Background Neurological symptoms are common manifestation in acute COVID-19. This includes hyper- and hypokinetic movement disorders. Data on their outcome, however, is limited. Methods Cases with new-onset COVID-19-associated movement disorders were identified by searching the literature. Authors were contacted for outcome data which were reviewed and analyzed. Results Movement disorders began 12.6 days on average after the initial onset of COVID-19. 92% of patients required hospital admission (mean duration 23 days). In a fraction of patients (6 of 27; 22%; 4 males/2 females, mean age 66.8 years) the movement disorder (ataxia, myoclonus, tremor, parkinsonism) was still present after a follow-up period of 7.5 ± 3 weeks. Severe COVID-19 in general and development of encephalopathy were risk factors, albeit not strong predictors, for the persistence. Conclusions The prognosis of new-onset COVID-19-associated movement disorder appears to be generally good. The majority recovered without residual symptoms within several weeks or months. Permanent cases may be due to unmasking of a previous subclinical movement disorder or due to vascular/demyelinating damage. Given the relatively low response rate of one third only and the heterogeneity of mechanisms firm conclusions on the (long-term) outome cannot, however, be drawn.

Cerebrotendinous xanthomatosis is a rare and underreported lipid storage disorder caused by various mutations in theCYP27A1gene. Here, we report a novel homozygous mutation in theCYP27A1gene in an Indian family. A 30-year-old man presented with childhood cataracts in both eyes; recurrent, intractable watery diarrhea; progressive cognitive impairment; bilateral patellar and Achilles tendon xanthomas; and ataxic speech and gait. Out of five siblings, four had similar symptoms. Three of the patient's siblings had the same novel mutation in theCYP27A1gene on the chromosome 2 region with c.301delG (Pro102LeufsTer5 protein change), which was homozygous. To date, the variant status of this mutation has not been reported in the Human Gene Mutation Database, the Exome Aggregation Consortium, and 1000 Genomes Project. Despite the clinical confirmation of the diagnosis and molecular analysis, our patient's symptoms did not improve with treatment for more than a year, because of delayed presentation with irreversible damage. Treatment with chenodeoxycholic acid and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors can reduce or reverse the progression of the disease; however, early diagnosis is key.

No abstract

No abstract