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Parkinsons Disease beginings,gut implicated.

Brain-gut axis dysregulation

Novel brain-gut neurotransmitter imaging and functional brain imaging show dysregulation of the brain-gut axis at the peripheral, spinal, and cerebral levels, all of which contribute toward the symptoms of Gastro Intestinal Disorders. particularly IBS Irritable bowel syndrome

Neurotransmitters such as serotonin, norepinephrine(Drug information on norepinephrine), corticotropin-releasing factor, and opioids modify both motility and sensation in the gut. Therapies that target the CNS are commonly used because of their effect on the serotonin and norepinephrine pathways, which cause direct modulation on all levels of the brain-gut axis. Serotonin and norepinephrine have been traditionally used to manage psychological and psychiatric disturbances that are commonly associated with GI disorders.⁶

Treatment of IBSs with psychiatric agents has grown significantly in the past 2 decades. Close to 15% of patients with IBS are offered an antidepressant, and in many of these patients, a gastroenterologist initiates the treatment,still regaded by some schools as aquestionable action

Past and Present

Since the days of Descartes, there has been a clear delineation in Western medicine between functional and organic conditions in the biomedical model of medicine.Using traditional diagnostic techniques, such as endoscopy and imaging, IBS were often considered at the functional end of the functional-organic spectrum. This would necessarily imply an absence of detectable structural abnormalities.

In the past 2 decades, there has been a great surge of research on motility, brain imaging, and neurotransmitters, which has given us the brain-gut axis—a working formulation now used ubiquitously by all international research groups.The pathophysiological understanding of the organic aspects of IBS has increased to such a degree that there is some debate whether we can still strictly call it a functional disorder.11 The time of Descartes is being challenged, but unfortunately the negative stigma associated with functional conditions still lingers in the minds of many clinicians and patients.

One of the most clinically useful ways to conceptualize IBS is with the biopsychosocial model. In this model, the influences of the CNS (at the spinal and cerebral levels), autonomic nervous system, and hypothalamic-pituitary-adrenal axis result in sensory and motor dysfunctions of the GI tract in a bidirectional way.

The trigger can be peripheral (eg, GI infection, abdominal surgery) or central (eg, sexual abuse, personal losses, separation, deprivation). Psychosocial factors, such as alexithymia, catastrophization, ongoing work stress, and life events, often play an important role in the perpetuation and clinical manifestation of IBS through centrally mediated pathways.

Persons with IBS commonly have a history of major stressful life events; those at the severe end of the spectrum may also perpetuate their symptoms by means of maladaptive illness behavior–like catastrophizing This groups inability to incorporate and successfully deal with these psychosocial factors leads to more gastroenterology referrals and needless investigations at great cost, both financial and in quality of life.

Stress can enable IBS symptoms. Likewise, chronic IBS symptoms can lead to physiological effects. In addition, stress aggravates motility, lowers pain thresholds, and increases gut inflammation.

It  is suggested that Patients with severe and  symptoms of IBS may have central dysregulation of their pain regulatory pathways (central sensitization).16 Because many of these pathways are activated by the same neurotransmitters  (eg, serotonin, norepinephrine, opiates)

Neuroplasticity

Perhaps the most striking rationale for the use of centrally acting treatments in recent years is the concept of neuroplasticity. Antidepressants, and possibly psychotherapy, can promote neurogenesis (ie, the regrowth of neurons) following the loss of cortical neurons in psychiatric trauma. Functional MRI studies have shown reduced neuron density in cortical brain regions involved in emotional and pain regulation in patients with pain disorders and with IBS. Pain and psychological trauma (and particularly the combination of both) can be neurodegenerative—much like Alzheimer disease and Parkinson disease are.

In these psychological and pain conditions, antidepressants and other CNS-targeted agents and methods might offer some remedy by stimulating an increase in the levels of brain-derived neurotrophic factor following treatment. Brain-derived neurotrophic factor is a precursor to neurogenesis, and with prolonged treatment, neural increases that correlate with the degree of recovery from depression are seen.

The duration of antidepressant treatment also correlates with decreased relapse frequencies and recurrence of depression. These findings provide insight into neuronal growth regulation in key areas of the central pain matrix and provide new and important opportunities for research and patient care using antidepressants for the treatment of IBS

Summary

As our understanding of the pathophysiology and psychopathology of IBS grows, it is becoming evident that the use of centrally acting psychopharmacological medications and concomitant psychotherapy should play an ever-increasing role in its treatment. Psychosocial factors play a key role in the etiology of IBS, especially at the more severe end of the spectrum Psychiatrists have an important role in understanding and treating patients.

November 20, 2011 - Posted by admin | Nutrition | gut