How does encephalitis present after a tick bite? - briefly
After a tick bite, encephalitis usually starts with sudden fever, intense headache, and neck stiffness, then advances to confusion, seizures, or focal neurological deficits. Laboratory analysis often shows lymphocytic pleocytosis and increased protein in the cerebrospinal fluid.
How does encephalitis present after a tick bite? - in detail
Encephalitis that follows a bite from an Ixodes tick typically emerges within a few days to several weeks after exposure. The initial phase often includes nonspecific systemic signs such as fever, headache, malaise, and myalgia. As the infection progresses, the central nervous system becomes involved, producing a characteristic constellation of neurological manifestations.
Early neurological symptoms
- Severe, throbbing headache that may be resistant to analgesics
- Photophobia and phonophobia
- Nausea and vomiting
Cognitive and behavioral changes
- Confusion or disorientation
- Impaired short‑term memory
- Agitation, irritability, or lethargy
Motor and sensory deficits
- Focal weakness, most commonly in the limbs contralateral to the affected brain region
- Ataxia and loss of coordination
- Paresthesias or hypoesthesia in a dermatomal distribution
Cranial nerve involvement
- Facial palsy (often unilateral)
- Diplopia due to ophthalmoplegia
- Dysphagia or dysarthria when bulbar nuclei are affected
Seizure activity
- Generalized tonic‑clonic seizures
- Focal seizures with or without secondary generalization
Autonomic disturbances
- Hypertension or tachycardia
- Sweating abnormalities
Diagnostic work‑up typically reveals lymphocytic pleocytosis in cerebrospinal fluid, elevated protein, and normal glucose levels. Polymerase chain reaction or serologic testing may identify tick‑borne pathogens such as Borrelia burgdorferi, Anaplasma phagocytophilum, or Babesia microti when co‑infection is present. Magnetic resonance imaging often shows hyperintense lesions on T2‑weighted and FLAIR sequences, frequently localized to the temporal lobes, basal ganglia, or brainstem.
Prognosis depends on rapid initiation of antimicrobial therapy and supportive care. Early administration of doxycycline, ceftriaxone, or combination regimens reduces morbidity. Persistent deficits may include memory impairment, chronic headache, or focal motor weakness. Regular follow‑up with neuropsychological assessment is recommended to monitor recovery.