Course and Outcome of Early European Lyme Neuroborreliosis (Bannwarth Syndrome): Clinical and Laboratory Findings

Ogrinc, Katarina; Lusa, Lara; Lotrič‐Furlan, Stanka; Bogovič, Petra; Stupica, Daša; Cerar, Tjaša; Ružić‐Sabljić, Eva; Strle, Franc

doi:10.1093/cid/ciw299

Cited by 119 publications

(101 citation statements)

References 26 publications

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“…In a 10–20-year follow-up study of patients with Lyme neuroborreliosis in the United States, most of whom were seen before knowledge of antibiotic treatment for the disease, 23% of patients with facial palsy had mild-to-moderate residual deficits of facial nerve function and 26% had subtle motor or sensory peripheral nerve abnormalities 172 . By contrast, in a study of antibiotic-treated European patients with Bannwarth syndrome, 7% with facial palsy and 50% with motor pareses of extremities had incomplete recoveries, although only one patient had motor weakness that was functionally limiting 95 . Similarly, in patients with late, stage 3 Lyme neuroborreliosis, antibiotic therapy halts disease progression and patients experience substantial improvement.…”

Section: Quality Of Lifementioning

confidence: 87%

“…Bannwarth syndrome begins with painful radiculoneuritis that is associated with lymphocytic meningitis, often without headache, and can be followed by cranial neuropathy or pareses of the extremities 95 . B. afzelii can also cause neuro logical involvement, but the clinical manifestations are not as clear as with B. garinii 96 .…”

Section: Diagnosis Screening and Preventionmentioning

confidence: 99%

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Lyme borreliosis

Steere

Strle

Wormser

et al. 2016

Nat Rev Dis Primers

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697

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Lyme borreliosis is a tick-borne disease that predominantly occurs in temperate regions of the northern hemisphere and is primarily caused by the bacterium Borrelia burgdorferi in North America and Borrelia afzelii or Borrelia garinii in Europe and Asia. Infection usually begins with an expanding skin lesion, known as erythema migrans (referred to as stage 1), which, if untreated, can be followed by early disseminated infection, particularly neurological abnormalities (stage 2), and by late infection, especially arthritis in North America or acrodermatitis chronica atrophicans in Europe (stage 3). However, the disease can present with any of these manifestations. During infection, the bacteria migrate through the host tissues, adhere to certain cells and can evade immune clearance. Yet, these organisms are eventually killed by both innate and adaptive immune responses and most inflammatory manifestations of the infection resolve. Except for patients with erythema migrans, Lyme borreliosis is diagnosed based on a characteristic clinical constellation of signs and symptoms with serological confirmation of infection. All manifestations of the infection can usually be treated with appropriate antibiotic regimens, but the disease can be followed by post-infectious sequelae in some patients. Prevention of Lyme borreliosis primarily involves the avoidance of tick bites by personal protective measures.

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Section: Quality Of Lifementioning

confidence: 87%

Section: Diagnosis Screening and Preventionmentioning

confidence: 99%

Lyme borreliosis

Steere

Strle

Wormser

et al. 2016

Nat Rev Dis Primers

Self Cite

644

697

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“…Detection of pleocytosis, blood-CSF-barrier dysfunction, intrathecal production of immunoglobulins (Ig) and especially an intrathecal synthesis of Borrelia specific antibodies in CSF are the best indicators for definitive diagnosis [10]. Once diagnosed, the majority of patients with neuroborreliosis experience a favorable outcome after antibiotic treatment [11–15]. However, in a small number of patients residual symptoms remain [16].…”

Section: Introductionmentioning

confidence: 99%

Common and uncommon neurological manifestations of neuroborreliosis leading to hospitalization

et al. 2017

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BackgroundNeuroborreliosis represents a relevant infectious disease and can cause a variety of neurological manifestations. Different stages and syndromes are described and atypical symptoms can result in diagnostic delay or misdiagnosis. The aim of this retrospective study was to define the pivotal neurological deficits in patients with neuroborreliosis that were the reason for admission in a hospital.MethodsWe retrospectively evaluated data of patients with neuroborreliosis. Only patients who fulfilled the diagnostic criteria of an intrathecal antibody production against Borrelia burgdorferi were included in the study.ResultsSixty-eight patients were identified with neuroborreliosis. Cranial nerve palsy was the most frequent deficit (50%) which caused admission to a hospital followed by painful radiculitis (25%), encephalitis (12%), myelitis (7%), and meningitis/headache (6%). In patients with a combination of deficits, back pain was the first symptom, followed by headache, and finally by cranial nerve palsy. Indeed, signs of meningitis were often found in patients with neuroborreliosis, but usually did not cause admission to a hospital. Unusual cases included patients with sudden onset paresis that were initially misdiagnosed as stroke and one patient with acute delirium. Cerebrospinal fluid (CSF) analysis revealed typical changes including elevated CSF cell count in all but one patient, a blood-CSF barrier dysfunction (87%), CSF oligoclonal bands (90%), and quantitative intrathecal synthesis of immunoglobulins (IgM in 74%, IgG in 47%, and IgA in 32% patients). Importantly, 6% of patients did not show Borrelia specific antibodies in the blood.ConclusionIn conclusion, the majority of patients presented with typical neurological deficits. However, unusual cases such as acute delirium indicate that neuroborreliosis has to be considered in a wide spectrum of neurological diseases. CSF analysis is essential for a reliable diagnosis of neuroborreliosis.

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“…Given the propensity for radiculitis, B. burgdorferi may access the central nervous system by tracking along peripheral nerves into the meninges, but more recent data challenge this model [6,7]. The prodrome of pain in this patient is consistent with an early radiculitis, followed by evolution into a poliomyelitis-myelitis syndrome.…”

Section: Discussionmentioning

confidence: 75%