الفهرس 
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Abstract
Background: A reciprocal interaction exists between sleep and epilepsy. Sleep disorders are frequently reported in patients with epilepsy. Patients and Methods: 90 epilepsy patients were included; 60 patients with drug refractory epilepsy and 30 patients with drug-controlled epilepsy. A healthy control group of 20 sex and age matched individuals was also included. All participants underwent detailed history taking, neurological examination. Psychiatric evaluation was done using Hamilton’s scale for anxiety (HAM-A) and Neurological disorders depression inventory for epilepsy (NDDI-E). Subjective sleep evaluation was done using Pittsburg Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS) then an overnight Polysomnographic (PSG) study. Radiological evaluation by MRI brain and MRS on both thalami, upper pons and both medial temporal lobes was also done, ratios of NAA/Creatine, NAA/Choline and Choline/Creatine were assessed at those sites. Results: Scores of PSQI, ESS, Hamilton anxiety rating scale (HAM-A) and Neurological disorders depression inventory for epilepsy (NDDI-E) were higher in the refractory epilepsy group. On PSG study; long N1, N2 sleep and decreased N3 percentage were found in both groups to a similar statistical degree, when compared to the healthy group. Patients in the refractory group had significantly decreased sleep efficiency, decreased total sleep time, delayed sleep onset latency and REM latency and decreased REM percentage. OSA was more significantly prevalent in the refractory epilepsy group. Increased number of used AEDs was significantly associated with higher scores of PSQI and ESS scores, increased sleep onset latency, decreased sleep efficiency and total sleep time. Increased seizure frequency was significantly associated with higher scores of ESS, delayed sleep onset, decreased sleep efficiency, and increased AHI. Increased duration of seizure control in the group of controlled epilepsy was more associated with lower percentage of N2 sleep, higher percentage of REM sleep and lower arousal index. In the group of refractory epilepsy, scores of HAM-A were significantly inversely correlated with percentage of sleep efficiency and significantly positively correlated with sleep onset latency. Moreover, scores of NDDI-E were significantly inversely correlated with total sleep time (TST), sleep efficiency and significantly positively correlated with Sleep onset latency. Using MRS, the refractory epilepsy group had statistically significantly decreased ratios of NAA/Cr and NAA/Choline, when compared to the healthy group, at bilateral thalami. NAA/Cr ratio was also decreased at a side of pons. In the controlled epilepsy group; ratio of NAA/Cr was statistically significantly decreased only at one thalamus and at a side of pons when compared to the healthy group. In refractory epilepsy; duration of epilepsy, duration of intractability and age at onset of epilepsy were associated with statistically significant decline in levels of neuronal viability markers at both thalami. Conclusion: Sleep architecture is also more widely disturbed in refractory epilepsy patients and may play a role in intractability. Causes of those sleep disturbances are diverse and multifactorial e.g.; seizure frequency, associated sleep disorders like OSA, associated psychiatric disorders e.g. anxiety and depression or due to used AEDs. In addition, neuronal loss at centers controlling sleep integrity e.g. thalamus and pons may complicate the disease leading to this disruption of sleep