Neuroborreliosis and stroke

David Goldemund M.D.
Updated on 10/03/2024, published on 22/02/2024


  • Lyme disease (borreliosis) is the most common anthropozoonosis; the typical vector of borrelia is the tick Ixodes ricinus
    • ticks, larvae, and nymphs are found in forested areas, parks, and suburban gardens from March to mid-November
    • Lyme disease is transmitted through tick bites, usually within 24 hours of attachment
  • Borrelia burgdorferi (BB), Borrelia garini (BG), and Borrelia afzelii (BA) belong to the order Spirochetales
    • Borrelia burgdorferi sensu lato (BG and BA) predominate in Europe, Borrelia burgdorferi sensu stricto in the USA
  • involvement of the nervous system is reported to occur in 10-15% of patients with Lyme disease  (Halperin, 2015)
  • stroke due to CNS vasculitis is a rare complication of the disease, single case reports or small series have been published  (Garkowski, 2017)
  • borreliosis-associated vasculitis should be excluded in all patients with vasculitic pattern on imaging and multiple ischemic lesions, especially in those living in endemic areas
  • remove attached ticks as quickly as possible, preferably with tweezers
  • do not remove the tick with unprotected fingers; rubber gloves are preferable
  • do not apply pressure to the tick; remove it with a rocking motion from side to side and a gentle pull
  • a circular motion is inappropriate, as is the use of oils or greasy creams
  • on the other hand, it is advisable to rub the wound with antiseptic
  • after removing the tick, treat the area with an antiseptic again


Tissue damage occurs in borreliosis due to:


Direct effect of Borrelia

  • direct cytotoxic effects are seen in erythema chronicum migrans (ECM) and other skin conditions, synovitis, arthritis, myocarditis, and endocarditis.

Autoimmune process

  • especially important in neuroborreliosis
  • mediated by the autoimmune action of T lymphocytes against neurons and glial cells
  • cross-reactivity of anti-Borrelia antibodies with myelin sheaths and neuroglia is also significant


  • commonly affects spinal roots, peripheral nerves, and muscles
  • vasculitis affecting cerebral arteries is rare, but possible

Neuroborreliosis and stroke

  • if parenchymal and vascular imaging suggest vasculitis, borreliosis should be excluded among other causes, especially in patients exposed to ticks or who live in areas with high prevalence of tick-borne diseases [Garkowski, 2017]
  • vasculitis is presumed to be caused by the inflammatory response to the spirochetal infection
  • symptoms of stroke in neuroborreliosis are similar to those of stroke from other causes
  • risk factors include:
    • delayed diagnosis and treatment of Lyme disease
    • severe systemic inflammation
    • involvement of large blood vessels by vasculitis
    • the presence of traditional cardiovascular risk factors
  • without proven vasculitis, the causal relationship between stroke and neuroborreliosis is unclear and other significant stroke etiologies must be excluded
clinical and radiological signs of stroke + vasculitic pattern of vascular imaging
confirmation of neuroborreliosis (according to EFNS guidelines)
exclusion of other etiologies (including other vasculitides!!)

Clinical presentation

Early localized stage

  • occurs days to weeks after a tick bite when borrelia multiply in the skin
  • the most typical manifestation is erythema (chronicum) migrans (EM or ECM)
    • appears within 4-5 weeks after a person has been bitten by an infected tick
    • a characteristic red expanding bull’s-eye rash, with a central clearing surrounded by a red outer ring
    • it often gradually enlarges and may reach sizes of up to several inches in diameter
    • a hallmark sign of Lyme disease, although not all individuals with Lyme disease develop this rash
  • general flu-like symptoms (subfebrile, fatigue, malaise, muscle, and joint pain, possibly regional lymphadenopathy) may occur
  • neurological involvement at this stage is less common but can include mild meningitis or cranial nerve palsies
  • early recognition and treatment of EM are crucial for preventing progression  to later stages of Lyme disease
Erythema chronicum migrans

Disseminated stage

Early disseminated stage (2-12 weeks)
Neurological Symptoms

  • Bannwarth’s syndrome (meningomyeloradiculitis)
  • encephalomyelitis
  • cranial neuritis (CN II, III, IV, VI, VII, VIII)
  • myositis, polyneuritis, radiculitis
Cardiac symptoms
  • arrhythmias
  • cardiomyopathy, myocarditis
Skin Symptoms
  • late rash
  • lymphadenosis benigna cutis (LBC)
  • regional lymphadenopathy
ENT Symptoms
  • cochlear lesions, tinnitus, labyrinth lesions (vertigo)
  • dysphonia
Late disseminated stage (> 6 months)
Neurological symptoms
  • chronic progressive encephalomyelitis with multifocal MS-like lesions
  • chronic asymmetric neuritis or chronic radiculopathy
  • myasthenic conditions, chronic fatigue syndrome
Other symptoms
  • chronic hepatopathy
  • cardiomyopathy, arrhythmias
  • immunodeficiency
  • polyarthritis, fibromyalgia, or recurrent monoarthritis
  • acrodermatitis chronica atrophicans

Diagnostic evaluation of borreliosis

Specific antibodies

  • specific antibodies (ELISA + Western blot confirmation) in serum and CSF
  • low sensitivity during the first weeks of infection
  • a positive result does not necessarily indicate the presence of bacteria in the organism – it may only indicate contact of the patient with the antigen of the infectious agent that led to the subsequent antibody response


  • false-positive and false-negative results in serum and especially in CSF, are common
  • PCR can be used in the early stages when there is no antibody response and in immunosuppressed individuals
  • testing is not recommended in the late stages

CSF analysis

  • cytology
    • lymphocytic pleocytosis, typically around 10-1000 / mm3 of elements
    • normal findings are rare in neuroborreliosis
  • elevated protein levels (reflecting disruption of the blood-brain barrier and inflammation in the central nervous system)
  • detection of specific antibodies (ELISA or Western blot) + assessment of intrathecal synthesis
    • the problem is a low sensitivity in the early stage and, conversely, their persistence after treatment
  • oligoclonal bands
    • indicate intrathecal antibody production
    • not specific for neuroborreliosis, can be found in other inflammatory diseases
  • electron microscopy (ELM) – low sensitivity/specificity
  • CSF analysis may be repeated during treatment to monitor response to therapy and guide further management decisions

Imaging methods

  • MRI
    • often non-specific findings
    • multifocal T2  periventricular/subcortical hyperintensities in the white matter (mostly in frontoparietal regions, sometimes in basal ganglia, thalamus, and brainstem) Neuroborreliosis on MRI
    • lesions may be present in the corpus callosum (differential diagnosis of MS)
    • cranial nerve enhancement Facial nerve enhancement in neuroborreliosis   [Hildernbrand, 2009]
    • leptomeningeal enhancement
    • CNS vasculitis is manifested by an ischemic lesion on DWI + vasculitic pattern on MRA/CTA (irregularities of the vessel lumen with occlusion or segmental narrowing or dilatation)
  • CT – usually a normal finding in neuroborreliosis, ischemic lesions can occur in CNS vasculitis

Other tests

  • EMG, evoked potentials, EEG
  • Holter ECG, echocardiography
  • skin biopsy, etc.


  • neuroborreliosis is typically treated with antibiotics
    • the choice of antibiotic and duration of treatment depend on factors such as the severity of the symptoms, the stage of the infection, and the patient’s medical history
    • commonly used antibiotics include doxycycline, ceftriaxone, and penicillin
    • intravenous administration of antibiotics may be necessary for more severe cases or if the infection involves the central nervous system
  • if stroke due to CNS vasculitis is suspected, corticosteroids and antiplatelet therapy should be added
  • use treatment regimens from evidence-based guidelines established by medical societies specializing in infectious diseases or neurology

Post-Lyme disease syndrome (PLDS)

  • difficulties (fatigue, joint and muscle pain, cognitive impairment, paresthesia) persisting for > 6 months after standard treatment of neuroborreliosis
  • recurrent or persistent infection must be excluded
  • prolonged antibiotic therapy has no effect in PLDS

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Neuroborreliosis and stroke