LETTER TO EDITOR
Year : 2016 | Volume
: 11 | Issue : 4 | Page : 384--385
Lyme polyradiculitis masquerading Guillain-Barre syndrome
Mritunjay Kumar, Ragini Singh, Mohsin Rashid
Department of Pediatrics, SGRR Institute of Medical and Health Sciences, Dehradun, Uttarakhand, India
Department of Pediatrics, SGRR Institute of Medical and Health Sciences, Patel Nagar, Dehradun - 248 001, Uttarakhand
|How to cite this article:|
Kumar M, Singh R, Rashid M. Lyme polyradiculitis masquerading Guillain-Barre syndrome.J Pediatr Neurosci 2016;11:384-385
|How to cite this URL:|
Kumar M, Singh R, Rashid M. Lyme polyradiculitis masquerading Guillain-Barre syndrome. J Pediatr Neurosci [serial online] 2016 [cited 2021 Jan 26 ];11:384-385
Available from: https://www.pediatricneurosciences.com/text.asp?2016/11/4/384/199483
Lyme disease, caused by the spirochete Borrelia burgdorferi, is a tick-borne disease, the global distribution of which corresponds to the distribution of Ixodes tick that transmits the organism. Although very commonly reported from the temperate regions of the world, the incidence has increased worldwide due to increasing travel and changing habitats of the vector. Neuroborreliosis, a common presentation of Lyme disease, is characterized by peripheral and cranial neuropathies, which may also be a presenting symptom of Guillain-Barre syndrome (GBS).
A 13-year-old girl presented with 7-day history of weakness of both lower limbs and nasal twang in speech which was followed by nasal regurgitation of feed and bilateral ptosis. There was no history of trauma, sore throat, ear discharge, photophobia, loose motion, and drug intoxication. At admission, she was conscious, oriented, and had apparent bilateral ptosis and dysarthria. She was able to stand with support with a wide swaying gait. She had a pulse rate of 110/min, respiratory rate of 23/min, blood pressure of 100/70 mm Hg, and SPO2 of 96% on room air. There were no signs of meningeal irritation, raised intracranial tension, and autonomic nervous system involvement. Power in lower and upper limbs was 3/5 and 4/5. There were hypotonia, areflexia, and flexor plantar response on both sides. Gag reflex was present, but uvula was deviated to the right side. Ophthalmological evaluation revealed impairment of bilateral medial and lateral rectus in addition to ptosis. Rest of the central nervous system and other systemic examinations were unremarkable. Investigations revealed hemoglobin 14.7 g/dl, total leukocyte count 12,580/mm 3 (polymorph 72% lymphocytes 25%), and platelet count 4.45 lac/mm 3. Serum electrolytes, kidney function test, and liver function test were normal. Cerebrospinal fluid (CSF) examination revealed sugar 57 mg/dl, protein 151 mg/dl, cell count 8 cells/mm 3 (all lymphocytes), ADA 3.98, and negative gram and acid-fast bacillus staining. Magnetic resonance imaging of the brain was unremarkable. In view of albuminocytological dissociation in CSF, possibility of GBS with polyneuropathy was kept and nerve conduction velocity (NCV) was conducted. NCV was suggestive of prolonged F-wave latency and bilateral common peroneal nerve axonal neuropathy. Intravenous immunoglobulin was started at 0.4 g/kg/dose and continued for 5 days after negative blood culture report. Neurology opinion was sought and during further interview with the parents, it was revealed that there was a history of insect bite over right great toe about 1 month back which was followed by local erythema, induration, and paresthesia. Lyme serology was sent and IgM and IgG B. burgdorferi antibody titer were measured using enzyme immunoassay. Borrelia IgM antibody titer was 1.5 U/ml (biological reference interval <0.90) and IgG antibody titer was 0.3 (biological reference interval <0.90). Final diagnosis of Lyme polyradiculitis was made and she was continued on ceftriaxone for 14 days as per standard protocol. Nasal regurgitation and speech improved, but there were residual ptosis and gait instability at the time of discharge. She was advised physiotherapy, neurorehabilitation, and regular follow-up.
Lyme disease is known as a great mimicker and it is, therefore, a vital diagnosis to bear in mind, especially as it can manifest with such disabling complications. Few cases have been reported from the Indian subcontinent too but mostly they are adult case reports with skin manifestations. Lyme disease, if untreated, can result in early localized signs such as a target-like erythema migrans rash, which is reported by almost 90% of patients. Early disseminated Lyme disease can present weeks or months after the initial tick bite and can cause neurological involvement such as mononeuritis multiplex, radiculopathies, and cranial nerve palsies (commonly facial palsy), collectively known as neuroborreliosis. It is a widely accepted hypothesis that B. burgdorferi is capable of producing an autoimmune response. It has been postulated that the components of the spirochete associated with Lyme disease may act as antigens or immune complexes, which facilitate production of antiganglioside antibodies implicated in the development of GBS in susceptible individuals. Lyme disease should be considered in anyone who presents with symptoms and signs suggestive of GBS and these patients should be questioned about possible tick bites in the preceding few months. In literature, there are reports in favor of Lyme disease triggering GBS, neuroborreliosis mimicking GBS, and cases where it was not possible to distinguish between these two entities.
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There are no conflicts of interest.
|1||Jairath V, Sehrawat M, Jindal N, Jain VK, Aggarwal P. Lyme disease in Haryana, India. Indian J Dermatol Venereol Leprol 2014;80:320-3.|
|2||Awan SF, Murphy FT. The development of Guillain-Barre syndrome (GBS) in association with confirmed Lyme disease. A potential autoimmune response in GBS secondary to Tick-Borne diseases? Clin Microbiol 2015;4:199. [Doi: 10.4172/2327-5073.1000199].|
|3||Halperin JJ, Shapiro ED, Logigian E, Belman AL, Dotevall L, Wormser GP, et al. Practice parameter: Treatment of nervous system Lyme disease (an evidence-based review): Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2007;69:91-102.|
|4||Vasudevan B, Chatterjee M. Lyme borreliosis and skin. Indian J Dermatol 2013;58:167-74.|
|5||Dubrey SW, Bhatia A, Woodham S, Rakowicz W. Lyme disease in the United Kingdom. Postgrad Med J 2014;90:33-42.|
|6||Cusick MF, Libbey JE, Fujinami RS. Molecular mimicry as a mechanism of autoimmune disease. Clin Rev Allergy Immunol 2012;42:102-11.|
|7||Stadsvold C. Poster 250: Guillain-Barré syndrome in the setting of acute CNS Lyme disease: A case report. PM R 2010;2:S113.|
|8||Horneff G, Huppertz HI, Müller K, Voit T, Karch H. Demonstration of Borrelia burgdorferi infection in a child with Guillain-Barré syndrome. Eur J Pediatr 1993;152:810-2.|