Unit 4, Group five: 

Could Mr. C.'s foot numbness be related to his stroke?
What other causes could there be for this pattern of
numbness? (From the last unit, remember his history of
alcohol intake, Type 2 diabetes and colorectal cancer.)

The case study indicates that Mr. C is experiencing
bilateral foot numbness.  When stroke patients (clients)
present themselves in a clinic or hospital setting they
may reveal problems controlling movement; sensory
disturbances including pain; problems using or
understanding language, disturbances with thinking and
memory.  In addition to this they may experience and
exhibit a sudden numbness or weakness of the face, arm
or leg; especially on one side of the body.  Knowing Mr.
C’s other medical conditions and associated disturbances
occurring with his activities of daily living, I believe
it is possible that his stroke can be causing a minimal
degree of numbness (in his case it would be the left)
but it is unlikely that the stroke is the primary cause
of the numbness occurring in both feet. 

Some stroke patients experience pain, numbness or odd
sensations of tingling or prickling in paralyzed or
weakened limbs, a condition known as paresthesia.  If
Mr. C’s left leg and foot is weakened and he is
experiencing constant numbness then paresthesia can be
responsible for the constant numb feeling. 

As we know, the other medical disorder that Mr. C has
been dealing with is his diabetes mellitus. Mr. C’s foot
numbness is likely primarily due to his Type 2 diabetes.
  Mr. C’s diabetes mellitus is affecting his central and
peripheral nervous systems, either directly or
indirectly and is causing many of his disturbances and
symptoms.    

In the context of pathophysiology, the factors leading
to the development of peripheral neuropathy in diabetes
are not understood completely but there are multiple
hypotheses.  It is generally accepted to be a
multifactorial process. The causes differ for different
varieties of diabetic peripheral neuropathy. 
Researchers are studying the effect of glucose on nerves
to find out exactly how prolonged exposure to high
glucose causes neuropathy. 

Thus far, McCance and Huether (2006) discuss the
pathophysiology of diabetic neuropathy in chapter 21. 
The symptoms that occur with diabetic neuropathy occur
as a result of Schwann cell abnormalities.  These
abnormalities result from the changes in the axons they
support.  In diabetic neuropathy, the metabolic activity
of the schawan cell is disturbed causing segmental loss
of myelin (McCance and Huether, 2006).  In Mr. C’s case
his numbness is “constant” which can lead us to believe
that he has developed a long term diabetic neuropathy. 
With this problem, there is a characteristic pattern of
demyelination and remyelination. (McCance and Huether,
2006).  However, Mr. C’s abnormalities can be improved
by good glucose control.  From the case study we see
that he is currently on medications to control his high
glucose levels.

Nerve damage is likely due to a combination of factors:

Such factors are:

1) Metabolic factors:  High blood glucose, long duration
of diabetes, possibly low levels of insulin, and
abnormal blood fat levels.

2) Neurovascular factors:  Leading to damage to the
blood vessels that carry oxygen and nutrients to the
nerves

3) Autoimmune factors that cause inflammation in nerves

Proposed theories include:

1) Metabolic theory 

The metabolic theory proposes that elevated glucose
levels cause increased levels of intracellular glucose
in nerves.  This leads to saturation of the normal
glycolytic pathway. From the case study we can see that
Mr. C’s sugars have been high consistently and he is now
taking medications to control his hyperglycemia.  This
theory proposes that the when Mr. C experiences periods
of hyperglycemia, the extra glucose is shunted into the
polyol pathway and converted to sorbitol and fructose.
Accumulation of sorbitol and fructose leads to decreased
membrane Na+/K+-ATPase activity, low levels of
myoinositaol.  This results in an altered sodium
transport resulting in an altered membrane potential and
slow nerve conduction. (McCance and Huether, 2006). 
This slow nerve conduction is likely to be responsible
for Mr. C’s constant numbness in his feet.  

2) Vascular (ischemic-hypoxic) theory 

This theory proposes that the endoneurial ischemia
develops because of increased endoneurial vascular
resistance to hyperglycemic blood. Metabolic factors,
including the formation of advanced glycosylation end
products have been implicated (Tomas, 1999).  The end
results are capillary damage, inhibition of axonal
transport, reduced Na+/K+-ATPase activity, and axonal
degeneration. 

3) The third theory proposes that ischemic injury and
demyelination occurs due to an increase of advanced
glycation end products that result from high glucose
levels.  This causes less Nitric Oxide to be present
which results in vasoconstriction of vessels.  In
response to the vasoconstriction there will be reduced
nerve blood flow and ischemic injury and demyelination.

I welcome your thoughts to this posting.  Thank you.


Inga


McCance, K. & Huether, S. (2006). Pathophysiology; the
biologic basis for disease in adults and children (5th
ed.). St. Louis, MS: Elsevier Mosby.

Thomas, K. P., Watkins, P.J., (1998). Diabetes and the
Nervous System.  Journal of Neurology, Neurosurgeon &
Psychiatry, 65; 620-632. Retreived May 22, 2007, from
JNNP online.