By Tom Grier
Over the past 23 years of running a Lyme disease support group and talking to thousands of patients, I have made many observations and conclusions about this complex disease that are often overlooked in the medical literature and text books.
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 firstname.lastname@example.org
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.
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.