Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 59, Num. 3, 2011, pp. 432-434

Neurology India, Vol. 59, No. 3, May-June, 2011, pp. 432-434

Case Report

Aphemia as a presenting symptom in acute stroke

Pawan K Ojha, Shobha Nandavar, Dawn M Pearson, Andrew M Demchuk

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

Correspondence Address: Pawan K Ojha Department of Neurology, Sir JJ Hospital, Byculla, Mumbai - 400 008, India ptojha@yahoo.co.in

Date of Submission: 23-Jan-2011
Date of Decision: 31-Jan-2011
Date of Acceptance: 15-Feb-2011

Code Number: ni11124

PMID: 21743177

DOI: 10.4103/0028-3886.82766

Abstract

Keywords: Aphemia, apraxia of speech, stroke

Introduction

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

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].

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.

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

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]

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

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