ABNORMALITIES OF NEURAL FUNCTION IN THE PRESENCE OF INADEQUATE NUTRITION 



1897 



Cobalt 



Signs of cobalt deficiency appear to be limited to 

 ruminants which need this trace element as a constit- 

 uent of vitamin B 12 , (277, p. 147). Failure of appetite 

 is an early and conspicuous symptom, and results in 

 extreme wasting. The mechanism involved in the 

 depression of appetite is not known. Anemia is a 

 later symptom which becomes progressively more 

 severe and the condition, if untreated, is likely to be 

 fatal. 



Cobalt has a protective action in a disease of sheep 

 and cattle called 'Phalaris staggers' in which a 

 marked incoordination of gait (staggers) and mus- 

 cular tremors are the characteristic symptoms, and 

 which develops in some areas where the animals 

 graze predominately on the grass Phalaris tuberosa. 

 The structural defect consists of demyelination of 

 nerve fibers of the spinal cord and medulla oblongata 

 (161). 



Copper 



Symptoms similar to those of cobalt deficiency, 

 ranging from spasticity to complete paralysis, were 

 reported in lambs from ewes pastured on lands defi- 

 cient in copper (156, p. 89). The structural lesions 

 involve a diffuse demyelination of the central nervous 

 system and of the motor tracts of the spinal cord. 



VITAMINS 



Thiamine 



Thiamine, as thiamine pyrophosphate and in 

 association with lipoic acid (in the form of lipothia- 

 mide pyrophosphate), is a catalyst which plays a 

 central role in pyruvate oxidation. Addition of 

 thiamine (84) or of diphosphothiaminc (cocarboxy- 

 lase) increases the oxygen consumption of the brain 

 tissue of Brdeficient animals ( 1 95). 



It is still unsettled as to whether the functional 

 alterations of the nervous system are due to the inter- 

 ruption of energy supply or to the accumulation of 

 intermediaries or to both. Peters (208) favored the 

 idea that the former represents the primary event in 

 the production of the nervous symptoms of thiamine 

 deficiency. Other authors believe that the accumula- 

 tion of pyruvic acid may be the cause of at least 

 some of the signs of the deficiency state, such as 

 anorexia (246). Other intermediary metabolites may 

 accumulate during thiamine deficiency, such as 



methylglyoxal (226, 281). The fact that the signs of 

 deficiency are aggravated by diets rich in carbohy- 

 drate may speak in favor of the pyruvate mechanism. 

 On the other hand, the lack of toxicity of pyruvic 

 acid (209), and the lack of parallelism between the 

 changes in pyruvate concentration in blood and the 

 signs of deficiency (51), make the role of pyruvic 

 acid somewhat doubtful. Extensive work on the 

 participation of thiamine in the transmission of the 

 nervous impulse in the peripheral nerve has been 

 carried out (175, 282). 



MANIFESTATIONS OF VITAMIN Bi DEFICIENCY IN ANI- 

 MALS. The classic picture of polyneuritis, produced in 

 pigeons and other birds when fed a diet consisting of 

 polished rice, begins with unsteady gait and weakness 

 which progresses until the animal is no longer able 

 to stand. Opisthotonus and convulsions are a charac- 

 teristic feature that can be reversed within 30 min. 

 by the injection of thiamine into the subarachnoid 

 space (209). 



Experimental production of polyneuritis gallinarum 

 in birds fed polished rice involves deficiency of other 

 vitamins besides B]. Moreover, since anorexia is one 

 of the principal and more constant signs of thiamine 

 deficiency, it is clear that starvation may be an 

 aggravating factor. The speed with which the defi- 

 ciency develops is also an important factor, and 

 differences in symptomatology are observed between 

 the acute and the chronic deficiencies. Also, the 

 presence of other nutrients in the diet may change the 

 pathology of thiamine deficiency to a considerable 

 extent (41. A summary of neurologic symptoms ob- 

 served in several species is presented in table 1. 



The signs of thiamine deficiency can be produced 

 by feeding thiamine-defieient diets, hv the presence 

 of thiaminase in food [e.g. Chastek paralysis of the 

 fox (98)] or by feeding analogues of thiamine (300). 

 The peripheral nerves and the proprioceptive nerve 

 endings are functionally normal, as shown by records 

 of nerve action potentials (39). Although some French 

 workers have reported changes of chronaxie in ihi.i- 

 mine deficient pigeons (184, 185), the conduction of 

 nervous impulses in peripheral nerves has been found 

 normal in thiamine deficient cats (15). The neurologic 

 signs of thiamine deficiency appear to be related to 

 alterations in the central nervous system, especially 

 the vestibular nuclei. 



The question of lesions in the peripheral nerves 

 has been a matter of lively controversy (164, 24111 

 Mannell & Rossiter (154) did not find chemical 

 siims of myelin degeneration in the rat under condi- 



