Well, it just keeps getting more and more interesting...

I seem to recall several people posting here whose tremor was not alleviated by PD drugs. Could it be in essence because all of the research is based on a premise that PD is due to mass death of dopamine neurons? Tossing l-dopa at our brain sure does help alleviate a lot of our symptoms but really it has taken
over 50 years to get here to proving that our little localized brain lesion is so much more?

Although it is very widely claimed that there is a massive loss of the brain cells involved in Parkinson's Disease, not a single piece of research has ever shown this. from that (******* site on all things PD)

Evidence that PD tremor did not stem from loss of dopamine was first published in the 60's by one person, then resurrected in the 80's by two intrepid researchers and now over 20 years later we have a replicating experiment that confirms "ta da" there is no correlation between loss of dopamine upon PET scan and presence of tremor. Absolutely no evidence that tremor is caused by dopamine loss. Along come these guys in 2012:

A role for locus coeruleus in Parkinson tremor

However, researchers studied the the Locus Coereleus (home of Norepinephrine) during an activity and found that intensity of tremor varied by task but frequency remained constant. The LC is where we process stress and where adrenalin is released. This all makes a lot of sense because my tremor has always and still does respond to a beta-blocker. Note: I initially had a diagnosis of ET that lasted five years.

Authors conclude:

The introduction of the LC in the neural network dynamics of parkinsonian tremor might well explain many of its remarkable features. In particular, (1) tremor would appear only in PD subject with no functional damages of the LC; (2) eventually, along with PD progression and a consequent degeneration of LC-NA system, tremor will diminish; (3) tremor will appear during maneuvers that trigger LC activity, above all stress; and (4) PD patients do not manifest tremor during sleep being the LC silent. Finally, given a putative neuroprotective and compensatory activity of LC-NA on its target cells (including the substantia nigra and the striatum), it is tempting to speculate that an intact, or hyperactive, LC-NA system might be responsible for a more benign progression of PD in patients with tremor.

All these pending questions obviously require further studies in the future both by imaging and laboratory techniques. On this track, we hypothesize that parkinsonian tremor might represent the clinical sign of an enhanced LC activity as possible compensatory process over dopaminergic loss.