Tegmental Lesions and REM Behavior Disorder
Yes, lesions in the pontine tegmentum are well-established causes of REM behavior disorder (RBD), with documented cases demonstrating this anatomical relationship through both animal models and human case reports.
Neuroanatomical Basis
The pontine tegmentum contains critical structures for REM sleep regulation that, when damaged, directly cause RBD:
The sublaterodorsal nucleus and precoeruleus region in the pontine tegmentum house glutamatergic "REM-on" neurons that generate and maintain normal REM sleep muscle atonia 1, 2
The pedunculopontine tegmental nucleus and laterodorsal tegmental nucleus contain cholinergic neurons essential for REM sleep regulation, and damage to these areas disrupts the normal suppression of muscle tone during REM sleep 1, 2
Lesions in the midrostral pontine tegmentum specifically impair the mechanisms that normally produce muscle atonia during REM sleep, allowing dream enactment behaviors to occur 3, 4
Clinical Evidence from Lesional Studies
Multiple documented cases confirm tegmental lesions as causative:
MRI studies in RBD patients have demonstrated multifocal lesions in dorsal pontomesencephalic areas (pontine tegmentum) in patients with confirmed RBD, with 3 out of 6 patients showing lesions specifically in these regions 4
Acute inflammatory lesions in the pontine tegmentum have been documented to cause severe RBD, with one case showing a small unilateral lesion in the right pontine tegmentum resulting in persistent RBD with nightly dream enactment and injury to bed partners 5
Ischemic pontine lesions have been reported to cause RBD with characteristic polysomnographic findings of REM sleep without atonia, even in the absence of neurodegenerative disease markers 6
Pathophysiological Mechanism
The mechanism by which tegmental lesions cause RBD is well-understood:
Damage to tegmentoreticular tracts or the midrostral tegmentum nuclei disrupts the descending inhibitory pathways that normally suppress motor activity during REM sleep 4
Loss of normal REM muscle atonia occurs when these pontine structures are damaged, allowing the motor manifestations of dreams to be physically enacted 3, 7
Animal models dating to 1965 demonstrated that bilateral pontine tegmentum lesions in cats produced "oneiric behaviors" identical to human RBD, establishing the causal relationship decades ago 7
Clinical Implications and Diagnostic Considerations
When evaluating RBD with suspected tegmental lesions:
Brain MRI is essential to identify structural lesions in the pontine tegmentum, particularly looking for signal intensity changes in dorsal pontomesencephalic areas and periventricular regions 4
Polysomnography must document REM sleep without atonia (either sustained tonic or excessive phasic muscle activity) to confirm the diagnosis 1, 8
Lesional RBD may present atypically compared to neurodegenerative RBD, sometimes with predominant nightmares or rapid onset following the acute lesion 5, 6
Absence of neurodegenerative markers (negative clinical, biological, and instrumental biomarkers at follow-up) supports a purely lesional etiology rather than prodromal synucleinopathy 6
Important Caveats
Lesional RBD is rare compared to neurodegenerative causes; most RBD cases (38-65%) are associated with α-synucleinopathies like Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy 1
Treatment response may differ: lesional RBD may not respond to standard clonazepam therapy but may improve with melatonin, as demonstrated in inflammatory pontine lesion cases 5
The location matters: while pontine tegmentum lesions are most clearly associated with RBD, lesions in the dorsal medulla have also been implicated in some cases 5