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Objective: This prospective study investigated the sensitivity of cone beam computed tomography (CBCT), a low dose technique recently made available for extremity examinations, in detecting scaphoid fractures. Magnetic resonance imaging (MRI) was used as gold standard for scaphoid fractures., Materials and Methods: A total of 95 patients with a clinically suspected scaphoid fracture were examined with radiography and CBCT in the acute setting. A negative CBCT exam was followed by an MRI within 2 weeks. When a scaphoid fracture was detected on MRI a new CBCT was performed., Results: Radiography depicted seven scaphoid fractures, all of which were also seen with CBCT. CBCT detected another four scaphoid fractures. With MRI another five scaphoid fractures were identified that were not seen with radiography or with CBCT. These were also not visible on the reexamination CBCT. Sensitivity for radiography was 44, 95 % confidence interval 21-69 %, and for CBCT 69 %, 95 % confidence interval 41-88 % (p = 0.12). Several non-scaphoid fractures in the carpal region were identified, radiography and CBCT depicted 7 and 34, respectively (p < 0.0001)., Conclusion: CBCT is a superior alternative to radiography, entailing more accurate diagnoses of carpal region fractures, and thereby requiring fewer follow-up MRI examinations. However, CBCT cannot be used to exclude scaphoid fractures, since MRI identified additional occult scaphoid fractures.

The first cases of early-onset progressive polyneuropathy appeared in the Alaskan Malamute population in Norway in the late 1970s. Affected dogs were of both sexes and were ambulatory paraparetic, progressing to non-ambulatory tetraparesis. On neurologic examination, affected dogs displayed predominantly laryngeal paresis, decreased postural reactions, decreased spinal reflexes and muscle atrophy. The disease was considered eradicated through breeding programmes but recently new cases have occurred in the Nordic countries and the USA. The N-myc downstream-regulated gene (NDRG1) is implicated in neuropathies with comparable symptoms or clinical signs both in humans and in Greyhound dogs. This gene was therefore considered a candidate gene for the polyneuropathy in Alaskan Malamutes. The coding sequence of the NDRG1 gene derived from one healthy and one affected Alaskan Malamute revealed a non-synonymous G>T mutation in exon 4 in the affected dog that causes a Gly98Val amino acid substitution. This substitution was categorized to be "probably damaging" to the protein function by PolyPhen2 (score: 1.000). Subsequently, 102 Alaskan Malamutes from the Nordic countries and the USA known to be either affected (n = 22), obligate carriers (n = 7) or healthy (n = 73) were genotyped for the SNP using TaqMan. All affected dogs had the T/T genotype, the obligate carriers had the G/T genotype and the healthy dogs had the G/G genotype except for 13 who had the G/T genotype. A protein alignment showed that residue 98 is conserved in mammals and also that the entire NDRG1 protein is highly conserved (94.7%) in mammals. We conclude that the G>T substitution is most likely the mutation that causes polyneuropathy in Alaskan Malamutes. Our characterization of a novel candidate causative mutation for polyneuropathy offers a new canine model that can provide further insight into pathobiology and therapy of human polyneuropathy. Furthermore, selection against this mutation can now be used to eliminate the disease in Alaskan Malamutes.