• Frontal cognitive functions;
  • Impairment;
  • Juvenile myoclonic epilepsy


  1. Top of page
  2. Methods
  3. Results
  4. Discussion
  5. Acknoledgments
  6. References

Purpose: The aim of the present study was to investigate the possible frontal cognitive dysfunction in patients with juvenile myoclonic epilepsy (JME) and to compare the results with those of patients with frontal lobe epilepsy (FLE) and temporal lobe epilepsy (TLE), as well as with controls.

Methods: A total of 50 patients with JME, 40 patients with FLE, 40 patients with TLE, and 40 normal controls, all matched for age, education, and IQ, were administered tests to assess frontal functions (the Word Fluency Test and the Wisconsin Card Sorting Test [WCST]). All participants had a normal intelligence level based on the Wechsler Adult Intelligence Scale, and did not take medications other than antiepileptics (AEDs) or have a psychiatric history.

Results: Patients with JME had severe impairment in all administered tasks, similar to that of patients with FLE; TLE patients and controls followed in order. Multiple regression analysis did not disclose any significant effect of clinical variables on the cognitive deficits.

Discussion: These results clearly suggest that JME patients can show some frontal dysfunction, which may affect both epileptogenic features and cognitive processes. Further studies are needed to confirm these findings.

Juvenile myoclonic epilepsy (JME) was first recognized as a syndrome by Janz and Christian in 1957 (Janz & Christian, 1957). According to the Revised Classification of Epilepsies and Epileptic Syndromes, JME is characterized by seizures with bilateral, single or repetitive, arrhythmic, irregular, myoclonic jerks, predominantly in the arms (Commission on Classification and Terminology of the International League Against Epilepsy, 1989). There are often generalized tonic–clonic seizures and, sometimes, absences. The seizures usually occur shortly after awakening and are often caused by sleep deprivation. Interictal and ictal EEG have rapid, generalized, often irregular, spike and polyspike waves. The disorder may be inherited and the gender distribution is equal. The response to appropriate drug treatment is generally good (Janz, 1997). It has been noted that JME may be related to some specific personality characteristics, such as impressionability, unreliability, emotional instability, characteristics which are similar to those observed in patients with frontal lobe lesions (Janz & Durner, 1997; Hommet et al., 2006). Some cognitive functions are impaired in patients with frontal lobe epilepsy (FLE); concept formation, abstract reasoning, mental flexibility, and planning have been reported to be dysfunctional in JME patients as well (Bech et al., 1977; Karachristianou et al., 2004).

The neuropsychiatric profiles of patients with JME have been evaluated in several studies (Perini et al., 1996; Trimble, 2000; Gelisse et al., 2001; de Araujo et al., 2006; Trinka et al., 2006; de Araujo et al., 2007; Plattner et al., 2007), while very few investigations have been dedicated to describing the cognitive deficits of this syndrome. Devinsky et al. administered a battery of neuropsychological tests sensitive to frontal dysfunction to 15 patients with JME and 15 patients with temporal lobe epilepsy (TLE) (Devinsky et al., 1997). The patients with JME performed worse than the TLE group on some frontal tasks, even though the results of the patients with JME were not homogeneous (Devinsky et al., 1997). Another study highlighted that patients with JME had impaired visual working memory; this deficit was intermediate between controls and FLE (Swartz et al., 1994). Sonmez et al. (2004) and Pascalicchio et al. (2007) reported similar results, confirmed by others published in abstract form, which pointed out the existence of specific disturbances in executive function processes in JME patients (Gershengorn et al., 1992; De Toffol et al., 1997; Lavandier et al., 2002). Savic et al., besides, found prefrontal cerebral changes in JME (Savic et al., 2000). More particularly, these authors noticed significantly reduced prefrontal concentrations of N-acetyl aspartate (NAA) in patients with JME compared to controls, which could indeed support the hypothesis of prefrontal neuronal lesion and, consecutively, the presence of a specific cognitive impairment related to this dysfunction.

Considering that all the previous investigations did not include large samples of patients and did not simultaneously analyze the neuropsychological data in different types of epilepsy, we initiated a new project on the possible neuropsychological dysfunction associated with JME in order to provide more detailed information. In fact, no study has been carried out thus far that has compared the cognitive profile of patients with JME with those of patients with FLE, TLE, and normal controls.


  1. Top of page
  2. Methods
  3. Results
  4. Discussion
  5. Acknoledgments
  6. References


All patients and controls gave informed consent prior to the psychological session. Consecutive patients treated at the Epilepsy Center, St. Paolo Hospital, were enrolled in the study according to the following criteria: age between 18 and 60 years, education level equal to or higher than elementary school, normal intelligence (IQ on the Wechsler Adult Intelligence Scale [WAIS] >85) (Wechsler, 1955), and a diagnosis of JME, TLE, or FLE according to the International League Against Epilepsy (ILAE) classification scheme (Commission on Classification and Terminology of the International League Against Epilepsy, 1989). More specifically, the diagnosis of JME was determined by history, clinical features, and EEG data. The diagnosis of TLE was made on the basis of a review of clinical semiology with characteristics related to complex partial seizures of temporal lobe origin together with interictal EEGs, MRI, and clinical history (Richardson et al., 2007). Cryptogenetic cases without clear-cut lateralizing features or with bilateral temporal involvement were excluded.

The diagnosis of FLE was performed by video-EEG recordings of the seizures and, when present, of structural lesions on MRI. If the ictal discharge was nonlateralizing, the site was considered to be the one with the structural lesion. Cryptogenetic cases without clear-cut lateralizing features were also excluded. Only patients meeting criteria for certain temporal or FLE were considered eligible for our study.

We excluded patients receiving medications other than antiepileptic drugs (AEDs), those with a psychiatric background, or those with progressive neurological pathologies. All patients were evaluated before any surgical treatment. Selection criteria for healthy controls included: age between 18 and 60 years, education level equal to or higher than elementary school, and normal intelligence (IQ on the WAIS >85). We excluded subjects with a medical or acute psychiatric condition or current substance abuse. Controls were acquired from a list of volunteers selected by the State University of Milan for research purposes. Table 1 provides the demographic and clinical characteristics of the patients with epilepsy and the controls.

Table 1.  Demographic and clinical characteristics of patients with epilepsy and controls
 JME (n = 50)TLE (n = 40)FLE (n = 40)Controls (n = 40)
  1. JME, juvenile myoclonic epilepsy; TLE, temporal lobe epilepsy; FLE, frontal lobe epilepsy; SD, standard deviation; WAIS, Wechsler Adult Intelligence Scale; SPS, simple partial seizures; CPS, complex partial seizures; SGS, secondarily generalized seizures; TCS, tonic–clonic seizures.

 Males21 15 18 17 
 Females29 25 22 23 
Age (years)
Level of education (years)
 Mean 9.910.1 9.810.1
 SD 2.6 3.5 3.2 2.1
 SD 2.3 3.5 3.1 3.4
Duration of epilepsy (years)
 SD 9.912.612.7 
Onset of epilepsy (years)
Frequency of seizures (monthly)
 Mean 0.4 5.6 6.3 
 SD 0.8 4.5 4.3 
 Cryptogenic 1317 
 Symptomatic 2723 
Number of medications
 CBZ 158 
 GBP  1 
 GVG  1 
 OXA  1 
 PB 3 3 2 
 PRM  1 4 
 PHT  2 1 
 VPA42  1 
Type of seizure
 SPS  3 2 
 CPS 1712 
 CPS and SPS 1320 
 CPS and SGS  7 6 
 Myoclonic 2 
 Myoclonic and absences 5 
 Myoclonic and TCS28 
 Myoclonic, absences, and TCS15 

There was no significant difference between the patients in the epilepsy groups and the controls in terms of socio-demographic features (age: F = 0.182, p = 0.908; education: F = 1.529, p = 0.210; intelligence level: WAIS: F = 1.687, p = 0.190).


Two main neuropsychological tests for the assessment of frontal functions, the Word Fluency Test (Novelli et al., 1986) and the Wisconsin Card Sorting Test (WCST) (Laiacona et al., 2000), were administered to patients with JME, FLE, TLE, and controls. All subjects were also administered the WAIS for determination of IQ (Wechsler, 1955). The Word Fluency Test consists of three word-naming trials. The examiner asks the subjects to say as many words as they can think of that begins with the given letter of the alphabet, excluding proper nouns and names of cities. The time allotted is 1 min for each trial. The WCST is a very well known instrument; patients are requested to sort at maximum two sets of 64 cards according to color, shape, and number. The number of trials achieved out of six is documented, along with the number of both perseverative responses and total errors.


A data analysis was performed using the Statistical Package for the Social Sciences (SPSS, Chicago, IL, U.S.A.) for Windows, version 13.0. Patients with epilepsy and controls were compared with respect to sociodemographic characteristics using MANOVA. The results of the neuropsychological tests were examined by a MANOVA and post hoc pairwise comparisons (LSD procedure) to evaluate frontal dysfunction.

A data set of independent variables for each participant was evaluated by linear regression analysis in the JME group. The set included the following variables: the duration of epilepsy, the frequency of seizures, the treatment and the type of seizures. The results of neuropsychological tests served as dependent variables. A stepwise selection procedure was used (pin < 0.05; pout < 0.10) to identify the factors, which significantly contributed to the explanation of variance in the cognitive variables.


  1. Top of page
  2. Methods
  3. Results
  4. Discussion
  5. Acknoledgments
  6. References

Patients with JME had a significant impairment in all the administered tasks assessing frontal functions compared to TLE patients and controls (p < 0.05). These deficits were similar to those of FLE patients (p > 0.05) (Table 2). A pairwise comparison between the controls and the epilepsy groups is reported in Table 3.

Table 2.  Cognitive performances of FLE, JME, TLE, and controls
 FLE (n = 40)JME (n = 50)TLE (n = 40)Controls (n = 40)Fp
  1. JME, juvenile myoclonic epilepsy; TLE, temporal lobe epilepsy; SD, standard deviation; WCST, Wisconsin Card Sorting Test.

 Categories (mean)<0.05
 Perseverative resp. (mean)29.328.211.86.841.831<0.05
 Errors (mean)46.846.216.67.573.602<0.05
• Word fluency (mean)15.516.725.626.719.675<0.05
Table 3.  Pairwise comparison between the controls and the epilepsy groups
 WCST categoriesWCST perseverative resp.WCST errorsWord fluency
  1. JME, juvenile myoclonic epilepsy; FLE, frontal lobe epilepsy; TLE, temporal lobe epilepsy; WCST, Wisconsin Card Sorting Test.

JME vs. FLEp = 0.089p = 0.447p = 0.653p = 0.563
JME vs. TLEp = 0.000p = 0.000p = 0.000p = 0.000
JME vs. controlsp = 0.000p = 0.000p = 0.000p = 0.000
FLE vs. TLEp = 0.000p = 0.000p = 0.000p = 0.000
FLE vs. controlsp = 0.000p = 0.000p = 0.000p = 0.000
TLE vs. controlsp = 0.090p = 0.000p = 0.003p = 0.513

The linear regression analysis performed in the JME group showed that no clinical variables, such as the duration of epilepsy, the frequency of seizures, the treatment, the type of seizures were associated with the neuropsychological impairment identified (Table 4).

Table 4.  Multiple regression analysis of four independent variables on frontal tests in patients with JME
 WCST categoriesWCST errorsWCST perseverative responsesWord Fluency Test
Duration of epilepsy0.4060.687−0.7560.452−0.9650.3400.6570.514
Frequency of seizures−0.3080.7590.1660.8690.6170.540−0.2790.781
Type of seizures−1.4760.1470.2100.8340.0390.969−1.2070.234


  1. Top of page
  2. Methods
  3. Results
  4. Discussion
  5. Acknoledgments
  6. References

Our data clearly demonstrate the existence of frontal cognitive dysfunction in patients with JME. The performance of patients with JME on frontal tests was similar to that of patients with FLE, and it was significantly more impaired than TLE patients' and controls' results. These findings are comparable to those reported by the literature (Gershengorn et al., 1992; Devinsky et al., 1997; De Toffol et al., 1997; Lavandier et al., 2002; Sonmez et al., 2004; Pascalicchio et al., 2007).

The linear regression analysis performed indicated that the frontal cognitive deficits in patients with JME were not associated with other clinical factors, such as the duration of the pathology, the frequency of seizures, the treatment or the type of seizures. Some authors have hypothesized that these deficits may be mainly due to some neuroanatomic changes or to the effect of interictal spike-wave discharge on metabolism (Engel et al., 1982; Theodore et al., 1985; Rodin & Ancheta, 1987; Savic & Pauli, 1994).

Our results testify that JME patients have a serious impairment in frontal functions, meaning deficits in the cognitive processes involved in planning, concepts formation, elaborating strategies for the attainment of immediate or future goals, and verbal fluidity (Hommet et al., 2006). Swartz et al. confirmed the existence of similar neuropsychological deficits in JME, probably due to a cortical disorganization, which deeply affects frontal lobe functioning (Swartz et al., 1996). In an 18FDG-PET study, these authors documented an inability to activate the dorsolateral prefrontal, premotor and basal frontal cortex during a visual working memory paradigm. During this task, patients with JME, unlike control subjects, activated medial temporal structures.

Neuropathological studies of the brain in JME patients have noted the presence of microdysgenetic lesions in the neocortex and subcortical white matter of the frontal lobes and the hippocampus, which suggests a disorder in neuron migration and cortical disorganization (Mencke & Janz, 1984; Meeke, 1995; Hommet et al., 2006). Similar results were reported also by Simister et al. (2003), who analyzed patients with idiopathic generalized epilepsy by a point-resolved spectroscopy (PRESS)-localized short echo time MR spectroscopy (MRS). Woermann et al. (1999), using an interactive anatomical segmentation technique and volume of interest measurements by MRI, noted an increase in cortical grey matter in the mesial frontal lobe of patients with JME, pointing out a structural cerebral abnormality with the involvement of mesiofrontal cortical structures as well.

The cognitive deficits which exist in patients with JME can also be ascribed to epileptiform activity, which in JME is typically generalized 4–6 Hz spike-wave activity, maximum in the frontocentral regions (de Araujo wt al., 2006; Devinsky et al., 1997). For this reason, it is possible to speculate that patients with JME may show some specific impairment that anatomically corresponds with the seizure area, considering that the interactions between epileptiform EEG discharges and cognitive performances are complex and reciprocal (Tassinari & Rubboli, 2006). Lavandier et al. (2002) further investigated the link between epileptiform EEG discharges and frontal cognitive dysfunctions in JME; they remarked, using continuous EEG and video monitoring, that some frontal tasks were more impaired in patients with epileptiform EEG activity during rest than in those without discharges. It is not clear whether the deficits are due to a static or irreversible disorder or they are related to the impact of interictal epileptiform EEG activity on mental processes (Hommet et al., 2006). Clemens et al. (2000) investigated the EEG frequency profiles in patients with juvenile absence epilepsy, JME and epilepsy with grand mal seizures in the awakening area. Statistically significant bilateral absolute power differences were found in the frontal delta in patients with JME, whereas relative power differences were frontal delta and beta. The authors hypothesized that this profile reflects a cortical dysfunction more localized in the frontal lobes.

We decided to exclude patients with a psychiatric condition, in order to reach cleaner cognitive profiles, unaffected by the psychiatric state. We are aware that this selection has not taken into account the incidence of such disorders within the whole JME population; however, our primary goal was to capture the cognitive dimension of JME per se.

In our study sample, patients with FLE were those with the most significant impairment, as expected, followed by patients with JME, TLE and controls, in that order. The fact that patients with TLE performed worse than controls may be accounted for by the “neural noise” hypothesis, i.e., a propagation of neural noise via pathways which links the anterior temporal lobe and hippocampus with the frontal area (Hermann et al., 1988). Hermann et al. (1988) found that patients with TLE showed marked deficits on the WCST compared to a control group of patients with generalized epilepsy; they suggested that this dysfunction could be a result of the propagation of epileptiform spike activity to distant brain areas from the site of the primary area via ipsilateral and controlateral pathways.

Our study has some strengths and limitations. It is one of the largest surveys on frontal cognitive dysfunction in patients with JME and the only study that simultaneously evaluated the cognitive performances in three different types of epilepsy, as well as in normal controls. A limitation of the study is the reduced number of neuropsychological tests used, but the WCST and the Word Fluency Test are considered the most reliable validated Italian instruments for the age group considered (Giovagnoli & Piazzini, 1995).

This investigation confirms the importance of considering neuropsychological profiles of patients with JME. A detailed description of these patients can provide relevant information on their pathophysiologic status and on the relationship between paroxysmal and neuroanatomic abnormalities and cognitive tasks. We believe that more attention should be paid to this subject, so as to deeply understand the cognitive mechanisms, their deficiencies and strengths, and to provide patients with JME a better clinical and psychological care.


  1. Top of page
  2. Methods
  3. Results
  4. Discussion
  5. Acknoledgments
  6. References

We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.

Conflict of interest: None of the authors has any conflicts of interest to disclose.


  1. Top of page
  2. Methods
  3. Results
  4. Discussion
  5. Acknoledgments
  6. References
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