Neurochemical Features of Rem Sleep Behaviour Disorder

Abstract

Dopaminergic deficiency, shown by many studies using functional neuroimaging with Single Photon Emission Computerized Tomography (SPECT) and Positron Emission Tomography (PET), is the most consistent neurochemical feature of rapid eye movement (REM) sleep behaviour disorder (RBD) and, together with transcranial ultrasonography, and determination of alpha-synuclein in certain tissues, should be considered as a reliable marker for the phenoconversion of idiopathic RBD (iRBD) to a synucleopathy (Parkinson’s disease –PD- or Lewy body dementia -LBD). The possible role in the pathogenesis of RBD of other neurotransmitters such as noradrenaline, acetylcholine, and excitatory and inhibitory neurotransmitters; hormones such as melatonin, and proinflammatory factors have also been suggested by recent reports. In general, brain perfusion and brain glucose metabolism studies have shown patterns resembling partially those of PD and LBD. Finally, the results of structural and functional MRI suggest the presence of structural changes in deep gray matter nuclei, cortical gray matter atrophy, and alterations in the functional connectivity within the basal ganglia, the cortico-striatal, and the cortico-cortical networks, but they should be considered as preliminary.

Current Treatment Options for REM Sleep Behaviour Disorder

“…Given the facts that PD is a very common neurological disorder and RBD is frequently associated with it before the onset of motor symptoms, it seems reasonable studies looking for neuroprotective strategies should include a selection of patients with polysomonographically confirmed iRBD and neurochemical and/or neuroimaging markers that suggest a high-risk of phenoconversion to synucleinopathies [15,91,97,99]. The combination of functional neuroimaging studies using different tracers, transcranial sonography, brain per-fusion and glucose metabolism studies, functional MRI, and the detection of α-synuclein in certain tissues should be useful for this purpose [15].…”

“…The neurochemical features of RBD include dopaminergic deficiency (the most consistent finding) and changes in noradrenaline, acetylcholine, excitatory and inhibitory neurotransmitters, hormones such as melatonin, and proinflammatory factors [15]. Patterns resembling those of PD and/or LBD have been found in brain glucose metabolism and brain perfusion studies, and cortical grey matter atrophy, structural changes in deep grey matter nuclei, and alterations in the functional connectivity between several networks including the basal ganglia and cerebral cortex have been found by using structural and functional MRI [15].…”

Emotional and Environmental Factors Aggravating Dream Enactment Behaviors in Patients with Isolated REM Sleep Behavior Disorder

“… 19 Furthermore, there is also evidence showing that psychological stress itself, regardless of PTSD, provokes disturbances of noradrenergic function in various brain regions. 20 Given the potential role of noradrenaline in the occurrence of RBD, 21 one can postulate that noradrenergic pathway alterations due to emotional stress contribute to the aggravation of DEBs in iRBD patients. Although stress has also been reported to increase serotonin turnover in the brain, 22 it remains debatable whether the serotonergic system is directly involved in RBD pathogenesis.…”

Sleep Disorders and Sleep Problems in Patients With Tourette Syndrome and Other Tic Disorders: Current Perspectives

“…Despite the fact that REM behaviour disorder is a very infrequent condition in children, 44 Trajanovic et al 45 described a boy diagnosed with TS who developed a clinical picture compatible with this disease aged 7 years. Modafferi et al 37 reported a frequency of 5.6% of sleep paralysis in patients with tic disorders and 2.6% in controls, although the difference did not reach statistical significance.…”