Structured cueing on a semantic fluency task differentiates patients with temporal versus frontal lobe seizure onset

Patients with frontal lobe dysfunction (e.g., Huntington’s disease) reportedly benefit more from cueing on measures of semantic fluency than do patients with damage to temporal lobe structures (e.g., Alzheimer’s disease). This differential benefit from cueing suggests that different neurocognitive functions are impaired in these two groups. Patients with frontal lobe dysfunction are presumed to have difficulty with the executive aspects of this generative fluency task, whereas patients with temporal lobe impairment are limited by deficits in semantic memory. We studied the performance of patients with complex partial seizures of frontal or temporal lobe onset, as determined by video/EEG monitoring, on standard and cued measures of semantic fluency administered in a counterbalanced sequence across groups. These groups did not differ significantly in terms of age, education, gender, age at seizure onset, total number of antiepileptic drugs, or IQ, and all patients subsequently underwent surgery for intractable epilepsy. Patients with frontal lobe dysfunction (FL group) performed significantly worse than patients with temporal lobe impairment (TL group) on the standard semantic fluency paradigm (TL group: M = 18.4, SD = 4.7; FL group: M = 11.1, SD = 5.3), t (27) = −3.75, P < 0.001. Nevertheless, results of an ANCOVA demonstrated that the FL group showed significantly greater performance improvement than the TL group when provided with a cued semantic fluency format, even after controlling for baseline differences in ability on the standard semantic fluency task (TL group: M = 0.45, SD = 3.8; FL M = 9.4, SD = 5.1), F (1, 29) = 12.37, P = 0.002. These findings support previous research suggesting that frontal and temporal structures contribute uniquely to semantic generative fluency and suggest that using a combination of standard and cued semantic fluency tasks may help confirm localization of seizure onset in partial epilepsy by localizing the associated cognitive dysfunction.