The association of gegenhalten in the upper limbs with dyspraxia.

Abstract

SUMMARY Ten patients with gegenhalten of the upper limb of mixed aetiology were studied, in nine of whom an association with dyspraxia was found. In four of the patients, the rigidity became more pronounced after the instruction to relax, and only one patient showed improvement after this instruction. In these patients, the resistance to movement, evident as gegenhalten, may be a direct consequence of the dyspraxia.Gegenhalten' and paratonic rigidity2 are terms used to describe an increase in muscle tone which occurs in response to passive movement, and which is proportional in degree to the stimulus applied. It is seen most commonly in the legs, but in some instances we have observed gegenhalten in the upper rather than the lower limbs in patients with dyspraxia. This observation, and the fact that gegenhalten is often exacerbated by the verbal command to relax, led to the investigation of the association between gegenhalten and dyspraxia. MethodsTen successive patients with gegenhalten of the upper limbs were assessed for dyspraxia. Patients who were unable to understand simple commands (that is, who were unable to respond appropriately to a command such as "clench your left fist") were excluded from the study, as were patients on psychotropic medication. Gegenhalten was defined as a rigidity of the limb detected on passive movement, occurring in the absence of cogwheeling or a spastic catch, that was not exacerbated by movement in the contralateral fist. Movements tested were wrist flexion and extension, forearm pronation and supination, elbow flexion and extension, flexion and extension of the knee, and rotation at the hip. Each movement was performed five times by the examiner, initially with no instruction to the patient. Elbow and knee flexion/extension were then repeated in turn, initially while the patient was opening and closing the contralateral fist, again while counting backwards from 10, and then after the instruction to relax. The limb placement manoeuvre was also assessed, because this has been used by others as a test for paratonia.34 The examiner held up the subject's arm and told him to relax, letting the examiner take the weight; the examiner then dropped his hands. The subject's arm should fall at the same time, and any delay in dropping of the arm was considered abnormal.3 Any patient with limb weakness, brisk reflexes, extensor plantar responses, or spastic catch or cogwheeling was excluded from the study. Dyspraxia was assessed on the basis of inability to copy gestures and commands,5 despite apparently normal coordination, sensation and power, in the upper and lower limbs, and orofacial muscles.The following movements were assessed.(1) Upper limb: Copying gestures: (with each hand in turn).

Progressive frontal gait disturbance with atypical Alzheimer's disease and corticobasal degeneration

“…Increased muscle tone was apparent later, particularly in the legs, at the time of the development of upper limb apraxia. It was thought, however, that this had the characteristics of Gegenhalten which may be found in association with dyspraxia 20. There were no cerebellar signs, prominent extrapyramidal features, or pyramidal signs.…”

Paratonia in Dementia: A Systematic Review

“…Three studies [ 23, 24, 38 ] expanded this description with that resistance occurs in the absence of cogwheeling or a spastic catch. Tyrrell and Rossor [ 38 ] supplemented this with that the resistance is not exacerbated by movement in the contralateral fist. Three studies [ 21, 33, 38 ] describe the limb placement maneuver, whereby the examiner passively lifts the patient’s arm with the instruction to relax.…”

Diagnosing paratonia in the demented elderly: reliability and validity of the Paratonia Assessment Instrument (PAI)

“…It has been suggested that patients who develop paratonia represent a subtype of Alzheimer's disease (AD) with a more rapid decline (Gladstone and Black, 2002), and that the presence of paratonia might be a marker for executive and planning impairments (Bennett et al, 2002). Unfortunately, definitions of paratonia used in the various published studies lack consistency and are, in some respects, even contradictory (Dupré, 1910;Kleist, 1927;Paulson and Gottlieb, 1968;Middelveld-Jacobs and Van den Boogerd, 1986;Tyrrell and Rossor, 1988;Franssen et al, 1993;Souren et al, 1997;Beversdorf and Heilman, 1998;Gladstone and Black, 2002). Unfortunately, definitions of paratonia used in the various published studies lack consistency and are, in some respects, even contradictory (Dupré, 1910;Kleist, 1927;Paulson and Gottlieb, 1968;Middelveld-Jacobs and Van den Boogerd, 1986;Tyrrell and Rossor, 1988;Franssen et al, 1993;Souren et al, 1997;Beversdorf and Heilman, 1998;Gladstone and Black, 2002).…”

“…Furthermore, it is hypothesized that the general decline of propriocepsis and exterocepsis invokes sensory deprivation, thus furthering the development of paratonia (Van de Rakt, 1997). Unfortunately, definitions of paratonia used in the various published studies lack consistency and are, in some respects, even contradictory (Dupré, 1910; Kleist, 1927; Paulson and Gottlieb, 1968; Middelveld-Jacobs and Van den Boogerd, 1986; Tyrrell and Rossor, 1988; Franssen et al ., 1993; Souren et al ., 1997; Beversdorf and Heilman, 1998; Gladstone and Black, 2002). Making clinical distinctions between paratonia, parkinsonian rigidity, and spasticity after stroke is therefore difficult.…”