Faculty Bibliography

INTRODUCTION: Depression and memory dysfunction significantly impact the quality of life of patients with epilepsy. Current therapies for these cognitive and psychiatric comorbidities are limited. We explored the efficacy and safety of transcranial direct current stimulation (TDCS) for treating depression and memory dysfunction in patients with temporal lobe epilepsy (TLE). METHODS: Thirty-seven (37) adults with well-controlled TLE were enrolled in a double-blinded, sham-controlled, randomized, parallel-group study of 5days of fixed-dose (2mA, 20min) TDCS. Subjects were randomized to receive either real or sham TDCS, both delivered over the left dorsolateral prefrontal cortex. Patients received neuropsychological testing and a 20-minute scalp EEG at baseline immediately after the TDCS course and at 2- and 4-week follow-up. RESULTS: There was improvement in depression scores immediately after real TDCS, but not sham TDCS, as measured by changes in the Beck Depression Inventory (BDI change: -1.68 vs. 1.27, p<0.05) and NDDI-E (-0.83 vs. 0.9091, p=0.05). There was no difference between the groups at the 2- or 4-week follow-up. There was no effect on delayed or working memory performance. Transcranial direct current stimulation was well-tolerated and did not increase seizure frequency or interictal discharge frequency. Transcranial direct current stimulation induced an increase in delta frequency band power over the frontal region and delta, alpha, and theta band power in the occipital region after real stimulation compared to sham stimulation, although the difference did not reach statistical significance. DISCUSSION: This study provides evidence for the use of TDCS as a safe and well-tolerated nonpharmacologic approach to improving depressive symptoms in patients with well-controlled TLE. However, there were no changes in memory function immediately following or persisting after a stimulation course. Further studies may determine optimal stimulation parameters for maximal mood benefit.

Introduction: The role of sleep in learning and memory has gained significant attention in cognitive neuroscience. We report our experience with a healthy subject population at a sleep research center. Methods: We recruited subjects for a daytime nap and overnight sleep study by advertising at an urban university over one year. Subjects were eligible if aged 18 to 35, English-speaking, and scored above 26 on the Montreal Cognitive Assessment (MOCA). They were excluded for any diagnosis of a neurologic or psychiatric disorder, including a sleep disorder (as identified by the insomnia symptom questionnaire, STOP-BANG, and Morningness-Eveningness scale); used psychoactive medications, alcohol or recreational drugs; or recent travel across time zones. Subjects participated in cognitive tasks and slept with simultaneous EEG-PSG, which was scored by a board-certified sleep neurologist. Results: We obtained 40 nap studies and 20 nighttime studies. Screening questionnaires identified eligible subjects with a low risk of insomnia (0.22 +/- 0.52), low r isk of sleep apnea (0.82 +/- 0.75), and inter mediate ci rcadian preferences (47.15 +/- 0.75). There was a wide var iance in sleep efficiency (0.68 +/- 0.29) and total sleep time (TST, 69.86 +/- 33.78 min) during naps; with less variance seen during nocturnal studies (SD 0.84 +/- 0.08; TST 454.13 +/- 45.0 min). Three (15%) nap subjects demonstrated excessive daytime REM. Two nap subjects (5%) and three (15%) nighttime subjects were diagnosed with OSA. One nap subject (2.5%) and two nighttime subjects (10%) were diagnosed with periodic limb movements of sleep (PLMS). Conclusion: Our experience with a healthy subject population suggests a wide variance in daytime sleep behavior and a notable prevalence of sleep disorders such as OSA, PLMS, and excessive daytime REM. These variables should be considered in planning and analysis of sleep and cognition studies

Transcranial magnetic stimulation (TMS) holds great potential in the treatment of a host of neurological conditions due to its ability to focally modulate-suppress or enhance-activity in targeted cortical brain regions and modify activity across specific brain networks. Results from early trials in a number of neurological indications are presented, including stroke rehabilitation, Parkinson's disease, tinnitus, chronic pain, migraine, and epilepsy. We emphasize both the challenges, such as the limited efficacy to date in tinnitus, as well as the opportunities, such as the use of TMS in epilepsy caused by focal/cortical lesions. However, to establish TMS as a clinically valuable neurological therapeutic intervention, a number of hurdles must be overcome, including accurate targeting of the treatment, characterization of its therapeutic benefit for specific patients/symptoms, proof of efficacy in multicenter trials that are adequately blinded and powered, proof of the durability of the effects, and assessment of potential adverse effects of cumulative dose and repeated application.

PURPOSE: To examine the efficacy and safety profile of antiepileptic repetitive transcranial magnetic stimulation (rTMS) for refractory status epilepticus (RSE) in the intensive care unit (ICU) setting. In addition, hypothetical concerns about electrical interference of rTMS with ICU equipment have been previously raised. METHODS: We describe two cases of RSE treated with rTMS in the ICU. RESULTS: In one case, rTMS contributed to decreased seizure frequency; in the second case, rTMS transiently decreased seizure frequency. In both cases, rTMS was safe and did not interfere with the functioning of the ICU equipment. CONCLUSION: rTMS is a potential therapy for RSE when conventional therapies have failed. Future studies should investigate the efficacy of various rTMS stimulation parameters, safety issues, and bioengineering considerations in the ICU setting.

Since the introduction of highly active antiretroviral therapy in 1996, the epidemiologic profile of HIV-associated neurocognitive disorder (HAND) has shifted drastically. Although HIV-associated dementia has nearly disappeared from clinical practice, presymptomatic and milder variants of HAND affect up to 50% of patients on chronic antiretroviral therapy.(1,2) Furthermore, the predominant phenotype has evolved from a subcortical dementia to a mixed cortical-subcortical cognitive syndrome affecting attention, executive, and memory systems, as well as slowing processing speed.(2) Yet, subtler forms of HAND often remain undetected. One Swedish HIV study found that only 27% of their patient cohort complained of cognitive dysfunction, but 67% actually demonstrated objective deficits on cognitive testing.(3.)