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Noradrenergic (NA) gating from the brainstem of the transmission of group II excitation (exerted pre- or post-synaptically) sketched in dashed green buy etodolac 400mg fast delivery. The double-headed horizontal dashed arrow indicates the lesion interrupting the descending projections quality etodolac 300 mg. Inanimalexperiments,such allows the selective assessment of motoneurone 562 Pathophysiology of movement disorders excitability in humans, and a change in the baseline (iv) When investigating the recovery cycle of the H excitability of motoneurones can only be inferred reflex (pp. Thisabnor- mality of the recovery cycle was taken as a sign Increased H reflex of increased motoneurone excitability (e. How- be explained by a change in transmission of the ever, it has been recently suggested that this afferent volley of the reflex. To do this requires elimi- apparentabnormalitywassimplyduetothefact nationof:(i)mechanismsactingontheIavolley(pre- that larger reflexes were used in the studies on synaptic inhibition of Ia terminals with PAD, post- spastic patients (Kagamihara et al. Hence, an duration and persistence was of the F wave are also increase in the Hmax/Mmax ratio by itself does not increased in patients with stroke (Milanov, 1992) establish increased motoneurone excitability. Sev- and spinal cord injury (Dressnandt, Auer & Con- eralmethodshavebeenproposedtoassesstheextent rad, 1995). However, these findings are not constant to which H reflexes are increased. Ithasbeen Sommerville & Ashby, 1978;Delwaide, 1985a, claimed that the F wave would provide a better mea- 1993;Yanagisawa et al. Because of the large interindividual the transmission of the afferent volley (Delwaide, variabilitydueinparttothedecreaseintheratio 1985a, 1993;Milanov & Georgiev, 1994). However, withage,thereisapoorcorrelationbetweenthis several factors limit the size of the F wave in spas- ratio and clinical spasticity. However, this fac- sensitivity of the F response to changes in motoneu- tor is correlated even less well with spasticity rone excitability is ten times less than that of the H than the Hmax/Mmax ratio (Angel & Hoffmann, reflex (see p. This ratio is increased motoneuronesthatcouldproduceanFresponse(see in stroke patients and may be better correlated pp. However, whether these changes reflect the upper motoneurone abnormality or the lower Plateau potentials motoneurone abnormality has not been clarified. In Motoneurones in reduced animal preparations can patients hemiparetic following a hemispheric stroke develop plateau potentials which amplify their thereisevidenceofadecreaseininwardrectification response to synaptic drive and can lead to peri- due to diminished activity of the hyperpolarisation- ods of sustained motor output. These changes occured in motor axons on spinal rats and may be an important factor in the the paretic side only. There is mounting evidence the findings for the two sides were compared and that plateau potentials can be induced in humans when the pathological side was compared with con- (see p. Plateau-like behaviour can be recorded trol data for healthy age-matched volunteers. In this respect, it is of interest that Conclusions the depression by baclofen of both spasticity and the H reflex has been ascribed to direct depression There are no methods to allow the assessment of motoneuronal excitability (Azouvi et al. Most experiments using the H reflex to inhibit plateau potentials in animals (Russo, Nagy have neglected to ensure that there were no asso- &Hounsgaard, 1998). One group reports that, if any- ciated changes in transmission in spinal pathways. However, this could have estimated, an increase in amplitude, duration and been due to a limitation of the technique of inducing persistence of the F wave in spastic patients might such behaviour, and the role of plateau potentials be a better argument in favour of motoneu- in spasticity remains to be clarified. To sum up, hyperexcitability chronic spinal rat, plateau potentials seem to play of motoneurones has never been demonstrated a significant role in spasticity (Bennett et al. Increased fusimotor activity If there were heightened fusimotor drive, particu- Changes in axonal excitability larly d, the response of primary endings to stretch Chronic changes in the excitability and activity of would be increased. As a result, the enhanced Ia dis- the motoneurone will lead to changes in the expres- charge would produce an increased stretch reflex sion of conductances and pumps on the motoneu- and exaggerated tendon jerks. As with the hyper- rone, and it is a reasonable assumption that there excitability of motoneurones (see above), that of 564 Pathophysiology of movement disorders d motoneurones might result from changes in their (ii)Doesincreasedfusimotordriveoccurinspastic intrinsic properties following their inactivation due patients? Vibration canproduceamoreintensespindledischargethanis everseeninhumansubjects,betheynormalorspas- Fusimotor overactivity as a cause of spasticity tic. Atmost,thevibrationwillproduceaTVRbutthat was a popular hypothesis in the 1960s can be readily controlled by normal subjects. Typi- This was primarily because of the superficial resem- cally spastic patients cannot control the TVR, and blance of human spasticity to decerebrate rigidity in this points to a defect in the control of spinal path- the cat, in which heightened fusimotor tonus con- ways in these patients. These arguments have been tributes to the exaggeration of the stretch reflex (see presentedelsewhere(Burke,1980,1983).