The most common etiological hypotheses involve dysregulated immune responses targeting myelin antigens, molecular mimicry following viral infections, or persistent low‑grade infection. In experimental settings, chronic experimental autoimmune encephalomyelitis (EAE) serves as a model for studying the disease, while in humans, conditions such as chronic relapsing inflammatory demyelinating polyradiculopathy or progressive multiple sclerosis are considered clinical analogues.
Clinically, patients may present with a combination of motor weakness, sensory disturbances, visual deficits, bladder dysfunction, and cognitive changes. Symptoms typically evolve over months to years, with periods of relative stability interspersed with relapses. Examination often reveals upper motor neuron signs, sensory level abnormalities, and sometimes cranial nerve involvement.
Diagnostic work‑up includes magnetic resonance imaging showing multifocal, often periventricular, lesions with variable enhancement, and cerebrospinal fluid analysis demonstrating oligoclonal bands or mild pleocytosis. Exclusion of infectious, neoplastic, and metabolic causes is essential. Neurophysiological testing may aid in assessing functional impairment.
Management is primarily immunomodulatory, employing disease‑modifying agents such as interferon‑β, glatiramer acetate, or newer monoclonal antibodies that target B‑cells or specific cytokine pathways. Symptomatic treatment addresses spasticity, pain, and fatigue, while rehabilitation supports functional recovery. Early initiation of therapy is associated with slower disability progression.
Epidemiologically, chronic encephalomyelitkronisk is relatively rare, with prevalence estimates varying according to diagnostic criteria and geographic region. Ongoing research focuses on elucidating immunogenetic risk factors, biomarkers for disease activity, and the development of neuroprotective therapies aiming to preserve axonal integrity and improve long‑term outcomes.