Chapter 22: Looking at my test results

According to the neurologist there are two possibilities.

Number I: I fell, hit my head (involving damage to several blood vessels) and suffered an acute traumatic brain injury.

Number 2: Cerebral Amyloid Angiopathy (CAA) had weakened some cerebral blood vessels causing several blood vessels to haemorrhage, causing a seizure, causing me to fall and hit my head. 

It is quite clear.  Head injury leads to an increase in total tau levels.  Many studies have shown this increase in Total Tau.  Tau levels increase early after trauma, peak in the second week and decrease slowly afterwards.  Tau levels in CSF is heading down about 40 days post trauma. The increase in Total Tau probably reflects axonal damage.  The Total Tau level is a marker for neural degeneration.

In one study the average CSF Total Tau level was >2,126 pg/mL on days 2 to 3 after trauma. The normal Total Tau level is less than 358 pg/ml.

Total Tau level also increases after an acute stroke with no external trauma.  In one study CFS Total Tau increased on day 2/3 to 179%, Day 7-9 to 257% and after three weeks 425% with return to normal 3/5 months later.

My Personal  Results:  CSF taken on 27/10 which is approximately three weeks post-accident  showed a total Tau level of >2279 which is an increase of about 634% above normal.  There is definitely proof of neural damage.  The damage may have come from the trauma of hitting my head either before or after a seizure. From CSF results there is no proof of anything except there was trauma involving my head.

The difference between the two original possibilities is CAA.  CAA is either present or not. That is what I need to find out. 

What is CAA? Cerebral Amyloid Angiopathy (CAA) is an angiopathy in which amyloid deposits form in the walls of blood vessels on the central nervous system. These deposits weaken the walls leading to breakage of the walls of the blood vessels. This manifests as a haemorrhagic stroke.

There is little information on levels of p-tau in CAA.  It is more likely to be increased but there is little evidence that says a certain level of p-tau means CAA. P-tau is a marker for the formation of neurofibrillary tangles.

My Personal Results:  I had a very low level of P-tau.  Suggests a low level of hyperphosphorylation of tau.

Levels of both Aβ40 and Aβ42 were lower in the CSF of CAA patients. These levels  probably relate to Aβ metabolism and the deposition of plaques containing Aβ40 and Aβ42 in the walls of the blood vessels.  A low level would probably indicate CAA as being more likely.

My Personal Results:  My results suggest a pretty normal level of Aβ40 and Aβ42 in the CSF. This suggests nothing except the need for further tests.

The final results of my investigations show a need for further tests. Within the next few weeks I will have a MRI taken of my brain. I will have a lumber puncture to obtain some CSF. I can’t wait for the tests and, even more importantly, I can’t wait for the results.