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Muscle spindle activity in motor disorders
$3 M i MICRONEUROGRAPHICSTUDY OF VESICO-SYMPATHETICREFLEXES IN SPINAL CORD INJURIED MAN BLUMBERG, H.*, STJERNBERG, L . * * , WALLIN, B.G.**~ *Department of Neurology, U n i v e r s i t y of Freiburg, 7800 Freiburg, FRG~ **Dept. of C l i n i c a l Neurophysiology, U n i v e r s i t y of Uppsala, S-75185 Uppsala, Sweden In para- or t e t r a p l e g i c patients distension of the urinary bladder sometimes evokes blood pressure increase, headache and excessive sweating. To i n v e s t i g a t e the e f f e c t of bladder s t i m u l a t i o n on sympathetic outflow in such patients recordings of muscle (MSA) and skin (SSA) sympathetic a c t i v i t y were made in 10 patients with complete spinal cord lesions (C6-Th8). Skin vasomotor a c t i v i t y was recorded by a photoelectric pulse plethysmogram from the f o o t . Stimulation of bladder afferents by pressure on the abdominal wall over the bladder or by f i l l i n g the bladder with CO2 e l i c i t e d short l a s t i n g sympathetic discharges in both skin and muscle nerves. Simultaneous recordings of MSA and SSA showed that the stimuli activated both sympathetic populations at the same time. The neural a c t i v i t y was followed by skin vasoconstriction l a s t i n g up to i - 2 min. In healthy man, MSA usually is not influenced by bladder stimulation and the stimulus does not cause long vasoconstriction. The results show that bladder s t i m u l i give r i s e to spinal sympathetic reflexes both in skin and muscle nerve. This coactivation together with the long duration of skin vasoconstriction may c o n t r i b u t e to a blood pressure increase.
M2
MUSCLESPINDLE ACTIVITY IN MOTORDISORDERS
BURKE D~ Unit of C l i n i c a l Neurophysiology, The Prince Henry Hospital, Sydney 2036, N.S.W.~ A u s t r a l i a Muscle spindles provide an essential a f f e r e n t input f o r stretch reflexes, but i t is not clear what r o l e , i f any, the fusimotor system plays in producing the abnormalities of tendon jerks and muscle tone seen in cerebellar disease, shock syndromes, Parkinsonian r i g i d i t y or s p a s t i c i t y . Previous studies suggesting a causal role were based l a r g e l y on " s e l e c t i v e " , fusimotor blocks with local anaesthetic or on comparisons of the tendon jerk and the H reflex.However recent studies have shown that the tendon jerk is not dependent on background fusimotor drive and that the mechanisms of the tendon jerk d i f f e r g r e a t l y from those of the H r e f l e x . The v a l i d i t y of the evidence implicating the fusimotor system in disorders of stretch r e f l e x a c t i v i t y can therefore be questioned. Recordings from human spindle afferents indicate that fusimotor hypofunction cannot be responsible f o r the hyporeflexia of shock syndromes and cerebellar disease. An excessive spindle input cannot, by i t s e l f , produce r i g i d i t y of s p a s t i c i t y . Fusimotor a c t i v i t y may accompany r i g i d i t y but does not cause i t . Current evidence is against fusimotor o v e r a c t i v i t y in spastic patients at r e s t , though the s i t u a t i o n could be d i f f e r e n t during movement, and i t is possible that fusimotor neurones are activated by cutaneous afferents as part of a f l e x o r spasm.
M2
MUSCLESPINDLE ACTIVITY IN MOTORDISORDERS
BURKE D~ Unit of C l i n i c a l Neurophysiology, The Prince Henry Hospital, Sydney 2036, N.S.W.~ A u s t r a l i a Muscle spindles provide an essential a f f e r e n t input f o r stretch reflexes, but i t is not clear what r o l e , i f any, the fusimotor system plays in producing the abnormalities of tendon jerks and muscle tone seen in cerebellar disease, shock syndromes, Parkinsonian r i g i d i t y or s p a s t i c i t y . Previous studies suggesting a causal role were based l a r g e l y on " s e l e c t i v e " , fusimotor blocks with local anaesthetic or on comparisons of the tendon jerk and the H reflex.However recent studies have shown that the tendon jerk is not dependent on background fusimotor drive and that the mechanisms of the tendon jerk d i f f e r g r e a t l y from those of the H r e f l e x . The v a l i d i t y of the evidence implicating the fusimotor system in disorders of stretch r e f l e x a c t i v i t y can therefore be questioned. Recordings from human spindle afferents indicate that fusimotor hypofunction cannot be responsible f o r the hyporeflexia of shock syndromes and cerebellar disease. An excessive spindle input cannot, by i t s e l f , produce r i g i d i t y of s p a s t i c i t y . Fusimotor a c t i v i t y may accompany r i g i d i t y but does not cause i t . Current evidence is against fusimotor o v e r a c t i v i t y in spastic patients at r e s t , though the s i t u a t i o n could be d i f f e r e n t during movement, and i t is possible that fusimotor neurones are activated by cutaneous afferents as part of a f l e x o r spasm.