Posttraumatic
Stress Disorder
and
Infectious
Encephalopathies
Summary:
This article explores the link between emotional
trauma and chronic relapsing tick-borne infectious disease affecting the brain.
Two case histories are presented. In these cases, posttraumatic stress disorder
(PTSD) is associated with increased symptoms of chronic, relapsing, infectious
diseases, and there is also greater difficulty recovering from the traumatic
event. These cases suggest psychic trauma contributes to the relapse of chronic
infectious tick-borne disease, and chronic infectious disease also appears to
contribute to the development of stress and posttraumatic stress symptoms. A
study of greater numbers in more depth is advised.
Introduction:
Studying the dynamics of stress is an area of great
interest in both biology and medicine. It is generally accepted knowledge that
individuals under greater stress are more susceptible to the common cold, the
flu, a relapse of a herpes simple fever blister, or a number of other acute and
chronic infectious diseases. Conversely, chronic illnesses such as chronic Lyme
disease can result in increased chronic stress, which may further reduce
immunocompetence, deter recovery, and contribute to a vicious cycle of chronic
illness, chronic stress, and lack of recovery from this illness.
Current research demonstrates that chronic stress,
sleep deprivation, and depression contribute to a decline in immunocompetence
and a decline in natural killer cell (NKC) activity. The presence of PTSD is
associated with a lower number of lymphocytes and T cells, decreased NKC
activity, and a reduction of the total amount of interferon gamma and IL-4. In
contrast, antidepressant treatment with fluoxetine (Prozac) has been
demonstrated to increase NKC activity in vivo (in a living person). Both
fluoxetine and paroxetine (Paxil) have increased NKC activity in vitro.
Improvement in immunocompetence in vivo appears, in part, associated with
serotonin 1-A receptor activity. Other indirect mechanisms through the
autonomic, neuroendocrine, and immune systems may also be significant in vivo.
Much has been written recently about the effect of
chronic, relapsing, infectious diseases upon the brain. There are a multitude
of journal citations, anecdotal reports on the Internet, and cases in clinical
practice of trauma contributing to a relapse of infectious disease symptoms.
The traumas involved may be psychic, somatic, or psychic and somatic (i.e.,
emotional trauma, childbirth, surgery, immunizations, or accidents).
Normally, we can peacefully co-exist with a multitude
of microbes within us and in our environment. In a state of severe or chronic
stress, there is a shift of allocation of resources towards dealing with the
acute stressor at the expense of an immunosuppressive effect, which can result
in an increased vulnerability to the pathogenic effect of microbes that might
otherwise be non-threatening. This increased vulnerability may trigger a
relapse of latent infections, resulting in a progression of symptoms from these
infections. The effect of the microbes, plus the body’s response to them,
results in the pathological symptoms associated with infectious disease.
Although we could focus on many facets of this disease process, this article
shall particularly focus upon mental symptoms, or more specifically, symptoms
associated with posttraumatic stress disorder (PTSD) and chronic, relapsing,
tick-borne diseases.
PTSD is an illness with a complex and puzzling
etiology when a traumatic event occurs, some recover with a healthy grief, and
a subsequent adaptive process. However, for a number of reasons others are not
able to integrate this experience into their lives in an adaptive manner. As a
result, patients with PTSD continue to experience symptoms of chronic stress,
accompanied by different combinations of re-experiencing of the trauma,
avoidance, hypervigilance, and psychic numbing. In a healthy adjustment to a
traumatic event there is, instead, a learning process accompanied by a change
of the neural architecture and neuro-chemistry of the brain, resulting in a
capacity to better differentiate and respond appropriately to specific threats.
However, in PTSD the fearfulness and response to the threat lacks adaptive
specificity. A dysfunction of the process of learned fear and the learned
response to this threat is, therefore, hypothesized as contributing to the
pathology of PTSD. A dysregulation of norepinephrine and cortisol are
particularly significant in understanding PTSD.
When a chronic, low-grade, relapsing infection
affecting the brain is present, brain functioning is impaired through a number
of pathophysiological processes. The presence of this impairment at the time of
psychic trauma may deter the normal recovery from trauma and contribute to the
development of PTSD.
Case
Histories:
Mrs. A is currently a 37-year-old white female with
an interest in outdoor activities. She was previously in good health until a
camping trip she took to a
In 1987, a bull’s-eye rash was noted on her right
leg. The multi-system illness progressed further after this time. She was seen
by a number of physician and was diagnosed with mitral valve prolapse, and
possible multiple sclerosis.
Symptoms continued to increase and she was eventually
diagnosed with Lyme disease (LD) in 1990 by a physician with experience in the
treatment of LD. The diagnosis was confirmed with a positive Lyme ELISA and
Lyme Western Blot. There were multiple other positive tests confirming Lyme
disease in the course of her illness. In addition, white matter lesions were
noted on an MRI of her brain. Over time, the prior lesions improved and new
ones appeared. The patient was stabilized in 1992 after antibiotic treatment,
including extended courses of IV antibiotics.
In 1994, while in a remission, the patient was in her
home and heard an explosion. Reportedly, outside the sky was orange, boulders
were flying in the air, and her car was melting and blistering. The patient
thought it was a nuclear blast. She embraced her son and husband and said, “I
love you. We’ll die. I’ll see you in Heaven.” The walls of her home were
burning, glass was cracking, and her skin was burning. At that point, they took
the risk of running from their home. As they left the house, it collapsed. The
patient and her family survived what was later found to have been a gas main
explosion.
After the incident, the patient experienced a number
of symptoms associated with a posttraumatic stress disorder (PTSD), including
flashbacks of running through fire, seeing the car melt, and telling her son
they would die. There was an exaggerated acoustic startle in response to noises
and she was distraught that all her possessions were lost in the explosion.
There was a return and increase of symptoms associated with LD immediately
after the explosion and a Lyme Western Blot both IgM and IgG were positive two
weeks after the trauma.
An exam in 1997 demonstrated the following signs and
symptoms:
·
Attention span symptoms include difficulty with cognitive
tracking and sustained attention, impaired ability to allocate attention,
impaired attention span when frustrated, and hyperacuity to sound, light,
touch, and smell. Memory symptoms include impairments of working memory,
working spatial memory, short-term memory, memory encoding, letter reversals,
spelling errors, word substitution errors, number reversals, and slowness
retrieving words, numbers, names, faces, and geographical memory.
·
Processing symptoms include impairments of reading
comprehension, auditory comprehension, transposition of laterality, left-right
discrimination, capacity for visual imagery, calculation, fluency of speech,
fluency of written language, handwriting, and spatial perceptual abilities.
There was stuttering, slurred speech, and optic ataxia. Executive functioning
symptoms included unfocused concentration, “brain fog,” difficulty prioritizing
multiple tasks, difficulty with multiple simultaneous tasks, and decreased
abstract reasoning.
·
The patient experienced depersonalization, derealization,
vivid nightmares, and illusions.
·
Mood symptoms included decreased frustration tolerance,
sudden abrupt mood swings, and hypervigilance.
·
Behavioral symptoms included disinhibition, exaggerated
startle reflex, suicidal tendencies, accident proneness, decreased job
performance, marital difficulties, compensatory compulsions, dropping objects
from her hands, and crying spells.
·
Psychiatric syndromes present including depression, panic
disorder, and posttraumatic stress disorder (PTSD).
·
The patient had insomnia and was not well-rested in the
morning. There was anorexia and weight loss. Capacity for pleasure, libido, and
social interests were all diminished.
·
There were body temperature fluctuations with intolerance to
heat and cold, decreased body temperature, low-grade fevers, night sweats, and
chills.
·
Headaches were in the neck, with sharp shooting pain
radiating to the scalp and eyes. In addition, there were TMJ and sinus
headaches.
·
Eye symptoms included blurred vision, sensitivity to bright
light, sensitivity to fluorescent light, floaters, eye pain, double vision, and
a lid drop.
·
A prior Bell’s palsy and loss of sensation on the side of
the face had not re-emerged. However, there was tinnitus, dizziness, vertigo,
motion sickness, choking on food, and difficulty swallowing.
·
Neurological symptoms Included numbness, tingling, sensory
loss, burning, crawling under the skin, stabbing sensations, weakness, tremors,
twitching, muscle tightness, muscle discomfort, and an odd sensation that her
head felt hollow. The patient fell backwards on Rhomberg testing when her eyes
were closed.
·
There was pain and tightness of multiple joints. There was
periosteal tenderness of the tibias, ribs, iliac crest, sternum, and clavicles.
In addition, there was chronic fatigue, muscle tenderness, and tenderness of
the
chostrochondal
joints.
·
There was mitral valve prolapse, a racing pulse,
pericarditis, and a heart murmur. Shortness of breath, a sore throat, and
swollen glands were present. Upper GI distress, irritable bowel syndrome, and
gallstones were also present. There was breast tenderness and irritable
bladder. In addition, alcohol intolerance, hair loss, tooth pain, multiple
chemical sensitivities, bruising, chronic pain, and an increase in allergies
were noted.
Symptoms were noted to have gradually evolved with
time, and they were sometimes subtle and variable. The symptoms were increased
by stress, they were exacerbated by antibiotic treatments, and they increased
in the perimenstrual period.
Laboratory testing demonstrate LUAT – 78, 110, and O
on samples collected at two days intervals – Lyme ELISA was positive at l.32.
Lyme Western Blot IgM was positive with reactivity of KDa 23-25, 31, 34, 39,
4l, and 58 bands. The patient also
tested
positive for babesiosis and human granulocytic ehrlichiosis (HGE). The
combination of problems from the LD and the explosion resulted in considerable
financial distress and difficulty paying for necessary medical care, which
further exacerbated symptoms. She has been treated with a combination of
antibiotics, psychotropics, and psychotherapy, with a partial response.
Mr. B is currently a 43-year-old white male who may have been infected
by tick-borne diseases thirteen years ago and eight years before diagnosis and
appropriate treatment. He, like many patients with these complex problems, had
been to numerous doctors. The illness also affected his marriage and his
occupational adjustment. His prior diagnosis was considered to be asthma,
irritable bowel syndrome, colitis, bipolar illness, and personality disorder
(NOS). He experienced many of the symptoms that Ms. A. described. Emotional
numbing, over-reactivity, hypervigilance, explosive outbursts, and vague
somatic symptoms give the impression of PTSD. In describing his temper, this
patient stated, “I was in a mind fog. I didn’t know what was right or wrong.”
He assaulted his wife and a restraining order was entered. He cut the phone
lines to his house, jumped up and down on his wife’s car, and put his foot
through her windshield. He was arrested three times and was committed to
psychiatric hospitals. The patient expressed the feeling he had no control.
After starting a suicide attempt, he regained some control,
drove to a hospital, and was committed to a state hospital, where an internist
diagnosed him with Lyme disease and started treatment. Mr. B began to respond,
was discharged, and pursued treatment with a doctor who had an extensive
reputation in the treatment of Lyme disease. The patient improved. Mr. B
developed a close working relationship with this treating physician, who
confided to him that he also suffered from Lyme disease. The patient felt his
doctor was showing increasing signs of Lyme disease. The State Board of Medical
Examiners investigated the doctor. Shortly thereafter, the doctor with whom Mr.
B identified committed suicide. The patient then suffered a relapse of symptoms
associated with PTSD. He was subsequently diagnosed with babesiosis and HGE and
stabilized with penicillin, Probenecid, Biaxin, and Paxil.
After stabilization, his medications were gradually reduced. He was stable
for a few years until experiencing a business failure. His symptoms increased
with a predominance of psychiatric symptoms. He experienced flashbacks,
hypervigilence, avoidance, and depression, and became increasingly isolated and
suicidal. He failed to respond to all psychiatric interventions and the
suicidal risk factors increased. He was given a shot of 2 grams of Rocephin IM
and three hours later, the depression improved and he was no longer suicidal.
He had since been stabilized on a combination of psychotropics and antibiotics.
There was a recent relapse related to stress from the
Discussion:
In the case of Ms. A, it appeared PTSD caused a
relapse of a chronic relapsing tick-borne disease. In the case of Mr. B, it
appeared a chronic relapsing tick-borne disease resulted in behavioral
symptoms, which resulted in a reciprocal intensification of both PTSD and the
tick-borne disease. After being stabilized, traumatic events resulted in
subsequent relapses of the tick-borne disease.
These cases suggest there is a reciprocal
intensification between chronic relapsing tick-borne diseases and PTSD.
Treatment of the chronic tick-borne disease with antimicrobial interventions
improved both the systemic infection and also the PTSD. In addition, treatment
of the PTSD with traditional psychiatric treatments improved both the PTSD and
the systemic infection. Further research is needed to study this link in more
detail.
Recent terrorist attacks against the
In working with patients directly and indirectly
affected by the events of
Patients with pre-existing psychiatric illness often
had an increase of symptoms, most notably anxiety, panic, phobias, paranoia,
depression, acoustic startle, and irritability. From similar events, such as
the
Contending with the threat of international terrorism
is a separate, but related, issue. Terrorism is “the use of force to threaten,
to frighten people, and cause them to obey, especially by a government or
political group” (Webster’s). Both violence and terrorism are an unfortunate
part of human nature. The degree of violence and magnitude of the attack of
September 11 is conducive to causing posttraumatic reaction in many, even those
far removed from the actual attack. Many patients with chronic tick-borne disease
and the physicians who treat them have prior experience and capability in
dealing with more subtle forms of terrorist tactics, which are implemented by
some to suppress freedom, access and ethics in the health care system, and
suppress the adequate recognition and treatment of tick-borne diseases. The
best defense against this threat is many of the same treatments used to combat
PTSD. This includes understanding the exact nature and extent of threats,
well-focused vigilance and response to threats, and approaches that restore and
maintain will, resolve, spirit, courage, self-esteem, and unity.