Previous studies have shown that patients with major depression have an interhemispheric imbalance between right and left prefrontal and motor cortex. We aimed to investigate the interhemispheric interactions in patients with major depression using repetitive transcranial magnetic stimulation (rTMS). Thirteen patients with major depression and 14 age-matched healthy subjects participated in this study. Corticospinal excitability before and after 1 Hz rTMS (applied to the left primary motor cortex) was assessed in the left and right motor cortex and these results were compared with those in healthy subjects. There was a significant difference in the interhemispheric effects between patients with depression and healthy subjects. In healthy subjects, 1 Hz rTMS significantly decreased corticospinal excitability in the stimulated, left hemisphere and increased it in the contralateral, right hemisphere. In depressed subjects, 1 Hz rTMS also decreased corticospinal excitability in the left hemisphere; however, it induced no significant changes in corticospinal excitability in the contralateral, right hemisphere. In addition, there was a significant correlation between the degree of interhemispheric modulation and the severity of the depression as indexed by the Beck Depression Inventory scores. Our findings showing a decreased interhemispheric modulation in patients with major depression are consistent with the notion that mood disorders are associated with slow interhemispheric switching mechanisms.

Objective: Sudden unexpected death in epilepsy (SUDEP) is a frequent cause of death in epilepsy. Respiratory dysfunction is implicated as a critical factor in SUDEP pathophysiology. Human studies have shown that electrical stimulation of the amygdala resulted in apnea, indicating that the amygdala has a role in respiration control.Unilateral amygdala stimulation resulted in immediate onset of respiratory dysfunction occurring only during nose breathing. In small numbers of patients, some but not all spontaneous seizures resulted in apnea occurring shortly after seizure spread to the amygdala. With this study we aimed to determine whether seizure onset or spread to the amygdala was necessary and sufficient to cause apnea. Methods: We investigated the temporal relationship between apnea/hypopnea (AH) onset and initial seizure involvement within the amygdala in patients with implanted depth electrodes. Results: Data from 17 patients (11 female) with 47 seizures were analyzed. With seven seizures (three patients), AH preceded amygdala seizure involvement by 2 to 55 seconds. There was no AH with four seizures (three patients) that involved the amygdala. With eight seizures (four patients) AH occurred within 2 seconds following amygdala seizure onset. With 28 seizures, AH started >2 seconds after amygdala seizure onset (range 3-158 seconds). Following seizure onset, there was a significant difference between AH onset time and amygdala seizure onset (P < .001). The mean ± standard deviation (SD) AH onset was 27.8 ± 41.06 seconds, and the mean time to amygdala involvement was 8.83 ± 20.19 seconds. Significance: There is a wide range of AH onset times relative to amygdala seizure involvement. With some seizures, amygdala seizure involvement occurs without AH. With other seizures, AH precedes amygdala seizures, suggesting that, with spontaneous seizures, involvement of the amygdala may not be crucial to induction of AH with all seizures. Other pathophysiology impacting brainstem respiratory networks may be of greater relevance to seizure-triggered apneas.

Introduction: Door-to-needle time (DTN) is associated with outcome in acute ischemic stroke (AIS) patients who are eligible to receive intravenous tissue plasminogen activator (IV tPA). Various factors have been shown to impact DTN time including patient-related factors such as initial refusal or management of hypertension, hospital-related factors such as laboratory tests; and system-related factors all potentially affecting clinical outcomes. Neurological deficits such as aphasia could potentially affect DTN through various mechanisms including difficulty in obtaining accurate last known well time (LKWT), discussing risks vs benefits of IV tPA, etc. We sought to investigate the association between aphasia as a presenting neurological deficit and DTN. Methods: This was a retrospective chart review of prospectively collected data through Get-with-the-Guidelines from 7/17 to 6/18 at our comprehensive stroke center. Data regarding patient demographics, medical history, last known well time (LKWT), arrival time, door-to-CT time, treatment time, admission National Institutes of Health stroke scale (NIHSS), pre-stroke modified Rankin scale (mRS) were analyzed. Pearson chi-square test was performed to determine association between aphasia and DTN time. Results: Out of 110 patients (mean age 72 years; 59% women) who received IV tPA; 40% had aphasia as part of their clinical presentation. Patients with aphasia were older (76 vs 69 years) and had higher admission NIHSS (13 vs 6). DTN times did not differ significantly between patients presenting with aphasia vs other neurological deficits (44 vs 45 minutes; p=0.84). No difference was observed between door-to-CT time (16 vs 18 minutes) and LKWT-to-treatment time (138 vs 142 minutes). Conclusion: We did not find significant differences in tPA treatment times in patients with AIS based on the presence or absence of aphasia. Although aphasia could present challenges in the evaluation of patients with AIS, the increased severity of neurological deficits inherent to aphasia may lead to a faster work flow. A small sample size is a major limitation of our study. Further research into the influence of aphasia and other presenting neurological symptoms on DTN is warranted.