A Companion Volume to Dr. Jay A. Goldstein's Betrayal by the Brain: A Guide for Patients and Their Physicians by Courmel Katie

Author:Courmel, Katie [Courmel, Katie]
Language: eng
Format: azw3
ISBN: 9781136374036
Publisher: Taylor and Francis
Published: 2013-04-02T16:00:00+00:00

Thalamic Reticular Nucleus (RT)

Normal Function—The thalamic reticular nucleus is a thin layer of cells wrapped around the dorsal thalamus. Providing the earliest developmental linkage between the thalamus and the cortex, the RT connects the numerous "relay nuclei" of the thalamus. The relay nuclei are the structures by which the thalamus receives sensory information from the body. The RT then regulates the transmission of pain and other signals to the cortex. The RT controls interneurons that release GABA, an inhibitory neurotransmitter whose selective secretion can send a sensory message of either pain or touch to the cortex. When the sensation is pain, GAB A inhibits messages regarding touch.

The RT also provides a pathway for crosstalk between the thalamus in each hemisphere, widening its sphere of influence to include the cerebral cortex and basal ganglia on both sides of the brain. The RT may help us focus our attention as well as regulate the connections that develop between the thalamus and the cortex.

The RT plays a role in the transition from waking to sleeping by regulating the action of thalamic interneurons that release the inhibitory neurotransmitter GABA. GABA deactivates the neurons that produce excitatory neurotransmitters such as acetylcholine and glutamate, inhibiting thalamocortical neurotransmissions and allowing uninterrupted sleep and REM sleep to occur.

Dysfunction in CFS/FMS—Dysfunction on in the RT, particularly related to secretion of GABA, could impede the onset of sleep as well as sleep maintenance, resulting in frequent awakenings or even nightmares.

With GABA secretion from the RT impaired, both touch and actual pain could produce the perception of pain. This could help explain the central pain mechanism of CFS/FMS.

The developmental plasticity of the RT makes it a probable structure for dysregulation in neurosomatic disorders. Inappropriate interconnections between the thalamus and the cortex might result from genetic factors or developmental and/or environmental stressors. A dysfunctional prefrontal cortex (PFC) could cause dysregulation in the RT's sensory gating functions. This could result in many of the bodily symptoms experienced by neurosomatic patients such as general pain, nerve pain, hot/cold sensations, and sleep disorders. It could also help explain the intermittent nature of these sensations and their tendency to move around the body without explanation.

The fatigue that CFS patients experience, along with their inability to focus attention, may relate to dysfunction in thalamic nuclei, because of dysregulation by the reticular nuclei and its cortical connections.

Drug Remediation—Gabapentin may enhance the function of the RT. Gabapentin increases GABA, inhibiting an inhibitory system in the RT, resulting in thalamocortical excitation.

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