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EMERGENCY:A person with new facial palsy, severe shooting arm or leg pains, and a history of tick exposure or a recent expanding red rash —call040-46324365immediately — 24 hours, 7 days— 24/7

NEUROINFECTIOUS DISORDERS & COMPLICATIONS

Lyme Neuroborreliosis in Hyderabad: Facial Palsy and Shooting Pains After a Tick Bite — Diagnosable, Treatable, Fully Reversible

Expert two-tier Lyme serology (ELISA + Western Blot), CSF evaluation with intrathecal antibody index, MRI brain and spine, and antibiotic treatment with IV ceftriaxone or oral doxycycline for facial palsy, Bannwarth syndrome radiculopathy, and Lyme meningitis at KIMS Neuroscience, Secunderabad, Hyderabad.

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Lyme neuroborreliosis (LNB) is neurological involvement in Lyme disease, caused by Borrelia burgdorferi (and related Borrelia species) transmitted by Ixodes tick bites. Lyme is endemic in temperate North America and Europe; cases in India are typically travel-related. Neurological manifestations occur in 10–15% of untreated Lyme. The classic presentation — Bannwarth syndrome — combines painful (often nocturnal) radiculopathy, facial palsy (commonly bilateral), and lymphocytic meningitis. Other presentations: cranial neuropathy (most often facial nerve), mononeuropathy multiplex, and rarely Lyme encephalitis or myelitis. Diagnosis uses a two-tier serology approach (ELISA then Western Blot); CSF antibody index (CSF:serum antibody ratio >1) confirms intrathecal antibody production. Treatment: doxycycline (oral) for facial palsy alone; IV ceftriaxone 2g/day for 14–28 days for Lyme meningitis, radiculopathy, or CNS disease. IgG remains positive lifelong after treatment (NOT a monitoring marker). PTLDS (post-treatment Lyme disease syndrome) does not respond to additional antibiotics.

Bannwarth syndrome = classic LNB triad: Nocturnal radicular pain (often severe, burning, worse at night) + facial palsy (often bilateral) + lymphocytic meningitis after a tick bite in an endemic area. The three together strongly suggest Lyme neuroborreliosis. Each can occur alone.
Bilateral facial palsy is the key clinical clue: 25–30% of Lyme facial palsy cases are bilateral — very rare in Bell's palsy. Any patient with bilateral facial palsy: think Lyme (also sarcoid, GBS, HIV). Tick exposure history is asked specifically.
Two-tier serology: Step 1: ELISA (sensitive but not specific) · Step 2: Western Blot to confirm a positive/equivocal ELISA · IgM in early disease; IgG in disseminated/late disease · CSF antibody index (CSF:serum) >1 = intrathecal production = confirms LNB
ELISA false negative window: First 2–4 weeks after infection: serology may be negative because antibodies have not yet developed. Clinical Lyme with classic features + tick exposure: treat empirically and repeat serology at 4–6 weeks if initial negative.
IgG stays reactive lifelong: Lyme IgG remains reactive lifelong after treatment. Cannot be used to monitor treatment success. Clinical resolution + normalising CSF (if LNB) = treatment success. Persistent IgG positivity is not treatment failure.
PTLDS — more antibiotics do not help: Post-Treatment Lyme Disease Syndrome: persistent fatigue, joint pains, cognitive symptoms in 10–20% after standard treatment. Multiple high-quality RCTs show additional antibiotics do NOT help and carry risks (line infection, C. difficile). Symptomatic management at KIMS.
Treatment: Doxycycline 200mg/day x 14–21 days (oral) for facial palsy alone or mild disease · IV ceftriaxone 2g/day x 14–28 days for Lyme meningitis, radiculopathy, or CNS Lyme · Bell's palsy alone but Lyme positive: oral doxycycline

Fact	Details
Pathogen + vector	Borrelia burgdorferi (and related Borrelia species) · Ixodes tick bite · Endemic in North America, Europe; sporadic in India · Travel history important
Bannwarth syndrome	Nocturnal radicular pain + facial palsy + lymphocytic meningitis · Classic LNB triad · Each component can occur alone
Bilateral facial palsy	25–30% of Lyme facial palsy is bilateral · Very rare in Bell's palsy · Bilateral facial palsy: think Lyme, sarcoid, GBS, HIV
Diagnosis	Two-tier serology: ELISA then Western Blot · CSF antibody index (CSF:serum) >1 confirms LNB · CSF lymphocytic pleocytosis + raised protein · ELISA false negative in first 2–4 weeks
Treatment	Doxycycline 200mg/day x 14–21 days (facial palsy alone, oral) · IV ceftriaxone 2g/day x 14–28 days (meningitis, radiculopathy, CNS) · Pregnant/lactating: ceftriaxone
Monitoring	Clinical resolution is the goal · CSF improvement (if LNB) by 3–6 months · IgG remains positive lifelong (NOT a treatment monitor) · Persistent IgG ≠ treatment failure
PTLDS	10–20% after treatment · Persistent fatigue, joint pains, cognitive symptoms · Multiple RCTs: more antibiotics do NOT help · Symptomatic management (physiotherapy, neuropsychological support)

About This Condition

Lyme Neuroborreliosis at a Glance

The essential facts that shape how Lyme neuroborreliosis is recognised, diagnosed, and managed at KIMS — from its transmission and Indian epidemiology, to the Bannwarth syndrome triad, two-tier serology, and the antibiotic regimens that produce complete recovery in most cases.

What it is

Lyme disease is a tick-borne bacterial infection caused by Borrelia burgdorferi, transmitted through the bite of Ixodes ticks (deer ticks). Neurological manifestations — collectively called Lyme neuroborreliosis (LNB) — occur in approximately 10–15% of untreated Lyme disease cases, typically weeks to months after the initial tick bite. LNB is the third most common manifestation of Lyme disease after the skin rash (erythema migrans) and joint involvement (Lyme arthritis).

Lyme disease in India

Lyme disease is not endemic across India in the way it is in North America or Europe, but it is reported. Cases have been documented in Himachal Pradesh, Uttarakhand, Jammu and Kashmir, and Rajasthan — regions with Ixodes tick populations. Cases in Hyderabad and other southern cities predominantly involve returning travellers from endemic areas (rural Europe, North America, parts of Central Asia) or from trekking and outdoor activity in the Indian Himalayan states. At KIMS, Lyme disease enters the differential diagnosis in any patient with unexplained facial palsy, painful radiculopathy, or lymphocytic meningitis with relevant exposure history.

The clinical triad of early LNB

The classic neurological triad of early Lyme neuroborreliosis (Bannwarth syndrome): (1) painful radiculopathy — severe, shooting, burning pains in the limbs or trunk, typically worse at night, often confused with disc prolapse; (2) facial palsy (cranial neuropathy — CN VII) — may be bilateral, which is uncommon in other causes; (3) lymphocytic meningitis — headache, neck stiffness, and mild fever with lymphocytic CSF pleocytosis. Not all three features need to be present simultaneously.

Diagnosis

Two-tier serology: ELISA for Borrelia antibodies (IgM and IgG) as the screening test; Western Blot (immunoblot) as the confirmatory test. A positive ELISA followed by a positive Western Blot is required for diagnosis. CSF analysis in LNB: lymphocytic pleocytosis, elevated protein, intrathecal Borrelia-specific antibody production (CSF:serum index). Serology can be falsely negative early in illness (within the first 2–4 weeks of infection) and may be equivocal in late disease.

Treatment

IV ceftriaxone 2g daily for 14–28 days for significant neurological involvement (meningitis, radiculopathy, facial palsy). Oral doxycycline 100mg twice daily for 14–28 days is equally effective for facial palsy and mild LNB in patients who can take oral medications. Oral amoxicillin is an alternative. The vast majority of LNB cases resolve completely with antibiotic treatment when diagnosed and treated promptly.

Appointment

040-44885000

About This Condition

The Face Drop That Was Not Bell's Palsy

A 38-year-old software engineer in Hyderabad returns from a 10-day trek in Himachal Pradesh. Three weeks later, he wakes with the right side of his face drooping. He cannot close his right eye completely, cannot smile symmetrically, and has difficulty eating. His GP diagnoses Bell's palsy and starts prednisolone.

Two weeks later, he attends KIMS because the prednisolone has not helped and he has developed severe shooting pains in his right arm and shoulder that are worst at night, waking him from sleep. He rates the pain 8/10. The pain is different from anything he has experienced — burning, electric, spreading down the arm in no particular nerve territory. He also has mild headache.

At KIMS, the clinical picture is re-examined. A facial palsy in a young person, following a trek in a forested hill area, combined with severe radicular pain and headache — this is the Bannwarth syndrome triad of Lyme neuroborreliosis. A careful history reveals he noticed a small tick attached to his leg on day 3 of the trek, removed it with his fingers. He did not notice a rash. Lyme serology is sent: ELISA is strongly positive for Borrelia IgG; Western Blot confirms bands at 23, 41, and 93 kDa. LP shows 84 lymphocytes, protein 0.9 g/L, with positive intrathecal Borrelia antibody index.

IV ceftriaxone 2g daily is started for 21 days. By day 14, the radicular pain has almost completely resolved. By week 6, the facial palsy has fully resolved. At his 3-month review, he is neurologically normal.

Book a Consultation

Speak directly with our Lyme neuroborreliosis specialist team — neurology, infectious diseases, and neuroradiology coordinated under one roof. Two-tier serology arranged for any suspicious presentation. No referral required. Monday to Saturday.

040-44885000Emergency: 040-46324365

Understanding the Disease

Stage-by-Stage Neurological Manifestations

Lyme disease evolves through three clinical stages with characteristic neurological involvement at each phase. The cards below summarise timing, clinical features, and the treatment approach used at KIMS for each stage.

Early localised (Stage 1)

Days to weeks after tick bite

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Erythema migrans (expanding red rash, often with central clearing — bull's-eye); flu-like illness.

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Neurological features absent or mild at this stage.

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Treatment: Oral doxycycline 100mg twice daily × 14–21 days.

Early disseminated (Stage 2)

1–8 weeks after bite

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Lyme neuroborreliosis begins here: lymphocytic meningitis; cranial neuropathies especially facial palsy (CN VII, often bilateral); painful radiculopathy (Bannwarth syndrome — severe shooting limb pain); less commonly encephalopathy.

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Heart: AV block (Lyme carditis) may occur in this stage.

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Treatment: IV ceftriaxone 2g/day × 14–28 days for neurological involvement; oral doxycycline for mild cases.

Late disseminated (Stage 3)

Months to years after infection

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Lyme arthritis (large joint, especially knee); encephalopathy (subtle cognitive problems, fatigue, poor concentration).

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Less commonly: progressive encephalomyelitis (rare, severe). May occur without recognisable earlier stages.

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Treatment: IV ceftriaxone 2g/day × 28 days; oral doxycycline for arthritis only.

Recognising Lyme Neuroborreliosis

The Key Neurological Features in Detail

The clinical profile of Lyme neuroborreliosis spans the recognisable cranial neuropathy of facial palsy, the painful nocturnal radiculopathy of Bannwarth syndrome, mild lymphocytic meningitis, the late encephalopathy and encephalomyelitis of untreated disease, and the important distinction of post-treatment Lyme disease syndrome — each of which is specifically assessed and managed at KIMS.

Facial palsy (CN VII) — the most recognisable sign

Peripheral facial palsy in Lyme disease is clinically identical to Bell's palsy: inability to close the eye, drooping of the mouth corner, loss of forehead wrinkle on the affected side. But several features should prompt Lyme serology in any facial palsy: (1) bilateral facial palsy — occurring in approximately 25–30% of LNB with facial involvement, which is extremely rare in Bell's palsy; (2) facial palsy occurring in the context of headache, neck stiffness, or limb pains; (3) exposure history — tick bite, outdoor activity in endemic areas, or travel to endemic regions. At KIMS, Lyme serology is sent routinely in any facial palsy with uncertain aetiology or with atypical features.

Bannwarth syndrome — the radiculopathy of Lyme

Severe, shooting, burning radicular pains affecting the limbs, shoulder girdle, or trunk, characteristically worse at night. The distribution does not always fit a single nerve root or dermatomal pattern — it is often multi-root, migrating, and intense enough to prevent sleep. It is the most common neurological feature of early LNB in European patients and is often misattributed to disc prolapse, cervical spondylosis, or neuropathic pain of other causes. The key distinction: onset in the context of a tick bite or rash history, often with mild CSF pleocytosis, and dramatic response to antibiotics within 1–2 weeks.

Lymphocytic meningitis — mild but important

Lyme meningitis presents as mild-to-moderate headache with neck stiffness, typically without the severity of bacterial meningitis. Fever, if present, is low-grade. CSF shows 100–200 lymphocytes, mildly elevated protein, and normal glucose. It is the CSF finding that most reliably prompts the Lyme diagnosis in a patient with unexplained lymphocytic meningitis after ruling out viral causes. At KIMS, Lyme serology is part of the unexplained lymphocytic meningitis panel.

Late neurological Lyme — encephalopathy and encephalomyelitis

A small proportion of patients with untreated or inadequately treated Lyme disease develop late neurological complications: subtle encephalopathy (cognitive slowing, memory difficulties, poor concentration, fatigue) or, rarely, an inflammatory encephalomyelitis with white matter changes on MRI resembling MS. These late manifestations are the most likely to present in India in patients who were bitten and infected abroad and received no treatment. Late Lyme encephalomyelitis responds to IV ceftriaxone but recovery is slower than early LNB.

"Post-treatment Lyme disease syndrome" — what it is and what it is not

Some patients continue to report fatigue, musculoskeletal pain, and cognitive difficulties for months to years after completing a full course of antibiotics for Lyme disease — a condition sometimes called Post-Treatment Lyme Disease Syndrome (PTLDS) or "chronic Lyme." The evidence from multiple controlled trials shows that prolonged further courses of antibiotics do not benefit these patients, and carry the risks of antibiotic resistance and serious complications. The symptoms likely reflect post-infectious immune dysregulation and require symptomatic management, not more antibiotics. At KIMS, this distinction is communicated clearly to patients with persistent symptoms after completed Lyme treatment.

Diagnosis at KIMS

Diagnosis at KIMS — Two-Tier Serology, CSF, MRI & Exposure History

Lyme neuroborreliosis diagnosis at KIMS combines two-tier serology (ELISA followed by Western Blot), CSF analysis with intrathecal Borrelia antibody index, MRI of brain and spine where indicated, and a careful exposure history — applied to the specific clinical picture of each presentation.

Two-tier serology — the standard diagnostic pathway

Step 1: ELISA for Borrelia burgdorferi IgM and IgG. If positive or equivocal: Step 2: Western Blot (immunoblot) for IgM (2+ of 3 specific bands) and IgG (5+ of 10 specific bands). Both tests positive = confirmed Lyme seropositivity. Important limitations: ELISA is negative in the first 2–4 weeks of infection (before antibodies develop) — do not exclude Lyme on a negative ELISA in the first month; a single test is not enough and repeat serology at 2–4 weeks later is indicated if clinical suspicion persists. At KIMS, Lyme serology is sent at specialist reference laboratories with established quality controls.

Lumbar puncture for CSF analysis

Indicated in any LNB patient with meningeal signs or significant neurological involvement. CSF: lymphocytic pleocytosis (typically 100–200 cells, predominantly lymphocytes); mildly raised protein; normal glucose. Intrathecal Borrelia-specific antibody production: calculating the CSF:serum Borrelia antibody index — a ratio above 1.3 (or the locally validated threshold) confirms intrathecal antibody synthesis and is evidence of active CNS Borrelia infection even when the serology is borderline. CSF culture for Borrelia is rarely positive and is not a routine test.

MRI brain and spine

MRI is arranged for LNB patients with encephalopathy, focal deficits, or progressive neurological deterioration. In early LNB (facial palsy, radiculopathy, meningitis): MRI is often normal or shows only meningeal enhancement. In late LNB: periventricular and white matter T2/FLAIR hyperintensities may be present, sometimes resembling MS. Gadolinium enhancement of cranial nerve roots (particularly CN VII in Lyme facial palsy) and nerve roots in the spine may be visible. MRI of the spine is arranged when radicular symptoms are prominent to exclude structural disc disease.

Exposure history — the most important part of the clinical assessment

A careful history of tick exposure is the foundation of LNB diagnosis. At KIMS: Was there a tick bite in the past 1–6 months? Did a red, expanding rash develop 3–30 days after the bite? Has the patient been in forested or grassy areas in India (Himalayan states, Western Ghats), Europe, North America, or Central Asia? The erythema migrans rash is pathognomonic of early Lyme disease and should be asked about specifically. Many patients do not notice the tick bite itself — Ixodes ticks are very small (2–3mm in the nymph stage).

Treatment

Treatment at KIMS — Antibiotics, Symptomatic Management & Monitoring Response

Antibiotic Treatment — Neurological Lyme

KIMS treatment protocol for Lyme neuroborreliosis

Significant neurological involvement (meningitis, radiculopathy, encephalopathy, encephalomyelitis): IV ceftriaxone 2g once daily for 14–28 days.

Facial palsy without meningitis or radiculopathy (mild LNB): Oral doxycycline 100mg twice daily for 14–28 days — equally effective and avoids IV access.

Alternative regimens: Oral amoxicillin 500mg three times daily for 14–28 days is an alternative for penicillin-tolerant patients who cannot take doxycycline (e.g., pregnancy). Longer courses beyond 28 days are not supported by evidence and are not prescribed at KIMS.

Symptomatic Management

Pain control, eye protection, fatigue rehabilitation

Radicular pain: Pregabalin 75–300mg/day or gabapentin 300–900mg three times daily during the antibiotic course, tapering as the antibiotics take effect (usually 1–2 weeks). NSAIDs for musculoskeletal pain.

Facial palsy: Eye protection is essential: lubricating eye drops hourly, eye ointment at night, and an eye patch at night to protect the cornea while the eyelid cannot close. Facial physiotherapy (neuromuscular re-education exercises). Most Lyme facial palsy resolves completely within 1–3 months of antibiotic treatment.

Post-treatment fatigue and cognitive symptoms: Graded exercise programme, sleep hygiene, treatment of co-morbid depression, and neuropsychological rehabilitation strategies. Not further antibiotics.

Monitoring Response

Clinical follow-up and serology interpretation

Follow-up at KIMS at 4–6 weeks after completing antibiotics and then at 3 months. The majority of LNB patients show clear clinical improvement within 4–6 weeks of starting treatment. Facial palsy recovery follows a longer timescale (1–3 months).

Serology: IgM antibodies usually decline and become negative within 6–12 months. IgG antibodies may remain positive for years after treatment and are not a marker of active infection — they should not be used to decide whether to re-treat.

Related Conditions

Lyme neuroborreliosis belongs to the family of infectious and post-infectious neurological disorders evaluated and managed at KIMS Neuroscience:

Neurocysticercosis Neuroinfectious Disorders & Complications (Master)

FAQs

Frequently Asked Questions

Yes — and this is exactly the clinical scenario that should prompt urgent Lyme serology at KIMS. You have the two hallmarks of Bannwarth syndrome (the neurological form of early Lyme disease): facial palsy and nocturnal radicular pain, occurring weeks after trekking in a forested Indian Himalayan state where Ixodes ticks are present. Even without a remembered tick bite or a bull's-eye rash — both of which can be absent — this presentation warrants two-tier Lyme serology and, if positive, an LP to assess for intrathecal Borrelia antibody production. Treatment with doxycycline or IV ceftriaxone, started now, will very likely produce complete resolution. Delay means the radiculopathy and facial palsy persist longer. Please call 040-44885000 urgently.

Bell's palsy (idiopathic peripheral facial palsy) and Lyme facial palsy are clinically identical — you cannot tell them apart from the appearance of the drooping face alone. The features that should prompt Lyme testing in any facial palsy: (1) recent tick exposure or travel to tick-endemic areas (forested regions of India, Europe, North America); (2) bilateral facial palsy — unusual in Bell's, occurs in 25–30% of Lyme facial palsy; (3) concurrent headache, neck stiffness, or limb pains; (4) onset during summer or autumn (peak tick season). If any of these features are present, Lyme serology should be sent before attributing the palsy to Bell's palsy. At KIMS, Lyme serology is sent for all facial palsies with any of the above features. Please call 040-44885000.

No — and this is one of the most important messages in Lyme disease management. What you describe is Post-Treatment Lyme Disease Syndrome (PTLDS) — persistent symptoms after a completed, adequate course of antibiotics. Multiple large, randomised controlled trials have shown that extending or repeating antibiotic courses does not improve these symptoms and carries significant risks (antibiotic resistance, serious side effects including Clostridium difficile colitis, and risks from prolonged IV access). The symptoms of PTLDS — fatigue, cognitive difficulties, and musculoskeletal pain — are real and disabling, but they appear to reflect post-infectious immune changes rather than ongoing active Borrelia infection. At KIMS, management focuses on graded exercise, cognitive rehabilitation, treatment of co-morbid depression or sleep disorder, and symptomatic relief — not further antibiotics. Please call 040-44885000 for a post-Lyme review.

No — particularly if you had the test within the first 2–4 weeks of possible infection. The ELISA test detects Borrelia antibodies, which the immune system takes 2–4 weeks to produce after infection. A negative ELISA in the first month of illness does not exclude Lyme disease. If your symptoms and exposure history are consistent with Lyme disease, the appropriate response is: (1) repeat the ELISA 2–4 weeks later; and (2) consider empirical treatment if the clinical picture is compelling and the risk of treatment is low. A negative ELISA 6–8 weeks after possible exposure, combined with a negative Western Blot, does effectively exclude Lyme disease. At KIMS, serological interpretation is always done in the context of the clinical history and exposure. Please call 040-44885000.

No — Lyme disease is not transmitted between people. It can only be acquired through the bite of an infected Ixodes tick. You cannot catch it from a family member, through sexual contact, through sharing food, or through any other person-to-person route. Your family members do not need Lyme testing unless they also had potential tick exposure in the same or another endemic area. If members of your family trekked in the same forested area, they should watch for the characteristic expanding red rash (erythema migrans) and any flu-like illness in the following weeks, and seek assessment if these develop. Tick prevention for future outdoor activities: light-coloured clothing (makes ticks easier to spot), insect repellent containing DEET, careful full-body skin checks after being in forested areas, and prompt removal of any ticks found. Please call 040-44885000 if you have concerns.

A drooping face after a tick bite. Shooting arm pains that wake you at night after a trek. A lymphocytic meningitis with no obvious cause.

Lyme neuroborreliosis responds completely to a course of doxycycline or IV ceftriaxone when diagnosed promptly. At KIMS Neuroscience, Secunderabad, Hyderabad, two-tier Lyme serology is arranged for any suspicious presentation, and treatment is started without delay when confirmed. Call 040-44885000 for a neurological assessment. Emergency: 040-46324365.

040-44885000

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