Echolalia Following Acute Ischemic Stroke

Case

A 66-year-old man, known to have hypertension and type II diabetes, presented to the Emergency Department with sudden onset right-sided weakness and speech disturbance. He was conscious, alert but not attentive. His initial National Institutes of Health Stroke Scale (NIHSS) was 17. The patient was noted to have severe aphasia, with poor comprehension and a tendency to echo the examiners’ speech sounds and words (videos 1). He also showed impairment in naming, reading, and writing. An upper motor neuron pattern right facial weakness was noted. His brain CT showed no hemorrhage or large vessel occlusion (LVO). He was treated with intravenous tissue plasminogen activator (tPA). MRI revealed acute infarction, predominantly involving the left parieto-occipital lobes (Figure 1). He improved dramatically within 8 days of rehabilitation and speech therapy (video 2).

Figure 1.

Diffusion-weighted imaging (DWI) sequence show infarction in the left inferior parietal lobule, parietooccipital lobes (arrows), internal capsule, and splenium of corpus callosum (arrowheads).

Transcortical sensory aphasia (TSA) is a rare form of aphasia, characterized by poor comprehension of spoken and written words with intact repetition, a feature that distinct TSA from Wernicke’s aphasia.¹ TSA is occasionally accompanied by echolalia, an extreme degree of repetition in which affected individuals echo words and phrases heard.^1,2 Echolalia has also been described during the recovery phase of classical, more common forms of aphasia (Broca, Wernicke, global, and conduction).¹ TSA is most often attributed to lesions in the posterior parietooccipital region with involvement of the left middle temporal gyrus, angular gyrus, white matter of the temporal isthmus, or posterior periventricular area.³ Other potential localization includes the thalamus, left mesial frontoparietal region, or inferolateral aspect of both temporal lobes. The most common etiology is territorial infarction in the middle or posterior cerebral arteries.³

Mirror neuron system (MNS) in the dominant hemisphere (located in the ventrolateral prefrontal cortex, superior temporal gyrus, and inferior parietal lobule) represents a complex network hypothesized to have a major role in integrating perception and action of visual and auditory stimuli for voluntary verbal control.^1,4 Pathological disruption of the audio-visual MNS is thought to be the cause of echolalia.¹ In our patient, the involvement of the thalamus and inferior parietal lobule has a potential contribution to cause TSA with echolalia.