Pusher symptoms
| Classification according to ICD-10 | |
|---|---|
| R29.3 | Abnormal posture |
| ICD-10 online (WHO version 2019) | |
The pusher symptoms (also pusher syndrome or pressure symptoms , from English to push = to push) occur in strokes with hemiplegia . It was first described by the physiotherapist Patricia M. Davies in 1985. It is a perception disorder for the upright body position of the patient concerned.
Symptoms
The symptoms are characterized by an (objectively, apparently unfounded) fear of the patient concerned sitting or standing, about falling to the non- paralyzed side. The person concerned counteracts this feeling by actively pressing ( " pushing " ) with the non-paralyzed extremities to the paralyzed side (by supporting the arm with the elbow joint extended, as well as by spreading the legs with knee and hip extension). This leads to the lateral inclination of the longitudinal axis of the body to the paralyzed (paretic) side up to falling to the paretic side. Despite the objectively clear disturbance, the patient is not aware of the problem. The patient thinks he is sitting or standing upright.
A passive correction of the lateral bending by the examiner is opposed to active resistance (increased pressure). In the case of active actions of the non-paralyzed extremities, however, an interruption in pushing can be observed, as well as in the absence of a firm support surface or lack of contact with the ground.
Active pushing to the paretic side differentiates the pusher symptoms from a possible loss of balance with falling to the affected side of the body simply due to paralysis.
It is a separate phenomenon that is not caused by neglect or anosognosia .
frequency
About 10% of all stroke patients suffer from pusher symptoms. There is no correlation with other symptoms such as neglect, aphasia, or apraxia . There are also no differences in terms of age, gender or handedness (right-handed or left-handed). On the other hand, 73% of pusher patients also suffer from sensitivity disorders (compared to 10–15% of all stroke patients).
Contrary to expectations, there is no difference between right and left-sided strokes. An apparent increase in right-brain infarcts (2: 1 according to Brandt / Dichgans) is due to accompanying spatial-constructive disorders of the right parietal lobe, which have an intensifying effect on the pusher symptoms (so-called "chaos syndrome" after right-brain damage).
Pathogenesis
Under laboratory conditions where the possibility of pressing is eliminated (lateral support of the trunk, no contact with the floor, arms on thighs), the patient can use the visual control to see whether he is in an upright position. The patient is thus cognitively able to distinguish an oblique from a vertical position. However, he is unable to maintain constant correction by visual inspection. Without visual inspection on a seat that can be tilted to the side , he evaluates a position inclined by approx. 18 ° to the non- paralyzed side as vertical. The subjective postural vertical is thus shifted. In the dark, however, he can bring a light stick into a vertical position at any time. The subjective visual vertical is therefore intact. Since he can see an objectively upright position of his body when illuminated, the visual-vestibular information processing is also intact.
The subjective postural vertical is tilted despite an intact visual-vestibular system. The reason for this is another graviceptive center for determining the orientation of the body. ( Graviception = recognition of the earth vertical )
A contraversive pressure is apparently due to a disproportion between the disturbed postural and the intact visual-vestibular information. Unexpectedly, the patient experiences a loss of balance in a position in the subjective postural vertical (which is inclined by 18 ° to the non-paralyzed side), which he tries to compensate by pushing towards the paralyzed side.
Location of the damage in the brain
In affected patients, magnetic resonance imaging or computed tomography shows a maximum of the superimposition of the findings in the area of the posterolateral (posterior and lateral) thalamus , more precisely the following core areas of the thalamus:
- Nucleus ventralis posterolateralis (VPL),
- Nucleus ventralis posteromedialis (VPM),
- Posterior lateral nucleus (LP).
Included in this maximum is the adjacent rear leg of the internal capsule , which explains the simultaneous hemiparesis. The inclusion of the VPL and the VPM with their lemniscal tributaries explains the correlation with simultaneously existing sensory disorders.
In patients without thalamus involvement, it was found that cortical structures in the area of the islet cortex and the postcentral gyrus are apparently involved in postural graviception.
therapy
The treatment is physiotherapeutic and occupational therapy . Meaningful actions with the non-paralyzed extremities appear important in order to suppress the pushing. It is necessary to reduce the tone of the non- paralyzed side and to activate the hypotonic paralyzed side by means of trunk movements in combination with movements of the non-paretic extremities.
Ultimately, the goal is to endure the subjective feeling of crookedness. Furthermore, the visual control can be used to a greater extent, for example through feedback processes, to compensate for the disturbed postural information .
Impact and forecast
The pusher symptoms have a good prognosis. Follow-up examinations after six months show complete or extensive regression in almost all patients.
In terms of everyday skills and walking ability, the result of stroke rehabilitation is in principle not worse than in patients without pusher symptoms. However, this requires an inpatient stay that is twice as long (on average 3.6 weeks longer).
literature
- Hans-Otto Karnath , Peter Thier: Neuropsychology . 2nd Edition. Springer Verlag, Berlin 2006, ISBN 3-540-28448-6 . (The full text of the book chapter with images is freely available as .pdf (279 kB))
Individual evidence
- ↑ Patricia M. Davies: Steps To Follow. A guide to the treatment of adult hemiplegia. Springer, New York 1985, ISBN 0-387-13436-0 .
- ^ A b Hans-Otto Karnath , S. Ferber, Johannes Dichgans : The neural representation of postural control in humans. In: Proceedings of the National Academy of Sciences . Volume 97, number 25, December 2000, pp. 13931-13936, doi : 10.1073 / pnas.240279997 , PMID 11087818 , PMC 17678 (free full text).
- ↑ a b P. M. Pedersen, A. Wandel, HS Jorgensen, H. Nakayama, HO Raaschou, TS Olsen: Ipsilateral pushing in stroke: incidence, relation to neuropsychological symptoms, and impact on rehabilitation. The Copenhagen Stroke Study. In: Arch Phys Med Rehabil. 1996; 77, pp. 25-28 PMID 8554469
- ↑ Thomas Brandt, Johannes Dichgans , Hans-Christoph Diener : Therapy and course of neurological diseases. 5th edition. Kohlhammer Verlag , 2007, ISBN 978-3-17-019074-0 .
- ↑ L. Johannsen, D. Broetz, T. Naegele, Hans-Otto Karnath : "Pusher syndrome" following cortical laesions that spare the thalamus. In: J Neurol. 2006; 253, pp. 455-463. PMID 16435080
- ↑ Hans-Otto Karnath , L. Johannsen, D. Broetz, S. Ferber, Johannes Dichgans : Prognosis of contraversive pushing. In: J Neurol. 2002; 249, pp. 1250-1253 PMID 12242549 .
