J. clin. Path., 23, Suppl. (Roy. Coll. Path.), 4, 166-171

Lesions in the cerebral hemispheresafter blunt head injury

SABINA J. STRICHFrom the Department of Neuropathology, Institute ofPsychiatry, London

Though this paper is limited to lesions in thecerebral hemispheres after non-penetrating headinjury, they are unlikely to be confined to thehemispheres, or to the brainstem for that matter.No attempt is made to deal with all the types oflesion which may occur, in particular those due tosystemic factors, such. as fat embolism or anoxiaand complications such as meningitis or epilepsy,are omitted. For further information the reader isreferred to Tomlinson (1964) and Strich (1969).Although some lesions due to head injury can beseen with the naked eye, many important ones canbe seen only with the microscope. Differentlesions will be described under separate headings,but often occur in various combinations withinthe same brain.

Contusions and Lacerations

Apart from subarachnoid haemorrhage, con-tusions are probably the most common macrosco-pic findings. They are areas of superficial damageconsisting of streaks or groups of punctatehaemorrhages accompanied by variable amountsof necrosis, and wedge-shaped areas of necrosiswithout haemorrhage also occur (Fig. 1). Likeother destructive lesions contusions are surround-ed by a zone of oedema (Fig. 1). Contusions arefound under fracture lines and under the site ofimpact, particularly if the head was struck by asmall, fast-moving object such as a cricket ballrather than a large one such as a brick wall. Mostcontusions, however, are found not near the siteof the impact but on the undersurfaces of thefrontal and temporal lobes and the sides and tipsofthetemporal lobes. These so-called 'contre-coup'contusions tend to occur in the same regions of thebrain no matter where the blow. The details of thedistribution vary. Contusions., are often moreextensive on the side opposite} the one which

received the blow. The mechanism of productionof 'contre-coup' contusions has puzzled patholo-gists for centuries. Several authors (Gross, 1958;Sellier and Unterharnscheidt, 1963) hold that theyare due to the collapse of bubbles formed at thesite of negative intracranial pressure which tendsto develop at a point diametrically opposite thesite of impact. There is, however, considerabledoubt amongst physicists (Holbourn, 1943;Goldsmith, 1966) that sufficient negative pressureto cause cavitation ever develops in the ordinaryrun of head injuries. Another difficulty is that,unless there are overlying fractures, contusions arerarely seen in the occipital lobes or the cerebellumafter frontal blows, nor are they seen on theconvexities of the hemispheres.The theory that contusions are rotational

injuries (Holbourn, 1943 and 1945) fits the factsbetter. Brain substance, like other fluids, is highly

Fig. 1 From a man aged 53 years who died in comaseven days after a road accident. Fractures of thevault of the skull over the sagittal sinus passed into therightfrontal region. Coronal section showing awedge-shaped area of necrosis (arrow) on the rightand a few small contusions (c). The right hemisphere isswollen. R = right.

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Lesions in the cerebral hemispheres after blunt head injury

incompressible, this means that the brain cannotreadily change in volume, it cannot draw awayfrom the skull. or lag behind when the head moves.Changes in brain volume due to displacement ofblood or of cerebrospinal fluid take place tooslowly to matter in this context. The brain is,however, easily changed in shape and distortedand is likely to undergo swirling movements,particularly when there is rotation of the head(Holbourn, 1945). Where the brain glides'over asmooth surface there may be subarachnoidhaemorrhage due to displacement of the brainrelative to the pia arachnoid and consequenttearing of blood vessels. But where the skull isuneven and is closely moulded to the convolutions,as in the floor of the anterior and middle fossae oraround the sphenoidal ridge, surface damageoccurs when the brain rotates.

Contusions heal in a few weeks after which timetheir age cannot be determined. The necrotictissue is removed and the floor of the defect iscovered by a glial or, occasionally, a thin collagen-ous scar. The end result is the characteristicshallow, often slightly yellow, defect running alongthe crests of gyri. In this, the scars differ fromthose left after necrosis due to small vascularlesions which are classically found at the bottomof sulci. The cortex at the edge of healed con-tusions is often gliosed and may contain calcifiedneurons. Healed contusions were an incidentalfinding in 25% of 2,000 consecutive necropsiesreported by Welte (1948).

In a laceration the surface of the brain and the

Fig. 2 From a man aged 55 years who had a largeright-sided subdural haematoma evacuated seven hoursafter a motorcycle accident. Marked brain swellingpostoperatively. Survival in a state of 'akineticmutism' for three months. Coronal section shows thatmuch of the right temporal lobe has disappeared (oldlaceration), the ventricles are dilated due to atrophyof white matter, and there are cysts in the whitematter on the right. Microscopically there wasevidence ofprevious severe, widespread cerebraloedema (Fig. 3). Healed brainstem haemorrhages werealso present. R = right.

overlying leptomeninges are torn. This constitutesa more serious degree of brain damage than thatdue to contusions partly because it entails a moreextensive loss of brain substance (Fig. 2). Lacera-tions leave a collagenous scar which may beattached to the dura, especially if this has also beentorn. Such lesions are more likely to be epilepto-genic than simple contusions. In the acute stagelacerations are surrounded by a larger zone ofoedema than contusions and this may turn thedamaged lobe into a significant space-occupyinglesion. Oozing from injured blood vessels will leadto the accumulation of subarachnoid blood, orworse, to the formation of a subdural haematomawith all its complications.

Cerebral Oedema

Current work on cerebral oedema surroundingdestructive lesions suggests that the leak of fluidoccurs from damaged vessels in the actual lesionand that it seeps from there, extracellularly, intothe surrounding white matter whose vascularpermeability is not in itself abnormal (Klatzo,1967). This has been demonstrated in experi-mentally produced necrotic brain lesions. Afluorescent dye which does not penetrate thenormal blood-brain barrier is injected intra-venously at the time of making the lesion. Somehours later, and shortly before killing the animal,a second dye fluorescing with a different colouris injected and the progress of the two substancescan be visualized. The spread of oedema fluid ispromoted by a high blood pressure (Klatzo, 1967).

Severe oedema of a hemisphere frequentlyoccurs after the evacuation of an intracranialhaematoma. This oedema does not respond wellto the usual treatments and is a serious complica-tion. Its pathogenesis is not understood. Swellingof the brain is not necessarily due to oedema fluid.It can be due to vascular engorgement which canbe severe enough to increase the brain volumesignificantly and therefore to raise the intracranialpressure. This congestion can be minimized byproviding a clear airway and good ventilation oreven by hyperventilation of the lungs.The accumulation of fluid in the white matter in

cerebral oedema is accompanied by histologicalchanges which can be seen with the light micro-scope. The astrocytes react quickly, that is, withinhours in the experimental situation (Klatzo,Piraux, and Laskowski, 1958). Their nuclei enlargeand the cytoplasm, which is normally not visible,swells to become a homogeneous, eosiniphilicmass. These are the 'plump', 'swollen', 'reactive',or 'gemistocytic' astrocytes (Fig. 3). Silverimpregnation shows that their processes alsoswell. The oedematous white matter looks pale instained sections; the myelin sheaths are pushedapart and may look irregular or beaded. Theastrocytes remain prominent for a long time (Fig.

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3). When the oedema resolves there is atrophy of glial fibrils (Mallory's phosphotengstic acidthe white matter and myelin actually disappears haematoxylin, Holzer).(Fig. 4) without the formation of the usualsudanophilic breakdown products. At the sametime an astrocytic fibrous gliosis develops whichmay be very dense and is seen with stains to show Ischaemic Necrosis

Areas of complete or partial tissue necrosis due toandischaemia are frequently seen after head injury.F0g# They may consist of small infarcts at the bottom

Fi sof sulci or they may involve part or the whole ofswollen astrocytes (arrowsthe territory supplied by one of the major cerebralfibresare sparse bat looknormal.NSatgranlecells. arteries. The cause of these vascular lesions is

unknown, but spasm due to distortion or stretch-The appearances aretypcalofongstadingoing of blood vessels or to direct damage of the

vessel by bone fragments, etc, must be considered.Ischaemia at the boundary zones between ad-

oedema.Survival time three months. Haematojacent arterial territories because of systemichypotension (Adams, Brierley, Connor, and Treip1966) is also an important factor.

Central Haemorrhages

Haemorrhages are a commnon macroscopicfeature of head injury but frequently microscopicones are also present. Haemorrhages are usuallymultiple and may occur anywhere but they havesome favourite sites, for instance, the corpuscallosum (Lindenberg, Fisher, Durlacher, Lovitt,and Freytag, 1955), usually on its undersurfaceand to one side of the midline (Fig. 5), or the

Fig.3 Sctino whte atte frm te bainsee insubcortical white matter. It is generally agreed that

Figures 2 and 4. There are large numbers ofplump, sc amrhgsadsm ftoei hswollen astrocytes (arrows to some). Myelinated nerve brainstem are of traumatic origin, that is, thatfibres are sparse, but look normal. No fat granule cells. they are due to tearing of blood vessels at the timeThe appearances are typical oflongstanding or resolved of the accident. Torn vessels have in fact beenoedema. Survival time three months. Haematoxylin demonstrated in serial sections in cases of headand eosin. X 300. injury (Krauland, 1950; Mayer, 1967). During

Fig. 5 From a man aged 25 years involved in a roadaccident and surviving in coma for five weeks. Coronalsection of brain showing a haemorrhage in one side of

Fig. 4 Section of cortex and white matter from the the corpus callosum and another in the parasagittalbrain seen in Figure 2. Myelin staining is pale and white matter on the right (R). There was severeblotchy. Healed contusions at arrows (cf. Fig. 3). degeneration of the white matter microscopically (seeMyelin stain x 1k7. Fig. 6).

Sabina J. Strich 168copyright.

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Lesions in the cerebral hemispheres after blunt head injury

Fig. 6 Section of hemisphere white matter of thebrain shown in Figure 5. There is a cluster of glialcells, one of which is in mitosis. Many astrocytes(arrows) have enlarged nuclei and swollen cytoplasm,evidence of degeneration in the white matter.Haematoxylin and eosin x 320.

Fig. 7 Section from cerebrum showing extensivemyelin degeneration in white matter and corpuscallosum (arrow). Myelin breakdown products show asblack dots (fat granule cells). From a boy aged 17years who fell from a height and survived for one yearin a state of 'akinetic mutism'. White matter andcortex were normal macroscopically. Marchi x 1-3.

Fig. 8 From a woman aged 35 years who died 11 days after a road accident without having recoveredconsciousness. Section through internal capsule. (a) Palmgren silver impregnation. There are many argyrophilicswellings (retraction balls), some clearly at the ends of ruptured nerve fibres. (b) Haematoxylin and eosin.Retraction balls are present (arrows) but are less conspicuous than in a. x 225.

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Sabina J. Strich

rotational acceleration of the skull and the swirl-ing motions of its contents the brain becomesdistorted, that is, its constituents become dis-placed relative to one another. The shear strainsproduced by this distortion are sufficient inordinary head injuries to tear blood vessels, nervefibres, and synapses. The physics of the processesinvolved and the reasons why linear accelerationand blows to the fixed head are unlikely toproduce generalized, as opposed to local, braindamage were set out very clearly by Holbourn(1943, 1944, and 1945). Holbourn's theoreticalconsiderations have been confirmed by experi-mental work on monkeys (Pudenz and Shelden,1946; Ommaya, 1966) whose skull caps had beenreplaced by transparent material. Considerableswirling and gliding of the convolutions was seen

when the head was free to move after a blow. Inother experiments concussion has been producedby rotational acceleration alone without impact tothe head (Ommaya, Faas, and Yarnell, 1968;Unterharnscheidt and Higgins, 1969). Significantrotational acceleration or deceleration of the headoccurs in a large proportion of human headinjuries.

Tearing of Nerve Fibres

There is now good clinical and pathologicalevidence that nerve fibres can be torn in the brainat the time of the accident (Strich, 1956 and 1961).This type of brain damage cannot be seen with thenaked eye even when severe. In many brains whichmacroscopically show a few haemorrhages onlywidespread damage to nerve fibres will be foundmicroscopically (Figs. 5, 6, 7, and 8). The histo-logical changes are the same as those followinginterruption of axons from any cause (Walleriandegeneration). When an axon is cut a bead of

Fig. 9 Section ofpons showing asymmetrical tractdegeneration. There was severe nerve fibre degenerationin both hemispheres. From a boy aged 18 involved in a

motorcycle accident. Became decerebrate andextremely demented, survival 13 months. 1, pyramidaltract; 2, medial lemniscus; 3, central tegmental tract.Marchi x 13.

eosiniphilic and argyrophilic axoplasm called aretraction ball or bulb (Fig. 8) forms at both cutends within hours (Cajal, 1928). The portion ofthe axon severed from the cell body becomesirregular and fragmented and is resorbed in a fewweeks. The retraction ball at the proximal endremains visible for months. Retraction balls donot invariably form. They are often absent undercortical contusions and at the edge of haemor-rhages, for example. Retraction balls are commonin cases of head injury (Nevin, 1967; Peerless andRewcastle, 1967). Their distribution depends onthe mechanics of the injury, and factors such asthe direction of the shear strains relative to fibredirection are probably important. Thus it is foundthat bundles of nerve fibres running in onedirection are damaged while nearby bundlesrunning in a different direction may be spared.Degeneration is often strikingly asymmetrical,certain anatomical tracts in one hemisphere or onone side of the brainstem (Fig. 9) being apparentlyselectively involved. Good places to look forretraction balls are the corpus callosum (even whenthere is no naked-eye lesion), the parasagittalareas of the hemispheres, the internal capsules,and the pons.

Wallerian Degeneration

When a severed axon degenerates, its myelinsheath also undergoes Wallerian degeneration. Inthe peripheral nervous system this process iscompleted in two or three weeks but in the centralnervous system Wallerian degeneration is a veryslow affair (Daniel and Strich, 1969, light micro-scopy; Bignami and Ralston, 1969, electronmicroscopy). The early stages are quite difficult torecognize in histological sections, though degener-ating tracts may look strikingly white macro-scopically. Under the microscope the affectedwhite matter or tract looks 'untidy'. The myelinsheaths are distended and later collapsed and theyare broken into spheres or sausages. The nuclei ofthe astrocytes enlarge and their cytoplasm becomevisible (Fig. 6); pyknotic nuclei and glial cells withoddly shaped nuclei can also be seen. Microglialcells (macrophages) are scanty in normal whitematter and their number does not increase duringthe first few weeks of Wallerian degeneration.There is at first no loss of myelin and stainablebreakdown products do not appear for severalweeks. After this, macrophages full of myelinbreakdown products (cholesterol esters) becomeprominent and the degeneration is easily seen insections stained with the Sudan dyes, Oil-red-O,or with osmium tetroxide (Figs. 7 and 9) as in theMarchi method (Strich, 1968). After some eightweeks loss of myelin is recognizable in paraffinsections. The pattern ofdegeneration does not nowreflect the pattern of the original damage. Thewhole length of the disconnected portion of thenerve fibre degenerates, the site or sites of inter-

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Lesions in the cerebral hemispheres after blunt head injury 171

ruption cannot usually be identified and degenera-tion of short fibres will be inconspicuous, whereasthat of long fibres will be obvious.

Microglial Reaction

Recently clusters of microgial cells have beendescribed scattered about in the brains of patientswith head injuries surviving for morethan 18 hours(Oppenheimer, 1968). These cells are probablyreacting to minute tissue tears and were found inabout two-thirds of the 59 cases examined. In theearly stages these microglial cells are most readilyseen in silver-impregnated sections (see Oppen-heimer, 1968 for Weil-Davenport's modifiedmethod, frozen sections; Gallyas 1963, paraffinsections). After three or four weeks smallcollections of glial cells are characteristically seenin routine paraffin sections of the white matter(Fig. 6) from cases with massive tearing of nervefibres.

Concussion

Concussion is supposed to be a completely revers-ible state. This does not exclude the occurrence ofsmall, irreversible lesions from which clinicalrecovery may be complete. It is of great interestthat clusters of microglial cells and retraction ballshave been described in the brainstem and hemis-pheres in cases ofconcussion (Oppenheimer, 1968),that is, in patients who were briefly unconsciousafter a head injury, recovered, and died of othercauses later. There is also the possibility ofreversible lesions, for instance due to stretchingrather than tearing of nerve fibres. Dislodging ofsynapses or displacement of cell organelles mayalso occur but such changes are unlikely ever to beseen in human necropsy material. The localizationof visible lesions in human concussion has notbeen mapped out in detail. The brainstem is usuallyregarded as the important site, but the retrogradeand posttraumatic amnesias and the confusionwhich are so prominent in concussion clinicallysuggest a more widespread cerebral dysfunction.The pathology of the postconcussion syndromehas not been investigated but it would be worthwhile to look for retraction balls and clusters ofmicroglial cells should such a patient die within afew weeks of a minor head injury.

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