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ARTICLES: Hans-Otto Karnath, Leif Johannsen, Doris Broetz, and Wilhelm Küker Posterior thalamic hemorrhage induces "pusher syndrome" Neurology 2005; 64: 1014-1019 [Abstract] [Full text] [PDF]

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Posterior thalamic hemorrhage induces "pusher syndrome"

Jose C. Masdeu, and Philip B. Gorelick   (11 May 2005)

Reply to Masdeu et al

Hans-Otto Karnath, Leif Johannsen, Doris Broetz, and Wilhelm Küker   (11 May 2005)

Posterior thalamic hemorrhage induces "pusher syndrome" 11 May 2005
Jose C. Masdeu, University of Navarre Department of Neurology, CUN, Pamplona, Spain, and Philip B. Gorelick Send Correspondence to journal: Re: Posterior thalamic hemorrhage induces "pusher syndrome" masdeu{at}unav.es Jose C. Masdeu, et al.	We read with interest the paper by Karnath et al describing the thalamic localization of the “pusher syndrome.” [1] Their careful study of the disturbed perception of the orientation in space experienced by these patients may partially explain their loss of stability. Postural instability with thalamic lesions (thalamic astasia) was present in 15 patients we described. [2] We selected our patients differently, paying attention to the presence of instability and the lack of sufficient weakness to explain it. However, the localization of the lesions reported by Karnath et al as causing the pusher syndrome coincides remarkably with the localization of the lesions in our patients. In both cases the postero -lateral portion of the thalamus and the suprathalamic white matter were maximally involved. Our patients also tended to fall to the affected side of the body. Although Karnath et al focus on the contraversive behavior, they also mention a lack of stability in their patients. In five of them pushing behavior while standing could not be quantified due to a complete inability to reach a standing position at the time of study. From a practical clinical standpoint, the instability of these patients, which hampers walking and predisposes them to falls, could be even more relevant than the pushing behavior. In order to try to understand whether there is a tie between the pushing behavior and instability, we would appreciate having the authors’ observations on the following two aspects: Did any of their thalamic-lesioned patients not have the pusher syndrome and yet lacked stability? Were all the pushers unsteady? References 1. Karnath HO, Johannsen L, Broetz D, Kuker W. Posterior thalamic hemorrhage induces "pusher syndrome". Neurology. 2005;64:1014-9 2. Masdeu JC, Gorelick PB. Thalamic astasia: inability to stand after unilateral thalamic lesions. Ann Neurol. 1988;23:596-603.
Reply to Masdeu et al 11 May 2005
Hans-Otto Karnath, Center of Neurology, University of Tuebingen Hoppe-Seyler Str. 3, D-72076 Tuebingen, Germany, Leif Johannsen, Doris Broetz, and Wilhelm Küker Send Correspondence to journal: Re: Reply to Masdeu et al karnath{at}uni-tuebingen.de Hans-Otto Karnath, et al.	We thank Drs. Masdeu and Gorelick for their interest and comments on our recent article on the "pusher syndrome." [1] They ask the interesting question whether contraversive pushing describes the same behavioral disorder that they had observed following thalamic lesions and had termed 'thalamic astasia'. [2] We discussed this issue more extensively in a previous study. [3] In 15 patients with unilateral, predominantly posterolateral thalamic lesions, Masdeu and Gorelick [2] found an inability to stand unsupported. Eight of the patients "could not even sit up by themselves and had marked truncal instability, falling backward or to the affected side from a sitting position when left without support. Typically, when asked to sit up, rather than using the axial muscles, these patients would grasp the side rail of the bed with the unaffected hand or with both hands to pull themselves up". [2] This detailed description of the typical characteristis of 'thalamic astasia' allows us to conclude that Masdeu and Gorelick obviously observed a behavior different from contraversive pushing. When patients with pusher syndrome are asked to sit up, they never grasp something "with the unaffected hand or with both hands to pull themselves up". Pusher patients do exactly the opposite: they show pushing not pulling behavior. When at rest and also when asked to sit up, pusher patients extend the unaffected arm and use it to push away actively from the non-paretic side. Moreover, they use the non-paretic arm to resist actively against attempts of passive correction towards the earth-vertical upright orientation. This typical combination of behavioral symptoms has been termed the "pusher syndrome". [4] The reason for this behavior is a disturbed perception of body posture in relation to gravity. [5] The patients experience their body as oriented 'upright' when actually tilted to the side of the brain lesion. Following the definition of Davies, [4] our present study diagnosed pusher behavior when the stroke patients showed the following combination: contraversive tilt of their spontaneous posture while sitting or standing, plus active use (abduction and extension) of the non- paretic arm, leg, or both to bring about the pathological lateral tilt of the body axis, plus resistance to passive correction of tilted posture when the examiner attempted to move the tilted body axis to an upright position by shifting the weight toward the non-paretic side. To be classified as a pusher patient, a subject thus was required to show all of these three criteria. Subjects who were classified as patients without pushing behaviour did not show noticable symptoms with respect to these variables. [1] Beyond the different clinical behavior, a further difference between patients with pusher syndrome and those patients described by Masdeu and Gorelick [2] is the presence of hemiparesis. While patients with contraversive pushing typically also suffer from severe paresis of the contralateral arm and leg [1,3] those patients of Masdeu and Gorelick had only very mild or no motor weakness. Like those patients studied by Masdeu and Gorelick, patients with pusher syndrome show an overlap of lesion location in the posterior thalamus. [1,3] However, it is obvious that patients with pusher syndrome are clinically not identical with those described by them as their patients exhibited the opposite motor behavior and showed severe hemiparesis. Further clarification is needed to determine whether different lesion sites in the posterior thalamus may result in different clinical syndromes. References 1. Karnath H-O, Johannsen L, Broetz D, Küker W. Posterior thalamic hemorrhage induces "pusher syndrome". Neurology 2005; 64: 1014-1019. 2. Masdeu JC, Gorelick PB. Thalamic astasia: inability to stand after unilateral thalamic lesions. Ann Neurol 1988; 23: 596-603. 3. Karnath H-O, Ferber S, Dichgans J. The neural representation of postural control in humans. Proceedings of the National Academy of Sciences of the USA 2000; 97: 13931-13936. 4. Davies PM. Steps to follow. A guide to the treatment of adult hemiplegia. New York: Springer, 1985. 5. Karnath H-O, Ferber S, Dichgans J. The origin of contraversive pushing: evidence for a second graviceptive system in humans. Neurology 2000; 55: 1298-1304.