Monica M Diaz1, Sarah F Wesley2. 1. Department of Neurosciences, University of California, San Diego, CA, USA; University of California San Diego Health, San Diego, CA, USA. Electronic address: mmdiaz@ucsd.edu. 2. Department of Neurology, Yale School of Medicine, New Haven, CT, USA; Yale New Haven Hospital, New Haven, CT, USA. Electronic address: sarah.wesley@yale.edu.
Abstract
BACKGROUND: Lyme disease is a common vector-borne illness in the U.S. caused by Borrelia species spirochetes. Neuroborreliosis has variable presentations, rarely manifesting as meningoradiculitis or "Bannwarth Syndrome", characterized by painful radiculopathy, neuropathy, varying degrees of motor weakness, peripheral facial nerve palsy and cerebrospinal fluid (CSF) lymphocytic pleocytosis. We present a case of Bannwarth Syndrome manifesting with transaminitis and significant weight loss. CASE PRESENTATION: A 60-year-old man with history of hypertension presented with 3 weeks of progressive back pain, bilateral arm and leg weakness, bilateral hand numbness and a right facial droop in absence of sphincter dysfunction. He reported an 11.3 kg unintentional weight loss and recent holiday to Egypt. Patient was afebrile with normal vital signs but with profound transaminitis on presentation. Exam revealed a lower motor neuron right facial nerve palsy, diffuse quadriparesis, areflexia but isolated brisk ankle reflexes. A left complete facial palsy developed shortly after admission. Concern for leptomeningeal plus peripheral nerve involvement led to consideration of oncologic, infectious and inflammatory etiologies, along with Guillain-Barre variants. Contrasted MRI of the brain and total spine was normal. CSF revealed lymphocytic pleocytosis (cell count 134), elevated protein (156) with normal glucose, cytology, AFB culture, viral PCRs and paraneoplastic antibodies. Serum and CSF Lyme IgG and IgM were positive. IV Ceftriaxone 2 g daily was started one day after admission. EMG/Nerve conduction studies showed diffuse polyradiculopathy without evidence of Guillain-Barre syndrome. Babesia co-infection was considered given unexplained transaminitis but PCR and quantitation were negative. CSF following 1 week of antibiotics showed improving cell and protein counts with resolving transaminitis. On follow-up at 2 months, facial paralysis, pain, motor and sensory deficits had resolved with return to baseline weight and liver function tests. CONCLUSIONS: Bannwarth syndrome, a subacute painful meningoradiculitis caused by Borrelia species infection, is an uncommon presentation of neuroborreliosis in the U.S. Our case demonstrates previously unreported features such as profound transaminitis and weight loss without evidence of co-infection. Clinical manifestations of neuroborreliosis are variable, thus it is important to consider Bannwarth syndrome in the differential of meningoradiculitis in areas where Lyme Disease is prevalent.
BACKGROUND:Lyme disease is a common vector-borne illness in the U.S. caused by Borrelia species spirochetes. Neuroborreliosis has variable presentations, rarely manifesting as meningoradiculitis or "Bannwarth Syndrome", characterized by painful radiculopathy, neuropathy, varying degrees of motor weakness, peripheral facial nerve palsy and cerebrospinal fluid (CSF) lymphocytic pleocytosis. We present a case of Bannwarth Syndrome manifesting with transaminitis and significant weight loss. CASE PRESENTATION: A 60-year-old man with history of hypertension presented with 3 weeks of progressive back pain, bilateral arm and leg weakness, bilateral hand numbness and a right facial droop in absence of sphincter dysfunction. He reported an 11.3 kg unintentional weight loss and recent holiday to Egypt. Patient was afebrile with normal vital signs but with profound transaminitis on presentation. Exam revealed a lower motor neuron right facial nerve palsy, diffuse quadriparesis, areflexia but isolated brisk ankle reflexes. A left complete facial palsy developed shortly after admission. Concern for leptomeningeal plus peripheral nerve involvement led to consideration of oncologic, infectious and inflammatory etiologies, along with Guillain-Barre variants. Contrasted MRI of the brain and total spine was normal. CSF revealed lymphocytic pleocytosis (cell count 134), elevated protein (156) with normal glucose, cytology, AFB culture, viral PCRs and paraneoplastic antibodies. Serum and CSF Lyme IgG and IgM were positive. IV Ceftriaxone 2 g daily was started one day after admission. EMG/Nerve conduction studies showed diffuse polyradiculopathy without evidence of Guillain-Barre syndrome. Babesia co-infection was considered given unexplained transaminitis but PCR and quantitation were negative. CSF following 1 week of antibiotics showed improving cell and protein counts with resolving transaminitis. On follow-up at 2 months, facial paralysis, pain, motor and sensory deficits had resolved with return to baseline weight and liver function tests. CONCLUSIONS: Bannwarth syndrome, a subacute painful meningoradiculitis caused by Borrelia species infection, is an uncommon presentation of neuroborreliosis in the U.S. Our case demonstrates previously unreported features such as profound transaminitis and weight loss without evidence of co-infection. Clinical manifestations of neuroborreliosis are variable, thus it is important to consider Bannwarth syndrome in the differential of meningoradiculitis in areas where Lyme Disease is prevalent.
Authors: Carol S Palackdkharry; Stephanie Wottrich; Erin Dienes; Mohamad Bydon; Michael P Steinmetz; Vincent C Traynelis Journal: PLoS One Date: 2022-09-30 Impact factor: 3.752