THE GENERAL PRINCIPLES OF MOTOR INTEGRATION 



783 



Spinal Shock 



The nature of spinal shock, the depression that 

 precedes recovery of spinal reflexes in the chronic 

 spinal state, is still obscure. It does not affect reflex 

 mechanisms rostral to the transection. Stimulation of 

 a large pathway such as the pyramidal tract still 

 provokes motor discharge. With facilitation by 

 strychnine the fle.xor and tendon reflexes can still be 

 obtained in the period of spinal shock. The motor 

 neurons preserve a natural histologic appearance. 

 The process of recovery of reflexes is a progressive 

 lowering of threshold, and spinal shock may there- 

 fore be regarded as a raised threshold of spinal 

 reflexes of unknown cause. It is observed at all levels 

 of transection caudal to the midpontine le\el, above 

 which a transection of the brain stem is followed 

 immediately by the selective heightening of reflexes 

 called decerebrate rigidity. The assimiption is there- 

 fore made that some mechanism in the tegmentum 

 of the upper pons and brain stem can counteract 

 spinal shock. The shrinkage of motor neuron pools 

 for measured fractions of the flexion reflex during 

 spinal shock suggests withdrawal of a 'subsidy' of 

 spinal excitatorv process (16). A lesser depression 

 of reflex function follows isolated section of cortico- 

 spinal innervation, suggesting that the chief element 

 in spinal shock is the sudden loss of any large facili- 

 tatory pathway (62). There is no evidence that any 

 of the events of spinal shock or reco\ery from it are 

 pharmacologic reactions comparable to the hyper- 

 sensitivity of cholinergic end organs following loss 

 of their innervation. The induction of parathyroid 

 tetany in the chronic spinal animal (103) after spinal 

 shock is associated with the development of clonic 

 tetanic spasms in the parts headward of the transec- 

 tion a little earlier than tho.se related to isolated 

 segments, but the general excitability is little if at all 

 lowered in the isolated segments. 



It has recently been demonstrated (ig, 34, 64) 

 that, at the motor nerve ending in muscle, very small 

 quanta of excitatory transmitter substance are con- 

 tinually bombarding the muscle membrane, regard- 

 less of the passage of nerve impulses. If such a phe- 

 nomenon can be shown at central synapses, it would 

 at once explain how the loss of a transmitting path- 

 way of potent effect could result in depression of all 

 other excitation of the motor or internuncial neuron. 



Deterioration of Spinal Reflexes 



Recovery of extensor reflexes in spinal inan pro- 

 ceeds to an optimum condition that is attained only 



with the most effective nursing care. It is commonly 

 observed that any intercurrent infection, particularly 

 that associated with trophic skin ulceration, results 

 in an enhancement of flexion reflexes with a loss of 

 extension reflexes, including diminution and ulti- 

 mate loss of knee jerks. The lower limbs then become 

 drawn up in continued flexion (paraplegia-in- 

 flexion). The flexion reflex can then be set off by 

 any stimulus, often in the form of 'spontaneous' 

 flexor spasms by the pressure of gravity on dependent 

 parts. With a strong stimulus it becomes associated 

 with urination and profuse sweating over the areas 

 of skin innervated by the sympathetic outflow from 

 the isolated segments of cord if these include L2 or 

 higher segments. If the midthoracic segments of 

 spinal cord are included, a rise in arterial pressure, 

 often extreme, is associated, owing to vasoconstriction 

 in the splanchnic area. This widespread reflex effect 

 from a single stimulus was termed the 'mass reflex' by 

 Head & Riddoch (48). In contrast to the state of 

 optimum recovery of spinal reflexes, where the re- 

 sponse is adapted to the locus and nature of the 

 stimulus, the mass reflex can be viewed as a loss of 

 'local sign.' It could be related to a breakdown of 

 canalization in the spinal nerve-net of such kind that 

 pharmacological alteration of selective transmission 

 could account for the change. The observation of a 

 comparable phenomenon in untreated combined 

 system disease of the spinal cord in man, where de- 

 generation of the dorsal column extends from the 

 thoracic to the lumbar and sacral segments and leads 

 to loss of spasticity and tendon reflexes with parallel 

 increase in flexion reflexes and ultimately para- 

 plegia-in-flexion, points to another mechanism. In 

 this case the progressive loss of the collateral branches 

 of dorsal column fibers responsible for extensor re- 

 flexes leads to reflex disequilibrium and flexor pre- 

 ponderance. It is likely that the emergence of the 

 mass reflex is always a siinilar disequilibrium. Con- 

 versely, ischemic damage to the lumbosacral inter- 

 mediate grey matter can, by selectively damaging 

 multisynaptic transmission, result in great exaggera- 

 tion of extensor postural reflexes at the expense of 

 nociceptive flexion, for this is our interpretation of 

 the phenomenon of Haggqvist (46) and van 

 Harreveld & Marmont (loi). 



Reflex Pattern 



Following his early studies in the spinal dog, 

 Sherrington successfully undertook a long series of 

 researches directed to the unra\elling of the pattern 



