Spinal Complications of Lyme Disease (Tick-Borne Borreliosis)
Myelitis (inflammation of the spinal cord) acts as one of the rare but extremely serious neurological manifestations of tick-borne borreliosis. When the pathogen enters the central nervous system, the pathological process can affect various segments.
In addition to classic myelitis, the list of rare neurological manifestations of Lyme disease includes:
- Involvement of cauda equina structures.
- Development of polymyositis.
- Formation of chronic Lyme encephalopathy, which clinically manifests as pronounced general weakness and progressive cognitive impairment.
To establish a provisional diagnosis, the physician must take a medical history. Key factors include a history of tick bite, the presence of erythema migrans, and the onset of somatic or neurological disorders. In the early stage, oral antibiotics (penicillin, tetracycline, or erythromycin) are prescribed to prevent cardiac, articular, and neurological complications.
Diagnosis and Treatment of Borrelia Myelitis
If spinal cord inflammation and other neurological disorders have already developed, the definitive confirmation of the diagnosis is based on positive serological tests for Borrelia and mandatory cerebrospinal fluid (CSF) analysis.
CSF analysis reveals characteristic changes:
- Lymphocytic pleocytosis: cell counts may reach 3,000 per 1 mm³.
- Elevated protein level.
- Preservation of normal glucose levels.
Treatment of overt neurological disorders requires high-dose intravenous (IV) antibiotic therapy. The standard course lasts 2 weeks and includes penicillin (20 million IU daily) or ceftriaxone (2 g daily).
Meningovascular Syphilis and Spinal Cord Ischemic Stroke
A second example of a specific infectious spinal cord lesion is neurosyphilis. Treponema pallidum (Treponema pallidum) crosses the blood-brain barrier, provoking inflammation of the meninges and blood vessels and degeneration of neural tissue. Currently, meningovascular syphilis is diagnosed most frequently (in 1–2% of patients with secondary syphilis).
- Timeline: 5 to 30 years from the moment of infection.
- Risk group: young and middle-aged patients.
- Pathogenesis: inflammatory lesion (narrowing and occlusion) of predominantly medium-sized arteries.
- Complications: cerebral and spinal endarteritis can provoke an ischemic stroke of the spinal cord or brain.
Tabes Dorsalis
Tabes dorsalis is a form of parenchymatous neurosyphilis that has become rare in the antibiotic era (developing 5–50 years after infection).
Pathomorphologically, the process begins with inflammatory lymphocytic and plasma cell infiltration, followed by degeneration of:
- Posterior spinal roots;
- Posterior columns of the spinal cord.
Most commonly, the lesion is localized at the level of the thoracic and lumbosacral segments.
Clinical picture:
- Piercing pains and sensory ataxia.
- Reduction or complete loss of deep sensitivity modalities.
- Loss of knee and ankle reflexes.
- Argyll Robertson sign: sluggish or absent pupillary light reflex with preserved reaction to convergence and accommodation (along with altered pupil shape and anisocoria).
Other Forms of Neurosyphilis
Spinal pathology may be combined with other manifestations:
- Latent (asymptomatic) neurosyphilis: clinical symptoms are absent, the diagnosis is made based on CSF changes (pleocytosis, elevated protein, positive Wassermann reaction). It is treated in the same way as clinically overt forms.
- Acute syphilitic meningitis: occurs on average one year after infection, presenting with symptoms of typical acute serous meningitis.
- General paresis: chronic meningoencephalitis with meningeal thickening, cortical atrophy, and hydrocephalus. It manifests as progressive dementia, gait disturbance, and impaired pelvic sphincter control.
- Syphilitic gumma: completely mimics the clinical presentation of a space-occupying brain lesion (tumor).
Briefly: answers to topical questions
What is the pathogenesis of nervous system involvement in Lyme disease?
Autoimmune reactions and prolonged persistence of the pathogen play a leading role in the pathogenesis of nervous system involvement in Lyme disease. The main mechanisms include:
- Molecular mimicry — the presence of shared antigenic determinants between the 41 kDa flagellar antigen of Borrelia burgdorferi and human tissues (myelin fibers of peripheral nerves, nerve cells, and CNS axons).
- Chronic inflammation — caused by prolonged persistence of Borrelia in the body.
- Autoantibodies — in the acute phase of the disease, their concentration increases against denatured DNA, mitochondria, and extractable nuclear antigens.
What diseases are included in the differential diagnosis of transverse myelitis?
Differential diagnosis of transverse myelitis is carried out with multiple sclerosis, polyradiculitis, neuromyelitis optica (Devic's disease / NMO), and neurosarcoidosis.
- In multiple sclerosis, CSF analysis data are taken into account, including the presence or absence of oligoclonal bands, as well as the clinical course of the disease.
- In transverse spinal cord lesions, the bulbocavernosus reflex is preserved, which helps distinguish it from polyradiculitis, in which this reflex is typically absent.
- Neuromyelitis optica and neurosarcoidosis are differentiated taking into account the contrast-enhancement pattern on MRI.
What is the antibiotic therapy regimen for neurosyphilis?
The antibiotic therapy regimen for neurosyphilis includes intravenous administration of penicillin or cephalosporin antibiotics for a 14-day course. The following options are used:
- Drug of choice — Benzylpenicillin at a dose of 12–24 million IU/day IV.
- Alternative regimen — Ceftriaxone (a cephalosporin) 1 g 4 times a day.
This treatment course is identical for both clinically overt forms and latent (asymptomatic) neurosyphilis.
For quick memorization of the classical manifestations of Tabes dorsalis, use the rule of three 'A's: Ataxia (sensory), Areflexia (loss of knee and ankle reflexes), and Analgesia (loss of deep sensation).
Class and exam questions
How does the cerebrospinal fluid change in borrelial myelitis?
Cerebrospinal fluid analysis reveals lymphocytic pleocytosis (up to 3,000 cells per 1 mm³), elevated protein levels, while glucose concentration remains normal.
Which spinal cord structures are affected in tabes dorsalis?
Inflammatory infiltration and degeneration of the posterior roots and posterior columns of the spinal cord occur. The lesion is localized at the level of the thoracic and lumbosacral segments.
What is the Argyll Robertson sign?
This is the absence or sluggishness of the pupillary light reflex with preserved accommodation and convergence reactions. It is characteristic of tabes dorsalis and general paresis.
What is the treatment regimen for neurological complications of Lyme disease?
High-dose intravenous antibiotics are prescribed for 2 weeks: penicillin (20 million IU/day) or ceftriaxone (2 g/day).
What else to study on this topic
- Mechanisms of spinal cord ischemic stroke in endarteritis.
- Chronic Lyme encephalopathy: clinical features and diagnosis.
- Progressive paralysis: motor and psychiatric disorders.
- Optic neuritis in neurosyphilis.
- Syphilitic gumma of the brain in the differential diagnosis of tumors.
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Other topics in "Chapter 23. Infectious Diseases of the Nervous System"
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