They include the classical Huntingtons disease mimic or phenocopy syndromes, called Huntingtons disease-like syndrome types 1, 2 and 3; inherited prion disease, the spinocerebellar ataxias type 1, 3 and 17, neuroacanthocytosis, dentatorubral-pallidoluysian atrophy (DRPLA), brain iron accumulation disorders, Wilsons disease, benign hereditary chorea, Friedreichs ataxia, mitochondrial disease and Rett syndrome. Acquired causes
The most common acquired causes of chorea are cerebrovascular disease and, in the developing world, HIV infection—usually through its association with cryptococcal disease.Sydenhams chorea occurs as a complication of streptococcal infection. Twenty percent (20%) of children and adolescents with rheumatic fever develop Sydenhams chorea as a complication. It is increasingly rare, which may be partially due to penicillin, improved social conditions, and/or a natural reduction in the bacteria (Streptococcus) it has stemmed from. Psychological symptoms may precede or accompany this acquired chorea and may be relapsing and remitting. The broader spectrum of paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection can cause chorea and are collectively referred to as PANDAS.Chorea gravidarum refers to choreic symptoms that occur during pregnancy. If left untreated, the disease resolves in 30% of patients before delivery but, in the other 70%, it persists. The symptoms then progressively disappear in the next few days following the delivery.Chorea may also be caused by drugs (commonly levodopa, anti-convulsants and anti-psychotics).Other acquired causes include CSF leak, systemic lupus erythematosus, antiphospholipid syndrome,  kappa light-chain monoclonal gammopathy of undetermined significance, thyrotoxicosis, polycythaemia rubra vera, transmissible spongiform encephalopathies and coeliac disease. Treatment
There is no standard course of treatment for chorea.
Individuals with genu valgum have larger than normal Q-angles causing the weight-bearing line to fall lateral to the centre of the knee causing overstretching of the MCL and stressing the lateral meniscus and cartilages.The cause of pain and dysfunction often results from either abnormal forces (e.g. increased pull of the lateral quadriceps retinaculum with acute or chronic lateral PF subluxation/dislocation) or prolonged repetitive compressive or shearing forces (running or jumping) on the PF joint. The result is synovial irritation and inflammation and subchondral bony changes in the distal femur or patella known as "bone bruises". Secondary causes of PF Syndrome are fractures, internal knee derangement, osteoarthritis of the knee and bony tumors in or around the knee. Diagnosis
Examination
People can be observed standing and walking to determine patellar alignment. The Q-angle, lateral hypermobility, and J-sign are commonly used determined to determine patellar maltracking. The patellofemoral glide, tilt, and grind tests (Clarkes sign), when performed, can provide strong evidence for PFPS. Lastly, lateral instability can be assessed via the patellar apprehension test, which is deemed positive when there is pain or discomfort associated with lateral translation of the patella. Various clinical tests have been investigated for diagnostic accuracy. The Active Instability Test, knee pain during stair climbing, Clarkes test, pain with prolonged sitting, patellar inferior pole tilt, and pain during squatting have demonstrated the best accuracy. However, careful consideration is still needed when using these tests to make a differential diagnosis of PFPS.