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NEW SERIES, VOL. XLVll JANUARY, 1940 NO. I D?h~~mtriwtiioultnsl ~‘QQ Copyright, ~gwa byThe American Journal of Surgen, Inc. A PRACTICAL JOURNAL BUILT ON MERIT NON#OPERABLE GROUP OF CRANIOCEREBRAL INJURIES W E are inciined, in present day meth- ods of teaching surgery, to resort considerabIy to groupings and cIas- sifications 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 patho- genesis 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 ex- ampIe, 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 com- pIete 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 stated that there is here an increase in brain voIume, which if suffIcientIy sus- tained, eventuates in intracortica1 hemor- rhage. 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 A uid 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 pro- found. There is a definite and prolonged period of unconsciousness, which may Iast for days. There is nausea and vomit- ing, 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 pres- sure is high, and the cerebrospina1 fluid contains bIood. It is thus quite obvious that the consider- ation 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 re- gards SymptomatoIogy. Both contusion and Iaceration are associated with edema and congestion, and these in turn incor- I

Non-operable group of craniocerebral injuries

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NEW SERIES, VOL. XLVll JANUARY, 1940 NO. I

D?h~~mtriwtiioultnsl ~‘QQ Copyright, ~gwa byThe American Journal of Surgen, Inc.

A PRACTICAL JOURNAL BUILT ON MERIT

NON#OPERABLE GROUP OF CRANIOCEREBRAL INJURIES

W E are inciined, in present day meth- ods of teaching surgery, to resort considerabIy to groupings and cIas-

sifications 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 patho- genesis 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 ex- ampIe, 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 com- pIete 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

stated that there is here an increase in brain voIume, which if suffIcientIy sus- tained, eventuates in intracortica1 hemor- rhage. 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 A uid 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 pro- found. There is a definite and prolonged period of unconsciousness, which may Iast

for days. There is nausea and vomit-

ing, 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 pres- sure is high, and the cerebrospina1 fluid

contains bIood. It is thus quite obvious that the consider-

ation 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 re- gards SymptomatoIogy. Both contusion and Iaceration are associated with edema

and congestion, and these in turn incor-

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 cIassifica- tion 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.