Table 1.
The use of P300 component for the assessment of cognitive functions in patients with epilepsy.
| S. No. | No. of Diseased Subjects | No. of Control Subjects | Site | Reference Electrode | Frequent/Rare Stimuli (Hz) | Intensity (dB) | Activity | Reference |
|---|---|---|---|---|---|---|---|---|
| 1 | 65 (39 TLE patients and 26 IGE patients) | 28 | Cz and Pz | A1 and A2 | 1000/2000 | 70 | In TLE patients with bilateral temporal EEG foci, significantly prolonged latencies were observed at Cz. | [31] |
| 2 | 68 | 30 | F3, F4, F7, F8, T3, T4, T5, T6, C3, Cz, C4, P3, Pz, P4, O1 and O2 | Cheeks | 1000/2000 | 70 | Patients with epilepsy had significantly prolonged latencies than controls. Latencies were significantly prolonged in patients with TLE compared to patients with IGE. | [32] |
| 3 | 23 | 54 | Pz | A2 | 1000/2000 | 65 | The latency was significantly prolonged in BCECT than in healthy controls. The latency prolongation was greatest during the course of therapy. The latency was shorter with age despite of continuous CBZ therapy. | [33] |
| 4 | 15 | - | 28 sites | A1 and A2 | 1000/2000 | 100 | The amplitude was significantly attenuated ipsilateral to the epileptic focus. | [34] |
| 5 | 50 (32 with IGE and 18 with TLE) | 39 | Cz and Pz | A1 and A2 | 1000/2000 | 70 | The age-corrected latencies were significantly longer in patients with IGE than in controls. The age-corrected latencies were not significantly differed with TLE and controls, or IGE and TLE. | [35] |
| 6 | 129 | 53 | Pz | - | 1000/2000 | 65 | The latency was significantly longer in patients with epilepsies than in controls. The prolongation of latency was greatest in patients with SPE, mild in those with IGE, and minimum in those with IPE. Abnormalities of latency were observed at all ages during childhood in patients with SPE, and at older ages in patients with IGE. | [36] |
| 7 | 90 | 63 | Pz | - | 1000/2000 | The degree of EEG slowing was associated with the prolongation of age-corrected latency. The latency was significantly prolonged in the patients with marked slowing than patients with no slowing. | [37] | |
| 8 | 72 (26 with IPE, and 46 with SPE) | 67 | Pz | - | 1000/2000 | 65 | The impact of EEG abnormalities (especially paroxysmal discharges) on the latency was comparatively minor, and the cognitive impairment in IPE or SPE predominantly originates from the epileptogenic lesion. | [38] |
| 9 | 72 | 67 | Pz | - | 1000/2000 | 65 | Patients with SPE found to have significantly prolonged age-corrected latency than in patients with IPE. No relationship with the prolongation of the latency and the frequency of seizure, seizure type and seizure duration. | [39] |
| 10 | 12 (6 epileptics whose mean IQ was 100 and 6 epileptics whose mean IQ was 52) | 9 | Fz, Cz and Pz | A1 and A2 | 1000/2000 | 50 | Latencies and amplitudes were not significantly differed among the three groups. | [40] |
| 11 | 50 | 38 | Fz, Cz, C3 and Oz | A1 and A2 | 1000/2000 | A positive correlation between prolongation of latencies and course of epilepsy. The latency was closely associated with arithmetic, digit symbol and picture arrangement. | [41] | |
| 12 | 46 unmedicated and 74 medicated patients | 78 | Fz, Cz, and Pz | A1 and A2 | 1000/2000 | 70 | The latency and amplitude were not significantly varied in the unmedicated group as well as in the control group. The latencies were significantly prolonged in the medicated group than in the control group. | [42] |
| 13 | 84 (55 TLE patients with and 29 without AHS) | - | - | A1 and A2 | - | - | Limbic amplitudes were decreased on the side of the epileptogenic focus only in patients with AHS. Latencies were prolonged bilaterally in AHS patients. Amplitudes were reduced bilaterally in patients with left-sided AHS. | [43] |
| 14 | 64 CPE patients and 52 IGE patients | - | Fz and Cz | A1 and A2 | 1000/8000 | 95 | Latencies were longer in IGE patients, and amplitudes were lower in both CPE and IGE groups than in controls. No correlation between the prolongation of latencies and the type, AED serum level, and seizure control. | [44] |
| 15 | 20 | 20 | Cz and Pz | A1 and A2 | 1000/2000 | 70 | Patients with epilepsy were found to possess significantly longer latencies and lower amplitudes. | [45] |
| 16 | 108 | 32 | Fz, Cz, Pz | A2 | 1000/2000 | 70 | The latency was significantly prolonged in patients with symptomatic epilepsy than in patients without detectable brain lesions. The prolonged latency was significantly correlated with epilepsy duration, seizure frequency and antiepileptic treatment. | [46] |
| 17 | 27 patients IGE and 13 patients with TLE | 60 | P3 and P4 | A1 and A2 | 125/750 | 70 | The age-corrected latencies were significantly prolonged in patients with TLE than in patients IGE and controls. | [47] |
| 18 | 24 | - | Fz and Pz | A1 and A2 | 500/1000 | 80 | Auditory amplitude was decreased in patients with schizophrenia as well as patients with EPI-SZ. Delay in P300 was related to patients with epilepsy and EPI-SZ with the exception of patients with schizophrenia. | [48] |
| 19 | 10 | 10 | F3 F4 FC3 FC4 C3 C4 CP3 CP4 P3 P4 | A1 and A2 | 1000 | - | The ERP amplitude was decreased in postictal recordings (9 out of 10 patients with TLE) when compared with preictal recordings. | [49] |
| 20 | 50 | 21 | Fz, Cz, and Pz | A1 and A2 | 1000/8000 | 70 | Epileptic activity, itself, leads to prolonged P300 components of auditory ERPs and visual ERPs. | [50] |
| 21 | 120 (55 with partial seizures, 45 with generalized seizures and 20 with intractable seizures) | 25 | Cz | A1 and A2 | 1000/8000 | 95 | Significantly longer latencies were observed in the intractable and partial groups. Delayed P300 latencies were not significantly correlated with epilepsy duration, frequency of seizure and cerebral imaging pathologies. | [51] |
| 22 | 30 | 25 | Fz and Cz | A1 and A2 | 1000/8000 | 95 | P300 latency was significantly longer in the childhood epilepsy with occipital paroxysms group. | [6] |
| 23 | 73 | 31 | Cz and Fz | A1 and A2 | 1000 /2000 | - | The effect of P300 on fatigue was superior, but depression had no effect on P300 in patients with epilepsy. | [52] |
| 24 | 30 | 30 | Fz, Czand Pz | A1 and A2 | 1000/2000 | 60 | The latency and amplitude were not significantly differed in groups of seizures and chronic use of AEDs. | [27] |
| 25 | 21 | 21 | Cz and Fz | A1 and A2 | 1000/2000 | 90 | The latency and amplitude were not significantly differed among the groups. | [53] |
| 26 | 40 (9 with IPGE and 31 with SGE) | 40 | Fz, Czand Pz | A1 and A2 | 1000/2000 | 70 | The latencies were longer in patients with epilepsy when compared to control subjects. Patients with IPGE had longer latencies than SGE. | [54] |
| 27 | 30 | - | C3, P3, C4 and P4 | Nose tip | - | - | The P300 was shorter in patients with epilepsy than in controls, but there was no change after the treatment of topiramate or VPA. | [55] |
| 28 | 10 | - | Frontal, central, parietal and temporal | A1 and A2 | 1000/1500 | 90 | Temporal lobe dysfunction would change the P300 source locations in patients with TLE. | [56] |
| 29 | 9 with absence epilepsy and 13with complex partial epilepsy | 10 | Frontal (Fpz, F3, Fz, F4), central (C3, Cz, C4), parietal(P3, Pz, P4), and occipital (Oz) | A1 and A2 | Low −600, medium −1050, or high −150 | 50 | A significant reduction of the P300 was observed in absence patients group than in healthy controls. A significant reduction in the amplitude on the visual continuous performance test in both groups of seizure patients than in controls. P300 on the auditory continuous performance test was reduced only in patients with absence seizures. | [25] |
| 30 | 35 (IGE) | 20 | Fz and Cz | - | 1000/2000 | 90 | The latency was significantly correlated with reaction time duration in patients with epilepsy. | [57] |
| 31 | 12 | 12 | C3A1, C3A2, C4A1 and C4A2 | - | 1000/1500 | 75 | In LMTS subjects, a greater latency and a lower amplitude were observed at all sites than controls with a significant difference at C3A1 and C4A2 sites. | [58] |
| 32 | 53 | 20 | Cz and Pz | A1 and A2 | 1000/2000 | 50 | The latency of patients receiving LEV was significantly shorter when compared with patients receiving VPA and CBZ. Latencies of these three groups were significantly longer than the control group. | [59] |
| 33 | 14 | 14 | Fz, Cz and Pz | Nose tip | 1000/1050 | - | Latencies were prolonged by the ylang-ylang aroma in both patients with TLE and controls. The amplitude was significantly reduced in controls. | [60] |
| 34 | 16 | 43 (12 men) | Pz | A1 and A2 | 1000/2000 | 40 | A decrease of amplitude and an increase of latency were observed in patients with MTS than in controls. There was no correlation between duration of disease and features. | [61] |
| 35 | 20 | - | CPz and AFz | CPz | 1024 | 50 | In VNS responders, the amplitude was significantly increased at the parietal midline electrode. | [62] |
| 36 | 19 | 16 | Fz | A1 and A2 | 1000/2000 | 75 | No significant difference in the latency and amplitude between the groups. | [63] |
| 37 | 20 | 16 | Fz | A1 and A2 | 1000/2000 | 75 | The latency was significantly prolonged in TLE patients than in control. | [12] |
| 38 | 75 | 30 | C3 and C4 | A1 and A2 | 1000/2000 | 80 | The prolongation of latency was declined in integral functions of the CNS and information processing mechanisms occurring in epilepsy. | [64] |
| 39 | 18 | - | Pz | CPz | - | 50 | The amplitude was significantly increased in responders and decreased in non-responders. Non-midline electrodes are better P300 biomarkers. | [65] |
AEDs, antiepileptic drugs; AHS, Ammon’s horn sclerosis; BCECT, Benign childhood epilepsy with centrotemporal spike; CBZ, carbamazepine; CNS, central nervous system; CPE, cryptogenic partial epilepsy; EEG, electroencephalography; EPI-SZ, epilepsy interictal chronic schizophrenia-like features; ERP, event-related potential; IGE, idiopathic generalized epilepsy; IPE, idiopathic partial epilepsies; IPGE, idiopathic primary generalized epilepsy; LEV, levetiracetam; LMTS, left mesial temporal sclerosis; MTS, mesial temporal sclerosis; VPA, sodium valproate; SGE, secondary generalized epilepsy; SPE, symptomatic partial epilepsies; TLE, temporal lobe epilepsy; VNS, vagus nerve stimulation; IQ, intelligence quotient