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. 

Chapter 21 : Tau Proteins

On this journey that I have been on I have kept coming across Tau proteins.  I have no alternative. I have to tell people a small part of what I have learnt about Tau proteins.

How many Tau proteins do you have? What are they? Tau is used to describe a group of proteins that exist in the cerebra-spinal fluid that primarily stabilize microtubules.  They are present in the liquid (the CSF) containing the nerves. They are not present in other fluids such as blood. When they are defective and don’t work properly it is commonly a sign that the person has Alzheimer’s Disease (AD) or Parkinson’s Disease.

One of the main functions of TAU proteins is to modulate the stability of axonal microtubules. In a healthy CNS the transport system is arranged in parallel rows. Food and waste travel along these rows or tracks. Tau proteins bind to microtubules to help keep the tracks straight.  Excessive or abnormal phosphorylation of tau results in the transformation of normal adult tau into PHF-tau (paired helical filament-Tau) and NFTs (neurofibrillary tangles) which don’t work as well. Phosphorylation of tau proteins means your brain doesn’t work as well. What causes phosphorylation of tau proteins? Kinases play a role. What are kinases and do you control them? That is a big question which I will look into.

Traumatic Brain Injury

High levels of tau in the CNS leads to poor recovery after head injury.  And head injury leads to high levels of tau in the CSF. Or head injuries can lead to a poor recovery from head injury. Repetitive mild trauma such as in boxing can lead to NFTs which can slow recovery from brain trauma.

When is a test for Tau proteins taken?

One time is Alzheimer Disease.  It is a supplemental test used to aid in diagnose. Typically done after a series of other tests where the practitioner first tests the function of the brain. In a symptomatic person a low Aβ 42 level along with a high tau level reflects an increased likelihood of AD. It may also indicate a rapid progression of the disease.

In Alzheimer’s disease (AD), total CSF beta amyloid (Aβ) is not significantly different from controls but Aβ42 is decreased probably because it is deposited in plaques and is not available in a diffusible form. Total-tau (t-tau) and phosphorylated tau (p-tau) are both increased in AD due to neural death and the release of tau into the extracellular space.

Another time a tau test is done is when trauma results in excess fluid in the ear or nose and it is not known where the fluid comes from.  A physical injury to the head will cause membranes covering the brain to break and CSF to leak out. A test to determine if the fluid is CSF is needed.  Time for a Tau test. 

Chapter 20: A customer of the Health System

In the past few weeks I have been a customer of the Health System.  This is the way things have gone.

Every disease varies from person to person and within the same person from time to time. The disease will constantly alters its appearance. It will not always appear typical or classic.  It will not always appear as described in the text books.

Management also depends on another person who is continuously changing and evolving: the clinician.  Clinicians all vary. They are not machines and some days they are feeling better than other days. Their emotional and physical state depends on both home and work, What happens at home and at work affects their work. In other words the work they do will affect their other work.Their knowledge about a particular topic varies for a multitude of reasons and may influence management.

The quality of your care depends on more than just you and the clinician. It depends on other people. Many times I have sat silently as the clinician has attempted to understand x-ray reports or lab results. The clinician has never told me what a good job these other people are doing.  He has never looked at the lab results and said, “We should be very grateful for these people. They are doing a great job and have come up with great results which make our job easier.”  They never say such things.  They always look at the results warily with a look of trepidation and fear. They are always suspicious. From this we can conclude one thing. Good care depends on a team working together. Another thing we can say is that good care depends on equipment that is understood and that works.

One of my favorite days was the day I had ultrasound on my arm. We argued and fought with people and their cars in order to get a suitable parking spot. We finally parked the car and sat in the waiting area downcast and wondering about a lot of things.  I was called for my scan which was done incredibly efficiently and effectively. I sat there overwhelmed by the quality of the machine and the pictures of my arm. I sat there thinking how far the medical system had come.  I was stunned. After the scan we exited the building in order to recommence our battles with the underwhelming parking system.

Sometimes my care has been diverted. It has lost sight of the ball game. Sometimes because of me. Sometimes the clinician. Sometimes for obscure nebulous reasons. At the moment the main issue is what happened on the 7/10/15. It is now five months later. Why did I collapse? Why did I become unconscious for two weeks? How do I prevent this happening again? 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 had weakened some cerebral blood vessels causing several blood vessels to haemorrhage causing me to fall. 

He doesn’t mention the third possibility which is the most likely.

Number 3:  Both Number 1 and 2 combined and occurring together.

I may have completely misquoted him for which I apologize. It is now five months since the beginning of my illness and he has ordered some MRI’s and lumbar punctures to try and diagnose the cause of my illness.

The last 5 months has taught me one thing (actually it is more than one thing). It is up to me to manage myself. This means I work with the professional staff where possible and where necessary. It is a collaborative effort involving a multitude of people but I am the one who needs to know everything.

My next task is to look over my lumbar puncture test results and see what I can deduce.  I have finally obtained copies of my test results (it was a long story). The main tests are for levels of TAU in my CSF.

I will go into more detail about TAU proteins in my next posts.  They are very interesting.