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HANDBOOK OF I'HYSK 'I 



NEUROPHYSIOLOGY III 



i ujll i. Nettrologu Sign* of Thiamine 

 Deficient, y in Animals 





Pigeon and 

 chick 



Cat 



Fox 



Monkey 

 Mouse 



Rat 



Signs 



References 



( .ill 



Leg weakness, ataxia, opisthotonus, Mi -<">. 

 convulsions, paralysis in chronic de- ^66, 268 

 ficiency (pigeon) 



Ataxia, abnormal posture, swaying 65, 196 



gait, pupil dilatation, torn 1 



vulsiv e seizures, coma 



Stiffness of gait, spastic paralysis, 35,63, 

 abnormal sensitivity to pain, con-; 96-98 

 vulsions 



Ptosis, ataxia, lack of coordination. 287 

 occasional convulsive seizures 



Tremor, occasional convulsions, 300 

 spasticity of legs, backward 

 jerking of the head, inability to 

 walk 



Incoordination of movements, sway- 39, 214 

 ing gait, head retraction, changes 

 in muscular tonus, ataxia, dis- 

 turbances of equilibrium, in- 

 creased duration of rotational 

 nystagmus 



Weakness, incoordination of legs, 

 convulsions, head retraction 



dons of acute thiamine deficiency. The lesions pro- 

 duced in central neural structures by thiamine 

 deficiency are summarized in table 2. In thiamine- 

 deficient monkeys (219), no clinical or histological 

 evidence of. peripheral neuropathy or of defeneration 

 of fillers in the spinal cord was observed. The authors 

 conclude thai the pathological picture is very similar 

 to Wernicke's disease in man. The main difference is 

 the absence in the monke) of vascular changes, so 

 impoi 1. mi in Wernicke's disease. 



As regards behavior, rats deprived of thiamine 

 [oi, 289) increased their running in a rotating 

 wheel until their activity fell off dramatical!) with the 

 onset of neuromuscular symptoms of thiamine defi- 

 ciency, culminating in spastic paralysis. Studies on 

 the impairment of the learning capacity in rats defi 



I ii hi in B complex vitamins were summarized by 

 M111111 (186, p. 541 ). 



iiiiwiiM deficiency in man. Thiamine deficiency is 



recognized .is the main etiological factor in the pro- 

 duction of two clinical conditions with characteristic 

 neurologic manifestations, beriberi and Wernicke's 

 encephalopathy, which have been well described in 

 medical literature (223, 242, 257, -'<|i Neurologi- 

 c.illv , beriberi is characterized b) peripheral, ascend- 



ing, symmetrical polyneuritis, with disturbances of 

 both the afferent and the motor systems. Wernicke's 

 encephalopathy is characterized by the clouding of 



consciousness and ophthalmoplegias, with poly- 

 neuritis and ataxia as less constant manifestations 



The effects of thiamine restriction in man have 

 been studied experimentally by several research 

 workers 1 i_>",, 292). Tin- effects of a prolonged partial 

 restriction and a brief total deprivation of dietary 

 thiamine were examined quantitatively in 10 young 

 men, clinically normal at the start of the experiment 

 (31). With other vitamins of the B complex made 

 available in adequate amounts, the intake of 0.2 m<i 

 of thiamine per 1000 Gal. for 168 days was on the 

 borderline of deficiency, as indicated by the level of 

 urinary thiamine (37)- In acute deprivation that 

 followed, definite signs of deficiency developed in 

 days or weeks, depending on the specific symptom. 

 The first signs were anorexia and nausea. Severe 

 deterioration observed on the 'psychoneurotic' 

 scales ("Hypochondriasis,' 'Depression,' "Hysteria" 1 

 of the Minnesota Multiphasic Personality Inventory 

 was subsequendy reversed by thiamine supplements. 

 On the other hand, changes in scores on the 'psy- 

 chotic' scales ("Paranoia," 'Schizophrenia," 'Hypo- 

 mania') were small. 



Performance on standardized tests of intelligence 

 was not affected adversely by thiamine deprivation. 

 In the sensory area the most consistent change, with 

 statistically significant decrement in deprivation and 



TABLE 2. l.< ^iiiis of the Central Xenons S) ftt m 

 in Thiamine Deficient r 



X = lesion present, no degree indicated. 



