Having a patient sit with their stronger side next to a wall and instructing them to lean towards the wall is an example of a possible treatment for pusher behaviour.A new (2003) physical therapy approach for patients with pusher syndrome suggests that the visual control of vertical upright orientation, which is undisturbed in these patients, is the central element of intervention in treatment. In sequential order, treatment is designed for patients to realize their altered perception of vertical, use visual aids for feedback about body orientation, learn the movements necessary to reach proper vertical position, and maintain vertical body position while performing other activities. Classification of pusher syndrome
Individuals who present with pusher syndrome or lateropulsion, as defined by Davies, vary in their degree and severity of this condition and therefore appropriate measures need to be implemented in order to evaluate the level of "pushing". There has been a shift towards early diagnosis and evaluation of functional status for individuals who have had a stroke and presenting with pusher syndrome in order to decrease the time spent as an in-patient at hospitals and promote the return to function as early as possible. Moreover, in order to assist therapists in the classification of pusher syndrome, specific scales have been developed with validity that coincides with the criteria set out by Davies definition of "pusher syndrome". In a study by Babyar et al., an examination of such scales helped determine the relevance, practical aspects and clinimetric properties of three specific scales existing today for lateropulsion.
For example, one study examined the retinal degeneration of SLOS, which in rats does not occur until at least one month after birth. Genetic models
Genetic models of SLOS are created by knocking out the DHCR7 gene. One study used homologous recombination to disrupt DCHR7 in mouse embryonic stem cells. Similar to what is found in humans, heterozygous mice (having only one mutated allele) were phentoypically normal, and were crossed to produce pups (young mice) homozygous for the mutated allele. Although these pups died within the first day of life due to their inability to feed, they showed characteristics similar to humans with SLOS. They had decreased levels of cholesterol, increased levels of 7- and 8DHC, showed less growth and smaller birth weights, had craniofacial malformations, and less movement. Many also had a cleft palate, and decreased neuronal responses to glutamate. Overall however, the pups had fewer dysmorphic features than human patients with SLOS; they did not present limb, renal, adrenal or central nervous system malformations. This is explained by the fact that in rodents, maternal cholesterol can cross the placenta, and actually appears to be essential for the development of the fetus. In humans, very little maternal cholesterol is transferred to the fetus. In sum, the genetic mouse model is helpful to explain the neuropathophysiology of SLOS. Discoveries
Many discoveries in SLOS research have been made using animal models. They have been used to study different treatment techniques, including the effectiveness of simvastatin therapy. Other studies have examined behavioural characteristics while attempting to explain their underlying pathogenesis.