DBN is frequently attributed to cerebellar pathology. Far less often, DBN arises from brainstem disease with midbrain etiologies being exceptionally rare and poorly characterized. In particular, DBN occurring with the dorsal midbrain syndrome has been reported only sporadically and has never been systematically examined.

Each of our three patients had aqueductal pathology: obstructive hydrocephalus from aqueductal stenosis, tectal glioma compressing the aqueduct, and infectious meningoencephalitis with secondary aqueductal narrowing. Upgaze paresis was evident in all three, skew deviation was present in two, and parkinsonism developed in two after shunt-related complications. 

Across all five patients, aqueductal stenosis or compression was observed, and upgaze paresis was a consistently associated clinical finding.

Involvement of the interstitial nucleus of Cajal, disruption of descending midbrain projections to paramedian tracts, or unstable cerebellar outflow could conceivably produce DBN at the level of the midbrain, but clinical and experimental evidence make these explanations less compelling. Converging evidence from our series, prior reports, and animal models, instead, points to posterior commissural dysfunction related to aqueductal pathology as the most plausible mechanism for DBN in association with the dorsal midbrain syndrome. Lesions of the posterior commissure may disrupt fibers responsible for vertical gaze holding and input from the vertical vestibular system, creating a rare imbalance that drives slow upward eye movement to create downbeat nystagmus, even with impaired upward range of eye movement.