvFTD (n = 24), AD (n = 28), and elderly healthy controls (HC; n = 35). Items were then selected based on discriminative value and psychometric properties. Items indicative of mild AD comprised spatially complex imitation of hand and finger postures and to a lesser degree, pantomime of common object-use. Buccofacial apraxia including imitation of face postures, emblematic face postures, and repetition of multisyllabic pseudowords differentiated bvFTD from HC and AD. The final test version consisting of 20 items proved highly efficient for the discrimination of biologically confirmed dementia patients from HC (sensitivity 91% , specificity 71%) but also for differential diagnosis of bvFTD and AD (sensitivity 74% , specificity 93%). Assessment of praxis profiles effectively contributes to diagnosis and differential diagnosis of AD and bvFTD. The Dementia Apraxia Test (DATE) is a brief and easy to administer cognitive tool for dementia assessment, has a high inter-rater reliability (Cohen's κ= 0.885) and demonstrates content validity.

The demise of Archbishop Wolf Dietrich--A historical note on a fatal status epilepticus documented at Salzburg in 1617.

Wolf Dietrich of Raitenau (WD) ruled the archiepiscopal Salzburg from March 2nd 1587 to December 17th 1611. He was condemned by his successor Archbishop Markus Sittikus of Hohenems to spend his last years imprisoned at the Fortress Hohensalzburg, where he died on January 16th 1617. This historical note describes the causes of his death. The original Latin handwriting, including the detailed medical history and the autopsy of the Archbishop's body performed by his personal physician, was analyzed in conjunction with historical handwritings provided by St. Peter's Abbey, Salzburg handwriting assigned to Markus Sittikus. Wolf Dietrich of Raitenau had his first well-documented left hemispheric stroke in winter 1604/05. He had palsy of his right arm, was unable to write, and, therefore, used a stamp instead of his signature until October 1605. After another stroke, right hemispheric in origin with persisting palsy of his left arm ["leva corporis pars iam pridem simili ex apoplectico assultu in paralysin resoluta"], he developed symptomatic epilepsy with recurring seizures ["epileptico insultu quo etiam alias correptus est"]. On January 15th 1617, he suffered from a secondarily generalized convulsive status epilepticus ["toto corpore convellitur epileptico insultu"] with stertorous breathing and distortion of his face ["spuma stertore insigni faciei perversione"] and was unconscious for 8h. He recovered from coma and showed dysphagia, buccofacial apraxia ["abolitam diglutiendi facultatem"], reversible speech disturbance ["accisa etiam verba loqui"], and left-sided hemiplegia ["leva corporis pars… immobilis prorsus est reddita"]. The following day, he had speech disturbances, and he died at noon. His autopsy showed large but intact liver ["hepar magnum sanum"] and heart ["cor magnum in quo lapsus nullus"]. There was intrapulmonal mucus ["pituita imbutus"], and part of the lungs adhered to its pleura. He had five kidney stones and a partly cirrhotic spleen. The cause of his death was assumed to be intracerebral ["causa mortis in capite requienda fuisset"]. The terminal suffering of Wolf Dietrich of Raitenau is the first witnessed case report on a fatal status epilepticus in Salzburg. Most likely, he suffered from vascular epilepsy due to a right hemispheric stroke, leading to status epilepticus with left-sided Todd's palsy and speech disturbances. An acute symptomatic etiology of this disease cannot be ruled out, as for religious reasons, the Archbishop's brain was not autopsied. Meticulous medical reporting including autopsy was already available in Salzburg in 1617, and the symptomatic etiology of epilepsy was diagnosed correctly. This article is part of a Special Issue entitled "Status Epilepticus".

Fahr's Disease Linked to a Novel SLC20A2 Gene Mutation Manifesting with Dynamic Aphasia

Background: Idiopathic basal ganglia calcification (IBGC), also known as Fahr's disease, is a rare disorder characterized by widespread cerebral calcifications, an autosomal dominant pattern of inheritance and clinical and genetic heterogeneity. The recently identified IBGC gene, SLC20A2, encodes for type III sodium-dependent phosphate transporter 2 and its loss-of-function mutations may lead to the regional accumulation of inorganic phosphate in the brain, causing calcium phosphate deposition. Objective: To describe the clinical, neuroimaging and genetic findings in an Italian family with IBGC. Methods: The family members underwent clinical and radiological examination in order to diagnose IBGC according to standard criteria and screening for SLC20A2 gene mutations. The affected subjects also underwent neuropsychological longitudinal assessments and functional neuroimaging investigations. Results: The 2 affected family members harbored a novel missense mutation, G1618A, in the SLC20A2 gene, leading to gly540-to-arg (G540R) substitution in a highly conserved residue. This is the first SLC20A2 gene mutation associated with familial IBGC reported in the Italian population and is damaging according to all prediction programs. In the index case we observed a fair correlation between cortical areas with no calcifications but with significant hypometabolism at [18F]FDG-PET (inferior frontal premotor cortex) and the neuropsychological picture dominated by dynamic aphasia and buccofacial apraxia. Conclusion: These findings expand the catalog of SLC20A2 mutations identified to date and add dynamic aphasia to the spectrum of neuropsychological deficits reported in IBGC, supporting the use of functional neuroimaging studies for better investigation of genotype-phenotype correlations.

Dysphagia Risk Assessment in Acute Left-Hemispheric Middle Cerebral Artery Stroke

Background and Purpose: Bedside evaluation of dysphagia may be challenging in left middle cerebral artery (MCA) stroke due to frequently existing aphasia. Here we analyse the predictive value of common bedside screening tests and of two items of cortical dysfunction, aphasia and buccofacial apraxia (BFA), for the detection of dysphagia. Methods: We prospectively examined 67 consecutive patients with clinical and imaging evidence of acute (<72 h) left MCA stroke. Dysphonia, dysarthria, abnormal volitional cough and abnormal gag reflex were assessed followed by a standardized 50-ml water-swallowing test determining the symptoms cough and voice change after swallow. Aphasia and BFA were assessed according to defined criteria. Fibre-optic endoscopic evaluation of swallowing (FEES) was performed for validation of dysphagia. Results: 41 (61%) patients had FEES-proven dysphagia. Abnormal gag reflex, abnormal volitional cough, cough after swallow, aphasia and BFA were significantly more frequent in dysphagic as compared to non-dysphagic patients, while dysphonia, dysarthria and voice change after swallow were not. Aphasia and BFA had the highest sensitivity (97 and 78%, respectively) and high negative predictive values (89 and 68%, respectively) for dysphagia. Multivariate regression analysis did not identify an independent predictor of dysphagia. Conclusions: In left MCA stroke, the sensitivity and specificity of common bedside dysphagia screening methods are low. In contrast, aphasia and BFA have a high sensitivity and high negative predictive power, presumably due to the neuro-anatomical overlap between cortical regions involved in swallowing, speech production, imitation and voluntary movement control.

An Elderly Woman With Difficulty Reading and Abnormal Eye Movements

An Elderly Woman With Difficulty Reading and Abnormal Eye Movements

Isolated buccofacial apraxia subsequent to a left ventral premotor cortex infarction

Buccofacial apraxia (BFA, or oral apraxia) is a nonspeech skilled movement disorder that involves orofacial structures in the absence of paresis. BFA usually co-occurs with aphasia or apraxia of speech (AOS) and isolated BFA is an extremely rare phenomenon. The brain regions correlated with BFA have been studied in patients with concomitant aphasia or limb apraxia. Therefore, the exact brain regions responsible for BFA remain unclear. We report a patient with pure BFA and discuss the localization of the brain lesion.

Primary progressive apraxia of speech (AOS) in a patient with Pick's disease with Pick bodies: a neuropsychological and anatomical study and review of literatures

A 56-year-old right-handed man suffered from progressive apraxia of speech (AOS), characterized by agrammatism and buccofacial apraxia. He also became mute at the later stages of the disease progression. At autopsy, the left precentral gyrus, pars opercularis, and hippocampus showed severe atrophy. Pick bodies and Pick cells were observed. In this report, we also review previous case reports of AOS. Pick's disease is among the most commonly associated of the major diseases. Brain lesions associated with AOS may be found in regions such as the precentral gyrus and the pars opercularis in the left hemisphere.

Cognitive performance is impaired in coeliac patients on gluten free diet: A case–control study in patients older than 65 years of age

IntroductionRetrospective studies and case reports suggest an association between coeliac disease and impaired cognitive function. AimTo evaluate functional and cognitive performances in coeliac disease vs. control patients older than 65 years. MethodEighteen coeliac disease patients (75±4 years, group A) on gluten free diet since 5.5±3 years and 18 age-sex matched controls (76±4 years, group B) were studied using a battery of neuropsychological tests. Results of functional and cognitive tests are expressed as “row scores” and as “equivalent scores” by relating “raw scores” to reference rank categories. ResultsBarthel Index of functional performance was similar in the 2 groups. “Raw score” was significantly lower in coeliac disease than controls for Mini Mental Test Examination (p=0.02), Trail Making Test (p=0.001), Semantic Fluency (p=0.03), Digit Symbol Test (p=0.007), Ideo-motor apraxia (p<0.001) and Bucco-facial apraxia (p<0.002). “Equivalent score” was also lower in coeliac disease than controls for Semantic memory (p<0.01) and for Ideo-motor apraxia (p=0.007). ConclusionCognitive performance is worse in elderly coeliac disease than control patients, despite prolonged gluten avoidance in coeliacs. Awareness on the increasing phenomenon of late-onset coeliac disease is important to minimize diagnostic delay and prolonged exposure to gluten that may adversely and irreversibly affect cognitive function.

Swallowing Disturbance Pattern Relates to Brain Lesion Location in Acute Stroke Patients

The relationship of brain lesion location and swallowing disturbance pattern has been poorly studied in acute stroke patients. Sixty patients with first-ever acute ischemic stroke at clearly assessed location and clinical signs of dysphagia were studied. Swallowing-related parameters rated clinically and fiberendoscopically were attention deficit, buccofacial apraxia, orofacial paresis, gag reflex, delay of pharyngeal swallow, pharyngeal contraction, larynx elevation, function of upper esophageal sphincter (UES), and aspiration severity. Attention deficit was independently predicted only by parietotemporal infarction, buccofacial apraxia by left-sided parietotemporal infarction, orofacial paresis by infarction encompassing upper motor neuron of cranial nerves, and impaired UES opening by lateral medullary infarction. Other swallowing parameters were not related to lesion topology. On posthoc analysis, pneumonia within 21 days after stroke was predicted only by insular lesion. Distinct acute brain lesion locations result in characteristic swallowing disturbance patterns. Dysphagic patients with insular stroke appear to have even higher risk of pneumonia suggesting a further associated factor promoting infection in these subjects.

Aphemia: an isolated disorder of speech associated with an ischemic lesion of the left precentral gyrus

Sirs, Aphemia, also termed apraxia of speech, cortical anarthria or pure word mutism, is an isolated disorder of coordinated speech articulation that results in severe affection of verbal motor output [8, 9]. This rare and possibly underdiagnosed syndrome was first postulated by Paul Broca in 1861 [1]; however, the definition remained imprecise during the course of history. Especially the differentiation between aphemia and aphasia—the latter of which was shortly after described by Armand Trousseau— as well as dysarthria has been in discussion since then. A 61-year-old right-handed dentist with treated hypertension awoke with acute loss of speech and saliva running out of the right corner of his mouth. He wrote ‘‘stroke’’ on a piece of paper for his wife, who called the ambulance. In the emergency room, he was nearly mute due to grossly distorted motor output, but he had full comprehension of speech, could communicate through gestures and intact, fluent writing (Fig. 1a). Speech was very difficult with strangled vowels, severe phonematic paraphasia and abnormal prosody that was not facilitated by singing, reading or repetition. This and the constant effort to correct himself cumulated in visible frustration, whereas, surprisingly, the patient was able to produce—apparently emotionally triggered—short, but intact and fluently articulated commentaries of the situation (e.g., ‘‘It’s not working!’’, ‘‘That’s terrible!’’). There was a mild right facial palsy without further affection of coordinated buccofacial movement (whistling, etc.) or oropharyngeal sensibility (NIHSS 4). Diffusion-weighted MRI performed shortly after presentation to the emergency room showed an acute ischemic lesion of the left precentral gyrus that was not yet visible on T2-weighted FLAIR images. The lesion extended slightly to the medial part of the premotor cortex (Fig. 2). Ultrasound and MRA demonstrated a highgrade stenosis of the left internal carotid artery (ICA). As extensive stroke workup failed to show an alternative source of embolism, symptomatic ICA stenosis was considered the most likely cause of stroke, and the patient was treated with endarterectomy on day 4. Under speech therapy, the symptoms improved gradually, and speech became more and more fluent after day 3. In the beginning, syntax presented incompletely because of the effort of speech, but became intact by day 3. From day 1, repeated dictations and spontaneous essays (see Fig. 1b) could demonstrate the constantly fluent and intact written language. During observation, dysarthric components never occurred. At 1 week, the patient recovered completely, including the right facial palsy. Still not clearly classified as an articulatory or language disorder, aphemia is today understood as an isolated disorder of the planning of motor articulation of speech. These patients, even when mute, can write correctly and have no difficulty in the production of verbal sequences as long as they do not have to articulate them, distinguishing the disorder from motor aphasia. The presentation of abnormal prosody, ‘‘false starts,’’ self corrections and the occurrence of undisturbed ‘‘insulas’’ in speech can help to differentiate it from dysarthria. Often, right-sided hemiparesis, limb apraxia, mild buccofacial apraxia and central right facial palsy are associated symptoms. The lesion of the precentral gyrus corresponds to recent data of the few similar cases published [2, 5, 7]. These case studies have linked the C. Ottomeyer (&) B. Reuter T. Jager C. Rosmanith M. G. Hennerici K. Szabo Department of Neurology, Universitatsklinikum Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany e-mail: c.ottomeyer@neuro.ma.uni-heidelberg.de

Ipsilateral ptosis as main feature of tuberothalamic artery infarction

Tuberothalamic artery infarction (TTAI) results mainly in a myriad of neuropsychological symptoms such as memory impairment, euphoria, apathy, verbal perseverations, constructional apraxia and lack of spontaneity. Language disturbances, acalculia, buccofacial and limb apraxia occur prominently after left TTAI while visual spatial processing deficits and hemispatial neglect occur prominently after the right one. Some cases of TTAI causing Horner's syndrome in addition of these wide-ranging neurobehavioral symptoms have been reported. Here, we report a case of TTAI with an ipsilateral ptosis as main clinical manifestation. This finding suggests that a Horner's syndrome can be the main feature of TTAI when neuropsychological manifestations are inconspicuous.