PEMF AND INFLAMATORY BOWEL DISEASE
Disclaimer: Please note that these pages are for general information purposes only. The opinions and information have not been evaluated by the FDA. They should not be considered complete in terms of the physical conditions discussed, or construed as healthcare advice.
Parkinson’s disease (PD) is a brain disorder affecting predominately the nerve cells in a specific area of the brain called the substantia nigra leading to damage to the basal ganglia. The basal ganglia controls much of the muscle movement of the body. Many of the symptoms of PD are due to the breakdown or death of neurons that produce a chemical messenger in the brain called dopamine. When dopamine levels decrease, it causes abnormal brain activity, leading to impaired movement and other symptoms of PD. Clumps of breakdown substances inside damaged brain cells are the microscopic markers of PD and are known as Lewy bodies. Inside the Lewy Bodies, is a protein, alpha-synuclein, which cannot be broken down and eliminated. PD is characterized by motor and non-motor symptoms. The main motor symptoms include bradykinesia (slow movement), tremor at rest (tremor affecting the body part that is relaxed or supported against gravity and not involved in purposeful activities ), rigidity and postural instability [2, 3, 4, 5, 6, 7]. However, motor symptoms are now considered only the “tip of the iceberg” of PD clinical manifestations. PD non-motor symptoms include cognitive decline, decrease in sleep efficiency, increased wake after sleep onset, sleep fragmentation, and vivid dreams as well as neuropsychiatric symptoms such as depression and psychosis, [8, 9, 10, 11, 12,13]. Pain syndromes and autonomic dysfunctions have also been observed in PD patients [14, 15, 16]. Individuals with PD are often impacted by their non-motor symptoms as much or more than motor symptoms. While Parkinson’s itself is not fatal, disease complications can be serious. Although there is no cure, treatment options vary and include medications, surgery and adjuncts for activities of daily living.
In vitro (cell-line studies) and in vivo (animal studies) treatment with pulsed electromagnetic fields (PEMF) has demonstrated potential neuroprotective effects. For example, PEMF was shown to regulate neutrophic factors such as brain derived neurotrophic factor, S100 and nerve growth factor. These three factors help create brain cells, regulate their function and stimulate the cells ability to adapt and grow [17,18]. PEMF enhances cell proliferation (growth) and differentiation [17,19], enhances neurite growth , reduces apoptosis (cell death) , stimulates angiogenesis (blood vessel growth) , increases microvascular perfusion and tissue oxygenation , and stimulates neurogenesis (nerve cell growth) in the hippocampal dentate gyrus  and in the sub ventricular zone after injury to the substantia nigra . The molecular mechanisms of PEMF are not yet fully understood. However, PEMF may affect the tissue directly by the interactions between the electromagnetic fields (EMF) and conductive tissue, and indirectly by initiating biological events leading to a physiologic response .
PEMF stimulation of the ventral intermediate nucleus of the thalamus can dramatically relieve PD associated tremor [26,27]. Similarly, stimulation of the Subthalamic nucleus or globus pallidus interna (GPi) can substantially reduce rigidity, tremor, gait difficulties, and slowness in movement in patients [26, 28, 29, 30, 31]. Moreover, PEMF therapy improved PD associated freezing (a symptom manifesting as a sudden attack of immobility usually experienced during walking ). Stimulation of the GPi also reduces all of the major PD motor manifestations, including the reduction of l-dopa-induced dyskinesias (medication induced muscle dysfunction) and involuntary movements produced by individual doses of dopaminergic medications that can limit treatment efficacy . PD patients treated with PEMF saw significant improvement in motor symptoms, tremor, rigidity and akinesia (loss of voluntary movement), which allowed the patient to decrease the amount of the medication l-dopa they were taking by a mean of 55% .
PEMF increases the release of dopamine in the striatum and frontal cortex, which in turn improves PD symptoms including motor performance . Furthermore, PEMF applied in the prefrontal cortex induces the release of endogenous (made by the body) dopamine in the ipsilateral caudate nucleus as observed by positron emission tomography (PET imaging) in healthy human subjects . PEMF application results in partial or complete disappearance of muscular pain and l-dopa-induced dyskinesia as well as the improvement of visuospatial (ability to see the space relationship of objects) impairment, suggesting that PEMF has a beneficial effect on corticostriatal (the pathway of information flow into the basal ganglia) interactions that play an important role in the pathophysiology (development and progression) of PD [37,38].
In 2008, the Food and Drug Administration approved the use of PEMF for major depressive disorder in PD patients who failed to achieve satisfactory improvement from very high dosages of antidepressant medications [39,40]. Several studies reported PEMF improved cognitive functions and motor symptoms. For example, an investigation involving three elderly PD patients with cognitive impairment assessed the effect of PEMF on macrosomatognosia, a disorder of body image in which the patient perceives a part or parts of his body as disproportionately large . PEMF applied to the frontal cortex can effectively alleviate PD associated depression as shown by a significant decrease in the Hamilton Depression Rating Scale (HDRS) scores . A further double blind, sham stimulation-controlled, randomized study, involving 42 PD patients affected by major or minor depression undergoing PEMF, evidenced a mean decrease in HDRS and Beck depression inventory after therapy .
PD affects the right prefrontal area, causing executive dysfunction which is characterized by deficits in internal control of attention, set shifting, planning, inhibitory control, dual task performance, decision-making and social cognition tasks [44,45]. PEMF sessions were found to enhance not only executive function, but subjective symptoms and objective findings of higher cognition, planning, personality, and proper social behavior [44,46].
Pulsed Electromagnetic fields (PEMF) opens a new avenue for PD treatment and can be tailored to the PD patient’s needs. Furthermore, PEMF can also be combined with pharmacological or non-pharmacological treatments, e.g., physical therapy and cognitive tasks, to produce additive or potentiated clinical effects.
In conclusion, pulsed electromagnetic fields represents a non-invasive, safe and promising approach that can be used alone or combined with conventional therapies for the challenging treatment of PD motor and non-motor symptoms.
Dr. Amanda Myers, MD, MSPH
Aura Medical Director
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