Dr. Robert Bransfield is a psychiatrist recognized in the Lyme community as
being at the forefront of treating patients with the neuropsychiatric symptoms
of tick-borne illness. When referring to Lyme disease in the interview that
follows, we are talking about multiple tick-borne infections, including Borrelia
and possibly some microorganisms that haven’t been identified yet.

How does Lyme disease affect the brain?

The early symptoms of Lyme that are perceived as diagnostic - the bull’s eye
rash, the arthritis, the bell’s palsy - these are not necessarily the difficult
symptoms. But when you look at a case that’s one, two, five, 10, 20 years out,
now you’re looking predominantly at the nervous system. So although there are
some people with significant musculoskeletal problems, the main impact of
late-stage disease is on the nervous system.
When we look at the cognitive and psychiatric symptoms, practitioners who
don’t understand them discount them as subjective and nonspecific - or
psychiatric. They’re discounted as the aches and pains of daily living, not
because they’re not objective and significant, but because they don’t know how
to interpret those findings.
If you look at how Lyme affects the brain and the nervous system, you have
to break the nervous system into different parts: the autonomic nervous system
(ANS), the peripheral nervous system, and the central nervous system. With the
ANS, you may have gastroparesis or irregular heart rhythms, where Lyme affects
the nerves that affect internal organs; that’s one cluster of symptoms.
Another cluster of symptoms involves the peripheral nervous system.
Neuropathy is one late-stage manifestation. You see numbness or tingling,
crawling and burning sensations, sensory loss or hypersensitivity.
There can also be irritation to the nerve roots where they come out of the
spinal cord; this is radiculopathy. That’s different from peripheral neuropathy
but it also gives symptoms in your arms and legs. You also see cranial nerve
symptoms, for example, Bells palsy effects the 7th cranial nerve. You tend to
see that early and there may be improvement and then some of those can re-
emerge years later.
The next thing is myelopathy, which involves the spinal cord. That’s not as
common. You’d see that as neurological symptoms from the point in the spine at
which that occurs and downward, and you may see numbness and weakness.
The symptoms that psychiatrists treat involve the limbic system. The limbic
system includes emotions, emotional reactivity, mood, and cognition. Cognitive
affects are seen somewhat sooner, and the emotional later. In the latest stages,
you can see dementia.
Executive functioning is one of the first things to go and involves the
prefrontal cortex. That’s your most complex, most sophisticated area of brain
functioning and that’s the most vulnerable when things go wrong. Executive
functioning’s the ability to create and sustain goal-directed behavior. You can
follow orders but it’s difficult to strategize. If doctors don’t know how to assess
these symptoms, they’ll dismiss them as subjective and nonspecific. It’s not just
subjective; you can make it objective and you can measure it. We can give you
a test for executive functioning.
You could also see slow processing speed in Lyme patients. That’s a different
cognitive capability and that’s a white matter problem; white matter is where
you form associations. So it takes longer to digest information and to express
information. That’s significant when you need to make decisions quickly or
absorb information quickly.

Regarding the limbic system, is there a pattern that you see in Lyme
patients?

Yes, the first thing you may see may be low tolerance to frustration, which can
result in irritability. Then you might see hyper-vigilance, low-grade anxiety, and
depression. Because there are cognitive problems with attention and
concentration and memory in addition to the executive functioning problems
and the slow processing - a person is not on top of things as they used to be.
What about brain fog? Brain fog’s different. With brain fog there's a
sluggishness, like a brain fatigue. A good way to replicate brain fog is if I give
you a hundred milligrams of Benadryl and then have you try to do some math
problems. You'd feel like your brain was stuck in molasses and it was hard to
make the connections work.

That's distinct from slow processing?

Right, it is different, and they may co-exist,
but anyone who has it can identify it. Many chronic illnesses have that.
Think of the terms fibro fog, lupus fog.

Is it possible to explain what's going on physiologically?

Yes, you see decreased activity on PET scans and SPECT scans. It’s similar to
what you see with fatigue. The most common complaint in a doctor’s office is
chest pain, the second most common is fatigue. Fatigue isn’t always specific.
There are a lot of things that cause fatigue, just like many things cause chest
pain. You don’t ignore chest pain because it’s nonspecific. But, if you have
chest pain that’s a certain quality, with pressure radiating down your left arm
and shortness of breath - that’s a pattern that makes you think of heart attack.
So, if you see fatigue associated with certain other symptoms, the pattern might
indicate Lyme disease - or some other condition. Fatigue is often one of the
worst symptoms (with Lyme disease). It's a very serious complaint and should
never be dismissed. Fatigue is part of the brain's functioning which involves
energy and coordinates with your circadian rhythm and your ability to get a
good night’s sleep - like recharging your batteries.

How is it that this tiny microbe can cause such problems?

Think of it this way. Everyone has symptoms that are a little bit different. You
see many common denominators, but how Lyme affects you depends in part on
your vulnerabilities and your strengths when you become infected. In some
people, one gene will make them more susceptible to one symptom, while some
people will be susceptible to other symptoms. If you got bit in the neck you
would have different symptoms than if you got bit in the toe. And it depends on
what co-infections are involved, how long before diagnosis - there are a lot of
variables in the equation.

How do you determine if someone has Lyme?

What you have to do is old-fashioned, basic medicine: do a thorough history, a
thorough review of symptoms, a thorough exam, and use a lot of thought and
judgment. You consider other things that might cause these symptoms. It’s
labor intensive, it takes a long exam, and then you have to put it all together
and look at pattern recognition. You can’t do a short cut. But the healthcare
system’s evolved with an emphasis on time efficiency and a reliance on testing.
That’s why a lot of cases are missed. What you don’t do is just the two-tier test,
and when the ELISA’s negative, say the patient doesn’t have Lyme. It’s
irresponsible to do that. The CDC says the test is not for screening but 3.4
million tests are done a year. So that may account for why you see 3.4 million
tests a year with only 30,000 cases reported to the CDC. That’s a hundred to
one ratio.

Why is there such a disparity between how many Lyme tests are done
and how many people are reported?

Instead you look for patterns. The typical pattern is someone is a high-
achiever, an active person who does a lot more things than the average person,
and then gradually they go downhill and now they have one hundred symptoms
that they didn’t have before. It’s not psychosomatic because psychosomatic
illness follows very clear recognizable patterns. When you see this multi-system
condition evolve, you know that it’s something that affects the entire body.
What affects the entire body? Infections are usually number one on your list. A
lot of doctors are used to dealing with acute infections, like bronchitis, where
you give 10 days of treatment. There’s difficulty diagnosing chronic, low-grade,
relapsing infections, but that's what makes the most sense.
Back to how Lyme affects the brain
There are three different ways Lyme infects the brain. One is where the
infection is within the brain, a second way is where the infection is in the blood
vessels leading to the brain causing vasculitis. A third way is when there’s
infection in the body that causes immune responses that in turn affect the
brain, that's what causes most cases of Lyme encephalopathy. For example, the
infection may throw off antigens that cross the blood-brain barrier and cause
inflammation within the brain. Or it may provoke the immune system and the
result of the immune provocation crosses the blood brain barrier and impacts
the brain through either inflammation and cytokines or autoimmune
mechanisms. Another theoretical idea is Lyme affects the brain with toxins, but
there has been little attention to this in recent years. That’s how some other
infections impact the brain. It's possible that antigens sloughed off by Borrelia
go to the brain and cause inflammation. A common mistake people make is
thinking that if there’s no bugs growing in the brain, it’s not affecting the
brain.
There are cases where Borrelia was found in the brain. Alan MacDonald
autopsied brains and showed that. In those cases you see more rapid
development of dementia and psychosis. Brain fog and executive functioning
problems are more likely due to the immune effect on the brain caused by
infection and subsequent inflammation in the body.
Normally when you acquire an infection, you have an early immune response,
which produces inflammation. Then there is a second response, which is
adaptive immunity, and then you’re fine. Unlike other infections, there’s never
adaptive immunity to Lyme disease. You see the inflammation but not the
adaptive immunity. That’s why people can be re-infected. That’s why the
vaccine required two boosters and even then people still were re-infected.
What you see instead of adaptive immunity is autoimmunity: anti-bodies
attacking the brain, causing another clusters of symptoms, like OCD (obsessive
compulsive disorder) or ticks, or some of the dyscontrol issues.

So there's still an infection and it might be low grade . . .

Yes, but it can provoke autoimmune symptoms, gliosis where the immune
system of the brain is activated from the infection in the body, and/or neural
functioning can be impaired from the impact of cytokines on the brain.

How about the coinfections?

When we look at psychiatric symptoms, we often see Babesia and Bartonella.
When infections impact the brain, they can cause cognitive impairment or
behavioral and psychiatric changes. Some of that is mood alteration or poor
impulse control, so some people might be apathetic and have decreased
initiative. It depends on how it impacts the circuitry, the neural networks. You
can see explosive rage. Invariably the rage you see with Lyme is bizarre and
senseless. So there’s a number of different patterns I’ve seen. Shoplifting, for
example, in someone who never shoplifted. Sometimes behavior stems from
confusion or impulsivity, urges to do harm. You can see domestic violence,
assaults, homicide, mass murder, serial killing; invariably it’s bizarre and
senseless. When you witness it first hand it’s very scary and very explosive in
quality.

Can someone who's progressed to that point recover?

I’ve done the same assessment on thousands of people and maybe 300 have
described rage. Your average person who acquires Lyme doesn’t show rage, but
a certain subset does. Again, when I say Lyme I mean tick-borne disease. What
is it that makes these people more susceptible? One adverse effect on the brain
is it gives you anxiety, depression, and bad behavior. So you see someone who
had no conduct problems in the past, now, all of a sudden has behavioral issues.
They become disinhibited. The average person who acquires Lyme isn’t
disinhibited, but you do see it more with Babesia and Bartonella patients.

Can Lyme alone cause it?

Difficult to say because so many people have
coinfections. Tick-borne infections push people in the direction of impaired
conduct along with impaired cognitive functioning. I’ve had people with homicidal
rage that were treated and the rage is gone.
It can be a phase of the illness that they go through and they can be treated,
but it isn’t always predictable. Same thing with suicide. We can correlate
suicide with inflammatory cytokines, particularly interleukin 6. When that’s
higher it can push someone towards violence and suicide. People with normal
brains don’t have obsessions to kill themselves. That’s invariably associated with
some kind of brain impairment.

How do you treat someone with Lyme that's gone undiagnosed for a long
while?

I treat what hasn’t been treated before. Usually what’s best is a combination of
antibiotics and psychotropics. Two basic strategies: One, you treat the
symptoms; this helps people function better. If they’re functioning better,
they’re less stressed, they’re sleeping better, and then their immune system’s
functioning better. So, addressing symptoms is an indirect treatment that
sometimes may be more effective than antibiotics. If you’re sleep deprived and
stressed, you will be immunocompromised. So, if a person’s not sleep deprived
and not overly stressed and they have good lifestyle habits, their immune
system is going to work better. In some ways it’s so simple that it’s often
overlooked, but it’s one of the first steps to take.
I don’t get too involved with antibiotic treatment but I will start them as a
test to see how the patient responds, which can help in diagnosis. But you
always have to look for the Herxheimer response. A neuropsychiatric
Herxheimer reaction can be fatal. Someone can become suicidal. So you start
with low-dose oral antibiotics and gradually increase. If they’re benefitting,
then a patient probably needs to see someone to take it to the next step with a
comprehensive antibiotic treatment. As long as someone’s improving from the
antibiotic treatment, you keep it up. If someone isn’t improving then you try a
different strategy. I do the psychiatric treatment, knowing that will help
overall.
Think of disease theory: there are predisposing factors and there are
precipitating factors. Then you have disease progression. What maintains or
contributes to disease progression isn’t necessarily what started it in the first
place. For example, someone with tick-borne disease may be sleep deprived,
which contributes to disease progression. So you need to deal with sleep
deprivation even though it isn’t what initially started it. That’s an example of
the part of treatment that I do.

Why is sleep such an issue?

Sleep does a few things: adaptive immunity occurs in deep sleep; it’s necessary
to overcome fatigue; it's critical for cognitive functioning and for mood stability;
it helps pain sensitivity. So there are a number of areas where it helps,
particularly with chronic disease.

How does Borrelia hijack sleep?

A study demonstrated 100 percent of Lyme patients have disturbed sleep.
Inflammation in general causes sleep deprivation, and sleep deprivation pushes
you further into an inflammatory state. So you need to try to break that cycle.
Is there anything to be said for a holistic approach?
That’s part of what I’m saying. There was a study that someone did a number of
years ago that compared a person that was 35 with someone who was 65. They
looked at good habits: limited alcohol consumption, exercising, getting
adequate sleep, not smoking, managing stress - all those things your mother told
you to do. The person who was 65 and did everything right was as healthy as the
person who was 35 and did everything wrong. If smart living can give you 30
years of health, that's important. When you have infection, health is a balancing
act, and you’re trying to tip the balance in your favor. Good diet also supports
that.

With tick-borne disease a holistic approach doesn't seem to go far enough.

Well, you have to think differently. The Human Microbiome Project recognized
that 90 percent of your body is microbes - by a ratio of ten to one - and you’re
in a dynamic balance with organisms within you. Certain pathological infections
throw off that healthy balance and you need to try to restore it. How can you
eradicate pathological organisms within you without doing harm to the
beneficial ones that you want? That can be a tricky. Increasing antibiotics has to
be a weighted decision in terms of are you harming organisms that are good for
you that sometimes keep certain pathogens at bay. For example, if you take a
lot of antibiotics, you get yeast overgrowth. Dr. Lida Mattman showed me a
slide that showed Lyme spirochetes growing inside of yeast cells. Lyme can grow
inside the yeast cells. When this happens antibiotics can potentially increase
yeast overgrowths.
Think of it like this, humans haven’t been on this planet as long as Borrelia,
and it didn’t survive for millions of years by being stupid. It’s not like they have
a brain but they have adaptive capabilities and can survive in many
environments. In some ways, that’s what humans are good at, being able to
survive in different environments: equatorial, polar, outer space. But
spirochetes have that same adaptive capability. It’s a formidable adversary in
ways that we don’t fully appreciate. So we can’t think of them in simplistic
terms like we used to.

Do psychotropic meds affect people with Lyme differently?

Lyme patients seem to be more drug sensitive. We might speculate that low
body temperature slows down chemical reactions, so people may be more drug
sensitive and need lower doses. Sometimes people pick the wrong psychotropic
medication but more often than not they were given too high a dose too fast.

Do you think that brain scans, SPECT scans and MRIs are useful diagnostic
tools?

Yes, within limits. The scans may support what you learned from your exam but
I think the most important thing is the comprehensive exam. Immune testing
also gives some information.

Where is the science going with tick-borne illness?

You have to look at a paradigm shift, recognizing complex contributors to
disease, complex mechanisms, pathophysiology, and the complex ways it
presents. So you need a different, more complicated disease formula. You can’t
use the simple disease formula anymore.

Is there a place for that in medicine today?

There are a lot of people that incorporate it in the way they think, but not
everybody does. I use a systems approach. In psychiatry we used to fight and say
well, there’s a psychoanalytic approach and then there’s people who think of
brain function; it’s not either or, you have to combine both. That’s how you
have to think of any disease, you have to use a complex system model. Similar
to the shift in math from Newton to Einstein, you need a more complicated
model, which is basically an ILADS approach.

But not an IDSA approach . . .

They’re still stuck in the simplistic approach. A big part of this is that Lyme
starts as a joint condition, and that gets doctors with that training involved in
treatment. But then it ends up as neuropsychiatric issues, and now you need a
different set of skills to deal with later disease than you did early disease. The
people who have placed themselves in the position of controlling that disease
are people who are not trained in comprehending the later stage
manifestations. That’s a big problem. I think there are issues with research
funding and people want to keep the funding in their category. If I define Lyme
as a neuropsychiatric illness then neuropsychiatrists should receive the research
money, not rheumatologist, and that may be threatening to people who are
currently receiving those grants. There’s a turf issue there; that’s a piece of it,
and there are people who can’t think of a multi-system approach.

Dr. Robert Bransfield practices psychiatric medicine in Red Bank, New Jersey

Janet Jemmott is editor of the Lyme Connection newsletter. To receive future online issues, sign up on our Home Page.