Abstract
Epilepsy is a network disease. The primary somatosensory cortex (S1) is usually considered to be intact, but could be subclinically disturbed based on abnormal functional connectivity in patients with temporal lobe epilepsy (TLE). We aimed to investigate if the S1 of TLE is abnormally modulated. Somatosensory evoked magnetic fields (SEFs) evoked by median nerve stimulation were recorded in each hemisphere of 15 TLE patients and 28 normal subjects. All responses were separately averaged in the awake state and light sleep using background magnetoencephalography. Latency and strength of the equivalent current dipole (ECD) was compared between the groups for the first (M1) and second peaks. Latencies showed no significant differences between the groups in either wakefulness or light sleep. ECD strengths were significantly lower in TLE patients than in controls only during wakefulness. The reduction of M1 ECD strength in the awake state is significantly correlated with duration of epilepsy. SEFs of TLE patients showed pure ECD strength reduction without latency delay. The phenomenon occurred exclusively during wakefulness, suggesting that a wakefulness-specific modulator of S1 is abnormal in TLE. Repetitive seizures may gradually insult the modulator of S1 distant from the epileptogenic network.
Highlights
No significant differences were found in latency of the M1 and M2 peaks of Somatosensory evoked magnetic fields (SEFs) between temporal lobe epilepsy (TLE) patients and normal subjects, during both the awake state and light sleep (Fig. 2)
The present study revealed that the equivalent current dipole (ECD) strength of SEFs was significantly lower in patients with TLE than in normal subjects exclusively during the awake state without prolongation of latency
These results imply that cortical function even outside the epileptogenic network (EN) is abnormal in TLE patients as a function of epilepsy duration
Summary
The primary somatosensory cortex (S1) is usually considered to be intact, but could be subclinically disturbed based on abnormal functional connectivity in patients with temporal lobe epilepsy (TLE). The ARAS widely projects to the cerebral cortex including the primary somatosensory cortex (S1) from the reticular formation in the brainstem[13], and modulates cortical function through the balance between excitatory and inhibitory synaptic transmissions mainly in the awake s tate[10,14,15]. The present study evaluated median nerve SEFs in the awake state and light sleep of patients with TLE to clarify whether the excitation level is abnormal in the S1 distant from the EN
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