Lebedev V.V., Krylov V.V., Martynenko A.V., Khalchevsky V.M.
Sklifosovsky Research Emergency Care Institute, Municipal Clinical Hospital N 33, Moscow
Brain contusions and processes due to secondary damaging factors are often of decisive importance in estimation of indications and contraindications for surgical treatment of a casualty. Not long ago intracranial hematoma was considered to be a key factor for performing an intervention in acute traumatic compression of the brain. Due to this fact, CT examination was first of all aimed at detection and description of such hematoma (its volume, thickness, dissemination, contents quality, i.e. heterogeneity, multiplicity of chambers, presence of a capsule, etc.). We are not going to diminish the role of hematoma proper in the process of brain compression. However, there are many cases when this process depends not so much on hematoma as on a pathologic focus on the whole (hematoma, contusion focus, concomitant brain edema, venous congestion, hypoperfusion, etc.). Prevention of secondary damaging factors and their sequelae results in 10-15% reduction of mortality [2, 3]. Thus, analyzing CT data in brain contusions, it is necessary to assess all components of a pathologic focus (areas of increased or diminished density, their volume both separately and in total) as well as signs of its effect on the brain (a value of transverse and axial dislocation, a state of the CSF system, etc.).One should keep in mind that a value of transverse dislocation (dislocation of brain median structures) obtained with CT is 2-5 mm larger than that got with echoencephalography. The explanation is that CT is a more precise method of dislocation assessment in comparison with echolocation.
One should define the term “brain contusion” more exactly before making any judgement on a contusion focus. It is of crucial importance for understanding this pathology, interpretation of pathogenesis of the brain injury, determination of indications for an operation and its volume, prognostication of an outcome of craniocerebral trauma (CCT) in a specific patient. Thus, it is necessary to work out classification of brain contusions based on CT data which would correspond to a clinical description of this injury, serve a guide for a neurosurgeon and make his work much easier. Achieving this goal is often hampered by discrepancies between a degree of an anatomic lesion and a clinical picture. Russian classifications of brain contusions based on CT findings, which were elaborated by Kornienko V.N., Vasin N.Ya. and Kuzmenko V.A.  and Kornienko V.N., Likhterman L.B., Kuzmenko V.A. and Turkin A.M. , do not always meet existing demands.
Thus, birth of a new classification of brain contusions based on clinical and CT data has to be preceded by clarification of the term “brain contusion”, otherwise all the attempts are doomed to failure.
It is supposed that contusion of the brain (a contusion focus) should be treated as its closed lesion characterized by macroscopic foci of destruction, hemorrhage and necrosis in its cortex [1, 19, 21]. Such an interpretation excludes the possibility of brain contusion in patients with open CCT. Besides, this definition does not comprise lesions accompanied by contusions not only of the cortex but also of the white matter.
It is oversimplification to view a contusion focus as an area of destruction of the brain substance watched macroscopically and imbibed with blood . This definition does not reflect its pathogenetic, clinical, morphologic manifestations and diagnostic (CT, MRT) findings.
Taking into account a mechanism of trauma, pathogenesis, evolution of a contusion focus it is absolutely correct to differentiate between primary traumatic foci of contusion and secondary necroses and hemorrhages . However, secondary necrotic foci are due to the effect of secondary mechanisms conditioned by cerebral trauma and cannot be regarded as a contusion focus.
As for the above definitions, they have one thing in common: there is always an area of anatomic destruction of the brain in its contusion (a contusion focus). According to our opinion, brain contusion should be treated as loss of its morphologic integrity at the moment of trauma. This very morphologic destruction of the brain emerging at the moment of trauma and caused by it is a peculiar feature of brain contusion distinguishing it from other destructive lesions. Morphologic destruction can take place both in closed and open CCT and involve the cortex or the cortex and subcortical structures. It is accompanied by hemorrhages of different severity into crushed areas of brain tissue or manifests itself as hemorrhagic softening (soaking).
Classification of brain contusions based of clinical and CT data can be impeded by possible absence of strict compliance of an anatomic lesion and a clinical picture. It depends on localization of a contusion focus, its size and, more often, on secondary processes taking place around it (severity of disorders of local and hemispheric blood circulation, regional or hemispheric brain edema causing various degrees of transverse or axial dislocation, etc.). S.V.Toutant et al.  report casualties in a comatose state (Glasgo coma score of 8 and lower) with a period of unconsciousness of not more than 2 days and unchanged basal cisterns. According to them, fatal outcomes or a vegetative state and good results were watched in 28% and 35% of these patients respectively. In case of compression of basal cisterns, these indices in the same category of patients are 46% and 19% respectively. If basal cisterns of such patients are not visualized, then the index of fatal outcomes or a vegetative state reaches 79% whereas the index of good results reduces up to 11%. Mortality in lateral dislocation of the median line exceeding 15 mm and absence of basal cisterns is as high as 100%. Our studies are indicative of an effect of brain dislocation on the outcome of its traumatic lesion as well . Thus, carrying out CT examination of a contusion focus one should pay attention not only to its dense (hemorrhagic) part but also to a size and dissemination of its hypodense component. Their volumes should be indicated in a description separately; besides, indication of their total volume is mandatory. It is also necessary to measure transverse dislocation of median structures of the brain in millimeters and to estimate axial dislocation (by deformity of a bordering cistern, possible foci of reduced density /ischemic edema/ in the area of the basilar artery branches). It is not a rare case when CT examination is repeated 2-3-4 times depending on clinical dynamics of a process; it is done with the purpose of clarifying indications for an operation. Primary CT examination carried out in 2-3 hours after trauma can reveal a limited focus of brain contusion without concomitant perifocal edema and dislocation or with minimum manifestations of the latter. When examination is repeated in 6-12 hours one can find growth of perifocal edema whose size is several times larger than that of a limited contusion focus; total volume of a hemorrhagic component and a size of its separate particles with increased density can become bigger resulting in a disseminated focus of brain contusion; there can appear transverse or axial dislocation. Levels (sections) of subsequent CT examination should not differ from those of previous studies. If necessary a number of sections can be increased.
Brain contusion is a nosologic entity with quite definite clinical and morphologic characteristics. It cannot be classified as brain contusion without compression and brain contusion with compression  or there should not be such a notion as “a hematoma type of a clinical course of brain contusion”  which, unfortunately, has been included into an official form describing activity of a neurosurgical department. Such trauma is always characterized by presence of a complex pathologic focus defined as a focus of brain contusion with hemorrhage into it and accompanying secondary processes. Definition of this complex focus given by Zotov Yu.V, et al.  makes a neurosurgeon to yield the palm to hematoma instead of a contusion focus with all resulting consequencies. Such a focus should be regarded as a complex combined lesion of the brain but not as a simple sum of two processes (a focus of brain contusion and intracranial hematoma). It is a specific form of combined traumatic lesion with its own morphologic and clinical peculiarities and secondary processes.
Clinical forms (diencephalic, mesencephalic, extrapyramidal, mesencephalobulbar) of brain contusion [8, 23] are not the definition of a form of brain contusion proper. They are reflection of a clinical picture conditioned by a degree of lesion of the brain stem which may be caused by any pathologic focus either with or without an area of brain contusion-crush (for example, intracranial hematoma). This focus can be localized in any part of cerebral hemispheres but not in defined sections of the brain stem. Depending on development of secondary processes (severity and dissemination of brain edema, severity of disorders of local and regional blood circulation, a degree of transverse and axial dislocation conditioned by these factors) an identical focus of brain contusion, which is “pure” from anatomic and CT points of view, can be a source of any of the above-mentioned neurologic symptoms. Besides, extremely marked symptoms indicative of the brain stem lesion can appear in the absence of transverse dislocation of the brain due to its compression by foci located in both hemispheres (on both sides). In essence, dislocation syndrome, which manifests itself clinically, is not a demonstration of a degree of brain dislocation but a reflection of severity of its stem lesion. Dislocation of the brain, its median structures is a secondary process conditioned by a primary pathologic focus, which leads to circulatory disorders in the brain stem and its dysfunction marked to a different degree. Thus, it is incorrect to speak of dependence of dysfunction severity on a size of transverse dislocation and, as a matter of fact, Zotov Yu.V. et al.  arrive at the same conclusion. As for the phase conception of a course of brain contusion  it has nothing to do with phases in a course of an anatomic focus of brain contusion proper but reflects changes of a clinical picture due to evolution of any acute pathologic focus (its progression or regression) and its effect, as well as that of concomitant secondary factors, on the function of vital centers of the brain stem.
If we stick to the notion of brain contusion given above, according to which it is always characterized by destruction of cerebral tissue at the moment of trauma, then it becomes quite evident that every focus of brain contusion is to have a hemorrhagic component. In this case the term “an edematous form of brain contusion” or “brain contusion of the first type” [10, 11] becomes incomprehensible. There is a uniform reduction of tissue density up to +18 - +25 H. units in such a focus; a hemorrhagic component and destruction of cerebral tissue are absent. This fact is confirmed by the authors of this classification themselves. They assert that foci of the first type are always subject to quick regression, though, according to our observations, it does not happen in all cases .
Usually, foci of diminished density are formed in frontal (polar-basal areas) and temporal lobes mostly by a counter-blow mechanism. Such foci correspond both to ischemia and brain edema. An attempt to explain formation of these foci by oscillatory movements of bony plates of the orbit roof, large and small wings of the sphenoid bone  is not very successful. It should be mentioned that foci under discussion are formed not only in the brain areas, adjacent to bony plates, but also on their polar and convexital surfaces where the brain borders a spongy bone which does not oscillate in trauma  and, thus, cannot be a cause of brain damage. Besides, some patients have no areas with diminished density of cerebral tissue during the first hours after trauma; they are watched later. One may conclude that foci of destruction with a hemorrhagic component appear not at the moment of trauma but after it has been inflicted.
Such secondary necrotic foci in the form of hemorrhagic softening, hemorrhagic infarction result from vascular spasm of long duration, stasis accompanied by ishchemic necrosis. Soaking of cerebral tissue with blood is due to diapedesis of erythrocytes through impaired walls of vessels located in such a focus [12, 22]. A pathophysiologic mechanism of its development comprises both primary (traumatic) vascular lesions and secondary lesions of vessels due to thrombosis and local vasomotor disorders which condition increase of an area of cerebral tissue necrosis . Studies of blood flow changes at a microcirculatory level allow to prognosticate a course of brain contusions . According to our experience , there was 56% increase of time of hemispheric and regional blood flow during the first two days after trauma in mild brain contusion. Normal indices of blood flow velocity were watched on the 7th-10th day. Thus, a zone of diminished density, revealed by CT in the absence of areas of increased density, is not a focus of brain contusion, as it has been thought before, but a focus of posttraumatic edema-ischemia. Thus, it cannot be categorized as brain contusion in the classification based on CT data.
Cavitation theory adapted to medicine [15, 26-29, 31, 32] explains the origin of this posttraumatic ischemic focus rather well.
Rotational movement of the brain or dislocation of its mass due to inertia (on the opposite side) or flexure of a cranial bone in the impact area followed by restoration of its former position (on a lesion side) results in generation of vacuum [27, 28]. Negative pressure watched during 1/700-1/1000 s causes formation of cavities in tissues and, first of all, in flowing fluid (blood). These cavities collapse as pressure reaches normal values (cavitation). Bubbles of steam or gas formed in blood are capable of unlimited growth. Blood delivers a cavitation bubble to a zone of higher pressure where it “slams” and produces a hydrodynamic shock wave which damages a vascular wall to this or that extent.
There appears a circulatory disorder in damaged vessels which depends on severity of a lesion of their wall and nervous parietal apparatus. It results in brain ischemia in this area. An ischemic focus on CT scan is described as brain contusion of the first type , though it is far from that. According to its etiology and pathogenesis it can be treated as a focus of posttraumatic hemoangiopathic ischemia (or, to put it briefly, posttraumatic ischemia). Later, this focus is subject to evolution in this or that direction conditioned by severity of a lesion of vascular walls as well as by a degree of disturbance of biochemical processes (proteolysis hyperreactivity, accumulation of secondary endotoxins of peptic origin, increasing concentration of products of lipid peroxidation in parallel with inhibition of antioxidant activity). These phenomena are accompanied by ultrastructural changes in mitochondria of brain cells and disorders of energy metabolism [7, 14, 18]. Changes of ultrastructure of nerve cells watched in a focus of ischemia are well described by Krylov V.V. et al. .
Kornienko V.N. et al. [10, 11] also mention contusion foci of the fourth type. According to them, in this case CT scans are indicative of single or, what is less frequent, multiple homogenous large round or oval foci with a density of +64 - +76 H. units (density of blood clots). From clinical and morphologic points of view these are not contusion foci, but intracerebral hematomas. This fact is acknowledged by the authors themselves. Thus, we consider that this category of “brain contusion” should be withdrawn from the classification as it does not reflect reality, misleads a clinician, reduces his alertness concerning necessity of an operation and fails to correspond to pathologic changes watched in a patient. Such foci of a traumatic lesion are to be classified as posttraumatic intracerebral hematomas.
Besides, Kornienko V.N. et al. [10, 11] describe foci of brain contusion of the second and third types. They treat foci of the second type as moderate brain contusion and of the third type as severe brain contusion or crush zone . It is not quite clear if the authors imply morphologic or clinical severity. Most likely, they speak of clinical severity as there is no such generally adopted notion as severe brain contusion in pathologic anatomy.
According to our opinion, changes observed on CT scans in brain contusion do not always coincide with their clinical manifestations. Thus, a contusion focus in the form of scattered inclusions with high density watched in a zone of diminished density  can give a clinical picture typical of mild, moderate and severe brain contusion. It depends on localization of this focus (for example, a frontal pole, a temporal lobe or brain stem), its spread (volume), severity of perifocal edema or its dissemination over the whole lobe or hemisphere, a tendency to progression or regression. Illustrations given by the authors demonstrate that difference on CT scans of brain contusions of the second and third type lies in quantity (a number of dense particles, their total volume) rather than in quality (a size of separate dense particles). From a practical point of view and taking into account CT data and morphologic changes, it is expedient to classify foci of brain contusion as follows:
As for their clinical or pathogenetic manifestations, multiple foci of brain contusion are not a simple sum of two or more of them. Their clinical course is always more severe than that of one focus of analogous volume. Peculiarities of a clinical course and impossibility to prognosticate further evolution of one of the foci, which is not a rare case, can result in inefficient surgical intervention. An operation performed on one focus only (when another focus is “calm”) can lead to a situation demanding secondary intervention. It can be conditioned by sudden “aggressiveness” of this “calm” focus in a postoperative period and especially if it is located on the opposite side. Traumatic subarachnoid hemorrhages without a focus of brain destruction revealed by CT should be categorized as brain contusions. CT examination carried out during the first hours and day after CCT is indicative of areas with increased density (from +64 up to +76 H. units) between gyri in basal bordering cisterns (blood or small clots). Subarachnoid hemorrhages can accompany other types of traumatic lesions of the brain which should be mentioned in description of CT scans of such a patient. These hemorrhages (as well as subarachnoid hemorrhages of non-traumatic genesis) cause vascular spasm and then degeneration of a vascular wall (hyperplasia) with subsequent persistent narrowing of an artery lumen [2, 12]. Depending on severity, dissemination and clinical manifestations of vascular spasm (local, regional, disseminated, compensated, decompensated), there appear ischemic foci which, in case of a persistent disorder of blood supply due to arterial spasm, can and do result in brain infarction in some patients. There is marked correlation between CCT outcomes and severity of angiospastic disturbances .
A peculiar type of brain contusion is isolated hemorrhages into a cerebral ventricle. They can manifest themselves as simple hemorrhages, when there is diffuse blood in ventricular liquor and sometimes small zones with increased density (small blood clots), as intensive filling of ventricles with blood or as intraventricular hematoma. CT reveals an increase of density of ventricular contents above +16 H. units (up to 44-50 of them depending on an amount of blood poured into ventricles). Some areas (clots) may have density of up to + 76 H. units. In case of hemotamponade of ventricles their whole cavity is filled with blood (density of +64 - +76 H. units). This pathology has a severe clinical course, is accompanied by a severe degree of consciousness disorders and extremely marked meningeal and cerebral symptoms. Blood and especially clots can thrombose tracts conducting liquor, in particular the aqueduct and Monro’s foramen, which results in symmetrical and asymmetrical internal hydrocephalus. Blood in ventricles makes a clinician search for a decision and choose a method of treatment (draining of ventricles, direct intervention with the purpose of blood removal, conservative treatment). Usually such patients develop hydrocephalus in a remote period (2-4 weeks) and some of them need surgical treatment (ventriculoperitoneal shunt).
Axonal lesions occupying a larger or smaller territory in a zone of a pathologic focus and, probably, outside it are watched in any traumatic destructive cerebral damage. However, they are limited. Axonal lesions with unlimited dissemination acquire an absolutely different quality. They are classified as a specific form of CCT called DIFFUSE AXONAL LESIONS OF THE BRAIN, characterized by an extremely severe clinical course and described not long ago by S.L. Strich at 1956. There are three types of such lesions :
Such lesions are the result of acceleration affecting the brain in saggital or coronary planes (lateral dislocation) or oblique acceleration . There is dislodgement of more mobile hemispheres relative to position of the immovable brain stem. It causes stretching and twisting of long axons connecting the cortex of hemispheres with subcortical layers. Disorganization of a neurofilamentous skeleton and membrane of axons progressing during 6-12 hours leads to disorders of axoplasmatic current, temporary block of stimulation, lysis and Wallerian degeneration of fibers. Axonal lesions are accompanied by simultaneous damage of small vessels resulting in petechial hemorrhages. There appears disconnection between the cortex and subcortical structures.
Clinical manifestation of these processes include a comatous state of long duration, signs of severe damage of vital centers of the brain stem and severe vegetative disorders. Unfortunately, this pathology is a frequent cause of vegetative states or fatal outcomes (diffuse axonal lesions are observed in 35% of patients who die of severe CCT). Changes revealed by CT do not seem to be very impressive. They comprise diffuse increase of the brain volume with compression of spaces conducting liquor (ventricles, subarachnoid fissures) or petechial hemorrhages located in the corpus callosum or subcortical ganglia against a background of marked (or absent) brain edema. Insignificant CT findings in diffuse axonal cerebral lesions prove once again that gross morphologic destruction of the brain watched on CT scans does not always correspond to a clinical picture of a disease.
CT assessment of foci of brain contusion discussed above meets the demands of practical neurosurgery to a great extent, helps a clinician to choose tactics of treatment of every particular patient and to prognosticate a possible outcome of this type of CCT.
Thus, the CT classification of brain contusions by Kornienko V.N. et al.  was justifiable and necessary at the first stage of CT introduction into clinical practice. Today it is to be revised and coordinated (if possible) with clinical needs.
Taking into account all the facts mentioned above, classification of CCT based on clinical and CT data can be as follows:
CRANIOCEREBRAL TRAUMA WITH A MILD CLINICAL COURSE
CRANIOCEREBRAL TRAUMA WITH A MODERATE CLINICAL COURSE
CRANIOCEREBRAL TRAUMA WIH A SEVERE CLINICAL COURSE
The definition of a contusion focus volumes of the brain in the allocated groups is based on their clinical importance counted in our department by A.A.Grin 
Distinguishing contusions of the brain stem and cerebellum into separate categories is conditioned by the following peculiarity: lesions of these structures are caharacterized by a severe clinical course with disorders of vital functions (especially in brain stem lesions irrespective of a contusion focus volume) and development of acute occlusive hydrocephalus in the absolute majority of cases.
Besides, a severe clinical course is typical of multiple contusions of the brain. A clinical picture is dependent not on a sum of contusion volumes but on secondary responses of the brain which are usually of extreme importance (development and progression of edema, brain dislocation). In contusions located in both hemispheres a degree of brain stem compression (in brain dislocation) does not always correspond to a value of transverse dislocation which can be minimum or absent. Such localization of contusion foci causes axial dislocation whose clinical course is more malignant than that of transverse dislocations.
We want to emphasize that clinical and CT data (severity of a clinical state and CT findings) disagree rather often. A clinical state of a patient in subarachnoid hemorrhages can be moderate or severe, and posttraumatic acute hydroma with one and the same volume can be characterized by brain compression or its absence, etc. Thus, results of any comparison of clinical characteristics of CCT with CT data should be regarded as relative. However, we consider it expedient to associate pathology, revealed by CT, with more severe clinical forms of its possible course.
Our classification based on clinical and CT data is not something invariable. Any category included into it is dynamic. Depending on direction of a process in every particular patient (progression or regression of pathology), one form can grow into another both from clinical and CT points of view (for example, posttraumatic edema can turn into a limited and even disseminated hemorrhagic focus; a local or limited contusion focus can regress without any intervention). In other words, CT diagnosis of a traumatic focus gives information on the brain state and the focus proper which is reliable only at the moment of examination. That is why assessment of indications for an operation and prognosis of trauma demands dynamic control both of a clinical picture and CT findings.