PURPOSE: The degree to which depression interacts with the cognitive deficits of epilepsy to alter cognitive skill and general functioning is unknown. Depression has significant negative effects on adaptive functioning including cognitive skills. Temporal lobe epilepsy (TLE) patients are known to possess cognitive dysfunction. Thus, TLE patients who are depressed may suffer a double burden of cognitive deficits. METHODS: We examined whether depressed patients show increased cognitive deficits relative to nondepressed TLE patients (n = 59). We then sought to determine if this effect varied for left versus right TLE patients utilizing preoperative depression and neuropsychological data. To accurately study the lateralization of any observed effects, we selected only patients with definitive evidence of unilateral pathology and seizure focus and utilized a two-year seizure-free postsurgical outcome to capture this. RESULTS: The data suggested that cognitive performance was not related to depression, and that depression did not reliably mediate the cognitive presentation of either our left or right TL patients. The notion of a double burden on cognition did not receive support from our data. The data did produce the expected advantage on verbal memory measures for right TLE patients. CONCLUSIONS: The reasons for the limited statistical effects are discussed and issues in unraveling the causal relationships between depression, cognition, and TLE are considered. We discussed the potential role depression may play in the cognitive skills of TLE patients, but the major implication is that depression and neurocognitive performance appear to bear a limited relationship in the context of TLE.
PURPOSE: The degree to which depression interacts with the cognitive deficits of epilepsy to alter cognitive skill and general functioning is unknown. Depression has significant negative effects on adaptive functioning including cognitive skills. Temporal lobe epilepsy (TLE) patients are known to possess cognitive dysfunction. Thus, TLEpatients who are depressed may suffer a double burden of cognitive deficits. METHODS: We examined whether depressedpatients show increased cognitive deficits relative to nondepressed TLEpatients (n = 59). We then sought to determine if this effect varied for left versus right TLEpatients utilizing preoperative depression and neuropsychological data. To accurately study the lateralization of any observed effects, we selected only patients with definitive evidence of unilateral pathology and seizure focus and utilized a two-year seizure-free postsurgical outcome to capture this. RESULTS: The data suggested that cognitive performance was not related to depression, and that depression did not reliably mediate the cognitive presentation of either our left or right TL patients. The notion of a double burden on cognition did not receive support from our data. The data did produce the expected advantage on verbal memory measures for right TLEpatients. CONCLUSIONS: The reasons for the limited statistical effects are discussed and issues in unraveling the causal relationships between depression, cognition, and TLE are considered. We discussed the potential role depression may play in the cognitive skills of TLEpatients, but the major implication is that depression and neurocognitive performance appear to bear a limited relationship in the context of TLE.
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