Over the past 23 years of running a Lyme disease support group and talking to thousands of patients, I have made man
Because of my own afflictions and severe neurological involvement; I
have paid special attention to patients with similar symptoms and
disabilities.
Even as far back as 1990, many researchers
observed and commented on UBOs (unidentified bright objects) that were
occasionally seen on Lyme patient’s brain MRIs.
Today decades
later after many debates and denials, these spots or lesions found in
the brains of Lyme patient’s, are now considered to be virtually
identical to MS lesions or areas of demyelination that started with
blood vessel inflammation.
I have also observed that in patients
who are early into their illness, that these areas of blood-vessel
inflammation appears to be mostly observed in the cerebral cortex or
grey-matter regions of the brain. (As seen on a T-2 Weighted gadolinium
contrast dye brain MRI) This also matches data from PET Scans of these
early patients that indicate metabolism or circulation disorders in the
same regions of the brain.
Interestingly since 1911 most
medical literature shows that when classical forms of spirochetes are
observed in the brain, they are found in the grey-matter and rarely seen
in the white-matter regions. Yet in late Lyme or Multiple Sclerosis we
mainly see and focus our attention on the white-matter lesions seen in
the central areas of the brain near the lateral or central ventricles.
It almost seems as though the infection in the brain may first gain a
foothold in the cortical regions (the outside layer of the brain or
grey-matter regions) and only later does the pathology seem move to the
white-matter regions. Interestingly we only seem to observe the
classical spiral form of the spirochete in the grey-matter and much more
rarely find this spiral form in the white matter. In other words the
conditions in the central part of the brain seems to favor the
non-spiral form or perhaps what we call the cystic form? This was
observed in 1922 and 1933 when Gabriel Steiner observed microscopic
“spherical” bodies that stained with Silver-Stain in the white-matter of
MS patient’s lesions during brain autopsies.
It is hard to
draw hard conclusions about the pathogenesis of Borrelia bacteria in the
human brain, because we have so little brain pathology autopsy data to
draw upon. Much less data than what was available pre-WWII from MS
brain autopsy studies done in Europe. In the end of his active career as
an Infectious Disease Pathologist and researcher, Dr. Gabriel Steiner
in 1954 stated in his American published position paper, that he felt
the spirochetes he observed in the brains of MS patients in Germany and
in Ann Arbor MI were in the family of Borrelia and related to Tick Borne
Relapsing Fevers.
Dr. Steiner was able to isolate the bacteria
from the brains of human MS patients, transfer the brain tissue to
animal models and recover the bacteria from the brains of animals
infected with human MS tissue. Yet a century later we only recognize him
for his work improving Silver-Stains. Steiner Silver Stain is still
used today in pathology to detect spirochetes in human tissue. It is
limited however like all silver-stains in that it is an extracellular
stain only, and cannot pass through the membranes of human cells.
One theory of why neurological Lyme patients have cognitive function
problems early involving the cerebral cortex, and lesions in the central
brain much later, may be explained by how the bacteria enters the human
brain and how it moves through the brain.
It has been observed
in animal models including dogs, that early in the infection when the
first symptoms are manifesting, that the classical spiral form of the
Lyme spirochete penetrates the Blood-Brain-Barrier mostly in the
cortical areas or outside layers of the brain. This might have to do
with the close association of brain microglia cells with these
particular blood vessels? The role of the microglia cells are not
entirely known, but they definitely play a role in vessel inflammation
and the production of a neuro excito-toxin called quinolinic acid.
Regardless of the exact mechanism, it appears that Borrelia enters the
grey-matter areas first, and it does this through creating holes in the
blood-brain-barrier (BBB).
Once the BBB becomes “leaky” some of
these early pathogens instead of entering brain tissue where it can
thrive, some of these highly motile spirochetes also randomly penetrate
into the CSF channels, and get trapped or isolated in the spinal fluid
or in the subarachnoid space where the conditions are unfavorable for
the bacteria to survive. We know by direct observation that we can
occasionally find and see Borrelia in the CSF of Lyme and MS patients,
but it is more likely the bacteria prefers the brain over the brain
fluid.
What we do not understand is how the spirochetes exit the CSF?
It is rare to find the bacteria in the CSF and it stands to reason that
the bacteria finds a way to re-enter the human brain. Perhaps by trial
and error, or perhaps by a use of receptors that latch on to cell
membranes? It is probable that some of these bacteria leave the spinal
fluid regions, and reenter the brain. Since we see the most notable
pathology near the central ventricles of the brain, it is plausible that
the bacteria re-enters the brain through the ependymal membrane of the
Lateral Ventricles where we see the most pathology in Lyme patient’s
brains.
The largest surface area where reentry to the brain can
occur, is the membrane that lines the lateral or central ventricles.
This would allow the bacteria to reenter the brain in the center of the
brain where the white-matter is most densely oriented. This would
explain why we see so many smokey-whispy flares and lesions surrounding
the lateral ventricles. Since the Lyme bacteria appear to react to
white-matter differently than grey-matter, the bacteria it appears
abandons its motile spiral form in favor of a cyst-like or L-forms.
(Lister forms are bacteria that shed their cell wall). Observations in
Syphilis suggest that treponemes can alter their spiral form depending
on the tissues that the Syphilis spirochete is found in. Perhaps it is
the same for Borrelia spirochetes?
Although on a brain MRI it
appears that the central part of the brain is the most affected,
virtually every part of the brain is at risk of invasion. While other
areas do not look as dramatic on a brain MRI, these other infected areas
are still under attack and can affect the Lyme patients in many ways.
Commonly reported neurological symptoms include numbness and tingling
of hands, feet and scalp. Patients often report memory loss, muscle
twitches, disorientation, sensitivity to bright lights, pressure inside
the head, eye disorders, and movement disorders. Also seen are the more
subtle changes like poor word retrieval, the reversal of letters, and
difficulty separating thoughts and images. Muscle weakness, loss of
ambulation and headaches are also sometimes reported. But a somewhat
nebulas symptom that is often overlooked and can linger for years is:
visual perception disorders, sometimes referred to as Visual-Spatial
Disorders ).
A neurological Lyme patient may describe this
disorder in a variety of lay-terms such as disorientation, surreal
perception, a sensation of feeling high and having impaired thinking and
memory problems. They may feel like a different person and exhibit
different emotional feelings than before being sick or even a complete
detached feeling that some have described as an emotional lobotomy. I
believe that the cause of these fuzzy indefinable symptoms that do not
readily respond to antibiotics, is micro-cellular damage in the brain
that causes small and numerous areas of brain damage.
Visual
perception disorders are not a physical disorder like double vision
because of crossed eyes, or headaches because of pressure inside the
cranium, but are more subtle and are probably caused by how the human
brain processes information. Another word often used by Lyme patients
to describe their condition is: surreal vision or surreal perception of
their visual field along with a feeling of floating, or emotional
detachment.
Unlike other symptoms of Lyme disease these symptom
do not have an immediate or positive response to antibiotics, and even
more distressing is that physicians who have no personal
frame-of-reference of these type of symptoms will simply trivialize the
condition as something they can understand like: depression, dizziness,
anxiety or seizure activity. Once they have reduced this complex
condition to something they are more familiar with, they will most often
try to treat it with a single treatment modality like antidepressants,
motion sickness tablets, or anti-seizure meds. Most of the time these
treatments are useless and the answer to ameliorating this surrealistic
vision that the patient is a useless endeavor.
Managing this
condition is frustrating for doctors and patients because there is
little that actually can be done to ameliorate this feeling of
surrealism either by the physician or the patient, but I will give some
suggestions that may help.
I often tell Lyme patients in Lyme
support group that the road to recovery takes three steps: First you
must derail the engine of destruction.
You must stop the active
progress of the pathogen. This I believe takes antibiotics, and may
require prolonged and aggressive treatment possibly with several
antibiotics. If the infection is active within the brain, no test short
of a brain autopsy can detect it. Also no test can tell us when active
infection is eradicated. So we must continue treatment based on symptoms
and response to symptoms.
The second step to recovery is: Give
the body whatever it needs to best heal itself. This will include proper
nutrition, vitamins, sleep, and possibly adjunct therapies like
alternative medicines, heat and exercise.
The third step is: TIME! It takes a long time to heal the human brain.
We once thought that the brain could not create new neurons or repair
itself. We now know that the brain can rebuild after it has been
damaged, but the brain takes much longer than other tissues to repair.
James Brady who was shot in the head during the President Reagan
assassination attempt, was told he would never talk or walk again. Ten
years later he walked to a podium, gave a speech, and said repeatedly
that the human brain takes time to repair! Lots and lots of time!
We know through the observations of stroke patients, that the brain can
and will re-route signals around the damaged areas of the brain. And
this may be where surreal perceptions or surreal visualizations begin.
This abstract idea might be hard to imagine so I will try to give some illustrations.
Imagine that a Lyme disease brain that has been attacked from within
and distinct areas of the brain are damaged: perhaps even destroyed.
Specific pieces of information may now be forever lost. Even things like
feelings and moods may be altered. This is why early stroke victims may
not recall certain memories, words, or may exhibit personality changes.
Whatever area of the brain is affected will affect the patient in a
unique way. But with time the brain finds a way to bypass the damaged
area. The brain can for lack of a better word use a patchcord to make
new connections to other areas of the brain.
The brain has the
ability to store information in several locations, and the brain has the
ability to reroute signals from damaged areas to healthy areas. This is
why a patient who may forget a word or stutter, might recall the word
if they try to sing it. The area of the brain that processes music might
store similar information as speech centers such as words, but to
access that information the patient must sing the words instead of
struggling to verbalize them through the speech center of the brain.
The bad news is that unlike a stroke patient that has just one area of
damage to reroute, a Lyme patient may have dozens of lesions that we can
see on an MRI, and perhaps hundreds of other smaller areas of damage
that we can’t detect with any MRI, SPECT scan or PET scan. These damaged
areas may be in visual centers, motor skills centers, or our emotional
centers of the brain. Regardless of where the damage is, the human brain
will try to compensate.
Now imagine this damaged brain with its
many lesions of focal areas of damage as it tries to compensate by
rerouting signals around these damaged areas. Where will the brain store
and retrieve data when there are so many areas that are not functioning
properly? Since the information comes from alien areas of the brain, it
can be expected that the information somehow “feels” different than
before the patient got infected.
As new more complex neural-nets
are created there may even be a different emotional attachment to the
final processed information.
For example a Lyme patient with
severe neurocognitive dysfunction may see a beautiful sunset and
intellectually the patient knows that it is a sunset and also knows that
it is beautiful, but emotionally the patient may be detached or have a
different emotional response to it than before being sick. This may be
because the brain has rerouted the visual information and the patient’s
stored information from new locations of the brain feels different. The
information is correct but the emotional quality of the sensation is
changed. The intellectual quality is also altered.
Many Lyme
patients have mentioned that they may start to cry or laugh
inappropriately for no rational reason? Yet over time and treatment they
improve. Sometime we try to blame this on hormonal changes, but I think
another component of these emotional mood-swings is from accessing
areas of the brain with newly forming neural-nets trying to compensate
for damaged areas.
Somewhere in the brain we gather thoughts and
images that forms our conscious mind. Where this is in the brain
exactly is unclear, but if you close your eyes you can see with the
mind’s eye and think in both words and pictures. But in the damaged
brain this internal mind’s-eye is now gathering information from new
pathways, and it makes sense that this will feel different.
Intellectually we still create thoughts and images and understand them
in an academic sense even though they have a different feeling to them.
In a Lyme patient where the brain has had many micro-alterations, the
imagery that the patient retrieves from their brain or the newly
observed information that is trying to be stored, is now slightly
altered. We feel different about our surroundings because we perceive
them differently than before the infection, we store the new data in new
locations of the brain, and we retrieve thoughts from entirely new
neural nets that are trying to make sense of the data as best it can.
The result is impaired thinking and a new or different emotional
attachment to the data that some patients refer to as: “surreal
perception”.
If you ask 10 small children to draw a star with a
crayon, you will mostly likely get 10 very different looking stars. You
know that they are all stars, but they may all vary in size, shape, and
color and each will affect you differently artistically. Well the human
brain that is damaged is acting a bit like there are ten different
children in your head presenting you with ten slightly different
presentations of that star. You know each one is a star, but it is
perceptually different than the star you once imagined before you ever
got sick.
Lets look at one last example of how rerouting signals
through the brain can result in impaired mental cognition. Imagine
looking though a telescope and seeing the world entirely through a lens
that magnifies. Now imagine seeing the world through a dozen different
glass lenses. One lens that distorts, a lens that creates multiple
images, a lens that shrinks things, a lens that adds color, or a lens
that adds rainbow like flares to reflections, or a lens that dims or is
blurry or seems to slow down images.
Now imagine all those
lenses as being places in the brain where we can process information.
Some areas process visual information, some areas process words, another
processes music or physical sensations. Now imagine that a single image
must now go through all these different lenses before it arrives to
that place inside your brain where you perceive all the collected data
and images as a thought.
The image that finally arrives as
perception, may be blurry, unfocused or a different color. It may be
louder or angry or detached and meaningless. The point is the message
may take on a surreal demeanor because it has travelled though regions
of the brain that is unfamiliar with processing raw data or visual
imagery. The net result is that the original image is now tainted and
skewed. It has now taken on the timbre and texture of the many lenses it
traveled through instead of the lens you normally used to see the
world.
Some Lyme patients have complained of audio and visual
hallucinations. Some may be sensitive to lights and even have seizures,
all of which are symptoms within the paradigm of thinking of most
doctors. But the patient who comes in and tries to explain that they
are disoriented, they feel different, and that they have a different
emotional response to everyday situations: this patient will seems odd
and disconnected to the physician who cannot understand or relate to
these fuzzy symptoms. Often these patients are categorized as having
psychological disorders when they most likely have areas of the brain
that can no longer process information without their brain rerouting the
message.
In most cases no medication can help with this, and
the attending physician may compartmentalize the patient’s affliction as
psychological or simply ignore the condition. They maybe labeled as
being depressed, as being anxious, or being a hypochondriac. When really
what the patient has is a form of brain trauma.
What can be done?
Time is the biggest factor to recovery. While it may take years or even
decades: over time the patient will start to feel more normal. The
expanding alternative neural nets will become the new normal way of
processing information. As this happens the patient establishes a new
set of emotional feeling to the things that they experience in life. In
other words the Lyme patient’s new and improved brain will feel more
normal with time, but certain feelings or memories may never feel the
same way to them as they once did. An emotional person might become
analytical, a spiritual person may become a doubting Thomas, a humorous
person may feel serious and somber and sunsets and birthdays may not
feel the same as they once did.
The other thing to do is to
treat this condition is to treat it as though it represented dozens of
tiny little strokes in the brain. The patient must rehabilitate
themselves with cognitive function exercises such as games, puzzles,
flash cards, reading and writing and creating new experiences for the
brain to process and store. One thing I did was I practiced focusing my
eyes to close objects because I lost the ability to focus closer than
two feet.
Most patients know intellectually where they have
changed, and what seems missing. It is up to the patient to design their
own recovery program to overcome the deficiencies they now face. No
doctor or psychologist will fully understand the patient’s deficits.
Before a patient puts all their faith in medications I recommend that
if a patient has lost some emotion like romance, humor or spirituality,
that they take up writing. Writing a short story that deals with
emotions will help you access those feelings. Force your brain to engage
these areas that are now diminished in your life, and see if you can
create new emotional neural-nets, and intellectual connections that you
feel are suppressed.
Most patients I have encountered that have
described surrealistic visual processing and feeling like a different
person have often compared it to drug experiences. Perhaps when on
mind-altering drugs we use neural pathways normally not experienced?
This would explain the similarities of being brain damaged to taking
mind altering-drugs, except the drugs wear off, and brain damage lingers
on for years.
To research this topic you may search under
Visual-Spatial disorders, cognitive dysfunction after brain trauma,
pugilistic dementia, and global cerebral atrophy following brain
infections. If you have more to contribute to this topic please contact:
Tom Grier donatebrain@gmail.com
Stroke-like Phenomena Revealing Multifocal Cerebral Vasculitis in Pediatric Lyme Neuroborreliosis.
Kurian M, Vitor MP, Maria V, Joel F.
Journal of Child Neurology, online before print, 2014 Oct 14. pii: 0883073814552104.
http://doi.org/10.1177/0883073814552104
Abstract
Stroke-like presentation in Lyme neuroborreliosis is rare in the pediatric age group.
We report a previously healthy 12-year-old boy who presented with acute
left hemiparesis and meningeal signs. Neuroimaging failed to reveal any
cerebral infarction but demonstrated a multifocal cerebral vasculitis
involving small, medium and large-sized vessels affecting both the
anterior and posterior circulation. Concentric contrast enhancement of
the basilar artery was also observed. Further investigations and
laboratory findings were consistent with Lyme neuroborreliosis.
