Focused ultrasound-mediated suppression of chemically-induced acute epileptic EEG activity
Byoung-Kyong Min, Alexander Bystritsky, Kwang-Ik Jung, Krisztina Fischer, Yongzhi Zhang, Lee-So Maeng, Sang In Park, Yong-An Chung, Ferenc A Jolesz, Seung-Schik Yoo
BMC Neuroscience 2011, 12 · 10.1186/1471-2202-12-23
Abstract
Background Epilepsy is a common neurological disorder, which is attributed to uncontrollable abnormal hyper-excitability of neurons. We investigated the feasibility of using low-intensity, pulsed radiation of focused ultrasound (FUS) to non-invasively suppress epileptic activity in an animal model (rat), which was induced by the intraperitonial injection of pentylenetetrazol (PTZ). Results After the onset of induced seizures, FUS was transcranially administered to the brain twice for three minutes each while undergoing electroencephalographic (EEG) monitoring. An air-backed, spherical segment ultrasound transducer (diameter: 6 cm; radius-of-curvature: 7 cm) operating at a fundamental frequency of 690 KHz was used to deliver a train of 0.5 msec-long pulses of sonication at a repetitive rate of 100 Hz to the thalamic areas of the brain. The acoustic intensity (130 mW/cm2) used in the experiment was sufficiently within the range of safety guidelines for the clinical ultrasound imaging. The occurrence of epileptic EEG bursts from epilepsy-induced rats significantly decreased after sonication when it was compared to the pre-sonication epileptic state. The PTZ-induced control group that did not receive any sonication showed a sustained number of epileptic EEG signal bursts. The animals that underwent sonication also showed less severe epileptic behavior, as assessed by the Racine score. Histological analysis confirmed that the sonication did not cause any damage to the brain tissue. Conclusions These results revealed that low-intensity, pulsed FUS sonication suppressed the number of epileptic signal bursts using acute epilepsy model in animal. Due to its non-invasiveness and spatial selectivity, FUS may offer new perspectives for a possible non-invasive treatment of epilepsy.
Abstract via europepmc.
Exposures
Exposure 1: 690 kHz pulsed FUS to rat thalamus, PTZ epilepsy model
Target: thalamus — “the thalamic areas of the brain”
Device: not reported
| Waveform | pulsed | |
|---|---|---|
| Fundamental frequency (kHz) | 690 | ✓✓✓ |
| Pulse duration (ms) | 0.5 | ✓✓✓ |
| Pulse repetition frequency (Hz) | 100 | ✓✓✓ |
| Duty cycle (%) | not reportedpulse duration × PRF gives 5% | ⚑ |
| Sonication duration (s) | 180 | ✓✓✓⚑ |
| Free-field pressure (kPa) | not reported | |
|---|---|---|
| Free-field Isppa (W/cm²) | not reported | |
| Free-field Ispta (W/cm²) | not reported | |
| In-situ estimate | not reported | |
| In-situ pressure (kPa) | not reported | |
| In-situ Isppa (W/cm²) | not reported | |
| In-situ Ispta (W/cm²) | not reported | |
| Pressure, domain unspecified (kPa) | 270 | ✓✓✓⚑ |
| Isppa, domain unspecified (W/cm²) | 2.6 | ✓✓✓ |
| Ispta, domain unspecified (W/cm²) | 0.13 | ✓✓✓⚑ |
A train of 0.5 ms tone bursts at 100 Hz PRF delivered twice for three minutes each after seizure onset, with ten minutes of EEG recording between and after sonications.
Flags from extraction
exposures[0].unspecified_domain.pressure_kpa— Peak negative pressure 0.27 MPa 'measured' with a hydrophone, but the paper also estimates pressure after rodent skull attenuation; domain not clear, so recorded as unspecified.exposures[0].unspecified_domain.ispta_w_cm2— Ispta 130 mW/cm2 converted to 0.13 W/cm2.exposures[0].timing.duty_cycle_pct— Duty cycle not stated; not computed.exposures[0].timing.sonication_duration_s— Two three-minute sonications separated by ten minutes of recording; duration recorded as the length of one sonication.exposures[0].device.family— Transducer described as air-backed spherical segment; no maker named (Sonomo is the control software).