Neurologic Manifestations Of Lyme Disease Research Articles

Common Neurologic Features of Lyme Disease That May Present to a Rheumatologist.

Lyme disease, caused by Borrelia burgdorferi (Bb) infection, has a broad spectrum of clinical manifestations and severity. Patients with possible Lyme disease may seek out or be referred to rheumatologists. Today, the most common reason to engage a rheumatologist is due to complaints of arthralgia. After skin, neurologic manifestations of Lyme disease are now among the most common. Therefore, it is important for rheumatologists to be aware of clues that suggest neurologic Lyme disease and prompt help from a neurologist experienced with Lyme disease.

Neurootological manifestations of Lyme borreliosis

Introduction: The incidence of tick-borne diseases in Poland and Europe is increasing which is considered to be due to climate warming which promotes the growth of tick populations. Lyme borreliosis is the most prevalent leptospirosis in the US and Europe. Due to the potential for serious complications and the lack of specific prevention, diagnostic vigilance is essential so as to ensure early diagnosis and implementation of treatment. The main pathogen-transmitting vector is the tick species Ixodex ricinus. The suborder of ticks (Ixodida) belongs to the Acari subclass of arachnids. The natural reservoir of B. burgdorferi consists of small and medium-sized mammals and birds. Around ¾ of patients with Lyme disease report complaints and present disease symptoms within in the head and neck. The symptoms are diverse and may occur at all stages of the disease. These include headaches, neck pain and stiffness, sore throat, dizziness, cervical lymphadenopathy, otalgia, tinnitus, sudden hearing loss, and facial muscle paresis. Despite numerous papers being published on neurological manifestations of Lyme disease, the issues regarding the location of damage within the course of the auditory pathway and the balance system remain unanswered. In some cases hearing disorders may be due to central damage while others may be due to peripheral damage. Objective: The article provides an overview of reports on the clinical course and manifestation of Lyme borreliosis.

UNTREATED NEUROBORRELIOSIS PRESENTING WITH SOMATIC DELUSIONS AND SUBJECTIVE MEMORY IMPAIRMENT

Introduction Lyme disease is a tick-borne spirochete illness with multi-system involvement. Although neurological manifestations of Lyme disease are becoming increasingly well recognized, its psychiatric presentations are not well known. Physicians need to be aware of its neuropsychiatric symptoms that may present months to years later. Endemic areas to Borellia Burgdorferi also have higher rates of schizophrenia. Prompt diagnosis and effective treatment is need to to avoid irreversible neuropsychiatric complications. Methods Case Report: We present a case of a 63 year old male with a psychiatric history of somatic delusions, pressured speech, disinhibition, subjective cognitive complaints with compensatory behavior, and pain on the anterior aspect of the upper torso. Patient believed symptoms stem from pesticide accumulation in fat cells after a single use of pesticides several years prior to initial somatic symptoms. Patient attempted to self treat with over-the-counter vitamins and supplements and sought the help of several internists and specialists. Patient discontinued follow up with several providers due to belief that physicians did not understand the association between his pesticide use and current symptoms. Results Upon psychiatric evaluation MMSE and MOCA were performed and found to be within normal limits. Subsequent Frontal Assessment Battery was found to be at threshold. Contact with current primary care provider to discuss concerns regarding possible neurologic etiology. Conclusions Prompt diagnosis and effective treatment is need to to avoid irreversible neuropsychiatric complications. This research was funded by: MRI of the brain was preformed that demonstrated a frontal lobe hyperintensity. Spinal tap was done which was within normal limits. Serology was remarkable for IgG antibodies consistent with Borreliosis. Course of Doxycycline for 4 weeks was completed. One month follow up patient had remission of pressured speech, disinhibition, and delusions regarding pesticide poisoning. Patient continued to experience chronic pain of the anterior upper torso and cognitive complaints without change in MOCA performance.

Lyme Neuroborreliosis.

Lyme disease, caused by the spirochete Borrelia burgdorferi, is the most common tick-borne illness in the United States and Europe. Lyme disease usually begins with the characteristic skin lesion, erythema migrans, at the site of the tick bite. Following hematogenous dissemination, neurologic, cardiac, and/or rheumatologic involvement may occur. Neurologic involvement occurs in up to 15% of untreated B. burgdorferi infection and neurologists should be familiar with its diagnosis and management. The most common early neurologic manifestations of Lyme disease are cranial neuropathy (particularly facial palsy), lymphocytic meningitis, and radiculoneuritis, which often occur in combination. Late neuroborreliosis occurs much less frequently than early disease. A combination of clinical and laboratory findings is recommended for the diagnosis of Lyme neuroborreliosis. Treatment with recommended antibiotic regimens is effective in Lyme neuroborreliosis, and patients with early disease usually have excellent outcomes. Recovery is slower and may be incomplete in patients with late disease. Nervous system involvement occurs in up to 15% of patients with untreated B. burgdorferi infection. This article reviews clinical aspects of the diagnosis and treatment of Lyme neuroborreliosis, with focus on the United States.

Neurologic Manifestations of Lyme Disease

Borrelia burgdorferi infection, the tick-borne spirochetosis known as Lyme disease or Lyme borreliosis, involves the nervous system (neuroborreliosis) in 10% to 15% of patients. Common manifestations include lymphocytic meningitis, cranial neuritis, mononeuropathy multiplex, and painful radiculoneuritis. Rare patients develop inflammation in the brain or spinal cord. Regardless of the form of involvement, neuroborreliosis can be microbiologically cured in virtually all patients using standard 2- to 4-week antimicrobial regimens. Oral regimens appear to be as effective as parenteral ones in most instances. Although patients ill with Lyme disease may have concomitant cognitive or memory difficulty, these symptoms are not specific to neuroborreliosis and, when present in isolation, should not be viewed as suggestive of this diagnosis. When present as part of Lyme disease, they do not require additional or different treatment.

J. Lawton Smith, MD (1929–2011)

J. Lawton Smith, MD (1929–2011)

Human brain microvascular endothelial cell traversal by Borrelia burgdorferi requires calcium signaling

Neurological manifestations of Lyme disease (or neuroborreliosis) occur variably and while it is clear that Borrelia burgdorferi can invade the nervous system, how it does so is not well understood. Pathogen penetration through the blood brain barrier (BBB) is often influenced by calcium signaling in the endothelial cells triggered by extracellular host-pathogen interactions. We examined the traversal of B. burgdorferi across the human BBB using in vitro model systems constructed of human brain microvascular endothelial cells (HBMEC) grown on Costar Transwell™ inserts. Pretreatment of the cell monolayers with BAPTA-AM (an intracellular calcium chelator) or phospholipase C (PLC) inhibitor U73122 inhibited B. burgdorferi transmigration. By 5 h, BAPTA-AM significantly inhibited (82–99%; p <0.017) spirochete traversal of HBMEC compared to DMSO controls. Spirochete traversal was almost totally blocked ≥99%; p <0.017) after pretreatment with the PLC-ß inhibitor U73122 as a result of barrier tightening based on electric cell-substrate impedance sensing (ECIS). The data suggest a role for calcium signaling in CNS spirochete invasion through endothelial cell barriers.

Lyme Disease Associated With Postganglionic Horner Syndrome and Raeder Paratrigeminal Neuralgia

A 55-year-old woman developed severe unilateral headaches, periocular numbness, and Horner syndrome after presenting with symptoms consistent with Lyme disease. The combination of Horner syndrome and periocular headache and numbness constituted a diagnosis of Raeder paratrigeminal neuralgia. Although the headaches resolved with antibiotic treatment, the Horner syndrome persisted for at least 1 year. This case expands the spectrum of neurologic manifestations of Lyme disease to include postganglionic Horner syndrome as well as Raeder paratrigeminal neuralgia.

The therapy of lyme neuroborreliosis

The challenge for the neurologist in the treatment of Lyme neuroborreliosis is not in the treatment per se, but in the diagnosis. Neurological manifestations of Lyme disease can present in many forms, and diagnostic techniques which detect the spirochete directly; the culture or polymerase chain reaction of the spirochete in cerebrospinal fluid, are of disappointingly low yield. Therefore, the diagnosis is frequently not easy. After the diagnosis is made, antibiotic therapy is straightforward; Lyme neuroborreliosis should be treated with at least 2 weeks of antibiotics. In the United States, intravenous therapy with ceftriaxone or penicillin for 2 weeks is the standard, whereas in Europe oral doxycycline therapy is commonly administered. Either is effective, and my choice of therapy generally depends on the patient. Many patients have symptoms which continue after antibiotic therapy referable to persistent inflammation, and, for those patients, I will commonly prescribe nonsteroidal anti-inflammatory medications.

Relation entre lombosciatique, hernie discale et neuroborréliose : à propos de quatre observations

We report four cases of sciatica in patients with same-level disk herniation confirmed by computed tomography and a final diagnosis of acute radiculitis caused by Borrelia burgdorferi, with a favorable response to ceftriaxone therapy. The neurological manifestations of Lyme disease are protean, and a potential contribution of concomitant disk disease to sciatica can lead to diagnostic wanderings. Disk lesions and infectious conditions that can cause sciatica are discussed. Whether a favorable response to antibiotic therapy should be taken as proof of B. burgdorferi radiculitis deserves discussion. In practice, in a patient with clinical manifestations suggesting disk-related nerve root pain and residing or having traveled to an endemic area, B. burgdorferi infection should be looked for, as both etiologies can coexist.

Sciatica, disk herniation, and neuroborreliosis. A report of four cases

We report four cases of sciatica in patients with same-level disk herniation confirmed by computed tomography and a final diagnosis of acute radiculitis caused by Borrelia burgdorferi, with a favorable response to ceftriaxone therapy. The neurological manifestations of Lyme disease are protean, and a potential contribution of concomitant disk disease to sciatica can lead to diagnostic wanderings. Disk lesions and infectious conditions that can cause sciatica are discussed. Whether a favorable response to antibiotic therapy should be taken as proof of B. burgdorferi radiculitis deserves discussion. In practice, in a patient with clinical manifestations suggesting disk-related nerve root pain and residing or having traveled to an endemic area, B. burgdorferi infection should be looked for, as both etiologies can coexist.

Síndrome cordonal posterior aislado en la enfermedad de Lyme: estudio cliniconeurofisiológico

Lyme disease, caused by spirochete Borrelia burgdorferi, is a multisystemic infectious disorder with prominent neurologic involvement, affecting both the peripheral and the central nervous system. Meningitis, cranial neuritis and radiculoneuritis are the usual manifestations in the acute phase, and peripheral neuropathy in the chronic phase. Other less common manifestations have been also described. Here we report one case of Lyme disease confirmed by PCR, with a previously undescribed neurological manifestation, and the neurophysiological studies performed before and after treatment.Our patient showed a chronic and progressive clinical picture consisting of instability on walking and distal paresthesia of lower limbs, suggestive of posterior column disfunction. The neurophysiological exam performed prior to treatment with ceftriaxone revealed bilateral absence of lower limbs somatosensory evoked potentials (SEPs), without alterations in the distal nervous conduction or in upper limbs SEPs. The exam performed after treatment revealed a partial recovery of lower limb SEP with presence of an evoked response in SEP of left lower limb, coincident with a transitory clinical improvement of paresthesia in the same extremity.Our findings reveal that posterior column disfunction can be a neurological manifestation of Lyme disease. Furthermore the neurophysiological study shows that this manifestation is partially reversible following treatment. Our study emphasize the importance of the neurophysiological tests for the diagnosis and follow up of neurological manifestations of Lyme disease.

H9724, a monoclonal antibody to Borrelia burgdorferi's flagellin, binds to heat shock protein 60 (HSP60) within live neuroblastoma cells: a potential role for HSP60 in peptide hormone signaling and in an autoimmune pathogenesis of the neuropathy of Lyme disease.

Although Borrelia burgdorferi, the causative agent of Lyme disease, is found at the site of many disease manifestations, local infection may not explain all its features. B. burgdorferi's flagellin cross-reacts with a component of human peripheral nerve axon, previously identified as heat shock protein 60 (HSP60). The cross-reacting epitopes are bound by a monoclonal antibody to B. burgdorferi's flagellin, H9724. Addition of H9724 to neuroblastoma cell cultures blocks in vitro spontaneous and peptide growth-factor-stimulated neuritogenesis. Withdrawal of H9724 allows return to normal growth and differentiation. Using electron microscopy, immunoprecipitation and immunoblotting, and FACS analysis we sought to identify the site of binding of H9724, with the starting hypotheses that the binding was intracellular and not identical to the binding site of II-13, a monoclonal anti-HSP60 antibody. The current studies show that H9724 binds to an intracellular target in cultured cells with negligible, if any, surface binding. We previously showed that sera from patients with neurological manifestations of Lyme disease bound to human axons in a pattern identical to H9724's binding; these same sera also bind to an intracellular neuroblastoma cell target. II-13 binds to a different HSP60 epitope than H9724: II-13 does not modify cellular function in vitro. As predicted, II-13 bound to mitochondria, in a pattern of cellular binding very different from H9724, which bound in a scattered cytoplasmic, nonorganelle-related pattern. H9724's effect is the first evidence that HSP60 may play a role in peptide-hormone-receptor function and demonstrates the modulatory potential of a monoclonal antibody on living cells.

Compartmentalization of antigen specific cytokine responses to the central nervous system in CNS borreliosis: secretion of IFN- γ predominates over IL-4 secretion in response to outer surface proteins of Lyme disease Borrelia spirochetes

The neurological manifestations of Lyme disease have been proposed to be partly due to cytokine-mediated immunopathological mechanisms. In this study, the number of Borrelia-specific cells secreting interferon- γ and interleukin-4 was determined in blood and cerebrospinal fluid from patients with CNS borreliosis ( n=23), other neurological diseases ( n=20), and in blood from healthy controls ( n=10), utilizing an ELISPOT-assay. Elevated specific secretion of IFN- γ was found in CNS borreliosis, most pronounced in cerebrospinal fluid, whereas secretion of IL-4 was strikingly low. This may indicate that symptoms are due to side effects of the immune response, since IFN- γ secretion in the absence of corresponding levels of IL-4 may be associated with tissue destruction.

Lyme disease in children.

Neurologic manifestations of Lyme disease are common in children, among whom the incidence of Lyme disease is higher than among adults. Cranioneuropathies, in particular palsy of the facial nerve, occur in approximately 3-5% of children with Lyme disease, followed in frequency by meningitis (1% of symptomatic children). Children with only non-specific symptoms such as headache, arthralgia or fatigue commonly are misdiagnosed as having Lyme disease. Although such non-specific symptoms often accompany more specific signs and symptoms (e.g., erythema migrans, arthritis) in children with Lyme disease, very rarely are non-specific symptoms the sole manifestation of Lyme disease. A number of carefully conducted follow-up studies have indicated that the prognosis is excellent for children with Lyme disease who have been treated with standard antimicrobial regimens.

Lyme disease presenting as isolated acute urinary retention caused by transverse myelitis: An electrophysiological and urodynamical study

Several neurological manifestations of Lyme disease, both central and peripheral, have been described. 1 Reported here is a case of acute transverse myelitis related to a Lyme neuroborreliosis that presented with isolated acute urinary retention and no lower-extremity impairment. This case, documented by urodynamic and electrophysiological investigations, partially resolved after 6 weeks of intravenous ceftriaxone, affording the removal of the indwelling catheter. Alpha blocker therapy was needed for 3 months, until the complete normalisation of urodynamic and electrophysiological records. This case study indicates that whenever urinary retention is encountered associated with acute transverse myelitis or alone, the patient should be investigated for Lyme disease.

Prevalence of Borrelia burgdorferi antibodies in Bell's palsy in a metropolitan area of northern Italy.

Borrelia burgdorferi is the causative agent of Lyme disease, a multiphasic disorder affecting the skin, heart, joint, muscle, and nervous systems [1]. Meningitis, cranial neuritis, and radiculoneuritis represent the clinical spectrum of neurological manifestations of Lyme disease [2]. Several reports from central and northern Europe indicate that Bell’s palsy (BP) may be caused by B. burgdorferi [3–5], giving a possible explanation for a consistent proportion of BP cases. The aim of this paper is to evaluate the prevalence of B. burgdorferi related cases in a consecutive series of BP observed in subjects living in a metropolitan area of northern Italy.

Rheumatic manifestations in Lyme borreliosis

Lyme arthritis was first described by Steere et al in 1976 as a previously unrecognized rheumatic disorder. 1 The primary credit for this goes to two concerned mothers from Old Lyme, Connecticut. They had called the attention of the state health department and the Yale Rheumatology Clinic to an unusual geographic clustering of individuals, mostly children, with arthritis in their small community. In most of the affected children the diagnosis of juvenile rheumatoid arthritis had been made. 2 Further studies of this epidemic form of arthritis then revealed that Lyme arthritis was only one expression of a complex multisystem disorder, thereafter called Lyme disease, that may also affect the skin, heart, and nervous system. 2,3 The cutaneous marker and the neurologic manifestations of Lyme disease were found to be consistent with entities well known in Europe since the early 1900s, erythema migrans 4 and lymphocytic meningopolyneuritis; 5,6 however, joint symptoms had hitherto only casually been mentioned in case reports on erythema migrans 7,8 and lymphocytic meningopolyneuritis. 6,9,10 Thus, it was for a long time thought that Lyme disease in North America differs from the corresponding European syndrome in the frequency and severity of arthritic manifestations. Following the description of Lyme arthritis in North America the first case reports on the association of erythema migrans and arthritis in Europe were published in 1980. 11,12 In the meantime, it is to be supposed that the presumed continental difference as regards arthritis merely reflected the lack of awareness of Lyme arthritis in Europe and that the rheumatologic spectrum of the disease is quite similar on both sides of the Atlantic. 13 With respect to historical notes on rheumatologic aspects of Lyme borreliosis, the earlier literature on aerodermatitis chronica atrophicans (ACA), now known to be caused by a chronic skin infection with Borrelia burgdorferi, 14,15 is of particular interest. First, because of the predilection of the skin lesions for extensor sites over the joints, the term arthrodermatitis was considered more appropriate. 16 Second, joint and bone abnormalities in association with ACA were described by several European authors 17–25 and also in a case report from North America. 26 This even led to proposal of the designation acrodermatitis chronica arthropathica. 22 Finally, it is noteworthy that histologic findings of myositis were noted in two case reports on ACA. 22,24

Chronic Neurologic Manifestations of Lyme Disease

Abstract Background and Methods. Lyme disease, caused by the tick-borne spirochete Borrelia burgdorferi, is associated with a wide variety of neurologic manifestations. To define further the chronic neurologic abnormalities of Lyme disease, we studied 27 patients (age range, 25 to 72 years) with previous signs of Lyme disease, current evidence of immunity to B. burgdorferi, and chronic neurologic symptoms with no other identifiable cause. Eight of the patients had been followed prospectively for 8 to 12 years after the onset of infection. Results. Of the 27 patients, 24 (89 percent) had a mild encephalopathy that began 1 month to 14 years after the onset of the disease and was characterized by memory loss, mood changes, or sleep disturbance. Of the 24 patients, 14 had memory impairment on neuropsychological tests, and 18 had increased cerebrospinal fluid protein levels, evidence of intrathecal production of antibody to B. burgdorferi, or both. Nineteen of the 27 patients (70 percent) had polyneuropathy wi...

Neurologic Manifestations of Lyme Disease

The chronic neurologic symptoms and signs in 27 patients with previous signs of Lyme disease and current evidence of immunity to Borrelia burgdorferi are reported from the Departments of Neurology and Medicine, Tufts University School of Medicine, New England Medical Center, Boston, MA.