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Sunday, August 16, 2015

Pushing Syndrome in stroke patient

Managing Pushing syndrome after stroke
Bismillahirahmanirrahim ....

lets go for another topic that are related in stroke management , there are calling a pusher syndrome...

  • Pusher syndrome in patients post-stroke is characterized by leaning and active pushing toward the hemiplegic side with no compensation for the instability,  and resistance to passive correction toward midline.
  • require longer than average to reach independence in activities of daily living and ambulation 
  • present primarily in patients with right hemispheric lesions centered in the area of the posterolateral thalamus. 
  • misperceive body orientation in space, 18° tilted toward the ipsilesional side
  • Visual cues and cognitive strategies as potential rehabilitation tools for correction of body posture.

Patients with pusher syndrome tend to have profound functional limitation(self transfering, standing and gait.
Purpose of this review
    -characteristic of pusher syndrome in post-
     stroke pt
    -location of stroke lesion
    -cause of behavior disorder
    -discussion of physical therapy intervention

Characteristic of Patient with Pusher Syndrome
  • left hemiplegia (right brain lesion)
  • spatial and sensory neglect of the hemiplegic side(physical and environmental)
  • postural asymmetries
  • shift of body weight toward the hemi-plegic side with no attempt to support or compensate for the resultant imbalance 
  • no protective responses when active pushing leads to postural instability in sitting and standing
    Therefore at high risk for falls. 
  • In severe case, sensory impaired(tactile, proprioceptive, visual and auditory stimuli)
  • However, all 23 of the patients with contraversive pushing in the study by Karnath et al displayed severe paresis of both the upper and lower contralesional extremities
  • The severity of paresis of the hemiplegic extremities has not been shown to directly influence the presence of pushing or body orientation with respect to gravity while seated.

How to Distinguish?

  • Active pushing with the nonparetic extremities : distinguish patients with pusher syndrome from patients with thalamic astasia and lateropulsion in Wallenberg's syndrome.
  • When asked to sit up, patients with astasia typically grasp the side rail of the bed with the unaffected hand or with both hands and pull themselves up, rather than using the available power of the trunk.
  • While patients with pusher syndrome extend the unaffected arm and using it to actively push away from the nonparetic side.
  • Patients with Wallenberg’s syndrome display a tilt in subjective visual vertical but in pusher syndrome, it is intact.
  • The tendency of patients with Wallenberg's syndrome is to fall sideways toward the side of the lesion, compared to patients with pusher syndrome who fall to the side opposite the lesion.
  • Able to maintain correct head orientation toward vertical in the presence of severe lateral lean

  • helps to differentiate patients with cerebral lesions in the posterior insula('vestibular cortex,‘),experience a perceived tilt of the subjective visual vertical
Location of Stroke Lesion.
  1.  infarctions clearly centered on the posterolateral thalamus
  2.  including the ventral posterior nucleus, lateral posterior nucleus(which seems to be critical in control of upright posture) .( Karnath et al,2002)
  3.  In another study shows that thalamic and extra-thalamic lesion also can cause pusher syndrome
  4.   Different types of imaging technology used to determine the structural damage as well as malperfused but structural intact tissue.
  5. Study shows that thalamic lesions did not show a systematic involvement of dysfunctional brain areas in addition to the ones found to be structurally damage   And in extra-thalamic lesion, thalamus was neither structurally damaged nor malperfused 
  6.    However, abnormality seen in these areas in extra-thalamic lesion in pusher syndrome’s patient.(inferior frontal gyrus, middle temporal gyrus, inferior parietal lobule, and parietal white matter.)
  7. Thus, these extra-thalamic brain areas contribute to the network controlling upright body posture. (Luca Francesco Ticini, Uwe Klose Thomas Nägele and Hans-Otto Karnath, 2009)
Causes of Pusher Syndrome
  1. results from a high-order disruption in the processing of somesthetic information originating in the contrale-sional hemibody.suspected that this could be gravi-ceptive neglect.
  2. The patients perceive their body as oriented 'upright' when it is tilted an average of 18° to the ipsilesional side severe misperception of body orientation in relation to gravity
  3. Pushing is a response of patients' unexpected experience of loss of lateral balance when trying to get up and sit upright in a vertically oriented room.

Scale for Contraversive Pushing (SCP)
3 criteria
(1) posture: symmetry of spontaneous posture while sitting and standing,
(2) extension: the use of the ipsilesional arm or leg to extend the area of physical contact to the ground while sitting and standing, and
(3) resistance: resistance to passive correction of posture while sitting and standing.

  1. Some patients with pusher syndrome can 'learn' to balance in standing with their feet apart within a half-hour session.(Bohannon RW, 1996)
  2. appropriate positioning over their feet, practicing and feedback to patients, they can achieve a short duration of independent static standing
  3. 3 stage of practices:back against wall,without support, during movement .
  4. Karnath et al, 2000 and Perennou, 2002 noted that patients able to align body axis with the use of visual cues from environment.
  5. Using the upright orientation of surrounding objects and persons.
  6. However, it is temporary. Thus, visual input alone not suffice to continuously control upright posture.
  7. It may be an effective training tool when combined with conscious strategies for postural control.
  8. It is believed that applying TENS by activating various afferent nerve fibers in the neck
    convey stimuli to the contralateral cerebral hemisphere, unmasking the patients' latent postural capabilities.
  9. TENS as substitution stimulus to reactivates the damaged neural network devoted to body orientation with respect to gravity.
     and lower initial activities of daily living (ADL) function scores as measured by the Barthel Index
  10. subjects with pusher syndrome had more severe strokes as expressed by lower neurological scores on the Scandinavian Stroke Scale
  11. According to Pedersen and colleagues(1996), pushing should first diminish in the supine position, then in the sitting position, and finally in the standing position.However, no supportive evidence.
  12. Pusher syndrome was found to slow the recovery process post-stroke,requiring an average of 3.6 weeks (63%) longer to reach highest ADL function
  •  patients with pusher syndrome display a misperception of body orientation in space, believing that the upright position is approximately 18° tilted toward the ipsilesional side.
  • suspected that is the result of 'graviceptive neglect' of signals originating in the contralesional trunk and pelvis
  • Pushing may be an attempt to compensate for a mismatch between an intact perception of the visual vertical and an impaired perception of postural vertical
  • Visual cues and cognitive strategies can be rehabilitation tool
  • Slow recovery process has been found in patient with pusher syndrome
  • Longer than average to reach independence ADL and ambulation

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