Question: List chromosomes that have been linked to Arnold Chiari syndrome in the literature.

Context:
Consistent with a genetic hypothesis for CMI, much of the PF morphology was found to be heritable and multiple genomic regions were strongly implicated from OSA, including regions on Chromosomes 1 (LOD = 3.07, p = 3 × 10(-3) ) and 22 (LOD = 3.45, p = 6 × 10(-5) ) containing several candidates warranting further investigation.
Furthermore, we report the first case of documented Arnold-Chiari malformation type I and increased factor XIII activity associated with 6p trisomy. 
Of particular interest were two regions (Chr8, Max LOD = 3.04; Chr12, Max LOD = 2.09) identified within the subset of "CTD-negative" families, both of which harbor growth differentiation factors (GDF6, GDF3) implicated in the development of Klippel-Feil syndrome (KFS).
Moreover, the performed DNA analysis showed interstitial duplication in chromosome 5 (5q35.1). 
CGH microarray showed a approximately 520.7 kb microdeletion on 16p13.3 involving CREBBP, ADCY9, and SRL genes. 
Pentasomy 49,XXXXY associated with a Chiari type 1 malformation and cervical syrinx.
A 13-year-old with pentasomy 49,XXXXY and a Chiari type 1 malformation with an associated cervical syrinx is presented.
Phenotypic definition of Chiari type I malformation coupled with high-density SNP genome screen shows significant evidence for linkage to regions on chromosomes 9 and 15.
Two-point LOD scores on chromosome 15 reached 3.3 and multipoint scores in this region identified a 13 cM region with LOD scores over 1 (15q21.1-22.3). 
Multipoint LOD scores on chromosome 9 maximized at 3.05, identifying a 40 cM region with LOD scores over 1 (9q21.33-33.1) and a tighter region with multipoint LOD scores over 2 that was only 8.5 cM. 
In addition, this child had an Arnold-Chiari type I malformation that required surgical decompression. FISH studies using BAC clones spanning the 5q15 to 5q22 region revealed that these were all present in both homologues. 
The karyotype showed 46, XY, del(1)(q23q31.2). 
Karyotype analysis showed inversion of Y chromosome. 
The clinical features and morphological findings in 31 Japanese infants with trisomy 18 are presented. The majority were small-for-date infants. There was no sex predominance in our series, as opposed to male:female ratios of 1:3 reported in the literature. The average age at death was greater in females than in males. Cardiovascular anomalies were consistently present; ventricular septar defect and patent ductus arteriosus being the most common malformations. Various other internal malformations including the Arnold-Chiari malformation were observed.
An unusual heterotopia of striated skeletal muscle and glial tissue occurred in the pontine meninges of a stillborn male showing feature of trisomy 13 and an Arnold-Chiari malformation.
Type II Arnold-Chiari malformation with normal spine in trisomy 18.
A variety of anomalies of the central nervous system are observed in trisomy 18. The present case describes an infant having a type II Arnold-Chiari malformation without spina bifida. One previous case of an Arnold-Chiari malformation was reported in trisomy 18 but that infant also had a lumbar meningomyelocoele. 
Recently, a child was reported who presented with a 3p13-14.1 deletion of four genes, including FOXP1, and a constellation of deficits that included speech delay. In this study, we report the case of a patient with a single deletion of FOXP1. This patient presented with speech and motor developmental delays, a Chiari I malformation, and epileptiform discharges.

Answer: Chromosomes 1, 3, 5, 6, 8, 9, 12, 13, 15, 16, 18, 22, X and Y have been reported in association with Arnold Chiari syndrome in genetic linkage studies and individual case reports.
Exact answer: 1, 3, 5, 6, 8, 9, 12, 13, 15, 16, 18, 22, X, Y