Imaging in Lyme neuroborreliosis

Abstract

Lyme neuroborreliosis (LNB) is a tick-borne spirochetal infection with a broad spectrum of imaging pathology. For individuals who live in or have travelled to areas where ticks reside, LNB should be considered among differential diagnoses when clinical manifestations from the nervous system occur. Radiculitis, meningitis and facial palsy are commonly encountered, while peripheral neuropathy, myelitis, meningoencephalitis and cerebral vasculitis are rarer manifestations of LNB. Cerebrospinal fluid (CSF) analysis and serology are key investigations in patient workup. The primary role of imaging is to rule out other reasons for the neurological symptoms. It is therefore important to know the diversity of possible imaging findings from the infection itself. There may be no imaging abnormality, or findings suggestive of neuritis, meningitis, myelitis, encephalitis or vasculitis. White matter lesions are not a prominent feature of LNB. Insight into LNB clinical presentation, laboratory test methods and spectrum of imaging pathology will aid in the multidisciplinary interaction that often is imperative to achieve an efficient patient workup and arrive at a correct diagnosis. This article can educate those engaged in imaging of the nervous system and serve as a comprehensive tool in clinical cases. KEY POINTS: • Diagnostic criteria for LNB emphasise exclusion of an alternative cause to the clinical symptoms. • MRI makes a crucial contribution in the diagnosis and follow-up of LNB. • MRI may have normal findings, or show neuritis, meningitis, myelitis, encephalitis or vasculitis. • White matter lesions are not a prominent feature of LNB.

Keywords: Encephalitis; Lyme neuroborreliosis; MRI; Myelitis; Neuritis.

Fig. 1

Meningoradiculitis due to Lyme neuroborreliosis (LNB) in a 73-year-old female. She experienced periods of strong superficial abdominal pain, reduced appetite and headache. Sagittal T2 (a) and T1 after gadolinium-based contrast agent injection (b, c) demonstrated normal cord parenchyma and diffuse leptomeningeal enhancement (arrows) of spinal cord and brain stem. Cerebrospinal fluid (CSF) analysis showed pleocytosis and intrathecal production of Borrelia burgdorferi (Bb)-specific IgM and IgG antibodies. No leptomeningeal enhancement was found 4 weeks after the treatment on post-contrast sagittal T1 weighted images (d, e)

Fig. 2

Facial neuritis in LNB with typical disease course in a 55-year-old female. She suffered from back pain radiating to chest, arms, head and neck, especially intense at night time, and after 2 weeks she also developed bilateral facial palsy. CSF analysis showed 594 cells/mm³ (normal range 0-5/mm³) and production of Bb specific IgG and IgM antibodies. Axial post-contrast fat suppressed T1-weighted image (a) showed intense enhancement in the distal intracanalicular, labyrinthine and geniculate ganglion segments of both facial nerves (arrows point to these structures which are mentioned from medial to lateral). 3 mm sagittal reformat (b) on the right side demonstrated the enhancement involving the tympanic and mastoid segment, as well as the parotid segment with the temporofacial and cervicofacial branches at the pes anserinus included (arrows point to these structures which are mentioned from cranial to caudal). Axial post-contrast fat suppressed T1-weighted image showed no abnormal enhancement of facial nerves 6 months after the treatment (c)

Fig. 3

LNB myelitis in a 35-year old female who presented with pain radiating in the right arm, neck stiffness and general symptoms of headache, fatigue, nausea and vomiting. T2 weighted images showed subtle spinal cord hyperintensity, on sagittal image (a) from C2-C5 centrally located (arrows), and on axial T2 gradient echo image at the C2/C3 level (b), dominant affection adjacent to the right anterior horn was seen (arrow). CSF analysis showed increased cell count as well as intrathecal production of Bb specific IgM and IgG antibodies. Two months after treatment she had fully recovered. Seven years has passed since her symptom debut, and there has been no further incidence of neurological affection

Fig. 4

Brachial plexus neuritis in a 74-year-old woman with acute distal right arm paresis. In the preceding weeks she had nausea, vomiting and weight loss, and felt increasingly forgetful and unsteady. A fluid-sensitive coronal STIR sequence showed diffusely increased signal of the nerve bundle on the right side (arrows) compared to the left side. Lumbar puncture followed, and showed cell count of 101/mm³ as well as a positive Bb IgG antibody index (AI)

Fig. 5

LNB meningoencephalitis in a 45-year-old female who presented with fatigue, headache, dizziness and vomiting. Neurological findings were tremor and unsteady gait. The CSF cell count was 270 cells/mm³ and there was a positive Bb IgG AI. Post-contrast sagittal (a) and axial (b) FLAIR images demonstrated patchy leptomeningeal enhancement over the cerebral convexities and in the posterior fossa (arrows). There was a hyperintense lesion in the left thalamus (arrow) on axial T2-weighted image (c) and coronal FLAIR image (d). There was no abnormality in the lesion on diffusion weighted images (not shown). Post-contrast axial (e) and coronal (f) T1-weighted images showed punctate and curvilinear uptake (arrows) in the thalamic lesion. Similar, subtle changes were present in the right thalamus. After 2 months there was only slight residual hyperintensity in the left thalamus (arrow) on axial FLAIR image (g) and no sign of enhancement on post-contrast axial T1 weighted image (h). One year after treatment there were no imaging abnormalities (i)

Fig. 6

LNB encephalitis in a 40-year-old woman. She presented with 1 day history of headache, vomiting, dizziness and personality change. The CSF cell count was 182 cells/mm³. MRI showed symmetric diffuse and patchy T2 (a) and FLAIR (b, c) hyperintensity of inferior thalami (arrows in a), cerebral peduncles, mesencephalon, pons (arrows in b) and cerebellar dentate nuclei (arrows in c). There were no abnormalities on diffusion-weighted or post-contrast images (not shown). Further clinical and laboratory investigations revealed erythema migrans on the right thigh and a positive CSF Bb IgG AI. Tests for TBE antibodies were negative. She received antimicrobial treatment, and repeated MRI 8 weeks after the initial scan was normal (d–f)

Fig. 7

LNB vasculitis in a 55-year-old woman with strange behaviour for 3 days preceding hospital admission. She had incoherent speech and was disorientated. CSF cell count was 213 cells/mm³ and Bb IgG AI was positive. MRI revealed ischemic lesions of different ages in thalamus bilaterally (a–f), right cerebral peduncle (g–i) and right occipital cortex (not shown). Axial T2-weighted images (a, d, g), diffusion weighted B1000 images (b, e, h) and ADC maps (c, f, i) demonstrated the lesions. In contrast to the hypointense lesions on ADC maps in the thalami (arrows in c and f) consistent with cytotoxic edema in recent infarcts, the lesion in the right cerebral peduncle was hyperintense on both B1000 image (arrow in h) and ADC map (arrow in i), consistent with vasogenic edema and a more advanced stage of ischemic lesion. 5 mm MIP coronal (j) and axial (k) reformats of CT angiography examination demonstrated several short stenotic segments of both posterior cereberal arteries (arrows), most pronounced on the right side