1298 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY II 



Tremor 



In 1950 Magoun (169) reviewed existing informa- 

 tion concerning mechanisms active in the experi- 

 mental production of an alternating tremor of rest 

 comparable to the tremor of parkinsonians. While 

 additional information on the subject has become 

 available since that time, the nature of the disorder 

 underlying this rhythmically iterated movement is 

 still far from clear. 



The tremor occurs during resting tonus and disap- 

 pears during the initial phases of activity and during 

 sleep (169). Antagonistic muscles are reciprocally 

 excited, creating the typical alternating movement 

 at the rate of 6 to 10 cps. The tremor exhibits no 

 constant rate, however, and frequency may differ in 

 various localities where it appears. It does relate to 

 muscle tension as increases in amplitude can be 

 demonstrated in muscles subjected to passive stretch. 



Tremor of this type has been induced experimen- 

 tally by lesions placed in the ventral paramedian 

 tegmentum at the level of the red nucleus in monkeys 

 (211, 279, 282). When tiie lesion is unilateral, the 

 tremor is displayed principally on the opposite side of 

 the body (211, 279). A similar disturbance is some- 

 times seen following lesions placed in the region of the 

 cerebellar nuclei (211) and superior cerebellar pe- 

 duncle (50), although such tremors are prone to be 

 complicated by accompanying dysynergia (211, 282). 

 Yet Carrea (49) proposes that interference with 

 portions of the brachium conjunctivum be considered 

 the principal cause of these experimental tremors. 



Ward & Jenkner (129, 281) have elicited a tremor, 

 comparable to those induced by brain-stem lesions, 

 in monkeys by stimulating rather than destroying the 

 reticular formation. As this tremor is reduced by 

 administration of cholinergic drugs, they suggest that 

 tegmental lesions inducing tremor isolate cells in 

 the reticular formation from higher structures; the 

 tremor is due, then, to rhythmical facilitatory activity 

 generated in these cells rendered hyperexcitable by 

 sensitization of denervation (129). 



Whether or not the above-mentioned concept is 

 correct, many observations suggest that these induced 

 disturbances have their origin in disordered reticular 

 system function. It has been pointed out (282) that a 

 supraspinal origin is clearly indicated by the persist- 

 ence of tremor after posterior rhyzotomy (214) which 

 eliminates the stretch reflex. It is possible that this 

 suprasegmental influence can be conducted by way of 

 the pyramidal tract, presumaljly because of abnormal- 

 itv induced in re-entrant circuits which traverse 



reticulocerebellothalamic structures (47). Credence 

 must be given this possibility as it is well known that 

 surgical lesions of the pyramidal system (47, 221) 

 will stop the tremor as it paralyzes the involved 

 musculature. Surgical lesions made in the nucleus 

 ventralis lateralis of the thalamus, however, do not 

 paralyze musculature but do eliminate the tremor in 

 certain instances (108), whether by pyramidal or 

 extrapyramidal conduction is not known. 



Evidence suggests that rhythmic activity can be 

 elicited in spinal motor pools through facilitatory 

 reticulospinal pathways. Lloyd (163) showed that 

 reticulospinal volleys have a pronounced synchro- 

 nizing effect upon anterior horn cell discharge through 

 propriospinal collaterals. Also, Gernandt & Thulin 

 (97) showed that prolonged stimulation of the bulbar 

 reticular formation resulted in a curious waxing and 

 waning of the intensity of the monosynaptic reflex. 

 Similarly, Kleyntjens et al. (144) reported the produc- 

 tion of oscillations or fluctuations in reflex spike 

 amplitude following stimulation of the reticular forma- 

 tion, related possibly to a recrudescence of augmenta- 

 tion which followed cessation of a short facilitating 

 volley to the brain stem. 



Such cx'idence suggests that imbalance within the 

 reticular formation is capable of inducing abnormal 

 brain-stem discharge of a facilitating nature. It is 

 anatomically possible for this disturbance to issue 

 toward the motor neuron both through pyramidal 

 and through reticulospinal channels. Both systems, 

 together with segmental reflex activity, sum their 

 effects at the motor neuron to create the nidus for 

 movement. Apparently, however, reticulospinal 

 mechanisms alone, if distorted, can reproduce rhyth- 

 mic excitatory states at segmental levels and such 

 oscillations doubtless contribute to tremor. 



There is no information to explain directly why 

 the addition of surgical destructive lesions to the 

 basal ganglia or its outflows induces improvement 

 not only in the tremor but also in the spasticity of 

 parkinsonism (57, 188, 257). That it does so should 

 create a vigorous stimulus for amplified investigations 

 into tiie problem. (See Chapter XXXV in this 

 Handbook on extrapyramidal mechanisms.) 



./AUTONOMIC MECH.'VNISMS MEDI.ATED BY 

 RETICLIL.\R F0RM.\T10N 



While neural mechanisms implicated in the func- 

 tion of the autonomic nervous system will be discussed 

 in detail elsewhere in this work, particularly by 



