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of fifth and


tween scrotum and


ing ; respiration slow






sixth cervi-


thigh.


and irregular ; pulse






cal verte-




weak ; countenance






brae.




livid ; death twenty-
four hours after acci-
dent.




m:.,28.


Crush at level
of fifth and
sixth cervi-
cal verte-


35° (95° F.), rectal.


Paralysis extended to 1
in. above nipple line ;
patient complained of
feeling cold.


Hutchinson. 2




brae.


35° (95° F.), rectal
and axillary just
before death.


Death on fifth day ; no
injury to other parts
of body.




M.,53.


Crusli at level


Below 35° (95°), 4


Complete paralysis of


J)




of fifth cer-


P.M., first day.


all limbs ; diaphrag-






vical verte-




matic breathing ; skin






bra.




cold and dry ; pulse
72.
Skin cold and clammy ;








Below 35° (95°), 6.30








p. M. , first day.


patient complains of
feeling cold.








Below 35°(95°),11. 30


Pulse 50.








P.M., first day.










36°-8 (98°-2), morn-


Skin warm and dry ;








ing, second day.


pulse 64.








36° '9 (98° -4), even-


Skin hot and dry.








ing, second day.










38°-9 (102°), after-


Death.








noon, third day.






M., 36.


Crush at level


36°-9 (9S°-4), sixth


Diaphragmatic breath-


J s




of seventh


hour after acci-


ing ; imperfect paraly-






cervical ver-


dent.


sis of arms ; patient






tebra.


38°-6 (10r°-5), third

day.
38°-0 (100° -4), fourth

day.
39°-0 (102°-2), fifth

day.
37° -45 (99° -4), sixth

day.


felt very cold.
Skin of natural warmth ;
pi;lse 72.

Pulse 99.

Face mottled ; pulse 84 ;
death.




M.


Crush at level


40°-0 (104°-0), first


Slight power of moving


Churchill. 3




of fifth cer-


day, axilla.


shoulders and upper






vical verte-




arms ; skin iiushed






bra.


40°-3 (104° -5), second

day.
38° -9 (102° -0), third

day.


and very hot.
Pulse 96, regular, quiet.





1 Med,. Chir. -Trans., London, 1837, p. 146.
"^ Lancet, Loudon, 1875, vol. i. pp. 713, 747.
3 Quoted from Hutchinson, loc. cit.



[Continued on next page.



NERVOUS CONTROL OF TEMPERATURE.



86i



Sex and
Age.


Seat of Injury.


Temperature.


Remarks.


Observer.


M.—


Crush at level


41" -1 (106°), fourth


40° -2 (104° -4) on foot;


Churchill. 1


contd.


of fifth cer-
vical verte-
bra.


day.


patient died soon after
in a violent spasm , and
a quarter of an hour
after death, tempera-
ture in axilla = 43°'3
(110°).




M., 48.


Crush at level


SS^-S (92°-3), on ad-


Temperature, taken in


Wagstafife. ^




of sixth cer-


mission to hos-


both rectum and ax-






vical verte-


pital.


illa, fell steadily until






bra ; frac-




death.






ture of skull.


27° -6 (81° -7), forty-
eight hours later.


Death,




M., 22.


Crush between


33°-9 (93°-0), on ad-


Patient drowsy and pro-


Le Gros Clarke.^




sixth and


mission.


strate.






seventh cer-


27°-8 (82°-0), a few


Death about forty-eight






vical verte-


liours before death.


hours after accident.






brae.








M., 39.


Crush at level
of fourth
and fifth
cervical ver-
tebrse.


34°-5 (94°-l), four

hours after the

accident.
36° -5 (97° -7), eighth

hour.
41°-6 (106°-9), 7

A.M., second day.
42°-4(108°-3),lp.M.,

second day.


Death at 2. 5 v. M. on sec-
ond day ; post-mortem
rise to 42°-9 (109°-2)
in ten minutes.


Billroth. 2


M.,34.


Crush at level


37°-6 (99°-7), five


Comjjlete paralysis of


Frerichs.^




of fifth and


hours after acci-


trunk and limbs ; dia-






sixth cervi-


dent.


phragmatic breathing.






cal verte-


40° -9 (105° -6), twelfth








br;e.


hour.

42° '1 (107°-8), fifth-
teenth hour.

43°-6 (110°-5), nine-
teenth hour,
eleventh minute.

43°-2 (109° -7), nine-
teenth hour,
thirty-fifth min-
ute.


1
Death.





These discordant results have to be explained. It is worse than useless to
say that the effects are due to the removal of the regulating influence of
" heat centres " in the brain, centres whose very existence is problematical.
Observations upon the deep and surface temperature, and upon the amount
of moisture given off by the skin, are needed to show whether the changes in
temperature are due to disturbance in the production or in the loss of heat,
or more probably in both. The data upon these points are insufficient, but,
recently, such observations have been made by Pembrey,* in the case of two



^ Quoted from Hutchinson, loc. cit.
2 Arch./. Jclin. Chir., Berlin, 1868, Bd. ix. S. 161.

^ Recorded by Lorain, " De la temperature du corps humain," tome i. p. 500.
■* "Proc. Physiol. Soc," Journ. Physiol.. Cambridge and London, 1897, vol.
Brit. Med. Journ., London, 1897, vol. ii. p. 883.



862 ANIMAL HEAT.

patients suffering from traumatic section of the spinal cord. The general result
is a subnormal temperature so long as the patient's condition is not complicated
by other internal or external disturbance. The subnormal temperatures are
due to excessive loss and diminished production of heat, owing to the
vasomotor and motor paralysis. The section of the spinal cord high up in the
cervical region abolishes the power of regulating temperature. When the
patient is exposed even to moderate cold, his temperature falls owing to the
increased loss of heat and to the diminished production of heat. On the
other hand, if the weather be hot and the patient be too well covered with
bedclothes, his temperature rises, and may reach a dangerous height, owing to
the diminished loss and the increased production of heat in the body. In the
paralysed man the production of heat rises and falls loitli the external tempera-
ture. In the case of the high temperatures there are several factors which
may play an important part ; the paralysed parts soon cease to sweat ; in fact,
Horsley has shown that, by the use of pilocarpine, it is possible to localise
the level of the injury to the cord. The respiration is hampered, it is only
diaphragmatic ; the ventilation of the lungs is therefore imperfect, and less
heat is lost by the cooling of the inspired air, and by the evaporation of
water from the respiratory tract to saturate the expired air with moisture.
Further, the warmer the paralysed tissues the greater is their metabolism and
production of heat.

It naturally follows that, in cases of section of the spinal cord in the
dorsal or lumbar regions, the regulation of temperature is less disturbed.

The influence of the brain upon the regulation of temperature.

— It is impossible to state concisely and dogmatically the influence of
the brain upon the temperatm-e of the body. With our present know-
ledge it is only permissible to revievv the chief results obtained by
various observers, and to draw some provisional conclusions.

In 1866, Tscheschichin ^ published the results of experiments, which
showed that a section between the medulla oblongata and the pons
Varolii caused a rise in the temperature of rabbits. In one case the
rectal temperature rose in two hours from 39 "^ to 42° "G, and at the
same time there was a corresponding increase in the rate of ■ the pulse
and respiration. On the other hand, section of the spinal cord between
the third and fourth cervical vertebrse caused, in another rabbit, a fall
in temperature from 38°'9 to 32°-I. From these experiments Tsches-
chichin concluded that a moderator centre exists in the brain, and pre-
vents the excessive activity of an augmentor heat centre in the medulla
oblongata. Lewizky ^ repeated but could not confirm these experi-
ments ; he observed a steady fall in temperature after the operation.
The subject was then taken up, under the guidance of Heidenhain, by
Bruck and Gtinther,^ who, working upon rabbits, obtained positive
results in eleven, negative in twelve cases. They found in one case a
rise from 39°'3I to 42°'5 in the rectal temperature, two or three hours
after the operation. These observers further found that simple puncture
with a probe between the pons and medulla was more effectual than
section, and they noticed that the rise in temperature occurred not only
in the interior, but also in the peripheral parts of the body, a fact which
indicates that the rise is due to increased production of heat. Bruck
and Giinther do not agree with Tscheschichin's view of a moderator
centre, for they point out that the results can be produced by electrical

' Arch. f. Anat., Physiol, u. wissensch. Med., 1866, S. 151.

^ Virchow's Archiv, 1869, Bd. xlvii. S. 3,57.

^ Arch, f, d. ges. Physiol,, Bonn, 1870, Bd. iii. S. 578.



INFL UENCE OF BRAIN ON HE A T REGULA TION 863

stimulation as well as by puncture of that portion of the nervous
system, and are probably due to traumatic stimulation. It is to be
noted that irregular muscular movements were observed in many of the
cases.

Schreiber/ from the results of experiments performed upon rabbits,
came to the conclusion that a rise of temperature followed injury
to all parts of the pons, to the pedunculi cerebri, cerebellum, and
cerebrum, when the animal was protected by a covering of wool or
flannel against excessive loss of heat ; injury between the medulla
oblongata and the pons always caused a rise in temperature. In most
cases, however, the rise in temperature was very small, and the experi-
ments were often complicated by spasms of the muscles.

Observations upon the production of heat, as determined by a
calorimeter, and also upon the animal's temperature after lesions of
various parts of the central nervous system, were made by Wood.^
Section of the spinal cord above the origin of the splanchnic nerves
produced an increase in the loss but a decrease in the production of
heat ; on the other hand, section between the medulla oblongata and the
pons caused an increase in both the production and loss of heat, and for
this reason Wood supported the view of Tscheschichin, that a moderator
centre exists in or above the pons.

Eulenberg and Landois ^ found that in dogs destruction of a jDortion
of the cortex of the brain in the neighbourhood of the sulcus cruciatus
caused a rise of temperature, which was most marked on the side of
the body opposite to the lesion ; they looked upon this effect as due to
vasomotor disturbance. These results were confirmed by Hitzig * and
Wood, but on rabbits Klissner ^ and H. Eosenthal ^ obtained negative
results.

Injury to the front of the brain was found by Eichet '' to produce a
rise of temperature, and Ott ^ obtained a similar result by injury to the
corpus striatum ; this observation was confirmed by Girard,^ Baginsky
and Lehmann.^*' In 1885, Aronsohn and Sachs ^^ published the results
of an important series of experiments upon rabbits; they found that
puncture with a probe, the greatest thickness of which was 3 mm.,
had no effect upon the temperature of the body when the operation was
performed upon the front part of the cerebral hemispheres, but a
puncture passing through the median side of the corpus striatum near
the nodus cursorius of Nothnagel caused, within a few hours, a rise of
temperature which persisted for two or three days. The rise varied
from l°-7 to TA, and could also be produced by electrical stimulation of
the corpus striatum. Control experiments showed that the injury to

1 Arch. f. d. ges. Physiol., Bouii, 1874, Bd. viii. S. 576.

^ "Fever, a Study in Morbid and Normal Physiology," Smithson. C'ontrib. KnoivL,
Washington, 1880.

'•^ Cevtralbl. f. d. mecl. Wissensch., Berlin, 1876, No. 15; Virchoio's Archiv, 187Q,
Bd. Ixviii. S. 245.

•* Centralhl. f. d. med. Wissensch., Berlin, 1876, No. 18.

5 lUd., 1877, No. 45.

*• " Einfluss des Grosshirns auf des Korperwarme," Diss., Berlin, 1877.

"^ Compt. rend. Soc. de bioL, Paris, 29th March 1884, p. 189 ; Compt. rend. Acad. d. sc,
Paris, 31st March 1884 ; Arch, de physiol. norm, etpath., Paris, tome vi.

8 Journ. Ncrv. and Ment. Dis., N. Y., 1884, Nos. 7 and 8 ; 1887, p. 152 ; 1888, p. 551 ;
Therap. Oaz., Detroit, 1887 ; Brain, London, 1889.

" Arch, de physiol. norm, et path., Paris, 1886, tome viii.

10 Virchovfs Archiv, 1886, Bd. cvi. S. 258.

^^ Arch. f. d. ges, Physiol., Bonn, 1885, Bd. xxxvii. S. 232.



864



ANIMAL HEAT.



the cortex during the performance of the puncture did not cause any
rise of temperature. The high internal temperature after puncture of
the corpus striatum was accompanied by an increase in the temperature
of the skin, and by an increase in the respiratory exchange, and in the
discharge of nitrogen in the urine. The mean result of the determina-
tions of the respiratory exchange was as follows : —





Rectal Temperature.


OXYGEX.


Carbon Dioxide.


in c.c. at 0° C, 760 m.m. per Kilo, and Hour.


Before puncture
After puncture


38° -5
39°-8


664°-0
749° -7


626°-7

715°'8



Aronsohn and Sachs conclude that the rise in temperature after the
puncture is due to increased production of heat, and increased metabolism,
arising from the stimulation of the corpus striatum.

These experiments have been repeated and extended by Hale White,^
who found no rise in the temperature of rabbits after lesions of the
white matter of the cerebrum, but an almost constant effect after injury
of the corpus striatum and optic thalamus. In the case of lesions of
the corpus striatum, the rectal temperature rose to 41°'6 in two cases,
to 41°"1 in eleven cases, and to 40° in eighteen ; while in three cases
there was a slight rise, and in two a fall in temperature. The average
rise was 1°"7, and was attained within four to sixteen and a half hours
after the operations, and persisted for about sixty-two hours. After
lesions of the optic thalamus, the average rise of temperature was 1°"4.
Hale White concludes that the corpus striatum and the optic thalamus
can modify the temperature of the body, and that they do not work
directly through the vasomotor system. No increase in the discharge of
carbon dioxide was observed in rabbits after damage to the corpus
striatum.-

Several cases of a rise in temperature in man after a hsemorrhage
into the corpus striatum have been recorded.^

Eecently Tangl * has observed the effect of puncture through the
anterior part of the optic thalamus in horses. In one case the tempera-
ture rose to 40''"8 within twenty-four hours, in another to 40°"4 within
sixteen hours of the operation, and in two other cases there was no
effect. The temperature remained only for a short time at the above
height, and then fell.

Fredericq^ found that removal of the cerebral hemispheres in pigeons
caused practically no difference in the daily curve of their rectal
temperature. This observation has been confirmed by Corin and Van
Beneden,^ who have, in addition, shown that the pigeons without their
cerebral hemispheres produce the same amount of carbon dioxide and heat

^ Journ. Physiol., Cambridge and London, 1890, vol. xi. p. 1.

-Hale White, Croonian Lectures, Lancet, London, 1894, July 10, and Brit. Med. Journ.,
London, 1897, vol. ii. p. 71.

^ Bourneville, Ferrier, J. H. Bryant, Hale White ; references given by Hale White, Brit.
Med. Journ., London, 1894, I7th Nov.

*Arch. f. d. ges. Physiol., Bonn, 1895, Bd. Ixi. S. 5r>9.

^ Arch, de bioL, Gand, 1882, tome iii. p. 747.

"Ibid., 1889, tome vii. p. 265.



DEVELOPMENT OF HEAT REGULATION. 865

as do normal pigeons. The rapid rise in temperature which occurs
when a hibernating marmot awakes, is not prevented by removal of the
cerebral hemispheres.

An impartial examination of the above evidence leads to the verdict
that the existence of the so-called " heat centres " in the brain has not
been proved. In the first place, the results, even in the hands of the
same experimenter, are inconsistent ; some observers obtain exactly
opposite effects from apparently similar lesions. Further, in many
cases rabbits have been used for these experiments, and it is notorious
that their temperature is liable to considerable variations during
operative procedures. Even if the existence of these centres lie
granted, even if it be allowed that after puncture there is an increase in
metabolism and in the production of heat, it by no means follows that
the centres are special centres for the regulation of temperature, and
give off " thermic nerves."

It seems more probable that the mechanism of heat regulation
has the same cerebral representation as the voluntary muscles. In
the lower warm-blooded animals the representation of these in the
cerebral cortex is not well developed, and it has likewise been shown
that the removal of the cortex in them has little or no effect upon
the regulation of temperature.



The Development of the Power of Maintaining a Constant

Tempeeature.

In the cold-blooded animals there are traces of the power of maintaining
a constant temperature, as shown by the high temperature which a female
python is able to maintain for many weeks when she is incubating her eggs.
This instance is the more remarkable because during that time the python
takes no food or exercise. Further instances have aheady been mentioned in
the case of bees, and some species of fish.

It is possible to trace in the warm-blooded animals the gradual develop-
ment of this power of regulation. Thus, during the development of a chick
there is first a stage in which the embryo responds to changes of temperature
in a similar manner to that of a cold-blooded animal ; then a stage of transition
in which there is a regulation for moderate changes of temperature ; and
finally, when a chick is hatched, the power of regulation resembles that of
a warm-blooded animal. ^ In 1824, Edwards^ pointed out that young
mammals and birds may be divided into two classes, the warm-blooded
and the cold-blooded, according as they are, or are not, able to maintain their
temperature when removed from the warmth of the parents. The difference
lies in the relative development of the two classes — active young animals
covered with fur or feathers, as in the case of the guinea-pig and chick, belong
to the former class ; while young animals born naked, blind, and helpless,
belong to the cold-blooded group. The inability to maintain a constant
temperature is due to diminished production of heat on exposure, and only
secondarily to excessive loss of heat. It has recently been shown that the
chick and guinea-pig can at birth regulate their production of heat, that young
cold-blooded mammals and birds are able to regulate only for moderate changes
of external temperature ; for, when exposed to cold, their temperature and

^ Pembrey, Gordon, and Warren, Journ. Physiol., Cambridge and London, 1894-95,
voL xvii. p. 331.

^ " De rinfluence des agens physiques sur la vie," 1824.

VOL. L— 55



866 ANIMAL HEAT.

production of carbon dioxide fall, and they resemble cold-blooded animals.
About the fifteenth day after birth, they respond to a fall in the temperature
of their surroundings with increased muscular actiAdty and output of carbon
dioxide, and thus maintain their temperature (Pembrey ^).

In the lowest mammals the temperature is much lower than in the higher
members of the group. Thus the temperature of the Echidna hystrix is 27° "5,
and that of the Ornithorhynchus, 24° '8. '^

Further, a hibernating mammal is an instance of an animal at one time warm-
blooded and at another time cold-blooded, and its power of regulation is in
many respects similar to that of an immature mammal.^ Additional proofs
of the gradual development of the power of maintaining a constant tempera-
ture are found in the unstable temperature of infants and animals. In
premature and weak infants the power is imperfect, and the temperature is
below the normal.''^ It is in man that the perfection of this power is reached ;
he of all animals has the most constant temperature under extreme differences
of external heat and cold.

It is impossible with our present knowledge to state what are the
structural differences which accompany the development of the power of
regulation. This much we may say : the power aj)pears to be associated
chiefly with the control of the nervous system over the skeletal muscles and
those of the blood vessels. An anaesthetic, or curari, or section of the spinal
cord reduces a warm-blooded animal to a cold-blooded condition ; its tempera-
ture and production of carbon dioxide vary Avith, and in the same direction as,
the temperature of its surroundings. In a hibernating animal the fall of
temperature is accompanied by greatly diminished activity of the muscular
and nervous systems ; and the sudden rise in temperature, when the animal
awakes from its torpidity, is marked by a sudden increase in the discharge
of carbon dioxide and in muscular activity. Those young mammals and birds
which are born with well-developed control over their muscular system, are
able to regulate their temperature even at birth, whereas those born in a
helpless condition do not attain this power until a week or two after birth,
at a time when their power of co-ordination is much increased.



The Tempeeatuke of the Body after Death.

After death the temperature of the body generally falls, the loss of heat
varying according to the difference between the temperature of the corpse
and that of its surroundings ; another important factor is the surface of the
body in relation to its mass, for the corpse of an infant or of a wasted
subject cools more rapidly than that of a well-developed adult. ^ In some
cases, however, a rise of temperature is observed in the corpse, especially
when death has resulted from tetanus, acute rheumatism, typhoid fever, small-
pox, cholera, or injuries to the brain and spinal cord. A few of the cases
recorded are given in the following table : —

^ Journ. Physiol., Cambridge and London, 1895, vol. xviii. ]). 363.

- Mikloncho Maclay, Froc. Linn. Soc. New South Wales, 1883, vol. viii. p. 425 ; vol. ix.
p. 1205 ; Semon, Arch. f. d. ges. Physiol., Bonn, 1894, Bd. Iviii. S. 229.

^Pembrey and Hale White, Journ. Physiol., Cambridge and London, 1896, vol. xix.
p. 477.

^ Cronibie, Indian Ann. Med. Sc, Calcutta, 1873, vol. xvi. ]>. 597; Raudnitz, Ztschr.
f. Biol., Miinchen. 1888, Bd. xxiv. S. 423.

^ Taylor and Wilks, Ouy's Hosp. Rep., London, 1863, p. 184 ; observations on one
hundred cases ; Sutton, Brit. Med. Journ., London, 1874, vol. i. p. 153 ; Bidder and
Schmidt, " Die Vcrdduungssaf'te und der Stoffwechsel," S. 323 ; Woniack, Bt. Bartli. Hosp.
Rep., London, 1887, vol. xxii. ji. 193; Niderkorn, " De la rigidity cadaverique chez
rhomme," Paris, 1872.



TEMPERATURE OF THE BODY AFTER DEATH. 867



Temperature


Temperature after


Disease.


Place of


Observer.


before Death.


Death.




Observation.






45°


Pyemia


Left ventricle.


Davy.i




(3i hrs. post-mortem)










42°-2


Sudden death, cause


) ?


,,




(5i hrs. post-mortem)


undetermined.








43° -75


Small-pox.


Axilla.


Simon. ^




(1 hour post-mortem)










44°-5


J


,,


,,


41°'-1


44°-5


Sunstroke.


^,


Levick.^


44°-75


45°-4
(57 mill, post-mortem)


Tetanus.


!>


Wunderlich.^




41°-2


Cholera.


Rectum.


Mackenzie.^


42°-3


43°-2
(15 mill, post-mortem)


Erysipelas.


Axilla.


Eulenburg.^


40°-4


42°-3
(20 min. post-mortem)


"


))


"




41°-8


Sunstroke.




Thompson.'''


36°-l


38° -3
(7imm. post-mortem)


Apoplexy.


))


De Haen.8


41°-6


43°
(30 min. post-mortem)


Tetanus.


"


Lehmann.^


43°-01


44°-03
(1 hour post-mortem)


Pyemia.


Rectum.


Quincke and
Brieger. ^°


42° -1


43°-4
(1 hour post-mortem)


Pneumonia
delirium tremens.


"


"


41°-1


43° -3
(15 min. post-mortem)


Crush of
spinal cord.


Axilla.


Churchill. ^



The causes of this post-mortem rise in temperature have been investigated
by various observers.^- The most important factors are these. When the
circulation and respiration cease at death, the normal loss of heat from these
causes and from sweating also comes to an end, but the tissues live for a short
time and produce heat even after the death of the organism as a whole. If
this production of heat is greater than the loss of heat from the corpse, the
temperature rises ; if, on the other hand, it is less, then the effect is only to
delay the fall of temperature. The next source of heat is in the muscles on
the onset of rigidity ; and, finally, when decomposition sets in, and this may



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