H. Jokeit et A. Ebner, Long term effects of refractory temporal lobe epilepsy on cognitive abilities: a cross sectional study, J NE NE PSY, 67(1), 1999, pp. 44-50
Objective-Intractable epilepsy is related to various transient and chronic
brain electric and neurochemical disturbances. There is increasing evidence
that chronic epilepsy induces secondary neuronal metabolic and structural
decline. However, there is no convincing evidence that the cognitive abilit
ies of patients deteriorate with increasing duration of intractable epileps
y.
Methods-To examine whether duration of refractory temporal lobe epilepsy (T
LE) is related to generalised cognitive impairment, psychometric intelligen
ce based on the full scale intelligence quotient (FSIQ, WAIS-R) was determi
ned in 209 patients with unilateral TLE. For analyses of variance (ANOVA) p
atients were grouped into three categories: <15, 15-30, and >30 years of re
fractory TLE.
Results-An ANOVA and a multiple regression analysis showed that duration of
TLE affects FSIQ. Patients with >30 years of TLE performed worse than pati
ents with 15 or 30 years of TLE. The factors side of seizure origin and typ
e of lesion an MRI did not reach significance. A second ANOVA including edu
cation as factor showed that in patients with higher educational attainment
, the mean FSIQ was stable for a longer duration of TLE than in less educat
ed patients. Retesting 6 months after anterior temporal lobectomy seizure f
ree patients (n=85 of 127) had an higher FSIQ but showed a similar duration
effect before and after anterior temporal lobectomy. The variables age at
epilepsy onset, education, frequency of interictal epileptiform discharges,
frequency of habitual and generalised seizures, serum concentration of ant
i-epileptic drugs, and polypharmacy were statistically controlled.
Conclusions-Psychometric intelligence of patients with a longer duration of
refractory TLE were most severely impaired. Consequently, refractory TLE s
eems to be associated with slow but ongoing cognitive deterioration. It is
assumed that epilepsy related noxious events and agents exhaust the compens
atory capacity of brain functions. However, as in dementia and Alzheimer's
disease, higher educational attainment as an indicator of higher brain rese
rve might delay the cognitive decline.