Non-operable group of craniocerebral injuries

JANUARY, 1940

NEW SERIES, VOL. XLVll

NO. I

D?h~~mtriwtiioultnsl ~‘QQ Copyright,

A

PRACTICAL

NON#OPERABLE

~gwa byThe American Journal of Surgen,

JOURNAL

BUILT

Inc.

ON

MERIT

GROUP OF CRANIOCEREBRAL

W

E are inciined, in present day methods of teaching surgery, to resort considerabIy to groupings and cIassifications of disease entities and pathoIogic pictures, and occasionaIIy mereIy aIIude to the fact that in some conditions, one cIinica1 picture “overIaps the other.” A cIearer understanding of the pathogenesis wiI1 undoubtedIy be foIlowed by a more accurate knowIedge of the pathologic findings, and this in turn wiI1 make more easiIy understandabIe the symptomatoIogy. With meticuIous pseudoprecision, for exampIe, we teach and Iearn the cIassifications of brain injuries, and ascribe to each entity a group of pathoIogic findings and the resuItant symptomatoIogy, as though each had its own cIassica1 story. In approximate order of increasing severity, we group the non-operabIe craniocerebra1 injuries as con’cussion, edema and congestion, and contusion and Iaceration. The pathoIogy of concussion is not def?niteIy known. Perhaps it is a reffex of some type resuIting in anoxemia. The chief symptom, however, is unconsciousness for a short period of time, foIIowed by compIete recovery. The pathoIogy of edema and congestion in themselves is rather diffxcuIt to evaluate, as edema and congestion are rareIy present without the accompaniment of more serious brain damage. It might perhaps be briefly

INJURIES

stated that there is here an increase in brain voIume, which if suffIcientIy sustained, eventuates in intracortica1 hemorrhage. The signs and symptoms, as is we11 known, are unconsciousness foIIowed by a return of consciousness, after which there is headache and dizziness, nausea, and some Ioss of memory. There is often increased intracrania1 pressure, but the cerebrospinal Auid is normaI. In contusion, there is some injury to the brain surface with torn cortica1 vesseIs. In laceration, the cortica1 surface is actuaIIy torn. Here the symptoms are more profound. There is a definite and prolonged period of unconsciousness, which may Iast for days. There is nausea and vomiting, and headache. In the more severe cases, there may be dilatation of the pupils, irreguIarity of respiration, and increase in puIse and temperature. Surgical shock is frequentIy present. The intracrania1 pressure is high, and the cerebrospina1 fluid contains bIood. It is thus quite obvious that the consideration of the pathoIogy of contusion and laceration incIudes that aIso occurring in edema and congestion, as we11 as that of concussion, The same can be said as regards SymptomatoIogy. Both contusion and Iaceration are associated with edema and these in turn incorand congestion, I

2

American Journal of Surgery

EditoriaI

porate concussion. Stating it in another way, following craniocerebra1 injuries, edema and congestion in&de concussion. For example, the unconsciousness in Iaceration is not necessariIy due to the tear in the brain cortex, as the concussion present was sufficient to cause it; the more severe pathoIogic findings and symptoms are due to the added damage, i.e., from the arbitrary division beyond concussion.

It is thus seen that the present cIassification is more of a didactic rather than either a true cIinica1 or pathoIogic one. If the foregoing is kept in mind, there wiI1 be a better understanding and appreciation of some of the non-operabIe craniocerebra1 injuries, and more important, a better rationaIization when thinking in terms of therapeutic measures. RAYMOND GREEN, M.D., F.A.C.S.