HFO are generated by different cellular mechanisms and can be detected in many brain areas. In
hippocampus, this fast neuronal activity is effect of the population synchronous
spiking of
pyramidal cells in the
CA3 region and
dendritic layer of the
CA1, which give rise to a characteristic oscillation pattern (see more in
sharp waves and ripples). The HFO occurrence during memory task (encoding and recalling images) was also reported in human patients from intracranial recordings in
primary visual,
limbic and higher order
cortical areas. Another example of physiological HFO of around 300 Hz, was found in
subthalamic nucleus, the brain region which is the main target for high-frequency (130 Hz)
deep brain stimulation treatment for patients with
Parkinson's disease.
Somatosensory evoked high-frequency oscillations ECoG recordings from human
somatosensory cortex, has shown HFO (reaching even 600 Hz) presence during
sensory evoked potentials and somatosensory evoked magnetic field after
median nerve stimulation. These bursts of activity are generated by thalamocortical loop and driven by highly synchronized
spiking of the thalamocortical fibres, and are thought to play a role in information processing. Somatosensory evoked HFO amplitude changes may be potentially used as biomarker for neurologic disorders, which can help in diagnosis in certain clinical contexts. Some oncology patients with
brain tumors showed higher HFOs amplitude on the same side, where the tumor was. Authors of this study also suggest contribution from the thalamocortical pathways to the fast oscillations. Interestingly, higher HFO amplitudes (between 400 and 800 Hz) after nerve stimulation were also reported in the EEG signal of healthy
football and
racquet sports players.
Pathological HFO There are many studies, that reports pathophysiological types of HFO in human patients and animal models of disease, which are related to different psychiatric or neurological disorders: • Amplitude aberrations of the sensory evoked HFOs (600 Hz) was reported in mild
demyelination in
multiple sclerosis patients. • HFO (>80 Hz) occur during epileptic seizure onset. • Disruption in the HFO (200–500 Hz) synchronization in
subthalamic nucleus is related to
Parkinson's disease symptoms. • High amplitude HFOs (80–200 Hz) bursts correlates with psychotic-like state evoked with
PCP or subanesthetic dose of
ketamine (and other
NMDA receptor blockers).
NMDA receptor hypofunction HFO reconstruction (done with kCSD method, red and blue dots) of the example HFO burst recorded (6 channel setup - green dots) from rat's brain (grey dots) There are increasing number of studies indicating that HFO rhythms (130–180 Hz) may arise due to the local NMDA receptor blockage, which is also a pharmacological model of schizophrenia.
nucleus accumbens Despite the fact that this type of HFO was not yet confirmed in human patients, second generation
antipsychotic drugs, widely used to treat schizophrenia and schizoaffective disorders (i.e.
Clozapine,
Risperidone), were shown to reduce HFO frequency. HFO in the bulb is generated by local excitatory-inhibitory circuits modulated by breathing rhythm and may be also recorded under ketamine-xylazine anesthesia. This findings may aid understanding early symptoms of schizophrenia patients and their relatives, that can suffer from olfactory system impairments. == See also ==