After reading my last post, you may be wondering if it’s just a coincidence that lesions in the cerebellum mimic many of the disinhibited behavioral features of PSP. It’s no coincidence, and here’s why.
The motor role of the cerebellum in effect acts as a “brake” on the actions of the cerebral motor cortex and basal ganglia. The “ataxic” gait of cerebellar disease is characterized by unchecked lateral movement of the center of gravity. Once the proprioceptive (joint position sense) and visual functions perceive that one is reeling to one side, a voluntary check and corrective action occur. But that correction, similarly, goes too far, producing a reeling in the other direction. This is the familiar gait of the drunk, as alcohol is an acute cerebellar toxin.
The same goes for other cerebellar motor deficits. The uncoordinated hand movements consist of overshooting a goal followed by a correction that itself overshoots, and the process repeats, producing a kind of tremor or wavering. The speech, besides its slurring, is degraded by an unintended, rapid grouping of syllables followed by a long pause. Try it — if you want to mimic drunkenness. The eyes exhibit a slow, involuntary movement of a few degrees to one side followed by a rapid correction. This is called “nystagmus” and can produce a constant jittering of the visual scene that may be described by the patient as “double vision.”
The behavioral aspects of cerebellar dysfunction are analogous. Just as they cause a loss of inhibition of an ongoing motor action, so do they cause a loss of inhibition on behavior, with inappropriate or repetitive comments, compulsive thoughts and incontinent laughter or crying.
So, yes, it makes sense.