972 



HANDBOOK OF I'inSICJLOaY 



NEUROI'HVSIOLOGV II 



turbance of the gastrointestinal tract due to autonomic 

 imbalance (see also Chapter XLV by Eliasson). 



The occurrence of pulmonary edema raises a num- 

 ber of questions. It has been found experimentally 

 that preoptic lesions in rats are followed by edema of 

 the lungs, and mid-line lesions dorsal to the chiasm 

 seem to be the most effective (io8, 109). This edema 

 is not influenced by vagotomy, but it is prevented by 

 cervical spinal transection or section of the splanchnic 

 nerves. Maire & Patton suggest that the preoptic 

 lung edema results from overloading of the pul- 

 monary circuit owing to splanchnic-mediated con- 

 striction of visceral venous reservoirs, since the liver 

 and spleen weights of animals dying from lung edema 

 are significantly less than normal. 



The hypothalamus is known to participate in so- 

 called stress reactions. Using eosinopenia as an index. 

 Porter (137) found that the response to epinephrine, 

 formalin and histamine in the cat was prevented by 

 lesions in the posterior part of the hypothalamus but 

 not by anterior hypothalamic lesions. He also found 

 that direct stimulation of the tuberal and mammillary 

 areas produced eosinopenia. Prcsumablv these effects 

 are mediated through the anterior lobe of the pitui- 

 tarv. Mirsky et al. (120) found that noxious stimula- 

 tion brought about increased production of anti- 

 diuretic hormone in rats. This was also true after 

 hypophvsectomy; presumably the sources of the 

 antidiuretic hormone were the neurons of the su- 

 praoptic nucleus. Mirsky suggests that possibly the 

 antidiuretic hormone may participate in the neuro- 

 humoral activation of the anterior lobe [cf. Martini 

 et al. (ill); Chapters XXXIX and XL of this work]. 

 McCann & Sydnor (112) were able to prevent the 

 rise of blood ACTH which ordinarily occurs during 

 stress by lesions which interrupted the supraoptico- 

 hypophysial tract. There may be a question here, 

 however, as to whether the lesions of the supraoptico- 

 hypophysial tract did not also interrupt the hypo- 

 physial portal system of \eins. 



CEREBR.'^L .^ND CEREBELL.XR .AUTONOMIC MECH.\NISMS 



A fairly extensive literature substantiates the par- 

 ticipation of the cerebral cortex in autonomic activi- 

 ties. A number of comprehensive reviews are avail- 

 able, including those of Fulton (56) and Kennard 

 (96). Other key references are Pinkston et al. (133), 

 Pinkston & Rioch (134) and Hoff (78). The subject 

 is discussed also in Chapters -L\T, LVII and LVIII 

 of this work. The observations upon which this litera- 



ture depends have been made upon patients in the 

 clinic and upon experimental animals. Physicians 

 have long been aware of the fact that following the 

 onset of hemiplegia the paralyzed extremities of a 

 patient show vasodilatation which later subsides as 

 the skin becomes paler and colder and increased 

 sweating appears. There is sometimes increased per- 

 meability of the capillaries with resultant edema. 

 Many experimental observations have been recorded 

 but no attempt will be made to summarize them here 

 except in a very general way, bringing into considera- 

 tion only a few relatively recent observations. 



Autonomic effects which may be elicited by stimu- 

 lation of the nonrhinencephalic cortex seem to be 

 most easily elicited from the frontal lobes, especially 

 from the anterior part of the motor area and extend- 

 ing into areas 6 and 8. From the latter, the frontal eye 

 fields, pupillary changes may be elicited; and it is in 

 connection with the pupil that an exception exists so 

 far as localization is concerned because constriction 

 can be produced in cats by stimulation in the occipital 

 region. Vascular changes in response to cortical 

 stimulation of the neopallium most commonly result 

 in increase in arterial pressure, and lesions of the same 

 areas in animals tend to produce a chronic vasodila- 

 tation. Howe\er, Uvnas (103) and his collaborators 

 have presented evidence for a sympathetic vaso- 

 dilator outflow originating in the motor cortex of the 

 dog, with relays in the hypothalamus and midbrain. 

 Uvnas discusses this system in detail in Chapter XLI V 

 of this work. 



Changes in activit\' ol the sweat glands may also 

 be produced bv stimulation of the motor areas in 

 animals, as indicated by the galvanic skin reflex of the 

 contralateral side. Increased sweating may appear 

 contralateral to lesions of the frontal lobe, while a 

 persistent piloerection may follow bilateral removal 

 of area 6 (96). Extensive bilateral lesions in the para- 

 central lobule result in loss of bladder control. 

 Respiratory changes are most readily obtained by 

 stimulation of the orljitofrontal cortex, and psychic 

 influences on respiration as well as on salivation and 

 other autonomic phenomena are well-known. 



Generally speaking, there is a fair amount of dis- 

 crete localization of autonomic areas in the motor and 

 premotor regions, usuallv in fairly close relation to 

 corresponding somatic representations. Kennard sug- 

 gests that such control as may exist from these areas 

 is that of regulation of finer autonomic adjustments; 

 when this control is lost, there is loss of inhibition and 

 there may be, as a result, overreactivity. Recently, 

 autonomic effects from other regions of the cortex 



