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We report the case of OTM who presented with dynamic aphasia following a stroke that occurred in the left basal ganglia. He showed drastically reduced spontaneous speech in the context of well preserved naming, repetition and comprehension skills. OTM was particularly impaired in generating words, sentences and phrases when cued by a stimulus allowing many response options. By contrast, when a single response was strongly suggested by a stimulus, he could generate verbal responses adequately. OTM's non-verbal response generation abilities varied across tasks. He performed in the normal range in a motor movement generation test and he produced as many figures as controls when tested on a figural fluency task. He showed, however, many perseverations on this test. Moreover in a random number generation task he produced more responses that were part of ascending and descending series of numbers. The patient's impairments are interpreted as a consequence of two deficits. The first of these consists of an inability to generate verbal responses particularly in situations of high competition and involves the function of left frontal regions. The second deficit is one of impaired novel thought generation as evidenced by perseverations. This second deficit has been proposed to be a function of basal ganglia damage.

The existence of semantic access disorders is now well established, however the precise cognitive and anatomical underpinnings are still debated. Here we describe the case of a patient that became aphasic after the resection of a left frontal glioma. Detailed lesion reconstruction indicates that the lesion was mostly restricted to the left dorsal and ventral prefrontal cortices and the underlying white matter, but sparing temporal lobes. Critically, the patient showed all the signs of refractory semantic access dysphasia, supporting the association between this syndrome and damage to left prefrontal areas likely to subserve retrieval and selection mechanisms for verbal material.

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