Scrub typhus is one of the most frequent causes of acute febrile illness in South and South-east Asian countries. Neurological features accompany 20% of scrub typhus infections, and may affect the central or peripheral nervous system, and sometime, may even occur in combination. Of late, its recognition among clinicians has increased with widening detection of its cutaneous hallmark, called eschar. Multiple mechanisms underlie neurological involvement, including direct invasion (meningitis, encephalitis), vasculitis (myositis) or immune-mediated mechanisms (opsoclonus, myoclonus, optic neuritis, Guillain–Barre syndrome). Despite an immunological basis for several neurological manifestations, response to doxycycline is remarkable, although immune therapy may be necessary for severe involvement. Scientific literature on scrub typhus neurology chiefly emanates from case reports, case series and small studies, and a comprehensive review is warranted to aid clinicians in recognising neurological involvement. This review aims at enriching this gap, and summarises clinical features, laboratory findings, and treatment options for various neurological facets of scrub typhus.

We aimed to evaluate the efficacy of the modified Atkins diet in children with epileptic spasms who had failed hormonal therapy. Children aged 9 months to 3 years having daily epileptic spasms despite a trial of ACTH or oral prednisolone and 1 additional anticonvulsant medication were enrolled. Children were randomly assigned to receive the modified Atkins diet either immediately or after a delay of 4 weeks. The ongoing anticonvulsant medications were continued unchanged. The primary outcome variable was the proportion of children who achieved spasm freedom as per parental reports at 4 weeks. Secondary outcomes included time to spasm cessation, proportion of children with electroclinical remission, the proportion of children with >50% reduction of spasms at 4 weeks, and adverse effects of the diet. (ClinicalTrials.gov Identifier: NCT03807141). A total of 91 children were enrolled in the study; 46 in the diet group and 45 in the control group. At the end of 4 weeks, 11 children in the diet group were spasm free compared with none in the control group (P ≤ .001). The median time to achieve spasm cessation was 10 days (interquartile range 9-20). Nine of these had resolution of hypsarrhythmia on electroencephalography (EEG). Thirty (65.2%) in the diet group had >50% reduction in spasms, compared with none in the control group (P < .001). The most common side effect was constipation, noted in 34.8% of the children. The modified Atkins diet was found to be effective and well tolerated in children with epileptic spasms refractory to hormonal therapy.

In this systematic review, we aim to describe the association between temporal lobe epilepsy (TLE) and sleep, with bidirectional links in mechanisms and therapeutic aspects. Sleep stages may variably impact seizure occurrence, secondary generalization and the development, frequency and distribution of interictal epileptiform discharges. Conversely, epilepsy affects sleep micro- and macroarchitecture. TLE, the most frequent form of drug resistant epilepsy (DRE), shares an enduring relationship with sleep, with some intriguing potential mechanisms specific to anatomic localization, linking the two. Sleep characteristics of TLE may also inform localizing properties in persons with DRE, since seizures arising from the temporal lobe seem to be more common during wakefulness, compared to seizures of extratemporal origin. Polysomnographic studies indicate that persons with TLE may experience excessive daytime somnolence, disrupted sleep architecture, increased wake after sleep onset, frequent shifts in sleep stages, lower sleep efficiency, decreased rapid eye movement (REM) sleep, and possibly, increased incidence of sleep apnea. Limited literature suggests that effective epilepsy surgery may remedy many of these objective and subjective sleep-related concerns, via multipronged effects, apart from reduced seizure frequency. Additionally, sleep abnormalities also seem to influence memory, language and cognitive-executive function in both medically controlled and refractory TLE. Another aspect of the relationship pertains to anti-seizure medications (ASMs), which may contribute significantly to sleep characteristics and abnormalities in persons with TLE. Literature focused on specific aspects of TLE and sleep is limited, and heterogeneous. Future investigations are essential to understand the pathogenetic mechanisms linking sleep abnormalities on epilepsy outcomes in the important sub-population of TLE.