Objective To assess the effectiveness and safety of melatonin in treating severe sleep problems in children with neurodevelopmental disorders.Design 12 week double masked randomised placebo controlled phase III trial.Setting 19 hospitals across England and Wales.Participants 146 children aged 3 years to 15 years 8 months were randomised. They had a range of neurological and developmental disorders and a severe sleep problem that had not responded to a standardised sleep behaviour advice booklet provided to parents four to six weeks before randomisation. A sleep problem was defined as the child not falling asleep within one hour of lights out or having less than six hours’ continuous sleep.Interventions Immediate release melatonin or matching placebo capsules administered 45 minutes before the child’s bedtime for a period of 12 weeks. All children started with a 0.5 mg capsule, which was increased through 2 mg, 6 mg, and 12 mg depending on their response to treatment.Main outcome measures Total sleep time at night after 12 weeks adjusted for baseline recorded in sleep diaries completed by the parent. Secondary outcomes included sleep onset latency, assessments of child behaviour, family functioning, and adverse events. Sleep was measured with diaries and actigraphy.Results Melatonin increased total sleep time by 22.4 minutes (95% confidence interval 0.5 to 44.3 minutes) measured by sleep diaries (n=110) and 13.3 (−15.5 to 42.2) measured by actigraphy (n=59). Melatonin reduced sleep onset latency measured by sleep diaries (−37.5 minutes, −55.3 to −19.7 minutes) and actigraphy (−45.3 minutes, −68.8 to −21.9 minutes) and was most effective for children with the longest sleep latency (P=0.009). Melatonin was associated with earlier waking times than placebo (29.9 minutes, 13.6 to 46.3 minutes). Child behaviour and family functioning outcomes showed some improvement and favoured use of melatonin. Adverse events were mild and similar between the two groups.Conclusions Children gained little additional sleep on melatonin; though they fell asleep significantly faster, waking times became earlier. Child behaviour and family functioning outcomes did not significantly improve. Melatonin was tolerable over this three month period. Comparisons with slow release melatonin preparations or melatonin analogues are required.Trial registration ISRCT No 05534585.

Painless idiopathic neuralgic amyotrophy after COVID-19 vaccination: A case reportOn December 11, 2020, the Food and Drug Administration issued an emergency use authorization of the Pfizer-BioNtech COVID-19 vaccine for coronavirus disease 2019 (COVID-19) infection prevention, consisting of two intramuscularly administered doses 21 days apart. 1 Large-scale placebo-controlled studies showed a 95% efficacy for COVID-19 infection prevention, with injection-site pain, fatigue, and headaches being commonly reported adverse events. 2 Although idiopathic neuralgic amyotrophy (INA) has been reported after COVID-19 infection, there are currently no published cases of INA occurring after COVID-19 vaccination. 3 A 35-year-old left-hand dominant woman presented with new-onset painless left-arm weakness, numbness, and paresthesias 9 days after receiving the Pfizer-BioNtech COVID-19 vaccine in the right deltoid. She had no history of neurologic diseases or allergies and denied recent trauma or infection. A detailed physical examination showed left upper extremity decreased antigravity strength in the deltoid, supraspinatus, biceps brachii, triceps brachii, extensor carpi radialis, extensor digitorum communis, extensor indicis proprius, flexor digitorum superficialis, and flexor digitorum profundus. Left-arm light touch sensation was decreased in the lateral antebrachial cutaneous (LAC), radial, and median nerve distributions. Hyporeflexia of the left biceps, brachioradialis, and triceps deep-tendon reflexes was present. Normal strength, sensation, and reflexes were present in the right upper extremity, without increased tone, fasciculations, or atrophy. She exhibited left medial scapular winging, with negative provocative tests for radiculopathy, musculoskeletal shoulder pathology, and peripheral nerve entrapment.Cervical spine computed tomography showed mild degenerative changes without foraminal narrowing. She was started on high-dose prednisone after neurology and physiatry evaluations, with paresthesia improvement and weakness stabilization within 1 week of medication initiation. Serologic evaluation including C-reactive protein, erythrocyte sedimentation rate, antinuclear antibody, rheumatoid factor, Lyme antibodies, and angiotensin-converting enzyme was negative. COVID-19 IgG and IgM antibodies were detected.The patient was reevaluated 6 weeks after symptom onset with significant strength improvement and resolved numbness and paresthesias. She underwent

There is emerging literature that coronavirus disease 2019 infections result in an increased incidence of thrombosis secondary to a prothrombotic state. Initial studies reported ischemic strokes primarily occurring in the critically ill coronavirus disease 2019 population. However, there have been reports of ischemic strokes as the presenting symptom in young noncritically ill coronavirus disease 2019 patients without significant risk factors. Further characterization of the coronavirus disease 2019 stroke population is needed. We present four cases of coronavirus disease 2019 ischemic strokes occurring in patients aged 37–68 yrs with varying coronavirus disease 2019 infection severities, premorbid risk factors, clinical presentations (eg, focal and nonfocal), and vascular distributions. These cases highlight the heterogeneity of coronavirus disease 2019 ischemic strokes. The duration of the coronavirus disease 2019–related prothrombotic state is unknown, and it is unclear whether patients are at risk for recurrent strokes. With more coronavirus disease 2019 patients recovering and being discharged to rehabilitation, physiatric awareness of this prothrombotic state and increased incidence of ischemic strokes is essential. Because of the variable presentation of coronavirus disease 2019 ischemic strokes, clinicians can consider neuroimaging as part of the evaluation in coronavirus disease 2019 patients with either acute focal or nonfocal neurologic symptoms. Additional studies are needed to clarify prothrombotic state duration, determine prognosis for recovery, and establish the physiatrist’s role in long-term disease management.

ObjectivesAntipsychotic-induced hypothermia is an uncommon type of secondary hypothermia resulting from neurotransmitter derangements within the nervous system thermoregulation pathway. The most common causative medications include olanzapine, haloperidol, and risperidone, with one published report of aripiprazole. Most individuals who develop antipsychotic-induced hypothermia receive neuroleptic treatment for psychiatric disorder management, with significantly fewer occurrences in those with neurologic disorders. There are currently no reports of antipsychotic-induced hypothermia after a traumatic brain injury (TBI), where antipsychotics are used for the off-label management of posttraumatic agitation.MethodsA retrospective chart review of the patient's medical record was performed.ResultsWe present a case of a 56-year-old man with a moderate TBI who developed recurrent episodes of antipsychotic-induced hypothermia after starting aripiprazole for posttraumatic agitation management.ConclusionsTo our knowledge, this is the first publication detailing antipsychotic-induced hypothermia occurring in a TBI patient. Clinicians who initiate antipsychotics for posttraumatic agitation in a TBI patient should be aware of this potential adverse effect, as well as clinical presentation, evaluation, and management strategies.