Pusher Syndrome

Original Editor - Your name will be added here if you created the original content for this page.

Top Contributors - Kate Sampson, Sehriban Ozmen, Kirenga Bamurange Liliane, Kim Jackson, Lizzie Cotton, Admin, Claire Knott, Dinu Dixon, 127.0.0.1, Evan Thomas, Oyemi Sillo, Naomi O'Reilly and WikiSysop  

References

References will automatically be added here, see adding references tutorial.

What is it?

A unique presentation of abnormal body posture seen in approximately 5-10% of post-stroke patients (Pedersen et al 1996, Roller 2004). First described by Patricia Davis in 1985, ‘Pusher Syndrome’ is a term used to describe the behaviour of individuals using their non-paretic limb to push themselves towards their paretic side. Left unsupported, these patients demonstrate a loss in lateral posture, falling on to their paretic side (Santos-Pontelli et al 2011). Pusher Syndrome is often accompanied by severe inattention and hemisensory impairments (Davies 1985, Perrennou et al 2002).

What causes it?

Karnath et al (2000) demonstrated that patients with Pusher Syndrome have a misperception of their upright body posture; with patient’s reporting an “upright” posture when actually tilted 18 degrees to the ipsilesional side. With MRI scanning, the patients included in this study typically demonstrate left or right posterolateral thalamus damage post stroke; suggesting that this area is involved in our control of upright body posture (Karnath et al 2005).

Diagnosis

Karnath and Broetz (2003) identify three diagnostic factors of Pusher syndrome, as shown below.

1) Spontaneous body posture- (severe/moderate and mild).
The patient’s initial posture shown immediately after a positional change (ideally supine to sit/ sit to stand) must be assessed for contralateral tilting. This can be seen with or without falling to the side contralateral to the brain lesion. It is felt that patient’s must demonstrate this postural abnormality regularly to be classified as suffering with Pusher Syndrome.

2) Abduction and Extension of the Nonparetic Extremities-
Patients demonstrate abnormal positioning of the side ipsilateral to the brain lesion. Typically the hand will be abducted away from the body, the elbow held in extension and the hand searching for contact with a surface on which to push oneself to the perceived upright position. The lower limb may be abducted, with the knee and hip held in extension (as with the upper limb).

3) Resistance to Passive Correction of Tilted Posture-
Patients will typically actively resist against therapist’s manual interventions to correct their body posture. The patient’s extended upper and lower limbs will be used to push their weight towards their paretic side.

Subsequently, the Standardized Scale for Contraversive Pushing (SCP), has been formulated on these 3 deficits. The SCP is a useful tool for clinicians to classify Pusher Syndrome, and is quick and easy to apply in both an acute and rehabilitation setting (Karnath, Ferber, and, Dichgans 2000.)

Rehabilitation

Karnath and Broetz (2003) conclude that the first goal of initial rehabilitation is to provide visual feedback of the patient’s altered body posture. Patient’s with Pusher Syndrome typically demonstrate a retained ability to align the longitudinal axis vertically with the help of visual cues. Consequently, visual feedback may be utilised by the use of a mirror or by using ground-vertical structures- ie a therapist’s arm held upright to demonstrate true upright orientation, a line on a wall or a door frame.
Although patients with Pusher Syndrome may initially need prompting with the use of visual feedback it is hoped that, with regular therapy, patients are able to apply training procedures independently and utilise their environment for gaining visual feedback from vertical structures.

Prognosis

There are conflicting opinions in the literature with regards to the persistence of Pusher Syndrome in the longer term and its impact on functional outcome. Some authors report that the presence of Pusher Syndrome is rarely seen 6 months post stroke and is shown to have no negative impact upon patients’ ultimate functional outcome, although it has been shown to slow rehabilitation by up to 3 weeks (Karnath and Broetz 2003). However, a case study by Santos-Pontelli et al (2011) reported the lingering presence of Pusher Syndrome in 3 patients up to two years post-stroke, with profound negative impacts upon their functional abilities.

References

(Davies PM. Steps to Follow: A Guide to the Treatment of Adult Hemiplegia. New York, NY: Springer;1985)
(Karnath H-O, Johannsen L, Broetz D, et al. Prognosis of contraversive pushing. J Neurol.2002 ;249:1250–1253.
(Karnath HO and Broetz D. Understanding and Treating “Pusher Syndrome. Physical Therapy. 2003;83:12:1119-1125 )

(Karnath HO, Ferber S, Dichgans J. The Origin of Contraversive Pushing: Evidence for a Second Graviceptive System in Humans. Neurology. 2000;55:1298-1304)
(Karnath H-O, Ferber S, Dichgans J. The neural representation of postural control in humans. Proc Natl Acad Sci U S A.2000 ;97:13931–13936.)
(Karnath HO, Johannsen L, Broetz D, Kuker W. Posterior thalamic hemorrhage induces “pusher syndrome”. Neurology. 2005;64:1014–9)
(Pedersen PM, Wandel A, Jorgensen HS, et al. Ipsilateral pushing in stroke: incidence, relation to neuropsychological symptoms, and impact on rehabilitation—the Copenhagen stroke study. Arch Phys Med Rehabil.1996 ;77:25–28).
(Perennou DA, Amblard B, Laassel el M, et al. Understanding the pusher behavior of some stroke patients with
spatial deficits: a pilot study. Arch Phys Med Rehabil. 2002;83:570-575.)
(Roller M. The ‘Pusher Syndrome. Journal of Neurological Physical Therapy. 2004; 28 (1): 29-34)
(Santos-Pontelli TEG, Pontes-Neto OM, de Araujo DB, Santos AC, and Leite JP. Persistent pusher behavior after a stroke. Clinics (Sao Paulo). 2011; 66(12): 2169–2171.)