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CASE REPORT
Year : 2011  |  Volume : 59  |  Issue : 3  |  Page : 432-434

Aphemia as a presenting symptom in acute stroke


Department of Clinical Neurosciences, University of Calgary, Calgary, AB, Canada

Date of Submission23-Jan-2011
Date of Decision31-Jan-2011
Date of Acceptance15-Feb-2011
Date of Web Publication7-Jul-2011

Correspondence Address:
Pawan K Ojha
Department of Neurology, Sir JJ Hospital, Byculla, Mumbai - 400 008, India

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.82766

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 » Abstract 

Aphemia is an apraxia of speech characterized by complete articulatory failure in the presence of preserved writing, comprehension and oropharyngeal function and can be the presenting manifestation of acute stroke. The responsible lesion is commonly in the left inferior frontal gyrus or the left motor cortex near the face M1 area. Three patients who developed aphemia due to acute ischemic stroke are described here. All had apraxia of speech due to acute infarct in the left motor cortex near face M1 area. Understanding the underlying speech disorder is crucial in planning the appropriate rehabilitation strategy.


Keywords: Aphemia, apraxia of speech, stroke


How to cite this article:
Ojha PK, Nandavar S, Pearson DM, Demchuk AM. Aphemia as a presenting symptom in acute stroke. Neurol India 2011;59:432-4

How to cite this URL:
Ojha PK, Nandavar S, Pearson DM, Demchuk AM. Aphemia as a presenting symptom in acute stroke. Neurol India [serial online] 2011 [cited 2019 Oct 21];59:432-4. Available from: http://www.neurologyindia.com/text.asp?2011/59/3/432/82766



 » Introduction Top


Aphemia is often a presenting symptom of acute stroke. In 1861, Broca coined this term to describe two patients, who could utter only a few words due to lesions in left fronto-parietal area. [1],[2] In modern literature, 'aphemia' is used to describe patients with initial mutism evolving to impaired articulation thereby manifesting speech which is effortful, slow and dysprosodic but with intact comprehension of spoken language, writing and buccolingual function. [3] Earlier, it was thought to be severe dysarthria linked to lesions of the left frontal lobe in the lower half of the primary motor cortex, posterior inferior frontal gyrus, and the underlying white matter but Wertz et al. proposed that it was in fact apraxia of speech. [4],[5],[6] The apparent cause of the conflicting opinions was the lack of clear diagnostic criteria for apraxia of speech, and many of the features used as inclusion criteria in studies for apraxia of speech were also shared by dysarthria and motor aphasia. We describe here three cases of aphemia due to acute ischemic stroke along with a discussion on the mechanism and lesion.


 » Case Reports Top


The first patient, an 85-year-old right-handed gentleman with a history of diabetes, hypertension and chronic renal failure, presented with sudden onset of dense right hemiplegia with no speech output. In the emergency room, his NIHSS was 18, but right hemiplegia improved spontaneously over the next hour. NIHSS improved to 6 but he had no speech output. He could not repeat words and his speech did not improve with repetition or singing. He had good language comprehension and could write well-formulated sentences. Neurological examination revealed right facial droop with subtle buccolingual apraxia without oropharyngeal weakness. An unenhanced computer tomography (CT) scan of brain showed early ischemic changes in the posterior left frontal lobe. In view of no clear time of onset, marked leukoaraiosis and renal failure, he was not treated with rt-PA. Over the next few days, he started speaking a few words in a slow, effortful and aprosodic manner. A follow-up CT scan confirmed an infarct in the left frontal lobe, predominantly in the precentral gyrus [Figure 1].
Figure 1: 24-h CT scan showing infarct in left frontal region involving the precentral gyrus and perisylvian region

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The second patient, a right-handed man, 80 years of age with hypertension and coronary artery disease, was brought to the emergency department for sudden onset of speech difficulty. On examination he only made grunting sounds, but could not produce any words. He had normal comprehension and wrote well-formulated sentences. No buccolingual apraxia or weakness was noted. He had a mild right supranuclear facial paresis. CT brain did not show any early ischemic changes [Figure 2]a. He received intravenous rt-PA at 3.18 h after onset and within 2 h spoke well albeit with a mild dysarthria that improved before discharge. CT brain done at 24 h revealed a small infarct mainly in the left precentral gyrus near the face M1 area.
Figure 2: (a) 24-h CT scan of second patient showing infarct predominantly involving the left precentral gyrus
(b) Diffusion-weighted MR brain image of third patient showing acute infarct predominantly involving the left precentral gyrus


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The third patient is a 58-year-old right-handed man who had diabetes mellitus, hypertension and mild left hemiataxia from two prior ischemic strokes. He was brought to the emergency department for inability to speak. On examination, he had no speech output but normal comprehension and writing. No oropharyngeal weakness, apraxia or limb deficit was observed. An unenhanced CT brain did not show any acute infarct. He did not receive rt-PA as the time of onset could not be ascertained. He needed feeding through nasogastric tube due to dysphagia. Magnetic resonance imaging (MRI) of brain after 24 h revealed an acute infarct in the left pre-central gyrus near face area M1 [Figure 2]b. He gradually recovered, evolving with an effortful, aprosodic and slow speech. [7]


 » Discussion Top


Our patients presented with aphemia as they had impairment of speech output in the absence of any impairment of voice, language, writing ability and cognition and had only mild buccofacial paresis. A language disorder is unlikely in our patients as they comprehended well and had normal writing. They were also not abulic as they showed adequate intention to speak and made the effort to write. The absence of severe oropharyngeal weakness made a diagnosis of anarthria unlikely. The most likely mechanism of aphemia in our patients is apraxia of speech. This apraxia of speech is characterized by distortions of phonemes that are perceived as sound substitutions and transpositions, occurs in the absence of paresis of speech articulators (lips, tongue, jaw and palate) or muscles controlling phonation. The subject knows what he wants to say and how it should sound, but cannot accurately program the articulators to make the desired sounds. [8],[9] As an example, on being asked to say "brush" - one patient uttered: "vois, uh, b---ush, wush, uh, uh, bois…" During the recovery phase, two patients with residual speech impairment demonstrated typical sound distortions and hesitant speech and fulfilled the Academy of Neurologic Communication Disorders and Sciences criteria for the diagnosis of apraxia of speech [Table 1]. [10]
Table 1: Voice characteristics of apraxia of speech

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In all the three patients, lesions were noted in the left frontal lobe, most prominently in the precentral gyrus near the face M1 area. Various lesion mapping techniques have been used to investigate the lesions associated with apraxia of speech. A well-designed CT lesion mapping study showed a robust association between chronic apraxia of speech and lesions in the superior tip of the precentral gyrus. [11],[12] An MR imaging study found lesions of the left inferior frontal gyrus (Broca's area) with acute apraxia of speech. [3],[8] Another MRI-based study revealed involvement of a localized cortical region near face-M1, which displayed high intensity on diffusion-weighted images, while the main portion of the corticobulbar fibers arising from the lower third of the motor cortex was preserved. [13]

The differentiation of apraxia of speech causing aphemia from conditions like non-fluent aphasia and severe dysarthria is important in planning speech rehabilitation. As we know, the main approach for speech therapy in aphasia is utilizing word meaning for learning and for dysarthria on speech muscle strengthening (e.g. Lee Silverman Voice Treatment). [14],[15],[16] In contrast, for apraxia of speech, articulatory kinematic approach is the most effective strategy. It involves repeated phoneme generation (exaggeration of words and sounds by the therapist allows imitation by the patient) and key word generation. [17]

 
 » References Top

1.Dronkers NF. The pursuit of brain-language relationships. Brain Lang 2000;71:59-61.  Back to cited text no. 1
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2.Dronkers NF, Plaisant O, Iba-Zizen MT, Cabanis EA. Paul Broca's historic cases: High resolution MR imaging of the brains of Leborgne and Lelong. Brain 2007;130:1432-41.  Back to cited text no. 2
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3.Urban PP, Rolke R, Wicht S, Keilmann A, Stoeter P, Hopf HC, et al. Left-hemispheric dominance for articulation: a prospective study on acute ischaemic dysarthria at different localizations. Brain 2006;129:767-77.  Back to cited text no. 3
    
4.Ure J, Morasso C, Funes J, Ollari J, Videla H, Diez M. Subcortical anarthria: A case report. Brain Lang 2001;78:43-52.  Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.Wertz RT LL, Rosenbek JC. Apraxia of speech in adults: The disorder and its management In: Apraxia of speech in adults: The disorder and its management. San Diego: Singular Publishing Group,Inc., 1984.  Back to cited text no. 5
    
6.Schiff HB, Alexander MP, Naeser MA, Galaburda AM. Aphemia. Clinical-anatomic correlations. Arch Neurol 1983;40:720-7.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.Shobha N, Smith EE. Thrombolysis in aphemia. N Z Med J 2009;122:96-8.  Back to cited text no. 7
[PUBMED]    
8.Hillis AE, Work M, Barker PB, Jacobs MA, Breese EL, Maurer K. Re-examining the brain regions crucial for orchestrating speech articulation. Brain 2004;127:1479-87.  Back to cited text no. 8
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9.Nadeau SE, Rothi LJ, Crosson B. Aphasia and language: theory to practice. In: The science and practice of neuropsychology. New York: Guilford Press, 2000. p. 221-65.  Back to cited text no. 9
    
10.Wambaugh JL, Duffy JR, McNeil MR, Robin DA, Rogers MA. Treatment guidelines for acquired apraxia of speech: A synthesis and evaluation of the evidence.(ANCDS Bulletin Board)(Academy of Neurologic Communication Disorders and Sciences). J Med Speech Lang Pathol 2006;14:xv(19).  Back to cited text no. 10
    
11.Dronkers NF. A new brain region for coordinating speech articulation. Nature 1996;384:159-61.  Back to cited text no. 11
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12.Dronkers N, Ogar J. Brain areas involved in speech production. Brain 2004;127:1461-2.  Back to cited text no. 12
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13.Terao Y, Ugawa Y, Yamamoto T, Sakurai Y, Masumoto T, Abe O, et al. Primary face motor area as the motor representation of articulation. J Neurol 2007;254:442-7.  Back to cited text no. 13
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14.Cicerone KD, Dahlberg C, Kalmar K, Langenbahn DM, Malec JF, Bergquist TF, et al. Evidence-based cognitive rehabilitation: Recommendations for clinical practice. Arch Phys Med Rehabil 2000;81:1596-615.  Back to cited text no. 14
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15.Doesborgh SJ, van de Sandt-Koenderman MW, Dippel DW, van Harskamp F, Koudstaal PJ, Visch-Brink EG. Effects of semantic treatment on verbal communication and linguistic processing in aphasia after stroke: A randomized controlled trial. Stroke 2004;35:141-6.  Back to cited text no. 15
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16.Hustad KC. Effects of speech stimuli and dysarthria severity on intelligibility scores and listener confidence ratings for speakers with cerebral palsy. Folia Phoniatr Logop 2007;59:306-17.  Back to cited text no. 16
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17.RK. Acquired apraxia of speech: Features, accounts, and treatment. Top Stroke Rehabil 2004;11:49-58.  Back to cited text no. 17
[PUBMED]  [FULLTEXT]  


    Figures

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    Tables

  [Table 1]

This article has been cited by
1 Acute transient aphemia
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Clinical Neurology and Neurosurgery. 2015; 131: 86
[Pubmed] | [DOI]



 

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