Musculoskeletal conditions

Glycogenosis (glycogen storage disease type IV)

Glycogen storage disease type IV of the Norwegian forest cat is an inherited abnormality of glucose metabolism. It is inherited as a simple autosomal recessive trait and can present in 2 types. By far the most common form is stillbirth or death within a few hours of birth. This probably results from the kittens having insufficient glucose to produce energy during the birth process and the first hours of life. On rare occasions, an affected kitten will survive the neonatal period and appear normal until 5 months of age. Though less common, this is the more devastating form of the disease because by this age new owners are attached to their kitten, and have to watch it go through months of neuromuscular degeneration. By 8 months of age, affected kittens have severe muscular weakness, atrophy and contractures, and inability to use their limbs. Affected cats may die suddenly from heart failure.

A DNA test is available for the diagnosis of affected kittens and the detection of carrier cats:
http://research.vet.upenn.edu/DiseaseInformation/BreedsbyDisease/tabid/2859/Default.aspx

Coates J R et al (1996) A case presentation and discussion of type IV glycogen storage disease in a Norwegian forest cat. Progress in Veterinary Neurology 7, 5-11
Fyfe JC et al (1992) Glycogen Storage Disease Type-IV - Inherited Deficiency of Branching Enzyme Activity in Cats. Pediatric Research 32:719-725.
Gashen F et al (2004) Congential diseases of feline muscle and neuromuscular junction. Journal of Feline Medicine and Surgery 6, 355 – 366

Cardiovascular Conditions

Hypertrophic cardiomyopathy (HCM)

An increased incidence of HCM has been reported in the Norwegian Forest cat, which may be due to an inherited gene defect.  However, to date, no specific defects have not been identified in this breed. 

See Screening scheme info on www.fabcats.org/hcm
Kittleson MD Feline Myocardial Disease, Textbook of Veterinary Internal Medicine. Editor:  Ettinger S.J, Feldman S.E., St Louis, Elsevier, 2000, pp 1082-1103