Brain-Gut Interactions And Visceral
Reflexes.
The similarities in neurotransmitters in the gut and CNS further
stimulated our understanding of the interactions of the brain and gut. Since
the time of Pavlov and Komarov and their colleagues, reflexes between the brain
and gut and within the gut have been shown to control much of normal physiology
and pathophysiology. Visceral reflexes explain a number of clinical signs, many
of which are controlled by complex interactions mediated by spinal or CNS
pathways. Such vagal or sympathetic reflexes initiate patterned behaviors that
often involve multiple organs. Such reflexive responses stimulated by extrinsic
neurons are then mediated locally by enteric neural pathways or intrinsic
hormones.
One of the most important and well-studied brain-gut reflexes is the one associated with
the control of gastric and pancreatic secretion. Sights, smells, sounds, and
even the anticipation of food serve as external cues that can stimulate vagally
mediated reflexes. Perhaps the best known is the reflexive increase in acid
secretion that prepares the stomach to begin digestion. These reflexes are both
instinctive and learned. Although it is initiated as an autonomic nervous
system vagal reflex, the release of acid is ultimately mediated by complex
interactions of histamine released from enteroendocrine cells and the systemic
release of gastrin. Excess stress is known to cause gastric upset. Such stress
is often attributed to “nerves” and dismissed, but it may be an important cause
of disease, including peptic ulcers, as described by Cushing. For example, the
incidence of perforating gastric and duodenal ulcers increased markedly in
England during the bombings of World War II.
Another very important visceral reflex is the gastrocolic reflex. This
normal physiologic response of post-prandial emptying of the colon occurs
gradually as a meal is consumed and colonic contractility increases
progressively over the next 30 to 60 minutes. The reflex is initiated by
specific receptors in the duodenum that respond to the intake of fatty acids
but not liquid alone or nonessential amino acids. Patients who suffer from
irritable bowel syndrome have an exaggerated gastrocolic reflex. Colonic
contractility is not only more forceful but begins sooner than normal. Spastic
contractions occur shortly after a meal is ingested and often peak in
intensity before the meal is complete, causing diarrhea, cramping pain, and/or
bloating. In this centrally initiated reflex, local serotonergic neurons in the
myenteric plexus stimulate propulsive and spastic contractions that at one time
may lead to constipation and at another, diarrhea. Afferent impulses from the
hypercontractile and often distended sigmoid colon initiate reflexes to the CNS
(e.g., headache, a strange feeling in the head), to the bronchial tree
(difficulty in breathing), to the stomach (epigastric distress, indigestion),
and to the abdominal skin (intolerance of constricting garments).
The afferent limb of viscerosomatic reflexes originates from gut
viscera and then affects other visceral and somatic structures; it may involve
sympathetic or parasympathetic nerves. The efferent limb is usually via
parasympathetic nerves. The viscerosensory reflexes result from shared afferent
pathways where C fibers in the dorsal horn that are not myelinated from
visceral organs comingle with somatic afferents in the dorsal horn or spinal
column. They explain the phenomena of “referred pain” and of “skin
hyperalgesia,” which, in the case of sympathetic reflexes, occurs in skin areas
(dermatomes) innervated by the same spinal segment from which the nerve supply
of the diseased viscus is derived.
Unusual and often dangerous viscerosomatic or viscerovisceral reflexes
are commonly encountered. Gas-trointestinal disorders leading to vasovagal
reflexes often lead to syncope in the setting of severe abdominal pain,
extremes of nausea, exposure to particularly noxious substances, and severe
diarrhea. In such settings, visceral “brain-gut” stimuli initiate vagally
mediated hypotension, bradycardia, and diaphoresis. Swallowing syncope, a
related reflex, occurs when a patient experiences an esophageal spasm,
irritation, or distention that leads to vagally induced arrhythmias or
bradycardia and syncope. Gastroesophageal reflux can rarely lead to a similar reflex.
