A Sporadic Case of LGI1 Autoimmune Encephalitis Feigning as Basal Ganglia Stroke

LG1 encephalitis is an immune mediated neurological disorder effecting temporal lobe and basal ganglia. The classic clinical syndrome comprises of myoclonic jerks of the ipsilateral upper arms, facial twitching, memory disturbances, behavioral disturbances and hyponatremia. With its overarching symptoms, it does not snug perfectly with either seizure or movement disorder. The main pathological basis is mass production of anti-LG1 auto-antibodies which strike the LG1 protein in the neuronal milieu and presynaptic membrane. On grounds of this immune mediated onslaught, LG1 protein injury transpires and slowing of signal conduction at the synaptic interface never ensues. In patients with aforementioned symptoms, a high degree of clinical suspicion necessitate MRI brain imaging which shows T2 hyperintensity in basal ganglia, temporal lobe and frontal lobe. This can be corroborated with assessing LGI antibody levels in the blood and CSF to monitor disease progression as well as treatment response. As soon as diagnosis is confirmed, intravenous corticosteroids, intravenous immunoglobulins or plasma exchange will reverse the epileptic activity and cognitive dysfunction. Long term immunosuppressive therapy is warranted as it is inclined to reduce the onset of temporal lobe epilepsy and hippocampal atrophy. Regular follow up to detect new clinical symptoms and brain lesions is recommended in these patients to reduce morbidity and mortality.