"Learning points

 a.. For patients with a brief history of poorly controlled
diabetes, the risk versus benefit analysis overwhelmingly
favours rapid glycaemic control.

 b.. In diabetic patients with chronically poor glycaemic
control, with the exceptions of hyperglycaemic emergencies
such as diabetic ketoacidosis or hyperglycaemic-hyperosmolar
non-ketototic coma, it is prudent to attain their glycaemic
targets over a gradual time frame to avoid acute
deterioration and precipitation of retinopathy and
neuropathy."

Hi Jan:

Under-recognised paradox of neuropathy from rapid glycaemic control

Your second excellent find on the subject of diabetic complications from
rapid glycemic control, the other being in the Retinopathy Progression
thread - http://medweb.bham.ac.uk/easdec/retinopathyprogression.htm.
Home page of the organization - http://medweb.bham.ac.uk/easdec/index.html

This graph at least shows a representation of the phenomena in question.
Figure 2  Hypothetical relation of risk of neuropathy with rate of
glycaemic control.-
http://pmj.bmjjournals.com/cgi/content/full/81/952/103/F2

While the question of optimal timing is not resolved in this article, it
does present the idea that studies should be done to get a better idea
of the "U" shaped curve conceptualized in figure 2, i.e., the
appropriate pacing of glycemic control in people with extreme hyperglycemia.

"This is usually a distal sensory polyneuropathy developing within a
month of aggressive diabetic control with intensive insulin therapy. ...

While evidence from studies such as the DCCT and UKPDS form the basis of
daily clinical practice, it is still largely oblivious to clinicians
that highly intensive treatment that rapidly achieves glycaemic targets
may ironically be undesirable and even have deleterious impacts on
microvascular outcomes. This is because neuropathy has been so well
established as a known microvascular complication of poorly controlled
diabetes that it becomes counter intuitive to imagine that rapid
glycaemic control should result in the very form of complication that
good control is supposed to prevent. ...

Diabetic neuropathy is an established microvascular complication related
to suboptimal glycaemic control. But hyperglycaemia is not the sole
factor in the pathogenesis of neuropathy in people with diabetes.1
Scattered throughout the medical literature are sporadic reports of
deterioration of neuropathy that apparently occurred during dramatic
resolution of chronic hyperglycaemia, associated with precipitous
declines in glycosylated haemoglobin (HbA1c) concentrations.2,3 This
unexpected phenomenon implicates hypoglycaemia in the precipitation of
neuropathy in both patients with pre-existing neuropathy and normal
baseline neurological status, given that those without a history of
neuropathy develop it after they become afflicted with insulinomas.4 It
is debatable as to whether the mere rapid attainment of euglycaemia,
associated with drastic decreases in HbA1c concentrations without
hypoglycaemic episodes punctuating the clinical course, can result in
this complication likewise. While the mechanisms of such seemingly
paradoxical results are being unravelled, it is prudent to instil in
clinicians the awareness of such entities and emphasise the dual edged
sword of rapid normalisation of chronically raised blood glucose
concentrations as the universal strive to reach satisfactory glycaemic
end points continues."

The list of references at the end of the article had many citations that
used terms like "hypoglycemic peripheral neuropathy."  It seems that
hypoglycemia can reduce blood supply to the nerves and cause neuropathy.
The author also cited studies that discounted the possibility that
hyperinsulinimea from a person's own insulin could have this effect.

I have heard people complain of this before--their blood sugar is
lowering and all of a sudden they experience neuropathy for the first
time. I have always thought this was because neuropathy, resulitng from
long term hyoerglycemia,  was about to become apparent anyway. In other
words the fact that they were achieving some control at the moment that
the neuropathy became evident was actually a coincidence.  I see the
possibliity in this thread that hypoglycemia can also cause neuropathy,
but is that common among hypoglycemics who are not diabetic?

Another thing that happens is that nerve damage can reverse as normal
blood sugar levels are restored. So that nerve pathways that had turned
off get turned back on.  Both the turning off and the subsequent
turning on are aaccompanied by electric jolts that are actually quite
similar. So in some cases the seemng onset of nueuropathy while
attaining glycemic control may actually be the reversal of previously
undiagnosed neuropathy.  To esperience this as something new would of
course require somebody to have not nnoticed the first round, but is
amazing how much can go undetected when we are stoic and don;t know
what to look for.

Morris