Lyme disease (LD) and dizziness and hearing loss


Timothy C. Hain, MD Return to Index. • Page last modified: July 20, 2019

Main Points:

Both syphilis and Lyme disease are spirochete illnesses. While syphilis usually is spread through contact with infectious lesions or body fluids, Lyme is mainly spread through insect (tick) bites. See here for a discussion of otosyphilis.

Lyme is caused by species of the genus Borrelia (burgdorferi, garinii, and afzelii). Oddly, "Borrelia" is sometimes spelled "Borellia" as well. The ticks that spread Lyme, of the genus Ixodes, are mainly found in wooded areas, and thus Lyme disease is somewhat localized to particular parts of the country in the US. In Europe, Borrelia garinii is the species mainly associated with neurological disease.

Other tick-borne diseases include Bartonella, babesia, ehrlichiosis.


The CDC reports about 30,000 cases of Lyme in the USA per year, but estimates that the true incidence is higher. (Garcia-Monco and Benach, 2019) According to Chavda and Patel, in 2019 "The prevalence of LD is swiftly mounting in present scenario in many countries from species to species."

In France, Septfons et al (2019) report that: "From 2011 to 2016, the mean yearly incidence rate of LB cases was 53 per 100,000 inhabitants (95% CI: 41-65) ranging from 41 in 2011 to 84 per 100 000 in 2016. " In Belgium, Geebelen et al (2019) reported "Applying these ratios to the EM incidence in Belgium resulted in an incidence estimation of 2.4/100,000 inhabitants (95% UI 1.5-3.7) for Lyme neuroborreliosis, 2.1/100,000 (95% UI 1.7-2.6) for Lyme arthritis and 1.4/100,000 (95% UI 1.1-1.7) for other less frequent manifestations." So roughly an order of magnitude difference.

Gordillo-Perez et al (2018) reported that "Lyme neuroborreliosis is a frequent condition in patients with neurological diseases in Mexico."


The clinical course of Lyme begins with a skin lesion (erythema migrans), several days after a tick bite. After this, neurological, cardiac, chronic skin, or joint involvement develops. Similar to the situation with syphilis, Lyme is divided into several stages -- an acute localized one, with later dissemination divided into early and late stages.

In the late stage (months to years), there may be chronic encephalomyelitis. Patients present with spastic paraparesis, ataxia, cranial nerve palsies such as facial weakness and deafness, bladder dysfunction, and cognitive impairment.

According to Garcia-Monco (2019), the most common clinical presentations are painful radiculitis, cranial palsy (43.4%; mostly facial), and headache. Thus these are symptoms primarily of nerve damage. In the US, lymphocytic meningitis is the most common and single early manifestation. Headache is the main complaint.


Sporadic case reports associate Lyme infections with sudden hearing loss, autoimmune inner ear disease, and bilateral vestibular loss. It seems likely that the damage of Lyme to the ear is through injury to the eighth nerve, rather than through damage to hair cells or inflammation within the inner ear.

Sowula et al (2018) reported that otological symptoms occurred frequently in tick-borne diseases. They reported in patient's with Lyme in Poland, "The most common complaint was tinnitus (76,5%) accompanied by vertigo and dizziness (53,7%), headache (39%), unilateral sensorineural hearing loss (16,7%). The patients also had tick-borne coinfections, among them the most common was Bartonella henselae (33,4%) and Bartonella quintana (13%)." Others have reported hearing loss accompanied by cochlear inflammation and polyneuritis (Ewers, 2015), as well as isolated sudden hearing loss (Espiney Amaro et al, 2015; Peeters et al, 2013). According to Bakker et al (2012), "Neuroborreliosis seems to be a rare cause of sudden SHL, and routine screening of patients for borrelia antibodies in serum should therefore not be recommended."

While it has been suggested that Lyme can cause vestibular loss, the evidence is slight. In areas where Lyme is endemic, positive blood tests for Lyme can wrongly be used to infer that Lyme caused vestibular loss. (Vos, 2016) When vestibular loss occurs, it is presumably from vestibular nerve radiculopathy (Farshad-Amacker et al, 2013).

Rare findings are infectious vasculitis, including for example, MRI enhancement of the basilar artery.



CSF studies may show lymphocytic mononuclear cell pleocytosis, sometimes with B burgdorferi specific oligoclonal bands as well as intrathecal synthesis of specific antibodies.

Lyme with CNS involvement requires demonstration of an inflammatory CSF as well as intrathecal synthesis of antibodies to B. Burgdorferi.

In endemic areas, the prevalence of antibodies may be high, and it may be difficult to prove that there is active Lyme vs. an old exposure.

Diagnosis of infection with B. Burgdorferi typically is done by a two-tiered approach. There is first ELISA positivity, followed by at least 2 of 3 signature bands on an immunoblot for IgM cases, and 5 of 10 cases for a positive IgG. A negative result early on does not rule out infection, and sensitivity improves with development of disseminated disease.

Intrathecal antibody production is considered a gold standard for the diagnosis of CNS infection in Europe. This can persist for a long time after successful treatment.



When treated within the first 4 weeks of infection, the vast majority of patients improve significantly. Most symptoms resolve spontaneously in 5-6 months without therapy. According to a panel of the AAN, LNB can be treated in both adults and children with intravenous penicillin, ceftriaxone, or cefotaxime.

European studies support use of doxycycline for adults with meningitis or nerve damage, and reserve intravenous regiments for patients with more severe neurological involvement. (Rauer et al, 2018)

It is controversial whether or not chronic CNS involvement of Lyme is responsive to antibiotics. According to Garcia-Monco, several controlled studies report comparable frequency of treated and untreated patients. This opinion is also held by Halperin (2019) who stated "Whether post treatment Lyme disease symptom (PTLDS) is an actual entity, or reflects anchoring bias when commonly occurring symptoms arise in patients previously treated for Lyme disease, remains to be determined. Regardless, these symptoms do not reflect CNS infection and do not respond to additional antimicrobial therapy."

Lyme disease involving the nervous system does not appear to be especially disabling. According to Obel et al (2018), "A verified diagnosis of Lyme neuroborreliosis had no substantial effect on long term survival, health, or educational/social functioning."