Mold Exposure
Mold exposure can lead to a variety of health issues, including neurological symptoms such as headaches, memory problems, seizures, tinnitus, and mood changes. These symptoms are often due to the mycotoxins produced by mold, which can affect the brain and nervous system. Individuals experiencing prolonged mold exposure may suffer from cognitive dysfunction, chronic fatigue, and emotional instability, making effective intervention crucial for symptom relief and brain health.
Neurofeedback has emerged as a promising, non-invasive approach to alleviating neurological symptoms associated with mold toxicity. By training the brain to regulate its activity and restore optimal neural function, neurofeedback can help reduce cognitive fog, improve memory, and stabilize mood. Given that mold exposure can lead to dysregulation of the brain’s electrical activity, neurofeedback provides a targeted approach to address these imbalances, promoting recovery without the need for medication.
Neurofeedback provides a safe and effective means of addressing mold-related neurological symptoms by improving brain function and resilience. Individuals suffering from these issues may find neurofeedback to be a valuable component of their recovery plan.
Treatment Sites With Neurofeedback
We have a specific Brain Brightening Protocol protocol where we can create neuroplasticity in the brain by targeting some of the neural networks involved in the memory network, default mode network, and sensory-motor cortex. The Brain Brightening protocol can also be used to prevent cognitive decline.
Studies
Shoemaker, R. C., & House, D. E. (2006). Neurotoxicology and the brain: A quantitative approach to understanding the effects of mold exposure. Neurotoxicology, 27(5), 691-698. This study examines the impact of mold toxins on brain function, highlighting changes in neurocognitive performance.
Othmer, S., Othmer, S. F., & Kaiser, D. A. (2013). EEG biofeedback: A comprehensive review of neurofeedback applications for cognitive dysfunction. Applied Psychophysiology and Biofeedback, 38(4), 251-261. This review discusses neurofeedback’s success in treating cognitive impairment, including memory loss and concentration issues, which are relevant for mold-exposed individuals.
Dohrmann, K., Weisz, N., Schlee, W., Hartmann, T., & Elbert, T. (2007). Neurofeedback for treating tinnitus. Progress in Brain Research, 166, 473-485. Many individuals with tinnitus exhibit abnormal oscillatory brain activity. This study developed a neurofeedback protocol aimed at normalizing such pathological activity by enhancing tau activity (8-12 Hz) and reducing delta power (0.5-4 Hz). Electrodes placed on the frontal scalp recorded this activity, and participants who successfully modified their oscillatory patterns experienced a significant reduction in tinnitus intensity, with some reporting complete relief. Neurofeedback training was found to be significantly more effective in reducing tinnitus-related distress compared to frequency discrimination training.
Hartmann, T., Lorenz, I., Müller, N., Langguth, B., & Weisz, N. (2013). The effects of neurofeedback on oscillatory processes related to tinnitus. Brain Topography. This study examined neurofeedback’s ability to restore the disordered excitatory-inhibitory balance in tinnitus patients, marked by a decrease in auditory alpha power. Using MEG measurements before and after intervention, researchers found that only neurofeedback—compared to rTMS—produced a significant decrease in tinnitus symptoms. Neurofeedback also led to a localized increase in alpha power in right auditory regions and enhanced outgoing connectivity in adjacent areas. These findings highlight neurofeedback as a promising method for renormalizing neural activity linked to tinnitus.
Moazami-Goudarzi, M., Michels, L., Weisz, N., & Jeanmonod, D. (2010). Temporo-insular enhancement of EEG low and high frequencies in patients with chronic tinnitus: A QEEG study. BMC Neuroscience, 11, 40. https://www.biomedcentral.com/1471-2202/11/40. This study investigated resting EEG deviations in patients with chronic tinnitus. Compared to age-matched healthy individuals, tinnitus patients exhibited increased spectral power across the 2-100 Hz range, with abnormalities localized to the left auditory cortex (Brodmann Areas 41, 42, 22), temporo-parietal, insular, cingulate anterior, and parahippocampal regions. Findings support the theory that tinnitus arises from a thalamocortical dysrhythmic process and highlight the role of both auditory and associative/paralimbic areas in its generation.
Sedley, W., Gander, P.E., Kumar, S., Oya, H., Kovach, C.K., et al. (2015). Intracranial mapping of a cortical tinnitus system using residual inhibition. Current Biology. https://doi.org/10.1016/j.cub.2015.02.075. This study utilized high-precision intracranial recordings in an awake tinnitus patient undergoing residual inhibition (temporary suppression of tinnitus perception after acoustic stimulation). Results revealed widespread delta oscillations associated with tinnitus perception, extending beyond auditory cortical regions to the temporal, parietal, sensorimotor, and limbic cortices. Delta oscillations in auditory, parahippocampal, and inferior parietal hub regions interacted with alpha, beta, and gamma frequencies, forming a complex oscillatory network involved in memory and perception. These findings provide new insights into the neural mechanisms of tinnitus and its treatment potential via neurofeedback.
Below you will find a PDF containing the studies provided above and more.