Treatment, Lyme Disease, CDC


People treated with appropriate antibiotics in the early stages of Lyme disease usually recover rapidly and completely. Antibiotics commonly used for oral treatment include doxycycline, amoxicillin, or cefuroxime axetil. People with certain neurological or cardiac forms of illness may require intravenous treatment with antibiotics such as ceftriaxone or penicillin.

Treatment regimens listed in the following table are for localized (early) Lyme disease. See references below (Hu 2016; Sanchez 2016) for treatment of patients with disseminated (late) Lyme disease. These regimens are guidelines only and may need to be adjusted depending on a person’s age, medical history, underlying health conditions, pregnancy status, or allergies.

Treatment regimens for localized (early) Lyme disease.

Age Category Drug Dosage Maximum Duration, Days
Adults Doxycycline 100 mg, twice per day orally N/A 10-21*
Cefuroxime axetil 500 mg, twice per day orally N/A 14-21
Amoxicillin 500 mg, three times per day orally N/A 14-21
Children Amoxicillin 50 mg/kg per day orally, divided into 3 doses 500 mg per dose 14-21
Doxycycline 4.4 mg/kg per day orally, divided into 2 doses 100 mg per dose 10-21*
Cefuroxime axetil 30 mg/kg per day orally, divided into 2 doses 500 mg per dose 14-21

*Recent publications suggest the efficacy of shorter courses of treatment for early Lyme disease.

NOTE: For people intolerant of amoxicillin, doxycycline, and cefuroxime axetil, the macrolides azithromycin, clarithromycin, or erythromycin may be used, although they have a lower efficacy. People treated with macrolides should be closely monitored to ensure that symptoms resolve

The National Institutes of Health (NIH) has funded several studies on the treatment of Lyme disease that show most people recover when treated within a few weeks of antibiotics taken by mouth. In a small percentage of cases, symptoms such as fatigue (being tired) and muscle aches can last for more than 6 months. This condition is known as “Post-treatment Lyme Disease Syndrome” (PTLDS), although it is often called “chronic Lyme disease.” For details on research into “chronic Lyme disease” and long-term treatment trials sponsored by NIH, visit the visit the National Institutes of Health Lyme Disease web site external icon .

From Lyme Disease to Borreliosis

Lyme disease is a tick-borne illness typically caused by spiral-shaped bacteria called Borrelia burgdorferi. It is transmitted from host species to humans primarily by ticks. The tick is known as the “vector” for the disease, thus it is a “vector-borne disease.”

Lyme disease is the most common vector-borne disease in the United States according to the CDC. It was first discovered in the mid-1970s during an epidemic of juvenile rheumatoid arthritis in Lyme, Connecticut. Since then, the number of people diagnosed with the illness has increased to an estimated 300,000 cases each year, accounting for more than 90% of all vector-borne disease in the U.S.

More than 20 species of Borrelia have been implicated in human and animal disease to date. Three genospecies of Borrelia cause most of the human disease:

  • B. burgdorferi sensu stricto (s.s.) in the U.S. and Europe
  • B. garinii and B. afzelii in Eurasia

Borrelia miyamotoi, first discovered in Japan in 1995, has been shown to cause Lyme-like symptoms in patients. In 2015, a series of case studies showed that patients who were seropositive for B. miyamotoi were more likely to experience joint pain and headaches. Furthermore, there is evidence for worse or more persistent symptoms when multiple Borrelia species are present. Borreliosis is a term used to describe infections with a single, or multiple, species of Borrelia.

Rarely, other species of Borrelia (B. valaisiana, B. lusitaniae, B. spielmanii, B. bissettii) have also been found in humans.


Borrelia species are transmitted via bites from hard ticks of the genus Ixodes that live in wooded areas and grasslands at temperate climates. Ixodes ticks are typically smaller than others, making them hard to detect. Additionally, they tend to feed in hard to find places and attach painlessly due to anti-inflammatory agents in their saliva.

I. scapularis and I. pacificus are common North American vectors, whereas I. ricinus and I. persulcatus are the main Eurasian vectors. In the United States, a majority of Lyme disease cases are reported in the Northeast and Midwest. However, studies have shown that this is slowly changing due to factors such as climate change and housing development.

Source: Tick-Borne Disease Working Group 2018 Report to Congress

The basic Ixodes tick lifecycle involves feeding on a mammal at each life stage and then mating once the adult stage is reached (Figure 1). A common misconception is that ticks carry Borrelia species bacteria from the moment they hatch. Actually, ticks capable of hosting the bacteria (“competent” tick species) acquire the bacteria by ingesting the blood of mammalian reservoirs, like mice, as they grow from nymphs to adults.

When the tick then feeds on another animal, including humans, the bacteria can be transferred from the tick’s saliva to the skin of the new host. Borrelia bacteria then migrate through the skin until they can penetrate the blood vessels and briefly use the bloodstream as transport to other tissues and organs. Once they leave the bloodstream, they are difficult to detect.


Lyme borreliosis symptoms are complex and can vary greatly between patients. Research has shown that Borrelia species cause a wide spectrum of symptoms because of their ability to cause inflammation in multiple areas of the body, including the eyes, brain, and heart. Complicating the situation further, multiple pathogens (generally, other species of bacteria) are often transmitted during a single tick bite.

Identifiable acute symptoms, like an erythema migrans (EM) rash, may appear a couple of weeks after a tick bite. Chronic symptoms of Lyme borreliosis can be mild and nonspecific, like headaches or joint pain. The list of possible symptoms includes, among others:

  • Headache
  • Fever
  • Malaise
  • Fatigue or chronic fatigue
  • Muscle soreness
  • Sleeplessness
  • Depression
  • Anorexia
  • Fibromyalgia
  • Localized or disseminated EM rash
  • Joint pain
  • Neurological symptoms (facial paralysis, blindness, memory loss, etc.)
  • Muscle impairment, limp, or paralysis
  • Arthritis
  • Carditis or heart block

Risk Factors

Ticks that transmit Lyme borreliosis can be found across the United States during the spring and summer months, but are increasingly being found year round. When ticks are “questing”, or looking for a mammal to feed on, they are able to sense breath, heat, and even shadows.

They tend to wait at the ends of blades of grass or tree limbs with two appendages reaching out to attach to the next passerby. People who spend time in grassy or wooded areas are at high risk of exposure to these ticks. Animal owners also face high risk because ticks can hitch a ride on the pet and affect a person in the household later. Although these are the areas of highest risk, ticks have been found in any environment where they can be transported by animals such as birds, including beaches.

The easiest way to reduce the risk of contracting Lyme borreliosis is to follow precautions such as the ones listed below:

  • Wear appropriate clothing (light colors, long sleeves, long pants, etc.) when outdoors to increase the chances of seeing a tick on you. Furthermore, reduce the amount of skin visible to decrease the likelihood of tick attachment.
  • Spray clothing with 0.5% permethrin.
  • Apply tick repellent that is at least 20-30% DEET.
  • Perform a thorough tick check shortly after finishing outdoor activities. Areas where ticks like to attach include the scalp, bellybutton, underarms and behind the knees or ears.
  • Shower, wash clothes in hot water, and dry with high heat for at least 10 minutes within two hours of arrival at home. This will reduce the chances of crawling ticks residing in the home and attaching later on.
  • Give an effective flea/tick preventative to your pets year-round. The preventative should kill tick species, including Ixodes ticks, within a couple hours of attachment to reduce the likelihood of pathogen transmission. Topical tick preventatives with permethrin may help ward off ticks as well.


Physicians typically diagnose and initiate treatment for Lyme disease based on a combination of clinical symptoms and results from laboratory testing, but there are some exceptions. For example, the Center for Disease Control (CDC) and International Lyme and Associated Diseases Society (ILADS) guidelines recommend starting antibiotic therapy, without laboratory evidence, if a patient presents with an EM rash. A large percentage of Lyme disease patients do not present with an EM rash, however, so physicians rely on diagnostic tests to aid in diagnosis. Organizations like the Infectious Diseases Society of America (IDSA) have also developed guidelines for physicians to follow when diagnosing Lyme borreliosis. For example, the IDSA suggests that physicians should consider the prevalence of ticks carrying Borrelia burgdorferi in the patient’s geographic region.

The CDC recommends that physicians follow a two-tier testing protocol to diagnose Lyme disease (See figure below).

The first tier utilizes IgM or IgG-based ELISAs, or IFA, to determine if antibodies from exposure to Lyme Borrelia are present in the patient’s serum. If it tests negative, then no further testing is required. However, the physician can have a convalescent sample drawn if acute infection is strongly suspected but the IgM ELISA was negative. Patient samples that are positive or equivocal should proceed to the second tier of the protocol.

The second tier is another round of immune response testing employing IgM and/or IgG Western blot methods. A Western blot looks for antibodies that are specific to different antigens produced by Borrelia burgdorferi. The CDC criteria for a surveillance case require that an IgM Western blot sample contain antibodies that are reactive to 2 out of 3 antigens to be considered positive. An IgG Western blot requires reactivity to 5 out of 10 antigens for a positive result that meets CDC criteria for surveillance reporting.

If the results for the ELISA and Western blot are “equivocal/positive” or “positive/positive”, then the patient satisfies CDC requirements for optimal laboratory evidence of Lyme disease. However, physicians often use different testing protocols and alternate guidelines to interpret test results. There are also specialty laboratories that utilize different criteria to report positive results. Galaxy Diagnostics’ in-house two-tier Lyme disease testing follows the current CDC standards for reporting positive lab results.

Source: CDC Website

What other laboratory tests are available for Lyme borreliosis?

There is an effort to develop novel diagnostic tools for Lyme Borrelia due to its increasing prevalence and incidence across the United States and the shortcomings of current testing methods. The mainstream recommended methods focus on exposure to specific species, but do not necessarily confirm active infection. There is a push to develop and utilize derivatives of molecular methods, like PCR, that target Borrelia DNA in the blood, serum, and/or tissues of patients.


Lyme disease is treated with antibiotic therapy, but the type(s) of antibiotics utilized and the duration of treatment vary with the nature of the infection and must be evaluated by a physician on a case-by-case basis.

Lyme disease (lime-borreliosis)

Medical expert of the article

Lyme disease (ixodid tick-borne borreliosis, systemic tick-borne borreliosis, lime-borreliosis) is an inflammatory disease caused by spirochetes and carried by mites; is characterized by early skin lesions and chronic migrating erythema (HME), after which, weeks and months after infection, pathological changes in the nervous system, heart and joints can develop. Diagnosis of Lyme disease is initially clinical, but the detection of antibody titers during illness and recovery can be used. Treatment of Lyme disease is carried out with antibiotics, such as doxycycline or in severe cases ceftriaxone.

ICD-10 codes

  • A69.2. Lyme disease. Chronic migratory erythema caused by Borrelia burgdorferi.
  • L90.4. Acrodermatitis is chronic atrophic.
  • M01.2. Arthritis in Lyme disease.

What causes Lyme disease?

Lyme disease (lime-borreliosis) was identified in 1975 when a number of cases were reported in the Old Lyme area of Connecticut. Since then, it has been encountered in 49 states of the USA, especially in the form of focal flares on the northeast coast from Massachusetts to Maryland, in Wisconsin, Minnesota, California and Oregon. It is also known in Europe and is found on the territory of the former USSR, in China, Japan. People fall ill usually in the summer or early autumn, regardless of gender and age, although in most cases children and young people living in the wooded area suffer.

Lime-borreliosis is transmitted by Ixodes Scapularis, a deer tick. In the United States, the natural reservoir of infection is mainly white-legged hamsters, they are the primary reservoir and the preferred host for nymphs and larvae of ticks. Deer are masters for adult mites, but do not wear Borrelia. Other mammals (eg dogs) can be accidental hosts, and they may develop Lyme disease. In Europe, the owners are sheep, but they never get sick.

B. Burgdorferi penetrate the skin in the place of a tick bite. After the incubation period lasting from 3 to 32 days, they spread in the skin around the bite along the lymphatic ways (regional lymphadenopathy) or with blood flow to other organs and skin areas. The relatively small number of microorganisms in tissues suggests that most clinical manifestations of the disease are associated with the host’s immune response, rather than the damaging role of microorganisms.

What are the symptoms of Lyme disease?

Lyme disease has three stages: early localized, early disseminated, late. Early and late stages are usually divided by an asymptomatic period.

Chronic migrans erythema (CML) is the most important clinical sign of Lyme disease in 75% of patients begins with the appearance of a red spot or papule, usually on the proximal limb or trunk (especially on the thighs, buttocks, in the armpits), between 30-32- m day after the tick bite. This formation increases (up to 50 cm in diameter), often pale in the center. Half of the cases soon after the first spot there are many such skin lesions, but smaller ones and without induration in the center. The cultivation of the biopsy material of these secondary lesions can be positive and indicate the dissemination of the infection. Chronic migratory erythema lasts, as a rule, several weeks; in the recovery period, rapid eruptions are possible. Changes in mucous membranes are not observed.

Symptoms of Lyme disease in the early disseminated phase begin several days or weeks after the primary lesions, when the bacteria spread throughout the body. Most often, HME accompanies (sometimes precedes for several days) a symptom complex resembling a flu-like syndrome and including weakness, malaise, chills, fever, headache, stiff neck, myalgia and arthralgia. Because the symptoms of Lyme disease are often nonspecific, the diagnosis is not always established; need a high alertness. At this stage, Frank’s arthritis is rare. Less often there are back pain, nausea and vomiting, pain or sore throat, lymphadenopathy and enlarged spleen. Most of the symptoms then appear, then disappear, except for weakness and malaise, which do not go away for weeks. Some patients develop symptoms of fibromyalgia. Rashes in the former places, but much less pronounced, may appear before the onset of arthritis. Severe neurologic disorders develop in about 15% of patients after a few weeks or months of CML (often before arthritis).

Neurological symptoms of Lyme disease develop in approximately 15% of patients, during weeks-months against a background of migrating erythema. Usually they last several months and pass without a trace. The most common are lymphocytic meningitis (pleocytosis in the CSF about 100 / μL), meningoencephalitis, neuritis of the cranial nerves (especially Bell’s paralysis, sometimes bilateral), sensory or motor radiculoneuropathies.

Disturbances in myocardial function are observed in 8% of patients a few weeks after the onset of chronic migratory erythema. They consist of symptoms of atrioventricular blockade with a variable degree of severity (1st degree, Wenkebach blockade, 3rd degree), less often — myopericarditis with a decrease in the left ventricular ejection fraction and cardiomegaly.

In untreated patients, the late stage begins months and years after the onset of the disease. Arthritis occurs in approximately 60% of patients with chronic migratory erythema several weeks or months after its onset, but sometimes even later — up to 2 years. Intermittent edema and pain in some large joints, especially in the knee, usually recur for several years. Edema is more pronounced than tenderness; joint hot, sometimes reddened. Baker’s cysts can be formed and torn. Such symptoms of Lyme disease as accompanying chronic migraine erythema, such as weakness, malaise and slight fever, may precede or accompany exacerbations of arthritis. Chronic arthritis of the knee joint (more than 6 months) develops in 10% of bumps. Of the late (after years) consequences, chronic atrophic acrodermatitis, susceptible to antibiotic therapy, and chronic neurological disorders such as polyneuropathy, encephalopathy, memory impairment, sleep are noted.

How is Lyme disease diagnosed?

Isolate the pathogen from tissues or body fluids is rarely possible; they should be used to diagnose other pathogens. Identification of the antibody titer at the height of the disease and during the recovery period is of diagnostic significance. If the titer is positive, there must be confirmation by western blotting. However, seroconversion may be late — more than 4 weeks or sometimes absent. A positive IgG antibody titer can talk about a previous infection. PCR analysis of CSF and synovial fluid often yields positive results with the interest of these structures. The diagnosis depends on the results of both tests and the availability of typical clinical data. Classical erythema indicates Lyme disease if there are other data (recent tick bite, stay in an endemic area, typical systemic symptoms).

In the absence of a rash, the diagnosis is difficult, because the remaining symptoms of Lyme disease may not be expressed. Previously, the disseminated phase can mimic juvenile RA in children, reactive arthritis, atypical RA in adults. These diseases can be excluded in the absence of morning stiffness, subcutaneous nodules, iridocyclitis, mucous membrane damage, rheumatoid factor, antinuclear antibodies. Lyme disease, manifested musculo-skeletal, influenza-like syndrome in the summer can be like erlichiosis, tick-borne rickettsiosis. The absence of leukopenia, thrombocytopenia, elevated transaminases and the incorporation of corpuscles into neutrophils make it possible to determine Lyme disease. In some cases, namely, with migrating polyarthritis with ECG changes (prolongation of PQ interval) or chorea (as manifestation of meningoencephalitis), the differential diagnosis includes acute rheumatic attack. When the disease of Lyme is rarely tapped heart murmur, and no indication of preceding streptococcal infection.

At a late stage, the axial skeleton is not involved, in contrast to spondyloarthropathy with lesion of peripheral joints. Lyme disease can cause Bell’s paralysis, fibromyalgia, chronic fatigue syndrome, and can mimic lymphocytic meningitis, peripheral neuropathies and similar syndromes of CNS diseases.

In endemic areas, Lyme disease may be suspected in many patients with arthralgia, chronic fatigue, difficulty concentrating, or other disorders. Despite the absence of history of erythema or other symptoms of an early localized or disseminated disease, these patients are really sick. In such patients, an increase in the IgG antibody titer indicates contact in the past, but not a persistent infection, and this often leads to prolonged and useless antibiotic therapy.


Lyme Neuroborreliosis

Lyme neuroborreliosis is a late manifestation of an infection by Borrelia spp., a tick-borne bacterial pathogen that is known for causing Lyme disease and a range of clinical syndromes. The ailment is primarily seen during the summer months and symptoms range from headaches and facial nerve palsy to severe sensory and motor deficits with altered consciousness. The diagnosis mandates a thorough clinical investigation, followed by microbiological studies.


Lyme neuroborreliosis (LN) is one of the many forms of Borrelia spp. infection, a spirochetal bacterial pathogen that is transmitted to the human host after a tick bite, specifically from Ixodes species [1] [2] [3] [4]. Higher prevalence is encountered in the United States (where Borrelia burgdorferi is the main causative agent, with an incidence rate of 9.1 cases per 100 000 individuals), and in Europe, where B. garinii, B. afzelii and B. burgdorferi sensu stricto are identified as main pathogenic species [2] [4]. In order for LN to occur, patients first pass through the initial stages of borreliosis (commonly known as Lyme disease) — the appearance of erythema migrans (a sharply-defined circular or «target» lesion that develops in the proximity of the tick bite) within a period of 3-30 days after the bite, and constitutional complaints such as fever, headaches, joint pain, and fever [1] [3] [4]. LN appears when bacteria are disseminated into the peripheral and central nervous system (CNS) and findings are seen either during early stages of dissemination or after a delayed period of weeks to years as a late manifestation [3] [4]. LN is frequently described as a complication of Lyme disease in Europe than in the United States (35% vs.

Entire Body System

Cranial paresis and other neurologic signs usually occur after the onset of pain. The present paper describes four patients who had severe pain as the main presenting symptom of Lyme neuroborreliosis. []

Elevated lactate levels were accompanied by fever and headache. In the Reiber nomograms, intrathecal immunoglobulin synthesis was found for IgM in 70.2% followed by IgG in 19.5%. []

headaches, joint pain, and fever. []

Five of the patients presented with severe fatigue, malaise, nausea, headache and fever. Four had recognised a tick bite recently, and two developed erythema migrans. []

Patients and healthy controls were assessed for quality of life [Short Form (36) with subscores for physical and mental components (PCS, MCS)], fatigue (fatigue severity scale), depression (Beck depression inventory), verbal memory and learning and cognitive []

The average Fatigue Severity Scale (FSS) score was 4.29. [8] Krupp defined severe fatigue 4.0 in her NIH sponsored clinical trial. [8] The 17 LBN subjects with residual symptoms also presented with a poor quality of life. []

Conclusions: LNB can present as acute ocular motor disorders in conjunction with fatigue and other clinical manifestations. []

A 15-year-old boy had onset of unilateral facial weakness. A few days later, he experienced mild vertigo, double vision, and headache. Examination confirmed a peripheral right seventh nerve weakness in addition to an internuclear ophthalmoplegia. []

Clinical examination revealed motor radiculopathy with bilateral areflexia of biceps reflex and asymmetric muscle weakness of shoulder elevation and flexion of the forearms. []

The rash is often accompanied by flulike symptoms, such as headache, fatigue, chills, loss of appetite, fever, and aching joints or muscles. []

Early localized stage (3-30 days post-tick bite) Red, expanding rash called erythema migrans (EM) Fatigue, chills, fever, headache, muscle and joint aches, and swollen lymph nodes Some people may get these general symptoms in addition to an EM rash, but []


The patient presented with dyspnea and pain behind the sternum, which had been occurring for several months, mainly during fast walking upstairs. The patient reported having no symptoms when he was motionless. []

[…] within one to two months after infection (range of less than one week to seven months). 17 – 19 Lyme carditis is a less common complication of systemic disease, occurring in approximately 4 to 10 percent of patients. 19 It may present as chest pain, dyspnea []

Hospitalization and continuous monitoring, with consideration for temporary pacing, are advisable for patients with any of the following: Associated symptoms (eg, syncope, dyspnea, or chest pain) Second-degree or third-degree AV block First-degree heart []


Five of the patients presented with severe fatigue, malaise, nausea, headache and fever. Four had recognised a tick bite recently, and two developed erythema migrans. []

Nausea and vomiting are rare. A solitary lesion is the most frequent presentation in both US (81%; 95% confidence interval [CI], 72%-87%) and European patients (88%; 95% CI, 81%-93%). []

Most of the predictive information was provided by the symptoms at 14 days: these included nausea, vomiting, memory and concentration disturbances, malaise, fatigue, headache, and arthralgia ( Supplementary Figure 2 ). []

A 26-kDa Borrelia glycosaminoglycan-binding (GAG-binding) protein, Bgp, binds to the GAG side chains of heparan sulfate on endothelial cells, and to both heparan sulfate and dermatan sulfate on neuronal cells ( 49, 50 ). []


Back pain is a common symptom among patients presenting to the acute medical unit. We describe the case of a 55-year-old man with a brief history of fatigue and severe back pain, unresponsive to escalating doses of opiate analgesia. []

 Flu-like illness  Headache  Extreme Fatigue  TMJ/ Jaw Pain (Temporomandibular Join)  Neck & Back Pain  Joint Pain & Swelling, Bone Pain (EM) Rash 6. []

Next day I was in agony with horrendous back pain. For the next two weeks I barely slept. Lying down was impossible. I got no relief from painkillers. A 24 hour bout of foul diarrhoea was distressing, and I felt ill. []

In comparison to patients with normal CSF cell counts, those with pleocytosis more often reported radicular pain, sleep disturbances, and lower back pain, and more often had meningeal signs and peripheral facial palsy (Table 1, Figure 2 ). []

Meningoradiculitis due to borreliosis presenting as low back pain only. Neuroradiology 1998 ; 40 : 126 –27 Ljostad U, Okstad S, Topstad T, et al. Acute peripheral facial palsy in adults. J Neurol 2005 ; 252 : 672 –76 Lesser RL. []

A 22-year-old male presented with history of flu-like illness and headache, accompanied by vertical binocular diplopia, worse on downgaze and better in upgaze and right head tilt. []

Other symptoms may include diplopia, hearing impairment, paralysis, altered sensation, difficulty in walking or cognitive impairment. []

She had experienced continuing headaches, lethargy and a self-limiting episode of diplopia that prompted her to see her general practitioner. []

A 71-year-old woman with headache, malaise, fever, and diplopia. Initial coronal postcontrast T1 MR imaging ( A and B ) with enhancing bilateral third and fifth cranial nerves. []

Two children presented with acquired nystagmus, one with combined nystagmus and partial sixth nerve palsy, one with partial sixth nerve palsy, one with ptosis and one with Adie’s pupil. []

Results: Two children presented with acquired nystagmus, one with combined nystagmus and partial sixth nerve palsy, one with partial sixth nerve palsy, one with ptosis and one with Adie’s pupil. []

Cranial nerve disorders: facial palsy (sometimes involving both sides of the face), double vision, drooping eyelid (ptosis), numbness pain and tingling of the face, hearing loss, dizziness and tinnitus. Seizures. []

Clinical record A 58-year-old woman of European ancestry presented to a rural hospital in New South Wales in May 2014 with an 8-month history of worsening motor instability, confusion and bilateral occipital headaches associated with photophobia, lethargy []

Photophobia As in various other infections and/or CNS disturbances (e.g. meningitis, migraine, psittacosis, typhus, Rocky Mountain Spotted Fever), photophobia may be a prominent feature. In our sample, 70% of respondents reported photophobia. []


We present two patients with monosymptomatic headache resembling chronic tension-type headache as the first manifestation of Lyme neuroborreliosis. []

The ailment is primarily seen during the summer months and symptoms range from headaches and facial nerve palsy to severe sensory and motor deficits with altered consciousness. []

Lyme Disease — Encephalopathies, Lyme Disease — Lyme Disease Encephalopathies — Lyme Disease Encephalopathy — Lyme Disease Mononeuritis Multiplex — Mononeuritis Multiplex, Lyme Disease — Peripheral Nervous System Lyme Disease — Lyme Meningoradiculitis []

The well-documented neurologic spectrum includes lymphocytic meningitis, cranial neuropathy, and radiculoneuritis in the early disseminated stage; and peripheral neuropathy, chronic encephalomyelitis, and mild encephalopathy in the late persistent stage []

Neurogenic pain with radiculitis is often the starting symptom in adult patients with tick-borne Lyme neuroborreliosis and in some cases the only clinical manifestation. []

Paresthesia, pain and persistent facial palsy was also significantly more common in patients treated because of neuroborreliosis. Our study shows that persisting neurological symptoms are common after a neuroborreliosis infection. []

Residual neurological symptoms, such as facial palsy, concentration disorder, paresthesia and/or neuropathy, were reported by 28/114 patients. []

In a multivariate analysis, both gender and having headache and neck stiffness were associated with a higher level of pleocytosis. []

stiffness during their acute illness (87% compared with 13%; odds ratio, 2.4 [CI, 1.0 to 5.5]; P 0.045); however, the performance of the two groups on neurocognitive tests did not significantly differ. []

stiffness due to meningitis (inflammation of the spinal cord) Pain and swelling in the large joints (such as knees) Shooting pains that may interfere with sleep Heart palpitations and dizziness due to changes in heartbeat Many of these symptoms will []


The diagnosis of LN is a difficult one to make without a proper clinical and microbiological investigation. The physician should first conduct a detailed patient interview during which the incidence of tick bites and typical skin lesions must be assessed, whereas a comprehensive travel history (given the fact that visiting endemic areas is a risk factor) may provide important clues as well [1] [4]. Tick-borne disease must be considered in all patients with undisclosed cutaneous and constitutional symptoms in the summer months, as the vast majority of such events occur from May to September [1] [2]. After a detailed physical examination (particularly focused on neurological evaluation), laboratory studies are the cornerstone for confirming the condition. Current recommendations advocate initial serological testing (through enzyme immunoassays or enzyme-linked immunosorbent assays — EIA and ELISA, respectively) of cerebrospinal fluid (CSF) or blood for immunoglobulin (Ig) G and IgM antibodies, followed by more sensitive methods such as Western blot [1] [4] [6] [7] [8]. CSF examination yields lymphocytic pleocytosis with normal biochemical composition [4], and the detection of neutrophilic predominance can firmly exclude Lyme disease as the etiology of neurologic infections [5]. Polymerase chain reaction (PCR) testing is a novel technique that allows identification of pathogenic DNA and its implementation is recommended whenever possible [4] [7]. Imaging studies of the endocranium and the CNS, magnetic resonance imaging (MRI) being the main candidate, reveal nonspecific findings and thus are of limited benefit for discriminating between etiologies of such symptoms [1] [9].

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