MRI Findings in Children Infected by Borrelia burgdorferi A n i t a L. B e l m a n , MD*+, P a t r i c i a K. Coyle, M D * , C l e m e n t R o q u e , MD~, a n d Eric C a n t o s , MD~
Cranial magnetic resonance imaging abnormalities were observed in 8 children (5 boys, 3 girls; ages 4-14 years) with neurologic problems following infection by Borrelia burgdorferi, the etiologic agent of Lyme disease. Neurologic features included headache (6), behavioral changes (5), facial palsy (2), papilledema (2), papilledema with diplopia (1), disturbance of sleep pattern (2), and carpal tunnel syndrome (1). Two MRI studies demonstrated multiple focal areas of increased signal intensity in white matter on long TR (both proton-density and T2-weighted) images. Belman AL, Coyle PK, Roque C, Cantos E. MRI findings in children infected by Borrelia burgdorferi. Pediatr Neurol 1992;8:428-31.
Introduction Lyme borreliosis is caused by infection with Borrelia burgdorferi, an arthropod-lransmitted spirochete. It is a
tal, Stony Brook. Reasons for consultation included headache and behavioral changes (3 patients), papilledema (2 patients), facial nerve palsy (2 patients), and sleep disturbance (1 patient). Medical histories compatible with systemic features of Lyme borreliosis included erythema migrans in 2 patients and a "flu-like" illness in 4 patients. The febrile illness was temporally related in 1 child to arthritis and in 2 to the onset of arthralgias and/or myalgias. At neurologic evaluation, 5 children were receiving or had received oral antibiotic therapy (Table 1). MRI. Cranial MRI was performed on a Sigma 1.5 T unit (General Electric Medical System, Milwaukee, WI), with a spin-echo technique using short and long TR/TE sequences. Ti-weighted images were obtained in both axial and sagittal planes (TR: 600 ms, TE: 20 ms). Proton density-weighted and T2-weighted axial images were also obtained (TR: 2,000-2,100 ms, TE: 25-30 ms, and TR: 2,000-2,100 ms, TE: 80 ms). Neuroh)gic Findings. Neurologic symptoms and signs are summarized in Table 1. Headaches were the most frequent symptom, most commonly described as frontal or occipital in location, intermittent, and not associated with nausea or vomiting. One child complained of transient neck pain as well. Behavioral changes in 5 patients included irritability and/or emotional lability. One child experienced a decline in school performance. In the two patients with papilledema, both had
multisystem disease of varying severity that may affect the skin, joints, heart, eye, and nervous system. In adult patients with Lyme borreliosis, neurologic involvement has been well described. Lymphocytic meningitis, cranial neuritis, radiculoneuritis, and peripheral neuropathy are the most frequent manifestations of neuroborreliosis [14]. Cranial magnetic resonance imaging (MRI) abnormalities also have been described in a few small series of patients [5,6]; however, relatively little attention has been given to the neurologic features and neuroimaging findings of this disease in children. We describe the MRI findings in 8 children who had neurologic involvement associated with B. burgdorferi infection. Methods Patients. This study included 3 girls and 5 boys whose ages ranged 4-14 years (median: 9 years). All were seropositive for anti-B, burgdorferi antibodies as measured by ELISA, in the Clinical Immunology Laboratory at University Hospital, Stony Brook. All of the children lived on Long Island, New York, an area highly endemic for Lyme borreliosis. Neurologic consultation was requested by the children's primary care physicians or by the physicians of the Lyme Center at University Hospi-
From the Departments of , Neurology, t Pediatrics, and CRadiology; School of Medicine; State University of New York; Stony Brook, New York. Presented in part at the 43rd Annual Meeting of the American Academy of Neurology, April, 1991, Boston.
428
PEDIATRIC NEUROLOGY
Vol. 8 No. 6
Figure 1. T2-weighted (TR: 2,100 ms, TE: 80 ms) axial MRI reveals bilateral punctate areas of hyperintense signal in the high convexity white matter (Patient 7).
Communications should be addressed to: Dr. Belman; Department of Neurology; Health Science Center, T-12-020; S.U.N.Y. at Stony Brook; Stony Brook, NY I 1794~ Received May 4, 1992; accepted June 29, 1992.
Table 1. Neurologic findings
Pt. No./ Age/Sex
Systemic Features of Lyme
Neurologic Syruptoms and Signs
Prior Antibiotic Treatment
Cerebrospinal Fluid LeukoProtein cytes/mm 3 (mg/dl)
1/4 yrs/F
Myalgias, arthralgias
Headache, behavioral changes, sleep disturbance
Amoxicillin
1
48
2/4 yrs/M
"Flu,"myalgias, arthralgias
Headache, behavioral changes
Amoxicillin
7
26
3/11 yrs/F
"Flu,"myalgias, arthralgias
$ School performance, sleep disorder (narcolepsy)
2
30
4/14 yrs/M
"Flu," arthritis, "rash"
Headache, behavioral changes, carpal tunnel syndrome
1
29
Cephalexin, amoxicillin
Headache, behavioral changes, papilledema, ? ICP
5/7 yrs/M
NA
6/9 yrs/M
ECM, "flu"
Headache, papilledema, "]"ICP (diplopia)
Amoxicillin
7/7 yrs/F
"Rash"
Facial palsy
Cephalexin
8/13 yrs/M
ECM
Headache, behavioral changes, facial palsy (bilateral)
9
35
130
30
9
32
Abbreviations: ECM = Erythrema chronicum migrans Flu = Flu-like illness ICP = Intracranial pressure documented increases in intracranial pressure. In addition, one of these children had diplopia due to a unilateral sixth cranial nerve palsy. In the two patients with seventh cranial nerve palsy (Bell's palsy), one had bilateral involvement. Two patients described intermittent paresthesias; carpal tunnel syndrome was documented in one of the children. The other child's symptoms were transient and had resolved prior to neurologic evaluation. Two children had changes in sleep patterns; one child resumed daytime naps, while the other experienced excessive daytime sleepiness and subsequently was diagnosed as having narcolepsy in addition to evidence of B. burgdorferi infection. At the time of MRI, 7 children (Patients 1-3,5-8) were considered to have early disease and one child (Patient 4) late disease. MRIs were obtained 1-7 months after the onset of signs and symptoms of Lyme disease in the children with early disease and approximately 5 years after the onset of the illness in the child with late disease. Cerebrospinal Fluid Findings. Examination of the cerebrospinal fluid (CSF) revealed lymphocytic pleocytosis in 4 children (7-130 leukocytes/mm3), with mild elevations in protein content in 6 (29-48 mg/dl; Table 1). Anti-B. burgdorferi antibodies were detected in the CSF of 7 patients. MRI Findings. MRI documented abnormal signal intensity (hyperintense signal relative to brain parenchyma) that was best visualized on T2-weighted images (long TR/TE). Lesions varied for a given individual based on size, shape, location, and number (i.e., single or multiple). When multiple lesions were present, they were either scattered or clus-
tered in a linear pattern. T2-weighted images in 4 children disclosed multiple, small (2-3 mm in diameter), round, punctate areas of increased signal intensity which were located in a linear pattern in the high convexity region of white matter consistent with dilated perivascular spaces (Fig 1); however, all 4 children also had larger lesions located predominantly in the deep white matter (Figs 2A,2B,3) which were focal, discrete, round, or ovoid "lesions" (4-6 mm in diameter) that were visualized on long TR (both proton-density and T2-weighted) images. One child also had a periventricular lesion and another child had a lesion in the brainstem. In addition to these lesions, MRIs of 6 children also revealed larger, irregularly shaped, patchy lesions in the deep or periventricular white matter. These lesions were also hyperintense on both proton-density and T2-weighted images (Figs 4A,4B).
Discussion W e r e p o r t 8 c h i l d r e n w i t h n e u r o l o g i c i n v o l v e m e n t ass o c i a t e d w i t h B. burgdorferi i n f e c t i o n w h o h a d a b n o r m a l ities o n c r a n i a l M R I . M R I f i n d i n g s w e r e l o c a t e d p r e d o m inantly in the deep white matter and were best visualized on T2-weighted images. Four children had multiple, small, punctate, linear areas o f i n c r e a s e d s i g n a l i n t e n s i t y in t h e h i g h p a r i e t a l c o n v e x i t y region that followed the distribution of perforating ves-
Belman et al: MRI and B. burgdorferi
429
A
B
Figure 2. Axial MRI of Patient 5 reveals focal, nodular lesions in the right centrum semiovah' observed o~t ¢A) both 7)-w~ O;ht4d ~7 le, 2,000, TE: 80) and (B) proton-densio, weighted (TR: 2,000, TE: 25) images.
sels. Such lesions probably represent dilated or prominent perivascular spaces (Virchow-Robin spaces). Because they are hyperintense on T2-weighted images and are not visualized on proton-density images, these lesions could simply reflect a normal variant. Alternatively, it is possible that they are associated with an inflammatory response. The pathophysiologic mechanism and significance of this finding is unknown and these MRI lesions cannot be classified as abnormal. As more experience is gained using high-field magnetic resonance units to image the brains of children who have a variety of neurologic conditions, the true significance of these findings should be resolved. Most of the children had small, nodular, discrete focal lesions that were hyperintense on both proton-density and Tz-weighted images. These MRI features have previously been described for brain lesions associated with inflammarion, demyelinarion, or gliosis [7,8]. In adults similar MRI lesions have been described for neuroborreliosis patients [4-6,9], elderly patients with microvascular disease [7], and normal aging brain [8]; however, all of our patients were young (median age: 9 years; oldest child: 14 years). In our experience, it is extremely unusual to see these MRI findings in otherwise healthy children who have no antecedent histories of vascular, infectious, or inflammatory conditions. Of note are similar MRI brain lesions described in one child with tick paralysis [ 10] and in one 4-year-old child and two teenagers with Lyme disease [5,6]. We believe that these brain lesions in our young patients most likely reflect a disease process that is associated with B. b u r g d o r f e r i infection. The larger, scattered, patchy white matter lesions that were reported in some of the children have a similar appearance to the MRI findings of childhood acute dissemi-
430 PEDIATRICNEUROLOGY Vol.8 No. 6
nated encephalomyelitis (parainfectious or postinfectious encephalomyelitis). In our patients we belicvc that this MRI pattern may be a reflection of a spirochete-triggered, immune-mediated neurologic process. Although immunemediated processes have been postulated to explain at least some of the neurologic features observed in patients with Lyme disease, to our knowledge this MRI pattern does not appear to occur frequently in adult neuroborreliosis patients. It may be an age-related phenomenon. The clinical and pathologic significance of these MRI f'mdings in our young patients with neurologic involve-
Figure 3. Axial T2-weighted (TR: 2,100, TE: 80) image demonstrates bilateral type 2 white matter lesions. Note also several smaller lesions in the right posterior centrura semiovale (Patient 7).
i ~ i~
A
~
B
Figure 4. High signal in the right and left posterior periventricular white matter of Patient 7 observed on both (A) T2-weighted (TR: 2,100, TE: 80), and (B) proton-density weighted (TR: 2,100, TE: 30) images.
ment is unknown. Our observations need to be extended to a larger cohort of children with Lyme disease; however, these MRI findings do suggest that neuroimaging may be a helpful adjunct in evaluating pediatric patients with neurologic involvement and B. burgdorferi infection. In children, as in adults, the neurologic manifestations and syndromes associated with B. burgdorferi infection may be quite varied [11-15]. In addition to meningitis, cranial neuritis, and radiculoneuropathy, syndromes that appear to be more common to the pediatric age group include a pseudotumor cerebri-like syndrome and disturbance of sleep patterns [15,16]. The pathogenetic mechanisms for these neurologic syndromes may include either direct or indirect spirochete-triggered immune processes. Continued investigations are required to delineate more fully the clinical neurologic syndromes associated with pediatric North American Lyme disease. Correlation of clinical syndromes with MRI findings, CSF changes, and the child's immune response to the spirochetal infection, should increase our understanding of the pathogenesis of pediatric Lyme neuroborreliosis. Such information will ultimately allow the design of rational and appropriate treatment protocols. Supported in part by a grant for Lyme Disease Research from the State of New York and in part by PHS RO1 AR40470 (PKC, ALB). References
[1] Reik L, Steere AC, Bartenhagen NH, Shope RE, Malawista SE. Neurologic abnormalities of Lyme disease. Medicine 1979;58:281-94. [2] Pachner AR, Steere AC. The triad of neurologic manifestations of Lyme disease: Meningitis, cranial neuritis and radiculoneuritis. Neurology 1985;35:47-53.
[3] Haiperin J, Luft BJ, Volkman DJ, Dattwyler 1LI. Lyme neuroborreliosis, peripheral nervous system manifestations. Brain 1990;113: 1207-21. [4] Reik L. Neurologic abnormalities in early and late Lyme disease. In: Lyme disease and the nervous system. New York: Thieme Medical Publishers, 1991;52-76,77-99. [5] Halperin JJ, Luft BJ, Anand AK, et al. Lyme neuroborreliosis: Central nervous system manifestations. Neurology 1989;39:753-9. [6] Fernandez RE, Rothberg M, Ferencz G, Wujack D. Lyme disease of the CNS: MR imaging findings in 14 cases. AJNR 1990;11: 479-81. [7] Braffman BH, Zimmerman RA, Trojanowski JQ, Gonatas NK, Hickey WF, Schlaepfer WW. Brain MR: Pathologic correlation with gross and histopathology 1. Lacunar infarction and Virchow-Robin spaces. AJNR 1988;9:621-8. [8] Ibid Brain MR: Pathologic correlation with gross and histopathology 2. Hypedntense white-matter foci in the elderly. AJNR 1988;9: 629-36. [9] Rafto SE, Milton WJ, Galetta SL, Grossman RI. Biopsy-confinned CNS Lyme disease: MR appearance at 1.5 T. AJNR 1990;11: 482-4. [10] Noweli AM, Grossman RI, Hackney DB, Zimmerman RA, Goldberg HI, Bilaniuk LT. MR imaging of white matter disease in children. AJNR 1988;9:503-9. [11] Christen HJ, Hanefeld E Neurologic complications of erythema-migrans-disease in childhood - Clinical aspects. Zentralbl Bakteriol Mikrobiol 1986;263:337-42. [12] Meissner HC, Gellis SE, Milliken JE Lyme disease first observed to be aseptic meningitis. Am J Dis Child 1982;136:465-7. [13] Left RD, Akre SP. Late stage Lyme borreliosis in children. South Med J 1989;82:954-6. [14] Feder HM, Zalneraitis EL, Reik L. Lyme disease: Acute focal meningoencephalitis in a child. Pediatrics 1988;82:931-4. [15] Raucher HS, Kaufman DM, Goldfarb J, Jacobson RI, Roseman B, Wolff RR. Pseudotumor cerebri and Lyme disease: A new association. J Pediatr 1985;107:931-3. [16] Belman AL, Coyle PK, Schutzer SE, Engel M, Dattwyler R. Neurological involvement in pediatric Lyme disease. Ann Neurol 1989; 26:476.
Belman et al: MRI and B. burgdorferi 431
Cranial magnetic resonance imaging abnormalities were observed in 8 children (5 boys, 3 girls; ages 4-14 years) with neurologic problems following infection by Borrelia burgdorferi, the etiologic agent of Lyme disease. Neurologic features included headache (6), behavioral changes (5), facial palsy (2), papilledema (2), papilledema with diplopia (1), disturbance of sleep pattern (2), and carpal tunnel syndrome (1). Two MRI studies demonstrated multiple focal areas of increased signal intensity in white matter on long TR (both proton-density and T2-weighted) images. Belman AL, Coyle PK, Roque C, Cantos E. MRI findings in children infected by Borrelia burgdorferi. Pediatr Neurol 1992;8:428-31.
Introduction Lyme borreliosis is caused by infection with Borrelia burgdorferi, an arthropod-lransmitted spirochete. It is a
tal, Stony Brook. Reasons for consultation included headache and behavioral changes (3 patients), papilledema (2 patients), facial nerve palsy (2 patients), and sleep disturbance (1 patient). Medical histories compatible with systemic features of Lyme borreliosis included erythema migrans in 2 patients and a "flu-like" illness in 4 patients. The febrile illness was temporally related in 1 child to arthritis and in 2 to the onset of arthralgias and/or myalgias. At neurologic evaluation, 5 children were receiving or had received oral antibiotic therapy (Table 1). MRI. Cranial MRI was performed on a Sigma 1.5 T unit (General Electric Medical System, Milwaukee, WI), with a spin-echo technique using short and long TR/TE sequences. Ti-weighted images were obtained in both axial and sagittal planes (TR: 600 ms, TE: 20 ms). Proton density-weighted and T2-weighted axial images were also obtained (TR: 2,000-2,100 ms, TE: 25-30 ms, and TR: 2,000-2,100 ms, TE: 80 ms). Neuroh)gic Findings. Neurologic symptoms and signs are summarized in Table 1. Headaches were the most frequent symptom, most commonly described as frontal or occipital in location, intermittent, and not associated with nausea or vomiting. One child complained of transient neck pain as well. Behavioral changes in 5 patients included irritability and/or emotional lability. One child experienced a decline in school performance. In the two patients with papilledema, both had
multisystem disease of varying severity that may affect the skin, joints, heart, eye, and nervous system. In adult patients with Lyme borreliosis, neurologic involvement has been well described. Lymphocytic meningitis, cranial neuritis, radiculoneuritis, and peripheral neuropathy are the most frequent manifestations of neuroborreliosis [14]. Cranial magnetic resonance imaging (MRI) abnormalities also have been described in a few small series of patients [5,6]; however, relatively little attention has been given to the neurologic features and neuroimaging findings of this disease in children. We describe the MRI findings in 8 children who had neurologic involvement associated with B. burgdorferi infection. Methods Patients. This study included 3 girls and 5 boys whose ages ranged 4-14 years (median: 9 years). All were seropositive for anti-B, burgdorferi antibodies as measured by ELISA, in the Clinical Immunology Laboratory at University Hospital, Stony Brook. All of the children lived on Long Island, New York, an area highly endemic for Lyme borreliosis. Neurologic consultation was requested by the children's primary care physicians or by the physicians of the Lyme Center at University Hospi-
From the Departments of , Neurology, t Pediatrics, and CRadiology; School of Medicine; State University of New York; Stony Brook, New York. Presented in part at the 43rd Annual Meeting of the American Academy of Neurology, April, 1991, Boston.
428
PEDIATRIC NEUROLOGY
Vol. 8 No. 6
Figure 1. T2-weighted (TR: 2,100 ms, TE: 80 ms) axial MRI reveals bilateral punctate areas of hyperintense signal in the high convexity white matter (Patient 7).
Communications should be addressed to: Dr. Belman; Department of Neurology; Health Science Center, T-12-020; S.U.N.Y. at Stony Brook; Stony Brook, NY I 1794~ Received May 4, 1992; accepted June 29, 1992.
Table 1. Neurologic findings
Pt. No./ Age/Sex
Systemic Features of Lyme
Neurologic Syruptoms and Signs
Prior Antibiotic Treatment
Cerebrospinal Fluid LeukoProtein cytes/mm 3 (mg/dl)
1/4 yrs/F
Myalgias, arthralgias
Headache, behavioral changes, sleep disturbance
Amoxicillin
1
48
2/4 yrs/M
"Flu,"myalgias, arthralgias
Headache, behavioral changes
Amoxicillin
7
26
3/11 yrs/F
"Flu,"myalgias, arthralgias
$ School performance, sleep disorder (narcolepsy)
2
30
4/14 yrs/M
"Flu," arthritis, "rash"
Headache, behavioral changes, carpal tunnel syndrome
1
29
Cephalexin, amoxicillin
Headache, behavioral changes, papilledema, ? ICP
5/7 yrs/M
NA
6/9 yrs/M
ECM, "flu"
Headache, papilledema, "]"ICP (diplopia)
Amoxicillin
7/7 yrs/F
"Rash"
Facial palsy
Cephalexin
8/13 yrs/M
ECM
Headache, behavioral changes, facial palsy (bilateral)
9
35
130
30
9
32
Abbreviations: ECM = Erythrema chronicum migrans Flu = Flu-like illness ICP = Intracranial pressure documented increases in intracranial pressure. In addition, one of these children had diplopia due to a unilateral sixth cranial nerve palsy. In the two patients with seventh cranial nerve palsy (Bell's palsy), one had bilateral involvement. Two patients described intermittent paresthesias; carpal tunnel syndrome was documented in one of the children. The other child's symptoms were transient and had resolved prior to neurologic evaluation. Two children had changes in sleep patterns; one child resumed daytime naps, while the other experienced excessive daytime sleepiness and subsequently was diagnosed as having narcolepsy in addition to evidence of B. burgdorferi infection. At the time of MRI, 7 children (Patients 1-3,5-8) were considered to have early disease and one child (Patient 4) late disease. MRIs were obtained 1-7 months after the onset of signs and symptoms of Lyme disease in the children with early disease and approximately 5 years after the onset of the illness in the child with late disease. Cerebrospinal Fluid Findings. Examination of the cerebrospinal fluid (CSF) revealed lymphocytic pleocytosis in 4 children (7-130 leukocytes/mm3), with mild elevations in protein content in 6 (29-48 mg/dl; Table 1). Anti-B. burgdorferi antibodies were detected in the CSF of 7 patients. MRI Findings. MRI documented abnormal signal intensity (hyperintense signal relative to brain parenchyma) that was best visualized on T2-weighted images (long TR/TE). Lesions varied for a given individual based on size, shape, location, and number (i.e., single or multiple). When multiple lesions were present, they were either scattered or clus-
tered in a linear pattern. T2-weighted images in 4 children disclosed multiple, small (2-3 mm in diameter), round, punctate areas of increased signal intensity which were located in a linear pattern in the high convexity region of white matter consistent with dilated perivascular spaces (Fig 1); however, all 4 children also had larger lesions located predominantly in the deep white matter (Figs 2A,2B,3) which were focal, discrete, round, or ovoid "lesions" (4-6 mm in diameter) that were visualized on long TR (both proton-density and T2-weighted) images. One child also had a periventricular lesion and another child had a lesion in the brainstem. In addition to these lesions, MRIs of 6 children also revealed larger, irregularly shaped, patchy lesions in the deep or periventricular white matter. These lesions were also hyperintense on both proton-density and T2-weighted images (Figs 4A,4B).
Discussion W e r e p o r t 8 c h i l d r e n w i t h n e u r o l o g i c i n v o l v e m e n t ass o c i a t e d w i t h B. burgdorferi i n f e c t i o n w h o h a d a b n o r m a l ities o n c r a n i a l M R I . M R I f i n d i n g s w e r e l o c a t e d p r e d o m inantly in the deep white matter and were best visualized on T2-weighted images. Four children had multiple, small, punctate, linear areas o f i n c r e a s e d s i g n a l i n t e n s i t y in t h e h i g h p a r i e t a l c o n v e x i t y region that followed the distribution of perforating ves-
Belman et al: MRI and B. burgdorferi
429
A
B
Figure 2. Axial MRI of Patient 5 reveals focal, nodular lesions in the right centrum semiovah' observed o~t ¢A) both 7)-w~ O;ht4d ~7 le, 2,000, TE: 80) and (B) proton-densio, weighted (TR: 2,000, TE: 25) images.
sels. Such lesions probably represent dilated or prominent perivascular spaces (Virchow-Robin spaces). Because they are hyperintense on T2-weighted images and are not visualized on proton-density images, these lesions could simply reflect a normal variant. Alternatively, it is possible that they are associated with an inflammatory response. The pathophysiologic mechanism and significance of this finding is unknown and these MRI lesions cannot be classified as abnormal. As more experience is gained using high-field magnetic resonance units to image the brains of children who have a variety of neurologic conditions, the true significance of these findings should be resolved. Most of the children had small, nodular, discrete focal lesions that were hyperintense on both proton-density and Tz-weighted images. These MRI features have previously been described for brain lesions associated with inflammarion, demyelinarion, or gliosis [7,8]. In adults similar MRI lesions have been described for neuroborreliosis patients [4-6,9], elderly patients with microvascular disease [7], and normal aging brain [8]; however, all of our patients were young (median age: 9 years; oldest child: 14 years). In our experience, it is extremely unusual to see these MRI findings in otherwise healthy children who have no antecedent histories of vascular, infectious, or inflammatory conditions. Of note are similar MRI brain lesions described in one child with tick paralysis [ 10] and in one 4-year-old child and two teenagers with Lyme disease [5,6]. We believe that these brain lesions in our young patients most likely reflect a disease process that is associated with B. b u r g d o r f e r i infection. The larger, scattered, patchy white matter lesions that were reported in some of the children have a similar appearance to the MRI findings of childhood acute dissemi-
430 PEDIATRICNEUROLOGY Vol.8 No. 6
nated encephalomyelitis (parainfectious or postinfectious encephalomyelitis). In our patients we belicvc that this MRI pattern may be a reflection of a spirochete-triggered, immune-mediated neurologic process. Although immunemediated processes have been postulated to explain at least some of the neurologic features observed in patients with Lyme disease, to our knowledge this MRI pattern does not appear to occur frequently in adult neuroborreliosis patients. It may be an age-related phenomenon. The clinical and pathologic significance of these MRI f'mdings in our young patients with neurologic involve-
Figure 3. Axial T2-weighted (TR: 2,100, TE: 80) image demonstrates bilateral type 2 white matter lesions. Note also several smaller lesions in the right posterior centrura semiovale (Patient 7).
i ~ i~
A
~
B
Figure 4. High signal in the right and left posterior periventricular white matter of Patient 7 observed on both (A) T2-weighted (TR: 2,100, TE: 80), and (B) proton-density weighted (TR: 2,100, TE: 30) images.
ment is unknown. Our observations need to be extended to a larger cohort of children with Lyme disease; however, these MRI findings do suggest that neuroimaging may be a helpful adjunct in evaluating pediatric patients with neurologic involvement and B. burgdorferi infection. In children, as in adults, the neurologic manifestations and syndromes associated with B. burgdorferi infection may be quite varied [11-15]. In addition to meningitis, cranial neuritis, and radiculoneuropathy, syndromes that appear to be more common to the pediatric age group include a pseudotumor cerebri-like syndrome and disturbance of sleep patterns [15,16]. The pathogenetic mechanisms for these neurologic syndromes may include either direct or indirect spirochete-triggered immune processes. Continued investigations are required to delineate more fully the clinical neurologic syndromes associated with pediatric North American Lyme disease. Correlation of clinical syndromes with MRI findings, CSF changes, and the child's immune response to the spirochetal infection, should increase our understanding of the pathogenesis of pediatric Lyme neuroborreliosis. Such information will ultimately allow the design of rational and appropriate treatment protocols. Supported in part by a grant for Lyme Disease Research from the State of New York and in part by PHS RO1 AR40470 (PKC, ALB). References
[1] Reik L, Steere AC, Bartenhagen NH, Shope RE, Malawista SE. Neurologic abnormalities of Lyme disease. Medicine 1979;58:281-94. [2] Pachner AR, Steere AC. The triad of neurologic manifestations of Lyme disease: Meningitis, cranial neuritis and radiculoneuritis. Neurology 1985;35:47-53.
[3] Haiperin J, Luft BJ, Volkman DJ, Dattwyler 1LI. Lyme neuroborreliosis, peripheral nervous system manifestations. Brain 1990;113: 1207-21. [4] Reik L. Neurologic abnormalities in early and late Lyme disease. In: Lyme disease and the nervous system. New York: Thieme Medical Publishers, 1991;52-76,77-99. [5] Halperin JJ, Luft BJ, Anand AK, et al. Lyme neuroborreliosis: Central nervous system manifestations. Neurology 1989;39:753-9. [6] Fernandez RE, Rothberg M, Ferencz G, Wujack D. Lyme disease of the CNS: MR imaging findings in 14 cases. AJNR 1990;11: 479-81. [7] Braffman BH, Zimmerman RA, Trojanowski JQ, Gonatas NK, Hickey WF, Schlaepfer WW. Brain MR: Pathologic correlation with gross and histopathology 1. Lacunar infarction and Virchow-Robin spaces. AJNR 1988;9:621-8. [8] Ibid Brain MR: Pathologic correlation with gross and histopathology 2. Hypedntense white-matter foci in the elderly. AJNR 1988;9: 629-36. [9] Rafto SE, Milton WJ, Galetta SL, Grossman RI. Biopsy-confinned CNS Lyme disease: MR appearance at 1.5 T. AJNR 1990;11: 482-4. [10] Noweli AM, Grossman RI, Hackney DB, Zimmerman RA, Goldberg HI, Bilaniuk LT. MR imaging of white matter disease in children. AJNR 1988;9:503-9. [11] Christen HJ, Hanefeld E Neurologic complications of erythema-migrans-disease in childhood - Clinical aspects. Zentralbl Bakteriol Mikrobiol 1986;263:337-42. [12] Meissner HC, Gellis SE, Milliken JE Lyme disease first observed to be aseptic meningitis. Am J Dis Child 1982;136:465-7. [13] Left RD, Akre SP. Late stage Lyme borreliosis in children. South Med J 1989;82:954-6. [14] Feder HM, Zalneraitis EL, Reik L. Lyme disease: Acute focal meningoencephalitis in a child. Pediatrics 1988;82:931-4. [15] Raucher HS, Kaufman DM, Goldfarb J, Jacobson RI, Roseman B, Wolff RR. Pseudotumor cerebri and Lyme disease: A new association. J Pediatr 1985;107:931-3. [16] Belman AL, Coyle PK, Schutzer SE, Engel M, Dattwyler R. Neurological involvement in pediatric Lyme disease. Ann Neurol 1989; 26:476.
Belman et al: MRI and B. burgdorferi 431
![[Ocular findings in infection with Borrelia burgdorferi].](/assets/img/hold.png)
