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Psychiatric Clinics of North America
Volume 21 . Number 3 . September 1998
Copyright 1998 W. B. Saunders Company

Brian A. Fallon 1 MD, MPH
Janice M. Kochevar 2 NP
Andrea Gaito 3 MD
Jenifer A. Nields 4 MD

1 Department of Psychiatry, Columbia University Medical Center and the
Lyme Disease Research Program New York, New York (BAF)
2 private practice Armonk, New York (JMK)
3 Department of Medicine, Seton Hall University, and private practice
Basking Ridge, New Jersey (AG)
4 Department of Psychiatry, Yale University School of Medicine New
Haven, Connecticut (JAN)
Address reprint requests to
Brian A. Fallon, MD, MPH
The NYS Psychiatric Institute
Lyme Disease Research Program
722 West 168th Street, #13
New York, NY 10032
This work has been supported by the Lyme Disease Association of New
Jersey and the Betz Family.

Lyme disease is a tick-borne illness caused by the spirochete Borrelia
burgdorferi. Reported throughout the United States, the greatest
incidence of Lyme disease occurs in certain areas, such as the
Northeast, the upper Midwest, and the Pacific Coastal states. It has
been dubbed "The New Great Imitator" because, like another spirochetal
illness neurosyphilis--the original Great Imitator, Lyme disease has a
vast array of multisystem manifestations, including neuropsychiatric
ones. [18] Failure to recognize Lyme disease early in its course can
result in the development of a chronic illness that is only temporarily
or partially responsive to antibiotic therapy. The goal of this article
is to present the typical and atypical manifestations of Lyme disease
in children and adults in order to help the clinician more rapidly
unmask the correct diagnosis behind the puzzling presentations of some


Whenever a disease exists for which serologic tests are unreliable in
determining the presence or absence of the disease process, frustration
and anxiety rise among both patients and doctors. When controversy
exists even among the leading academic researchers as to the validity
and reliability of these tests, a battleground is then set in which
doctors dispute amongst themselves over the diagnosis while the patient
is left with an uncertain clinical syndrome in which treatment
recommendations vary widely depending on the physician chosen. If this
particular disease process also has psychiatric manifestations that
lower the patient's frustration tolerance, increase irritability, and
impair cognitive functioning, then the stage is set for a referral to a
psychiatrist to address a presumed psychogenic or functional disorder.
Such is the situation when dealing with Lyme disease. For example, in
1991, an essay appeared in a major medical journal entitled, From the
Centers for Fatigue Control (CFC) Weekly Report. Lime disease-- United
States, in which patients with unexplained persistent fatigue were
mocked for wondering whether or not they had Lyme disease, suggesting
that they were clinging to a stylish diagnosis unable to accept that
they actually suffered from a fictitious "Lime Disease." [14] This
sarcastic essay resulted perhaps from a sense that the medical
scientific community had full knowledge about this disease. Such was
(and is) clearly not the case. The observation that fatigue after Lyme
disease is a significant problem, that many of these patients would
meet clinical criteria for chronic fatigue syndrome (CFS), and that a
substantial portion of these patients appear to have signs in
experimental CSF studies of persistent infection with B. burgdorferi
has led the National Institute of Health to fund major research studies
investigating the extent to which ongoing symptoms are due to
persistent infection versus a "post-Lyme" syndrome.

Overdiagnosis of Lyme disease has been reported in rheumatology
clinics. In 1990, a report [20] summarizing a chart review of 100
patients referred to a New Jersey Lyme Clinic indicated that only 25%
had a history explicitly suggestive of Lyme disease. The most common
other diagnosis was fibromyalgia. In 1993, an article [21] describing a
retrospective case survey of 788 patients referred to another Lyme
disease center revealed that only a minority (23%) of the patients met
diagnostic criteria for active Lyme disease. An additional 20% of the
788 patients had confirmed previous Lyme disease with concurrent or
residual symptoms and an additional 45% of the patients who were
determined not to have ever had Lyme disease had negative serologic
results in the authors' laboratory, but had had positive serologic
results in other laboratories. Patients with fibromyalgia or CFS
constituted the majority of cases of presumed misdiagnosis. Given that
the symptoms of fatigue, myalgia, arthalgia, sleep disturbance, and
persistent headaches are common during active Lyme disease and that
both CFS and fibromyalgia are thought by some researchers to be
triggered and perhaps perpetuated by infectious agents, excluding CFS
and fibromyalgia as aspects of the syndrome of active Lyme disease
seems premature in the history of our understanding of this illness.

Data to support the clinical speculation that many persistently
symptomatic Lyme disease patients have one disease process and not
multiple concomitant diseases was provided in 1994 by the results of a
case-controlled community epidemiologic study. [19] Compared to
controls, patients with a history of previously treated well-defined
Lyme disease had significantly increased frequency of fatigue,
arthralgias, paresthesias, poor coordination, inattention, emotional
lability, and sleep disturbances. Less than half of these patients at
follow-up were seropositive for Lyme disease. Among the 10 persistently
symptomatic patients who were retreated, five improved. Although not a
placebo-controlled study, the latter finding suggests that
neuropsychiatric symptoms may persist in some patients despite prior
therapy and that retreatment with antibiotics may result in further

Possible misdiagnosis of Lyme disease and failure to identify another
concurrent disease need to be considered seriously among patients who do not have
a typical profile, whose tests are equivocal, or who are not responding
to antibiotic treatment. In certain Lyme endemic areas, for example,
approximately 10% of patients with Lyme disease may be coinfected with
babesiosis, a comorbid infection which worsens the course of Lyme
disease resulting in more frequent symptoms (fatigue, headaches,
sweats, chills, anorexia, emotional lability, nausea) and a longer
duration of illness. [13] Patients with major depression alone may have
prominent fatigue, anorexia, emotional lability, myalgias, and
insomnia, all symptoms that overlap with Lyme disease but by themselves
do not make the diagnosis. Because a medical diagnosis is more socially
acceptable, disabling major depression may go untreated for years. One
patient, who consulted with one of the authors, with a prior history of
Lyme disease was given long courses of antibiotic treatment for a
constellation of symptoms, among which were prominent panic attacks and
agoraphobia. After treatment with pharmacotherapy and behavior therapy,
her panic attacks and medical condition dramatically improved. Although
panic attacks and severe anxiety may be a symptom of untreated Lyme
disease, when the Lyme disease has been treated but the anxiety
persists physicians should suspect that an underlying Lyme-triggered or
unrelated-but-concomitant psychiatric disorder exists.

Underdiagnosis of Lyme disease, however, is also a problem,
particularly when the symptoms are primarily neuropsychiatric. In a
survey of 193 patients with seropositive chronic Lyme disease, [7]
patients reported having been sick for approximately 1 year and having
had to consult with a mean of two doctors before the diagnosis of Lyme
disease was made. Prior to diagnosis, 42.5% of these seropositive
patients were thought to have had only a psychiatric disorder. Although
this survey sample undoubtedly included some seropositive patients who
may not have had Lyme disease, the results do suggest that
neuropsychiatric problems are common in chronic Lyme disease, and that
mental health professionals can play a critical role in the initial

In this article, the authors describe the typical clinical profile of
Lyme disease and the tests that exist to support the diagnosis. They
conclude with case studies of three patients who were initially thought
to have other diagnoses: attention deficit disorder (ADD), depression,
and multiple sclerosis (MS).


In the early phase of infection after being bitten by an infected
ixodes scapularis tick, common signs and symptoms include an
erythematous annular rash (erythema migrans) followed by mild to severe
flu-like symptoms. Hematogenous dissemination of the spirochete can
occur within days to weeks of the tick bite. The organism may then
lodge within the heart, eyes, joints, muscles, or central and
peripheral nervous system. Although manifestations of target organ
involvement may occur early, B. burgdorferi may remain quiescent for
months to years before producing symptoms. Because of the potentially
long latency period before disease onset, the fact that approximately
one third of patients do not recall the tick-bite or rash, and the
nonspecific nature of the early flu-like syndrome, infection by B.
burgdorferi may not be recognized until long after the initial tick

Approximately 15% to 40% of patients with Lyme disease develop
neurologic problems. [4] Initially patients may complain of a bad
headache without any signs of inflammation in the CSF. Early neurologic
Lyme disease may be manifest thereafter by meningitis, encephalitis,
cranial neuritis, and motor or sensory radiculitis. Patients with
meningitis often complain of a headache and stiff neck while the
patients with encephalitis may have mood lability, irritability,
confusional states, and poor sleep. Involvement of the seventh cranial
nerve should automatically lead the clinician to test for Lyme disease,
however only 5% to 10% of patients with neurologic Lyme disease have a
Bell's palsy. Peripheral neuropathies (motor or sensory) may result in
sharp shooting or stabbing pains, burning pains, paresthesias,
weakness, or fasciculations. Later stage neurologic Lyme disease may
result in a chronic encephalopathy (see below) or an encephalomyelitis.
Encephalomyelitis, markedly less common, may be characterized by
spastic paraparesis, transverse myelitis, cerebellar syndromes,
hemiparesis, or movement disorders. Rarely patients with neurologic
Lyme disease may have strokes, seizures, or severe dementia.

Lyme encephalopathy is characterized by subtle to severe disturbances
in cognition, affecting primarily short-term memory, verbal fluency,
attention and concentration, and processing speed. Patients may
complain that their brains are "in a fog" or that their reaction time
is slower. Recitation of their history may be very disorganized because
these patients have a hard time keeping track of their thoughts. Some
of these patients are so distractible that they may appear to have new-
onset attention deficit disorder. Although memory storage is often not
impaired, patients may have a hard time retrieving information. Word
transpositions are not uncommon, such that a patient might say, "I put
the microwave in the dinner" instead of "I put the dinner in the
microwave." Other concomitant symptoms associated with late Lyme
disease include profound fatigue, sleep disturbance, photophobia,
hyperacusis, periods of geographic disorientation, and disturbances of

The plethora of psychiatric problems associated with Lyme disease were
first reviewed in 1990 in the European medical literature by Drs.
Kohler [12] and Omasits. [17] Kohler attempted to categorize the
psychiatric symptoms by stage, listing depressive mood in early
disease, organic personality disorders in mid-stage disease, and
organic psychoses, dementia, and anorexia in the later phase of the
illness. Omasits stated that psychiatric manifestations can be
predominant and that the clinical spectrum of Lyme disease ranges from
agitated depressive states with suicidal ideas to the clinical picture
of dementia. A review of the medical literature [8] revealed that, in
addition to the disorders listed by Kohler and Omasits, Lyme disease
appear to be capable of causing syndromes which manifest as personality
change, depersonalization, mania, hallucinations (auditory, visual, and
olfactory), paranoia, catatonia with stupor and mutism, somatization
disorder, obsessive compulsive disorder, violent outbursts, panic
attacks, and disorientation.

In children and adolescents with neurologic Lyme disease, behavioral or
mood disturbances are the second most frequently reported symptom. [1]
Common neuropsychiatric symptoms include headaches, fatigue, difficulty
with concentration in school, irritability, oppositional behavior, and
new onset anxiety disorders. When the onset of illness is not dramatic,
but characterized by gradually increasing fatigue, disinterest, and
inattention, children may begin to label themselves as incompetent as
they realize they can no longer keep up with the rest of their
classmates academically. While developmental and family issues always
need to be considered when there is a change in a child's behavior or
mood, in endemic areas Lyme disease should be considered as well,
particularly because delays in diagnosis are associated with greater


When Lyme disease is suspected clinically, the clinician should order a
Lyme ELISA and a Lyme Western Blot, both indirect serologic tests that
detect the presence of antibodies against B. burgdorferi. Whereas the
ELISA is a less expensive screening test, it is less specific (and
perhaps less sensitive) than the Western blot, resulting in false
positives among patients infected with other spirochetal conditions,
such as syphilis or periodontal disease. Because patients can have a
negative ELISA but a positive Western blot, polymerase chain reaction
(PCR) assay, or culture, and both an ELISA and Western blot should be
ordered. [11] [16] The test should be sent to a laboratory with
established reliability in conducting Lyme assays. The Centers for
Disease Control (CDC) guidelines currently used by many commercial
laboratories for the interpretation of the Western blot are overly
restrictive in that patients with active Lyme disease may not have the
requisite 5 of 10 specific bands. In addition, certain bands not listed
as specific such as the 31 Kd (Osp A) and 34 kD (Osp B) bands are in
fact highly specific, the former being used to create the new Lyme
vaccines. Other tests that may be helpful include more direct tests
such as the PCR assay that detects the presence of the DNA of the
spirochete and antigen detection assays (in urine or cerebrospinal
fluid [CSF]) which detect pieces of the spirochete itself. These tests
are stronger indications that the organism may in fact be present;
however, they do not necessarily indicate that the spirochete is alive.
The best and most definitive test is based on culture, although this
test has a very low yield in late Lyme disease.

Overutilization of Lyme serologic tests can lead to a higher likelihood
of false positive results. When tests are used as an indiscriminate
screen, ordered without regard for clinical presentation, risk factors,
and history, one report indicates that the positive predictive value of
a test falls to 7%. [10] When tests are ordered for patients with a
typical clinical history of Lyme disease, the positive predictive value
rises to over 96%. The clinical history therefore is extremely

A recent FDA Public Health Advisory statement [3] on assays for Lyme
disease warned: "A positive result does not necessarily indicate
current infection with B. burgdorferi, and patients with active Lyme
disease may have a negative test result." For example, in early Lyme
disease with erythema migrans, patients are expected to have negative
serologies because detectable levels of borrelia-specific antibodies
have not yet been produced. In later chronic Lyme disease, among
patients who were treated early in their illness, negative or equivocal
serologies may result presumably because the early antibiotic treatment
abrogated the immune response. In one recent study, [15] of 8 patients
with late Lyme encephalopathy who had CSF evidence of active central
nervous system (CNS) infection, half of the patients had equivocal
serologic results and one quarter were seronegative. This study, in
addition to demonstrating the presence of seronegative Lyme disease,
points out the importance of spinal fluid assays among patients with
suspected central nervous system involvement.

Other tests that are a key part of the evaluation include
neuropsychologic testing, CSF studies, and structural and functional
imaging. Neuropsychologic tests of memory, attention, processing speed,
and verbal fluency can detect objective evidence of cognitive
dysfunction that may not be immediately observable on clinical exam.
The most common problems are in memory retrieval and attention. CSF
tests in early neurologic Lyme disease may demonstrate intrathecal
antibody production, although in later Lyme disease the results of CSF
antibody studies may be negative up to 43% of the time. [5] More
commonly the CSF may reveal a mild increase in protein or a
pleocytosis. Because a normal CSF may be seen in 20% of patients with
active central nervous system infection with B. burgdorferi, this test
cannot be used to exclude the diagnosis of Lyme disease. MRI scans may
reveal T2 weighted white matter hyperintensities similar to the
demyelinating lesions associated with MS. Functional imaging may reveal
a diffuse pattern of heterogeneous uptake, resembling patients with
vasculitides. [9] [15] In late neurologic Lyme disease, SPECT and PET
imaging appear to be more sensitive in detecting objective
abnormalities than MRI scans. Neuropsychiatrists therefore may find
functional imaging particularly helpful in the effort to tease out
whether a patient's problems are primarily psychiatric or owing to
another more diffuse central nervous system process.


Three cases are presented below, one child, one adolescent, and one
adult. Each demonstrates the complexity of presentation, diagnosis, and

Case Study 1

Attention Deficit Disorder Versus Lyme Disease

At age 7, Susan who lived in a Lyme endemic area developed problems
focusing in school. A neuropsychologist diagnosed probable ADD. Other
symptoms included lethargy, irritability, forgetfulness, headaches,
poor coordination, joint pain, word-finding difficulties, and light and
sound sensitivity. A comprehensive medical work-up, including EEG and
MRI, were within normal limits, except for a positive Lyme ELISA. Once
Lyme disease was diagnosed and treated, her symptoms of attention
deficit disorder resolved and her school grades returned to their pre-
Lyme disease level of excellence. Her course over the subsequent 2
years appeared to be antibiotic-dependent, such that she would do well
as long as she stayed on antibiotics and relapse when taken off. At age
9, she was able to come off antibiotics and remained symptom free for 3
years, performing in the A/A+ range academically. Knee pain, frequent
headaches, and poor concentration re-emerged at age 12. Serologic tests
revealed a positive ELISA with fully reactive IgG and IgM Western
blots. A brain SPECT revealed normal perfusion. Treatment with oral
cefuroxime for 2 months led to a rapid improvement in all symptoms,
however within 2 weeks of stopping antibiotics her symptoms returned.
During the following months, her teachers recorded a variety of
problems: "trouble with consistency in day-to-day work; careless; head
in the clouds; scattered and sloppy work; assignments are late,
forgotten, or lost; difficult time following directions; more forgetful
and disorganized." Her parents noted that Susan would go to school with
homework in her bag but once there have no idea where it was or whether
she had done it. Emotionally, she had become frustrated, overwhelmed,
tearful, aggressive, and fearful with new onset phobias and nightmares.
Physically, she had knee pain with mild swelling, paresthesias,
headaches, moderate fatigue, insomnia, and trouble focusing.

On mental status examination, Susan acknowledged having problems in 6
of the 9 inattention areas identified in the DSM-IV criteria for
attention deficit hyperactivity disorder (ADHD), thereby qualifying for
the diagnosis. She denied significant depression or suicidal feelings
but acknowledged feeling overwhelmed. Cognitive testing after being off
of antibiotics for 4 months revealed that she had a very superior
baseline intelligence (verbal IQ 132) but significant deficits in
visual motor planning, speed of processing, visual scanning, attention,
visual memory, and learning. She was diagnosed then as having a
persistent encephalopathy secondary to Lyme disease and treated with
additional oral antibiotics. She continues on oral cefuroxime several
months later and has had a full return to her prior level of health and
academic excellence, with no evidence of the prior ADHD symptoms.

Case Study 2

Depression Versus Lyme Disease

David, a 16-year-old boy who lived in a Lyme endemic area, presented
complaining of long-standing depression, exacerbated recently when he
stopped dating a girl after only 2 weeks because he felt too tired and
not smart enough. He reported anger, frustration, insomnia, poor
appetite, mild weight loss, and passive suicidal ideation: "I wish I
could just die in my sleep." He was oriented to person and place, but
when asked the date he said 1977 instead of 1997. He reported feeling
spaced out all the time, as if in a fog.

David's recent medical history was notable for painful knees throughout
much of 7th grade, such that he had to quit sports. A previous A/A-
student, his grades declined to Bs. He appeared lazy because he found
it hard to get out of bed in the morning and often forgot to hand in
assignments that he had in fact completed. His grades declined during
8th and 9th grades such that by 10th grade he was nearly failing most
of his courses. The presumed cause of his poor performance was either
laziness or mild depression. When asked about his school difficulties,
he reported trouble staying awake in class and trouble concentrating.
When asked about his physical and cognitive status, he acknowledged
severe headaches; facial fasciculations; myalgias; stiff neck;
hyperacusis; episodic paresthesias of his face and hands; sudden
sweating; painful joints; sore throats; palpitations; electric shock-
like pains; word-finding problems such that it was hard to finish
sentences; semantic paraphasias; short-term memory problems such that
he could not recall conversations; and testicular pain. David had had
embedded tick bites, but he could not recall ever having had an
erythema migrans rash.

Given the suspicious clinical history, further testing was done.
Although a Lyme ELISA was negative twice in the prior 3 months, his IgG
Western blot revealed 4 of the 5 requisite CDC specific bands. Other
tests, including TFTs, heterophile antibodies, and brain MRI with FLAIR
sequences were unremarkable. Neuropsychologic testing revealed
significant deficits in processing speed and visual spatial memory, in
a young man whose premorbid intellectual capacity was estimated to be
in the 85th percentile. A brain SPECT was ordered that revealed
moderate to severe diffusely and heterogeneously decreased perfusion in
the cortex and the central white matter, consistent with encephalitis,
vasculitis, and Lyme disease. Based on these findings, a diagnosis of
probable Lyme encephalopathy was made and he was treated with 12 weeks
of IV ceftriaxone with excellent results physically (sleep, appetite,
headaches, joint pains, distractibility, numbness), cognitively
(distractibility, short-term memory), and emotionally. Anti-depressant
medications had been recommended prior to IV treatment, but were not
taken. The patient was no longer depressed after the IV antibiotic
regimen and his school performance markedly improved. David's follow-up
neuropsychologic testing revealed an improvement of 22 full-scale IQ

Case Study 3

Multiple Sclerosis Versus Lyme Disease

Mr. B, a 45-year-old research scientist recently diagnosed as having
MS, presented asking whether any of his current symptoms might be
related to a diagnosis of Lyme disease 6 years earlier. Current
symptoms included headaches, arthritis, sleeping difficulties,
paresthesias, tremors, fasciculations, irritability, visual problems,
and short-term memory difficulties.

At age 39, shortly after two tick bites from a Lyme endemic area, the
patient experienced a severe flu and myalgias, followed by marked
headaches, fatigue, leg weakness, migratory lower extremity
polyarthritis, paresthesias, loss of touch, and temperature sensation
below the hips, and urinary sphincter dysfunction. Serologic tests were
unremarkable, including a Lyme ELISA and rheumatoid factor. Although
some CSF studies (including VDRL, Lyme titers, and oligoclonal bands)
were within normal limits or nonreactive, he did have a pleocytosis of
7 white blood cell (WBC) count and mildly elevated myelin basic
protein. A neurologist diagnosed transverse myelitis, secondary to
presumed seronegative Lyme disease. He was treated with intramuscular
ceftriaxone for 2 weeks followed by 4 weeks of oral doxycycline with
resolution of his headaches. This was followed by oral prednisone with
resolution of his leg weakness and foot drag. Although markedly
improved, over the subsequent 5 years he was intermittently symptomatic
with ankle pain, headaches, night sweats, fasciculations, paresthesias
below the waist, insomnia, and testicular pain. The cause of these
persistent symptoms was unclear.

At age 44, his symptom profile worsened: more severe headaches, slurred
speech, left facial and upper extremity tingling, double-vision, poor
coordination with poor postural balance, and lightheadedness.
Neurologic examination revealed dysarthric speech, decreased pain, and
temperature sensation and a delayed corneal reflex on the left side of
his face, decreased temperature sensation in the lower extremities, and
a markedly abnormal cerebellar examination. A brain MRI revealed
multiple areas of focal white matter disease extending from the brain
stem to the parieto-occipital lobe. Median nerve somatosensory evoked
potential studies were within normal limits. Visual evoked potential
studies were abnormal suggestive of optic nerve or severe retinal
disease on the left and axonal optic nerve dysfunction on the right.
CSF was within normal limits with no evidence of Lyme antibodies,
oligoclonal bands, or elevated myelin basic protein. Despite the normal
CSF, he was diagnosed clinically as having probable MS. After treatment
with prednisone, he experienced improved energy and vision, but
continued to have diffuse multisystemic symptoms.

Now at age 45, he presented with the symptoms identified above. Lyme
serologies revealed a Western blot IgG that met full CDC criteria for
reactivity. Other laboratory tests were within normal limits (including
FTA, ANA, RF, ACE, anti-cardiolipin antibody) except for a mild
polyclonal increase of IgM. Brain SPECT revealed decreased perfusion
diffusely throughout the cortex, the white matter, and the basal
ganglia bilaterally. The diagnosis of Lyme disease was made, although
concurrent MS could not be excluded.

Over the subsequent 9 months, off all steroids, Mr. B was treated with
high dosages of oral cefuroxime and minocycline. Although improvement
occurred in all symptoms such that he was able to return to work, a
return of left-sided paresthesias and weakness led to a repeat MRI
which showed a worsening of demyelination in the brainstem. He was then
started on a regimen of intravenous ceftriaxone (2 g IV qd) and
clarithromycin (500 mg po BID), both of which he continues on now 12
months later. Since the IV antibiotics were started, serial MRI scans
at the same center revealed progressive diminution in the size of all
white matter lesions and the development of no new lesions. Based on
the history, Lyme serologies, and antibiotic responsiveness, both his
neurologist and infectious disease doctors changed their diagnosis from
MS to a resolving antibiotic responsive Lyme encephalomyelitis.


These three cases demonstrate that patients with Lyme disease may have
variable neuropsychiatric presentations, equivocal or negative
serologic test results, incomplete treatment response and subsequent
relapses. As is true for most patients with neuropsychiatric Lyme
disease, each of these patients had a history of multisystemic symptoms
after exposure to a Lyme endemic area. In the absence of such a
history, Lyme disease is not likely to be the correct diagnosis.

Inattention and poor mental tracking are common features of Lyme
encephalopathy in both children and adults. Although impulsivity and
hyperactivity may be seen, more often children with Lyme-induced ADHD
meet criteria for only the inattention subtype. The initial treatment
should be antibiotics, followed later by psychopharmacologic approaches
to help diminish any residual problems with inattention.

The optimal duration of antibiotic treatment in chronic Lyme disease is
unknown, although typically patients are initially given 4 to 6 weeks
followed by longer courses if relapse occurs. [2] [6] [13A] In case 1,
Susan appeared to need long courses of oral antibiotics to remain
symptom free. An understanding of the microbiology of this spirochete
sheds light on why Lyme disease may require longer courses of
treatment. Borrelia burgdorferi has many features that are typical of
organisms that are difficult to eradicate: a slow rate of growth;
ability to remain dormant for long periods; intracellular invasion;
and, sequestration in areas where antibiotic penetration is more
difficult, such as the central nervous system or the anterior chamber
of the eye. Case study 2 demonstrated that even among patients who have
had Lyme disease undetected for long periods, antibiotic treatment can
be helpful although perhaps not curative.

The depression associated with the earlier encephalitic phase of
neurologic Lyme disease is characterized by marked irritability and
mood lability. Later, in the setting of encephalopathy, the depression
is often more mild, characterized primarily by anhedonia, low energy,
hopelessness regarding the future, and a diminished sex drive. In case
study 2, David's long-standing depressive state appeared to be a
chronic dysthymia. The diagnosis of Lyme disease would have been missed
had the physician not asked explicitly about specific cognitive and
physical symptoms. After the initiation of antibiotic treatment, he had
to be carefully educated about the fact that he had been suffering from
an undiagnosed infectious illness over the last few years that had been
draining his energy. Rather than being lazy and incompetent, he had
been sick. With this new understanding, David was able to perceive
himself in a new way and once again apply himself to his studies,
working hard to make up for the years of illness.

Differentiating Lyme encephalomyelitis from MS can be difficult. Mr. B
in case study 3 had many of the clinical features of MS, including
double vision, optic neuritis, paresthesias in one half of the body,
disturbed micturition initially, cerebellar involvement, and diffuse
white matter disease. Mr. B's CSF however did not have the
characteristic oligoclonal bands which are seen in over 90% of patients
with MS but in fewer than 5% of patients with neurologic Lyme disease.
Nor did his CSF demonstrate the common finding in MS of a marked
elevation in myelin basic protein. The negative CSF results for MS, the
positive serologic tests for Lyme disease, clinical improvement with
antibiotics, and progressive diminution of MRI hyperintensities
together confirmed the diagnosis of Lyme encephalomyelitis.

Although none of the three patients in this report took psychiatric
medications, psychopharmacology can be very valuable adjunctively for
patients dealing with persistent or severe neuropsychiatric symptoms.
For example, carbamazepine may help to reduce paroxysmal pain or
hyperacusis. Bupropion may help to diminish depression and enhance

In conclusion, in endemic areas, although Lyme disease may be an
overdiagnosed disorder in rheumatology clinics, it may be an
underdiagnosed disorder in child and adults psychiatry clinics.
Although none of the currently available tests for Lyme disease other
than direct culture definitively indicates active infection, the
clinical presentation and the multiplicity of tests taken together can
serve as guideposts for the clinician.


1. Belman AL, Iyer M, Coyle PK, et al: Neurologic manifestations in
children with North American Lyme Disease. Neurology 43:2609-2614, 1993

2. Burrascano JJ: Lyme disease. In Conn's Current Therapy.
Philadelphia, WB Saunders Company, 1997, pp 140-143

3. Burlington DB: FDA Public Health Advisory: Assays for Antibodies to
Borrelia burgdorferi: Limitations, Use, and Interpretation for
Supporting a Clinical Diagnosis of Lyme Disease. Department of Health
and Human Services, United States Public Health Service, Food and Drug
Administration, July, 1997

4. Coyle PK: Neurologic Lyme Disease. Semin Neurol 12:200-208, 1992

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[This message has been edited by pacbird (edited 28 December 2000).]

Posts: 733 | From CT | Registered: Oct 2000  |  IP: Logged | Report this post to a Moderator
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pacbird- great info, as usual, from you to us! I benefit greatly from reviewing and rereading articles every so often. It refreshes my memory and implants a broader reference source for later use. (Not that us Lymies have any memory problems you know! ) Very much appreciate the effort. Wonderin' if Cathy T has seen this recently? With her may help her. Think I will give her a yell...Take care of you.
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Very interesting info Pacbird.

I was dx with Transverse Myelitis in August. The neuro then said MS, prescribed Rebiff and then phoned a few days later and changed his mind because MRI and LP were clean. My original spinal lesion at T5 had even disappeared! He said that cannot happen with MS(actually seemed angry about it - like I have any control over it! Ha!)

I think that intensive blood work should be the standard protocol with anyone who presents with MS like symptoms.

I am seeing an LLMD now. About 35 vials of blood were taken and he is testing for everyhing under the sun, including Lyme.

His hunch is actually another bacterial infection called Brucellosis, caused from unpasteurized milk.

It is so sad, and such a loss to society that people are not being tested adequately.

Thanks again for the info!

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I have most of the Late Lyme symtoms ,although my neuro thinks I have early lyme b/c of positive IGM only.
Reading thismade me think I had lyme for a while. Ihad severe panic attacks at 18, now 25 and have had recurrent bouts of extreme anxiety, anger depression and not to mention
parasthesias! Nightmares are common for me, unfortunatly.Except in my case the ANA was + and FTA for syphilis.I know Syphilis was ruled out but Lupus is still a posibility, though I don' have the joint pain.
Thanks for the info, I'd like to send this to my friends' husband who told me he didn't believe I was sick or had Lyme. He said this to my face last night and both my friend and him were laughing at the whole painful ordeal I've had to endure. What ignorrance!

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Gisells2500......yes, it is ignorance. We will never laugh at you here........just understanding and support!
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Gosh, I am sorry that your friends were less than supportive. These symptoms are so hard to cope with and our lives are so affected. How is all the testing going? Are you being treated for the Lyme yet?
Take Care,

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yes, I got some treament, 1 month of 300mg Doxy. But this really isn't going to cure me.
So I need a good LLMD to direct me in the right path as far is this really lyme and stronger ABX.

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wow . . . I wish the 1 million or so doctors I've seen had read that pacbird!!! So what if I'm a little crazy . . . it is entirely possible that I'm sick as well - that's what I've been trying to tell them!!!

gisells - I'm living the "noone believes I'm sick dream" for about the last 13+ years!!! Now, I've been walking around w/ a PIC line in my arm for the last 3 or so weeks and there are still some that feel I'm imagining all of this or trying to get attention! Go figure . . . be true to you and know that at least I believe you!!! Sherry R

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Wowe, 13yrs of no one beleveing me would sure drive me to despair but you are a trooper! How is the IVABX, do you get a Herx right away? I'm GLAD that this forum is here.
Imagine dealing with all those symtoms and people thinking you nuts!

[This message has been edited by gisells2500 (edited 01 January 2001).]

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Top again..
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This is funny I just saw a child psyhc doctor for my two boys last week and the doctor pulled up the very same article. He told me he wants to see all the Lyme test results before he decides what to do for them.

I think this is a great paper, he had no understanding about Lyme before I saw him and while I was in the office he read this article and was supportive of the position. This doctor is also a professor at UCLA been around the block so I was impressed.

We had a very long talk about Lyme, it so happens he is doing a study on ADD/ADHD and the effect the gland system has on it. It opend his eyes that was for sure.

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Thanks for bringing this to the attention of us "newbies"...


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