Lyme Disease and Complex Partial Seizures

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Case Report: Lyme Disease and Complex Partial Seizures

C. Bransfield, MD, Associate Director of Psychiatry, Riverview

Medical Center, Red Bank, New Jersey.

[Journal of Spirochetal and Tick-Borne Diseases 6(4):123-125, 1999. © 1999

Lyme Disease Foundation, Inc.]

Abstract

A case of complex partial seizure disorder associated with late stage

neuropsychiatric Lyme disease is presented. The patient showed a progressive

development of somatic, cognitive, psychiatric, and neurologic symptoms.

Reliance upon a conservative criteria for the interpretation of

immunological testing caused an initial delay in diagnosis and treatment,

resulting in more severe symptoms including a complex partial seizure

disorder. Early diagnosis and treatment of Lyme disease is suggested to

prevent the development of more severe sequelae, such as complex partial

seizure disorder. When patients present with a complex partial seizure

disorder and a multisystem illness, Lyme disease should be considered in the

differential diagnosis.

Introduction

Seizure disorders are sometimes a manifestation of late stage

neuropsychiatric Lyme disease. There are a number of references to this

association in the medical literature.[1-17] A case history is presented to

describe the emergence of a seizure disorder in association with late stage

Lyme disease.

Case Report

A 46-year-old female patient lived in a Lyme endemic area and recalled an

incident in which she and her 8-year-old daughter sustained multiple tick

bites at the same time approximately 5 years previously (the daughter was

subsequently diagnosed with Lyme disease). The patient did not recall any

ECM-like bulls eye rash or flu-like illness at the time. However, she

noticed the gradual onset of increasing symptoms over the next two years

which initially included arthralgias of the thumbs and aching hands

bilaterally, night sweats, shortened menstrual cycles, insomnia, and

unexplained irritability and anger.

Two years after the tick bite, the patient sprained her ankle and had

difficulty healing from this injury. She also noted the uninjured ankle was

hurting as well.

Following the ankle injury, there was a rapid increase in the development of

symptoms including memory impairments; spelling difficulties; loss of

executive functioning; becoming lost in familiar places; depression;

numbness and tingling of the left side of her face; pain under her left eye;

twitching of her left eye; tinnitus; ear pain; myoclonic jerks; jerking

movements of the left shoulder; involuntary movements of her fingers, hands,

arms, and legs; burning pain of her right hip; lower back pain on her right

side; nerve pain; numbness and tingling of both legs; restless leg syndrome;

a pulling in of the right foot followed by a jerking of the right leg;

involuntary toe movement; chills; and fatigue.

She saw several physicians and had multiple diagnoses including an

adjustment reaction from a fertility problem, multiple sclerosis,

Huntington's, and moving toe and painful leg syndrome.

She was referred to a neurologist who ordered serology testing for Borrelia

burgdorferi antibodies. A reactive enzyme immunoassay (1.11) was confirmed

by repeat analysis (> 0.99 positive), IgM Western blot was reactive (39 and

41 kd bands), and IgG Western blot was interpreted as negative (23, 28, 41,

93 kd bands were present) by Kline Beecham Labs. The testing was

considered negative since there were only four bands on the Western blot

IgG.

A magnetic resonance imaging (MRI) scan was also negative. The strobe light

during an electroencephalogram (EEG) resulted in a seizure-like episode.

Although spikes were seen on the EEG, no seizure was recorded. During a

subsequent lumbar puncture, an apparent complex partial seizure occurred.

A second MRI scan a year later demonstrated scattered foci of abnormal

signal within the periventricular white matter, more confluent in the

periatrial region. However, a second physician interpreted this MRI as

normal.

Subsequently, a family physician diagnosed the patient with Lyme disease

based upon clinical grounds and started treatment with intravenous

ceftriaxone. A second seizure occurred during intravenous treatment. There

was a significant clinical improvement with 10 weeks of intravenous

treatment. After discontinuing the intravenous antibiotics, the patient

relapsed and was treated with a second 10-week course of ceftriaxone. The

patient again improved but more slowly. The patient recorded her symptoms

and reported improvement of cognitive and emotional symptoms. After

discontinuing the second course of intravenous antibiotics, there was a

return of myoclonic jerks, and later seizure activity on a daily basis.

Seizures were triggered by caffeine, light flickering through a row of trees

on the highway, exercise, or during symptom flares associated with

antibiotic treatment (apparent Jarish-Herxheimer reactions). They sometimes

began with blurred vision, followed by increasing tinnitus, drowsiness, and

a sense that her body was floating. During these episodes, her right arm

stiffened accompanied by a twitching of her right toes, which progressed to

her feet and calf muscles. The right foot then bent inward, and her legs

began jerking. After her legs stopped jerking, her head turned from side to

side as far as her head could turn. After the head movements stopped, her

abdomen contracted, as if doing sit-ups. These contractions forced the air

out of her lungs. After several minutes, the seizures stopped. She felt

tired after these episodes.

The patient was referred to another physician experienced in the evaluation

and treatment of Lyme disease. The Lyme IgG/IgM antibody test was equivocal

at 1.03 with a reactive cut off of 1.2. Lyme Western blot testing for IgM

was positive with 23-25, 31, 37, 41, and 58 Kd bands. IgG was positive with

23-25, 28, 31, 34, 41, 58, 73, and 83 kd bands (Ingenex, Menlo Park, CA).

The Babesia microti IgM titer was negative, and the IgG titer was reactive

at 1:80. There was a confirmation with positive B microti-in situ (RNA),

multiple merozoites only (Ingenex). No blood smear was reported. Human

granulocytic ehrlicheosis (HGE) titer was 1:40 for IgM and 1:80 for IgG.

Human monocytic ehrlicheosis (HME) titer was 1:80 for IgM and 1:80 for IgG

(Ingenex). The findings of the Babesia, HGE, and HME testing added support

for the presence of tick-borne diseases. However, it should be noted that a

negative blood smear and nonreactive IgM test of Babesia antibody does not

support the diagnosis of acute babesiosis.

A psychiatric assessment performed 6 months after intravenous antibiotic

treatment was discontinued demonstrated the following signs and symptoms:

decreased ability to sustain attention span, decreased ability to allocate

and prioritize attention, easily distracted by frustration, auditory

hyperacusis, visual hyperacusis, decreased working memory, decreased

short-term memory, slowness retrieving words and names, becoming lost in

familiar locations, letter reversals, spelling errors, word substitution

errors, depersonalization, poor concentration, " brain fog " (slowness and

inaccuracy of processing), decreased capacity to plan and prioritize,

obsessive thoughts, mental apathy, decreased frustration tolerance, sudden

abrupt mood swings, exaggerated startle reflex (including acoustic startle),

explosive anger, decreased social functioning, decreased job performance,

family problems, compensatory compulsions, dropping objects from her hand,

crying spells, depression, panic attacks, generalized anxiety, not well

rested in the morning, mid and early insomnia accompanied by seizures,

episodes of anorexia and weight loss, episodes of overeating accompanied by

weight gain, decreased libido, decreased capacity for pleasure, menstrual

irregularity, intolerance to cold, decreased body temperature (average

97.6°F), night sweats, chills, cervical radiculopathy, tension headaches,

intolerance to bright light and fluorescent lights, conjunctivitis, eye

pain, dry eyes, left sided Bell's palsy, tinnitus, hearing loss, dizziness,

low threshold for motion sickness, choking on food, absence and complex

partial seizures, numbness, tingling, sensory loss, burning, stabbing

sensations, paresis, tremor, twitching, muscle tightness, restless leg,

myoclonic jerks, herniated discs, equivocal Rhomberg, a sensation of being

bit by fleas, vibration sensations on the bottom of the feet, a sensation of

an outer ear infection, tightness and crepitations of joints, periostitis of

the right tibia, myalgia, tarsal tunnel syndrome, chest pain, racing pulse,

shortness of breath, cough, sinusitis confirmed by MRI, recurrent urinary

track infections, and vaginal pain.

It was noted that the symptoms gradually progressed over a period of 5 years

since the initial onset of the illness. Symptoms fluctuated throughout the

day and were increa