Medico-Legal Aspect of Head Injuries
Of all the regional injuries suffered by the body the head and neck injuries are by far the most common and important in Forensic Practice.
The reasons for this include
1. The head contains the most vital organ in the body. An injury which may not be fatal on other areas may be fatal on the head and neck.
2. Knowing that it contains the most vital organ and an injury can be easily fatal it is targeted in assaults, especially in blunt force trauma and even in firearm injuries.
3. In road traffic accidents and falls death is often caused by head and neck injuries.
Therefore, a sound knowledge and understanding of head and neck trauma is essential to deal with the medico-legal issues raised by such injuries.
This should start with understanding the anatomy of head and spine. The unique nature of injuries to this area partly depends on its anatomy.
The easiest and most practical way to classify injuries to head and neck is to go layer by layer, starting with the most external, which is the scalp.
Since this is the way the forensic pathologist is supposed to describe head and neck injuries in their medico-legal reports and even in oral evidence in high court.
Injury to Scalp
Forensic Anatomy of Scalp
The most important differences in the scalp compared to the skin are as follows:-
1. The scalp covers the cranial vault extending from external occipital protuberance and superior nuchal lines to the supraorbital margins. It consists of 5 layers : the skin, connective tissue, epicranial aponeurosis, loose areolar tissue, and pericranium. The first 3 layers are bound together as a single unit. This single unit can move along the loose areolar tissue over the pericranium, which is adherent to the calvaria.
2. The skin of the scalp is thick and hair bearing and contains numerous sebaceous glands. As a result, the scalp is a common site for sebaceous cysts.
3. Connective tissue (superficial fascia). It is a fibrofatty layer that connects skin to the underlying aponeurosis of the occipitofrontalis muscle and provides a passageway for nerves and blood vessels. Blood vessels are attached to this fibrous connective tissue. If the vessels are cut, this attachment prevents vasospasm, which could lead to profuse bleeding after injury.
4. Epicranial aponeurosis (galea aponeurotica) is a thin, tendinous structure that provides an insertion site for the occipitofrontalis muscle. Posterolaterally, the epicranial aponeurosis attachment extends from the superior nuchal line to the superior temporal line. Laterally, the epicranial aponeurosis continues as the temporal fascia. Anteriorly, the subaponeurotic space extends to the upper eyelids due to the lack of a bony insertion. This loose areolar tissue provides a potential subaponeurotic space that allows fluids and blood to pass from the scalp to the upper eyelids.
5. Loose areolar tissue - Areolar tissue loosely connects the epicranial aponeurosis to the pericranium and allows the superficial 3 layers of the scalp to move over the pericranium. Scalp flaps are elevated along a relatively avascular plane in craniofacial and neurosurgical procedures. However, certain emissary veins traverse this layer, which connects the scalp veins to the diploic veins and intracranial venous sinuses.
6. Pericranium is the periosteum of the skull bones. Along the suture lines, the pericranium becomes continuous with the endosteum. A subperiosteal hematoma, therefore, forms in the shape of the skull bones.
7. Occipitofrontalis muscle consists of 2 occipital bellies and 2 frontal bellies. The occipital bellies arise from the superior nuchal lines on the occipital bone. The frontal bellies originate from the skin and superficial fascia of the upper eyelids. The occipital and frontal bellies insert into the epicranial aponeurosis. (http://emedicine.medscape.com/article/834808-overview)
Abrasion of the Scalp
Production of abrasions is modified by the presence of hair. Even if present, the examiner may miss them as they are obscured by the hair unless the scalp is closely shaven using a sharp scalpel.
Bruising of the Scalp
The same obscuring effect of hair may hide the presence of bruises on the scalp unless it is carefully palpated and shaven.
Since the bruises in scalp can only disseminate sideways and not vertically into the skull they are usually easily detectable and last longer.
Most bruises are confined to the tissues between the epidermis and epicranial aponeurosis. Sometimes they can be seen below the aponeurosis and even beneath the epicranium. In infants with skull fractures the haematoma may occur beneath the epicrainium. Since it is attached to the suture lines it can be well-circumscribed and limited to a single skull bone.
The shape and size of the instrument (weapon or object) are not usually reproduced on the scalp due to the presence of the hair, which acts as a cushion and the dissemination of bruise due to gravity through tissue planes. As a result of this phenomenon bruises on the skull can gravitate around the eyes causing ‘black eyes’ or peri-orbital haematoma.
Laceration of the Scalp
They bleed profusely and may cause death by blood loss if large enough and not treated early. If the head is in dependent position they may bleed profusely even after death making the calculation of ante mortem blood loss by the amount of blood present at the scene more difficult. Sometimes, a scalp laceration inflicted after death (post-mortem laceration) may bleed considerably. This may cause confusion as to the ante mortem or post-mortem nature of the injury.
Unlike bruises scalp lacerations may reproduce the size and shape of the instrument e.g. a hammer blow onto the scalp may produce either a circular or semi-circular laceration depending on whether the full or part of the face of the hammer struck the scalp.
Scalp laceration may look like an incised wound. Scalp is stretched overlying the skull, which may act like an anvil trapping the scalp between it and the offending object. This may produce a nice and clean split mimicking an incised wound. However, as in the case of any laceration the following features may distinguish it from an incised wound.
1. Bruised margins
2. Presence of tissues bridging (fascia, nerves, blood vessels and hair bulbs) in the wound depth
3. Uncut head hair crossing the wound
Black Eyes (Peri-orbital Haematoma)
Black eye is an appearance caused by blood in the soft tissues around the eye. It is usually caused by a direct trauma onto the eye socket such as a punch or kick. However it can also be caused by following mechanisms.
1. Gravitational seepage of blood from a bruise or laceration on the scalp or eye brow. The victim should have been upright at least for some minutes before death (in a case of a dead victim).
2. Leakage of blood into to the eye from a fractured anterior fossa of the skull.
Facial Injuries
Facial injuries can be part of the injuries to the head. However, they are rarely fatal by themselves unless the victim has asphyxiated from the blood entering into the air passages.
The face has many prominences with complex contours such as chin, nose, cheekbones, eyebrows, ears and lips. They may be the ones first to receive blows directed at the face producing characteristic injuries.
Eyebrows are injured during falls and blows producing lacerations and fractures of the frontal bone and orbital margin.
Although the cartilaginous part of the nose escapes from being serious damaged nasal bone is fractured causing dangerous bleeding into the nasal passages if the victim is unconscious.
Direct impacts on the face can cause fractures of the mandible and maxilla. This also can cause dangerous bleeding in to air passages. Severe impacts like kicking and road traffic accidents may totally detach the maxilla from the face.
Injuries to the mouth and lips are very common in ‘physical assaults’ such as child abuse, wife battering etc. Punching or kicking on the mouth injures the lips when compressed between the inflicting weapon and teeth. Rupture of the frenulum in a child is considered to be pathognomonic in child abuse.
Fracture of Skull
Forensic Anatomy
The adult skull bone is consistent of two tables, outer and inner. The outer is twice the thicknness the inner. In between these two tables is a central zone of soft cancellous bone called ‘diploẽ’. This is interrupted at suture line and absent in thin areas such as the squamous temporal bone and base.
The thickness of the skull varies from area to area even within the same bone. Thin areas or plates lie in the paeietotemporal, lateral frontal and lateral occiptial regions. They are supported by strong thick bones such as petrous temporal, greater wing of sphenoid, saggital ridge, occipital protuberance and glabella.
Thickness of the skull ranges from 6 to 10mm in frontal and parietal regions, 4 mm in temporal bone and 15 mm or more occipital bone at the midline.
Mechanism of Skull Fractures
The experimental studies done in the past revealed following facts.
1. A fairly rapidly moving blunt object such as a baseball bat, brick, hammer may cause an area of depression and most of the expended energy is absorbed in producing this depression. When the area under the point of impact is ‘inbended’ the immediate periphery is ‘outbended’. When this force exceeds the limit of elasticity of the bone fracture occurrs.
2. In the inbended area the bone is concave and compressed. As result of ‘tearing apart forces’ acting on the inner table multiple radial fracures occurr. Immediately away from the impact the bone is convex and streched. As a result of the ‘tearing apart forces’ acting on the outer table a circular fracture occurr. Combination of these two mechanisms ultimately produces a deprrssed communited fractur, which circular in the case of a hammer blow.
3. A slowly moving object causing a localized blow may produce a depression at the site of impact but failied to cause a depressed communited fracture as in the case of hammer blow as not enough energy is expended. However, the energy of the blow may cause the skull to ‘out bend’ away from the site of intact. This is called ‘struck hoop’ anology. These‘outbended’ areas may produce linear fractures due to ‘tearing apart forces’acting on the outer table, which may extend towards the point of impact. If the energy is more there may be more than one linear fracture produced as a result of outbending away from the site of impact.
4. A slow moving high kinetic energy blunt surface (e.g. deceleration fall on a flat surface) would result in extensive communition with radial fracture lines extending from centre of impact and circular fracture lines at varying distances around the area of impact (stellate fracture). At the point of impact the inbending fails and a comminuted fracture occur due to tensile stresses of the inner table with several (3-6) linear fractures, which would extend outward from the centre of impact. Simultaneously linear fracture occur in the periphery due to outbending, which may extend towards the point of impact and merge with the linear fractures of the inner table. If the energy is adequate there is a failure of the bone from inbending immediately around the point of impact at the junction between inbending and ‘not-yet-inbended’ bone causinng a circular or curvilinnear fracture lines at various distances from the point of impact. These semicircular fractures are initiated on the external surface of the skull.
5. It was found that impacts on certain areas of the skull produce fractures in specific areas of the skull e.g. impact on upper temporal or parieto-temporal areas cause fissured fractures running obliquely downward across the temporal area.If impact is severe there will be another fissured fracture, which would run to the other side across the vertex.
6. When there is heavy impact on the top or side of the skull a linear or fissured fracture would run down to the middle cranial fossa, crosses the middle cranial foss along the petrous temporal bone or greater wings of the phenoid to enter the pituitary fossa. Then it crosses the pitiuitary fossa to enter into the contralateral middle cranial fossa, sometimes dividing the base of the skull in to two justifying the label‘hinged fracture’. According to the rule these fracture do not initiate at the point of impact instead they originate away and extend toward the point of impact.
7. When the impact is on the frontal area a linear fracture would exend downward to the orbital margin, turn inwards and extends into the anterior cranial fossa. When the impact is on the occipital area a linear fracture would typically extend vertically downward just to the side of the midline to the posterior cranial fossa and reaches the foramen magnum.
8. It should be noted that when there are two successive impacts on the head the linear fractures caused by the second impact will terminates at those from the first impact when they meet, which is called ‘Puppe’s rule’. By knowing this seemingly common sense rule one would be able to identify the first impact from the second.
Types of Skull Fractures
1. Linear Fracture
They can be either curved or linear usually present in the weaker unsupported bones although can be present in any bone. According to the mechanisms described above they can either radiates from the site of impact, which is depressed, or they can originate at a site away from the point of impact due to outbending of the periphery. They may be confined to either outer or inner table but commonly involves both tables.
A typical linear fracture is the ‘hinged fracture’ wich has been described earlier. It is also called ‘motorcyclist’s fracture’ for obvious reasons.
Sometimes, when a linear fracture reaches the skull sutures it opens up the suture line causing ‘diastasis’. This is often seen in the sagittal suture but rarely already closed metopic suture inbetween the frontal bones can also be opened.
2. Ring Fracture
This is a fracture in the posterior cranial foss, which encircle the foramen magnum. A fall on to the feet from a height is the usual cause. The transmitted force through the feet, pelvis and the spine may ram the cervical spine into to the base of the skull taking a ring of bone around the foramen magnum with it. A heavy impact on the vertex may also produce this fracture in some occasions.
3. Pond Fracture
This is basically a depression of the bone with no fractures. The mechanism is same as in depressed fractures but the skull fail to fracture due to its elasticity especially in infants.
4. Mosaic or Spider’s-Web Fractures
The mechanism of this fracture has been described above. Multiple linear fractures, which are connected to each other by one or more rings of succesive circular fractures, extend outward from a central comminuted depressed fracture is called a mosaic or spider-web fracture. Sometimes the central depression minimal or absent.
5. Depressed Fracture
As described above they are usually caused by weapons with small striking surfaces such as baseball bats and hammers.Some times they can be confined only to the outer table. A depressed fracture caused by a hammer may not be circular as expected instead it was a semic circle with more depression at one end. This occurs when only a part of the hammer head strikes the skull. Where the maximum depression is seen is usually the hammer strikes the skull first.
6. Liverage Fractures
When a heavy sharp cutting weapon, sword, axe, ‘manna knife’ etc. strikes the skull it usually cause a more or less a clean cut on the skull. In some of these cases in addition to the‘clean’ cut there are two linear fractures on the either side of the cut, which seperates a flap of bone to one side of the cut. They are called ‘liverage fractures’. They occur as a result of movment of the weapon side ways deliberately or unitnetionally in order to release it from the skull during the process of withdrawal of the weapon after striking the skull.
Complications of Skull Fracturs
Although the factures are not dangerous to life by themselves they are indicators of the severity of the head injury.
1. If the fractures cross a branch of middle meningeal artery and/or dural sinus it might give rise to Extra dural haemorrhage.
2. Factures, especially depressed fractures can damage the brain by impinging of fractured bones.
3. Traumatic Epilepsy – This may be a sequalae of depressed fracture. When this has occurred following an assault or accident the victim can claim monentary compensation for the long term neurological disability.
4. Infection – Infection can spread to the intracranial tissue from all kinds of fracures. Not only the meninges are affected but also the brain itself. The infection spread through a compund fracture or through nasal cavity when the anterior cranial fossa is fractured or paranasal sinuses, mastoid air cells or middle ear cavity especially with the basal fracures.
Intra-Cranial Injuries
The brian, its membranes and blood vessles are said to be the most fragile of all the organs of the body. That is why they are encased in a rigid bony box.
Forensic Anatomy of Brain Membranes
Dura Mater
This is the outer most pachymeninges. It consist of two layers. The outer layer is firmly attched to the skull and acts as the internl periosteum. The innerlayer merges with the arachnoid. The subdural space is really a potential cleavage plane.
The falx and tentorium are formed by dura, in which the cerebral venous sinuses run. Branches of meningeal vessles run over and through it. Bridging veins traverse the dura to enter the venous sinuses especially along the vertex and the tips of temporal poles.
Arachnoid mater
This is the outer of the two leptomeninges. The other is the pia mater. It is a thin vascular meshwork closely applied to the dura mater. Although there is not true subdural space in normal conditions they can easily split apart as the attachment is weak.
Blood vessels carries a sheaths of arachnoid when penetrates the brain. The vessels and thin connective tissues strands anchor the brain within the subarachnoid space.The width of the subarachnoid space vary from few millimeters in the young to a centimeter or more in the old. In them the bridging vessels are vulnearable to rotatory and shearing forces.
Pia Mater
This is not a true membrane.
Intra-Cranial Haemorrhages
Extradural Haemorrhage
This is the collection of blood between the skull and dura mater and is the least common of three types of brain membrane haemorrhages.
Since the dura is closely applied to the skull in the base it does not occur on the base except on the posterior fossa. On the vault the potential space between dura and skull can be seperated by arterial blood and less often by venous blood also.
Most extradural haemorrhages are associated with skull fracture but about 15% occurr in intact skull. 10% of extradural haemorrhages are associated with subdural haemorrhages. Bilateral extradural haemorrhages are rare.
The commonest site is pareito-temporal area where rupture of a branch of middle meningeal artery is associated with a fracture line.
Leakage from the ruptured artery strips the dura from the skull due to its high pressure. The minimum collection of blood may vary from 35 – 100 ml before clinical signs appear. Less common fronal or occipital areas the bleeding is either from smaller branches of meningeal artieris or from venous sinuses, in which a fracture is not essential and bleeding is much more slower.
Clinical Signs
The classical clinical sign of extradural haemorrhage is ‘lucid interval’. The victim recovers from intitial concussion to deteriorate after the latent period (lucid interval) with the advent of raised intracranial pressure to unconsciouness and subsequent death.
In should be noted that in some cases this lucid interval is absent as concussion merges with unconscousness caused by raised intra cranial pressure.
The lucid interval may be of variable duration from as little as half and hour to more than a day depending on how quick or slow the bleed is. However the average interval is thought be 4 hours.
Medico-Legal Importance of Extradural Haemorrhage
A doctor may be accused of medical negligence if a patient is discharged from the hospital after the reovery of the concussion and died at home from complications of extradural haemorrhage.
A question may be asked from a doctor in a court trial about the volitional activity of a person who died from extradural haemorrhage. For instance the court might want to know whether it was possible for a man who died from extradural haematoma to talk to a person after hours of assult and died at home later.
Extradural haemorrhage is never considered to be a ‘contrecoup’ injury. (Contrecoup injuries will be discussed later.)
Heat Haematoma
This is a collection of altered blood in the extradural space in a severly burnt body with burning of salp and skull mimicking extradural haematoma and considered to be a postmorem artefact.
Subdural Haemorrhage
This is collection of blood in the sudural space and it is much more common than extradural haemorrhage. Compared to the latter it is less often associated with skull fractures.
It can be classified in to acute and chronic.
It is more common in both extremes of life. In young it is infamously associated with fatal child abuse. Rediscovery of syndrome of child abuse by Caffey in 1946 was prompted by his observation of association of subdural haemorrhage with long bone fractures.
In old people it commonly exist in chronic form, which may be mistaken either for ‘strokes’ or senile dementia.
This lesion is always due to trauma. Probably there is no entity called ‘spontaneous subdural haemarrhage’.The reason for not having a history of trauma in some cases is that it has been such mild in form that the victims or others can not recall it. As with extradural haemorrhage the minimal amount of blood before the clinical symptoms appear is thought to be between 35 – 100 ml.
As with extradural haemorrhage the position of subdural haemorrhage should never be interpreted as ‘contrecoup’.
Acute Subdural Haemorrhage
This is a common result of any significant head injury. Presence or absence of skull fracture is immaterial as it does not have any role in mechanism of the haemorrhage. After all skull fracture is only an indication of the severity of trauma.
The lesion is often seen alone in a close head injury with no skull fractures and scalp injuries.
The source of bleeding is ruptured bridging or communiating veins in the subdural space due to shear stresses caused by the acceleration or deceleration of the head with rotational component. This moves the bridging veins laterlly enough to rupture them from their junction at the cortical vein.
Unlike extradural haemorrhage which is confined to one place by the dura annd the skull, subdural haemorrhage can move.
Clinical Signs
As with extradural haemorrhage there can be a latent period or ‘lucid interval’ after the initial concussion. When there is ‘lucid interval’ it should be longer than the average 4 hours for the more rapid arterial bleeding of extradural bleeding. Infact this does not have a upper limit as acute subdural haemorrhae can merge with the chronic variety.
Chronic Subdural Haemorrhage
This is usually lesion of old people and often an incidental finding,which does not have any association with the cause of death.
Most of these lesions are small and do not give rise to any neurological symptoms. Therefore, in these individuals cause of death should be sought in some other place and this should not be given as the cause of death.
Some chronic subdural haematomas may reach volumes of 100-150 ml but still they can remain asymptomatic. When they are symptomatic they can mimick ‘strokes’ and ‘senile dementia’ an so on.
Some times they can become large and act as space occupying lesions with associated changes of raised intra-cranial pressure such as tonsillar and uncal hernatiations. How they enalrge is not known but thought to be due to repeated further bleeding and/or osmosis of fluid from the CSF to the haematoma.
Chronc extradural haemorrhage, when recent, up to several weeks old are tan or red-brown colour with a gelatinous membrane covering the surface. Older haematoma, up to months or even a year old, is firmer, with tough membrane around both surfaces. The conent may be brown or even straw coloured.
Medico-Legal Significance
As with extradural haemorrhage a doctor would be held responsible for a death of a patient from acute subdural haemorrhage, who had been discharged after the recovery of initial concussion.
As with the extradural haemorhage a question may be asked from the doctor about the possible volitional activity of a person who died from acute subdural haemorrhage.
In a person who died from chronic subdural haematoma a question will be raised as to when the bleeding started and what prompted the bleed.Was it the alleged assult on such and such date and time or was it the fall caused by the road traffic accident on such and such date and time?
In that case accurate dating of the chronic subdural haematoma becomes crucial.
Subarachnoid Haemorrhage
This is commoner than other two haemorrhages. Any form of trauma to brain, either it is blunt, sharp or penetrating, which give rise to brain injuries, extradural haemorrhage and subdural haemrrhage, can be associated with subarachnoid haemorrhage.
It even can occurrr as a pure lesion without any other assoicated memebrane haemorrhages or brain injuries following trauma.
Subarachnoid haemorrhage differes from other two haemorrhages as unlike the latter it can occur as a result of natural causes such as rupture of berry aneurysm and arterior-venous malformations.
Appearance & Mechanism of causation
Subarachnoid haemorrhage is caused by the same mechanism as that in the subdural haemorrhage. The rotational movement of the brain and the shearing forces it generates rupture the bridging veins that crosses the subarachnoid space from the cortex to enter the large draining veins and sinuses in the dura. Small cortical arteries also contribute to haemarrhage. In subarachnoid haemorrhages associated with brain injuries such as lacerations, contusions the haemorrhage comes from cortical veins and small arteries. Sometimes intracerebral haemorrhges rupture through the cortex to produce subarachnoid haemorrhages.
When it occurs as result of contusion and lacerations they are present around these injuries. When it occurs due to a blunt impact, with or without other membrane bleeding or cortical bruising it can occur in anywhere on the brain.
The bood in the subarachnoid space tend to mix with CSF. Therefore unlike other haemorrhage less likely to clot. Like subdural haemorrhage it can gravitate down to lower position.
In head injury, death is usually more likely due to associated membrane haemorrhages and brain injuries than the subarachnoid haemorrhage itself. In the unlikely case of pure traumatic subarachnoid haemorrhage it must be accepted as cause of death.
Rotational Trauma to the Head and Upper Neck: Basilovertebral Artery Injury (Traumatic Basilar Subarachnoid Haemorrhage)
It has been a well-recognized fact for the last few years that a blow to the side neck/or head give rise to fatal subarachnoid bleeding.
The cause for this phenomenon is thought to be due to tear or dissection of the vertebral artery, which allows the blood to tract along the upper part of the vessel and enter cranial cavity causing basilar subarachnoid haemorrhge.
Some of this cases have frctured transverse process of the 1st vertebra.Hence it was called CV-One Syndrome.
The mechanical force initiated by the blow to the side of the neck may cause tilting and rotation of the neck could damage the vertebral artery in the vertebral canal in addition to producing skin and soft tissue injuries on the side of the necck at the site of the blow. However, in some cases there may not be any external sign at all.
A blow can be from a fist, foot, or any blunt object, which land in the side of the back of the neck in the region between the angle of the jaw and ear.
However, some pathologist believe that the vertebral artery damage is just a concomitant finding. They believe the subarachnoid haemorrhge is due to the damage to the intra-cranial vessels and not due to the vertebral artery damage. They both, they think, are parellel findings and not cause and effect events.
Autopsy Demonstration of Bsilo-Vertebral Artery Damage
When history suggests a traumatic subarachnoid haemorrhage following a blow to the side of the neck or external examiantion shows a bruise on the side of the neck in a case of sudden death vertebral artery damage should be suspected and demonstrated at autopsy.
There are several ways of demonstrating vertebral artery damage
As soon as the subarachnoid haemorrhage is found when the skull cap is removed precations should be made to demonstrate the vertebral artery damage.
The brain is lifted from the skull carefully and basilar artery is clamped off with surgical forceps.Then the brain is removed after cutting the basilar artery off above the clamps.
1. Radiography of upper neck to demonstrate the fracture of the 1st cervical transverse process. It should be remembered the fractures are only presnt in a small number of cases.
2. Postmortem angiogram
3. Dissection of the upper cervical spine.
Method- Upper cervical spine is exposed posteriorly. Spine is exposed and sawed C4 level or lower. A cut is made around the foramen magnum and the occipital bone around the foramen magnum is revomved with the attached cervical spine.
The block is decalcified in 10% formic acid for few weeks. Then vertebral is opened and vertebral artery is dissected.
Mechanism of Death
Most of the traumatic basilar subarachnoid haemorrhges cause immediate death. When the amount of blood is considered it is sometimes suprising to see such immediate death as the amount of blood is not enough to act as a space occupying lesion. Since these hamorrhages are seen in the basal cisterns bathing root of the cranial nerves and brain stem bathed in blood it is thought that it acts as an irritant and death is caused by rapid cardio-respiratory failure.
Cerebral Injuries
Although many different types of injuries and their complications such as bleeding and infection of scalp wounds, membrane haemorrhages, meningitis can cause death in majority of fatal head injuries death is caused by brain injuries and its complications.
Mechanism of Brain Injury
The following point should be appreciated to understand the mechanism of brain injury
1. The actual physical disruption of the brain tissue is caused by
a. Compression– by being froced together
b. Tension– By being pulled apart
c. Sliding or ‘shear’ strains – Movement of one layer laterally on the other layer.
2. Brain can be injured by direct intrusion of a foreign body such as a penetrating weapon, bullet, or fragment of a fractured skull. This may be due to different mechanism and may be called ‘mechanical seperation’.
3. Intrusion of the skull during the transient deformation resulting from a blunt impact may cause a cone shape bruises on the cortex with the apex pointing towards interior and base at the exterior are caused by this mechanism. This seems to be the result of compression of the brain tissue together.
4. When the skull is locally deformed the compensatory bulging out of the skull in other areas (the so-called ‘struck-hoop action) rarefaction away from the site of impact may cause ‘tension’ damage.
5. In a closed head injury mechanism of brain injury is complicated. The brain is almost incompressible. It is placed in a hard bony case, divided into several compartments by dural sheaths such as falx and tentorium.
6. A pure axial impact may inflict only a little or no damage.
7. It is hard to find a impact which does not give the brain a rotatory movement. This is thought to be the kind of movement, which caused brain injury.
8. It is no need for the head to receive a actual blow or to fall to cause a fatal brain injury. It is the change of velocity, acceleration or decelaration with rotatory movement rather than the axial movement that causes brain damage.
9. However, impact is always releases more energy to cause brain damage than pure movement of the head with no impact.
10. When the head is accelerated in a blow to the head or decelerated in a fall or road traffic accident application of force on the scalp and skull is tranmitted to the brain through the anatomical suspensory systems in side the skull such as falx and tentorium. These relative movements between the brain and these structures, when violent, may cause injury to the brain.
11. In these instances the brain damage is due to ‘shear stress’ caused by angular rotation of the head. Since the head is fixed to the neck at one point almost any impact on the jaw, face, cranium would give rise to angular movement.
12. The brain and the skull can not suddenly change their velocities simultaneously in acceleration and deceleeration both .For instance, in a fall when the movement of the head is suddenly arrested the movement of the brain will continue even after the skull ceased to move with possible rotatory movments.
13. These shering forces act first on the superficial layers of the brain and will gradully spread to the more deeper layers causing laminer tearing of brain tissue and blood vessels.
14. In addition to these shearing forces brain get damages by contact with the sharp edges of dural folds such as falx and tenotrium and the inerior of the skull, especially base of the skull where anterior and middle cranial fossa are particulary demonstrate a rugged surfaces.
There are few theories which try to explain the how the brain is injured. They are:-
1. The rotational shear force theory
2. The pressure gradient theory
3. The vibration theory
4. The transmitted wave force theory
5. The brain displacement theory
6. The skull deformation theory
Brain Contusions
They are caused by linear or more often laminar sresses (shear stresses). When it retains its shape, bruised and swollen it is called ‘contusion’. When the disruption is greater to produce macroscopic tearing it is called laceration. As mentioned ealier they are cone shape with base on the surface.
Brain Lacerations
When they are mild they look like red velvet. Severe lacerations are fissured with fragmented coretex. They sometimes extend into the deapth of the brain. The pia and arachnoid are torn.
Traumatic Brain Haemorrhages
They can be either infiltrating brain tissue or forming actual haematoma in the brain tissue. Some are primary either occuring at the time of impact or immediately after. Some are secondary caused by changes in intra-cranial pressure or bleeding into the infarcts caused by vascular damage.
In the cerebral hemispheres, deep haemorrhages can be caused by conrecoup or coup mechanism and may situate in anywhere.
In severe contrecoup lesions, the frontal lobes may have large haematomas with overlying contusions and laceratinon. They may rupture through the cortex into meningeal space causing a‘burst lobe’. When they occur in older people with a past history of atherosclerosis and hypertension, it may be difficult to separate a traumatic cerebral haemorrrhage from a spontaneous haemorrhge. Even if there is a scalp injury and perhaps a skull fracture present it is difficult to decide the cause and effect relationship of them. A man fell after suffereing a spontaneous haemorrhage or had a fall, which cuased the traumatic brain injury.
Primary Brain Stem Haemorrhages
Two types of haemorrhges occur in the brain stem, primary and secondary haemorrhages. Secondary haemorrhages occur as a consequence of raised intracranial pressure, which will be dealt with later, and primary haemorrhage occur at the time of injury.
The spontaneous haemorrhges occur in hypertenives can occur in midbrain especially pons. They are large, explosive lesions,which swell the pons and disrupt the cental parts of the brain stem with a ragged rim of white matter around.
Primary traumatic brain stem haemorrhages are often well circumscribed lesions sometimes rounded, which lie lateraly in the tegmentum. The shape of the midbrain is undistorted.
The typical site is between the aqueduct and the outer end of the subtantia nigra. They are usually associaed with occipital impacts and victim is often unconscious from the time of injury.
Coup and Contrecoup damage
This is of tremendous practical importance for the pathologist to decide whether the head injury was due to a fall or assault.
When a mobile head is struck with an object the site of maximum cortical injuries is most likely to be beneath the site of impact or atleast on the same side. This is the so-called coup injury.
When a moving head is suddenly decelerated as in a fall, there is often cortical damage on the opposite side of the impact. This may be in addition to a possible coup injury caused by a blow. This is called contre-coup injury.
The mechanism of these injuries is still debatable.
However the following points need to be remembered.
1. There may be no coup damage at all only contrecoup
2. There need be no fractures of skull even in severe coup and contrecoup injuries
3. The most common site of coup injury is in the frontal and temporal lonbes if the fall was on the occiput.
4. In temporal and parietal impacts contrecoup lesions ae likely to be diametrically opposite contralateral side of the brain
5. Fall on the frontal region does not produce conrecoup injuries on the occiptial lobes
6. In a temporal impact the contrecoup injury may be on the opposite side of the ipsilateral hemisphere due to friction against thefalx
7. In falls on the occiput the transmitted forces might fracture the orbital plates or the floor of the anterior cranial fossa.
8. When a fixed head is struk contrecoup injuries can be produced
Concussion
Definition
A transient paralytic state due to head injury which is of instaneous onset, does not show any evidence of structural cerebral injury and is always followed by amnesia from the actual moment of the accident.
It is a common sequalae of tauma to head but it is not an inevitable phenomenon. The duration is generally considered to be proportionate to the severity of trauma. But exceptions occur.
True conscussion may last few seconds of minutes. If unconsciousness extends to hours or days there should be strucural damage to brain. Sometimes a concussion may cause death by respiratory paralysis and autopsy would fail to show a significant lesion.
The cause of the concussion is thought to be due to shear stress causing neuronal damage precipitated by rotational movement of the brain as there seems to be a connection between the rotatory movements of the head and concussion.
Concssion may be followed by postconcussional state charachterized by headaches, unsteadines, anxiety and retrograde amnesia.
Medico-Legal Imporance
Since concussion can cause death, though rarely, by respiraory paralysis it should be considered as an injury endangering life.
Doctors have to be aware of the people who demonstrate false symptoms of postconcussional syndrom to claim compensation.
Focal and Diffuse Brain Injury
Brain injuries can also be classified as focal and diffuse injury.
Focal lesions are associated with contact forces and are most likely to result from falls, while diffuse damage is more commonly associated with acceleration/deceleration factors operating in road traffic accidents and similar events.
Focal Brain Injury
e.g. Injury to scalp, Facture of skull, Surface contusions/ lacerations, intra-cranial haematoma, raised intra-cranial pressure and associated vascular changes
Diffuse Brain Injury
e.g. ischaemic damage, axonal injury, brain swelling, meningitis
Diffuse Axonal Injury
Axonal injury (AI) is a non-specific term referring to damage to axons of any aetiology.
Traumatic Axonal Injury (TAI) is damage to axons caused by trauma, which may vary from small foci of axons to more widespread brain damage. Diffuse TAI is more severe form of traumatic axonal injury.
Diffuse Axonal Injury is primarily caused by non-impact rotational deceleration-deceleration phenomenon. Deformation by stretching is the possible mechanism.
Cerebral Oedema
Swelling of the brain can be a local phenomenon such as seen around contusion, laceration, infarction etc. but here we are concerned with the general brain swelling.
Although it can be associated with other lesion as a local or general phenomenon it can occur as a sole abnormality, which can be fatal not infrequently especially in young victims.
Cerebral oedema can be related to concussion and DAI. It is the most common reason for raised intracranial pressure and seen more often than space occupying lesions.
As with concussion the cause is obscure.
Autopsy features
On the removal of the skull cap dura is stretched and tense. The brain is bulging. Gyri are pale and flattened. Sulci are filled giving the normal corrugated appearance smoothness. The cut surface is pale and ventricles are reduced in size.
Cerebral hemispheres are pressed down causing uncal and tonsillar herniation.
Cerebral oedema may be the only intracranial abnormality found at autopsy after substantial head injury. This is seen more commonly in children.
Cerebral oedema may be self-potentiating. Once it starts after brain trauma it impairs the venous return. Since the pressure is insufficient to restrict the arterial flow further congestion and swelling occur. This may lead to worsening of cerebral hypoxia and oedema to actual cerebral infarction and brain death.
Secondary Brain Stem Lesions
When there is raised intracranial pressure due to supratentorial space occupying lesions the possible sequalae are as follows. One cerebral hemisphere is pushed to the other side accompanying with subfalcine herniation of cingulate gyrus. The midbrain is compressed against the edge of the tentorium forming a notch which is called‘Kernohan’s notch’. Hippocampal gyrus may press through the tentorial opening herniating the uncus. This would elongate the midbrain in antero-posterior direction. The distortion stretches the and compresses the paramedian and nigal vessels that supply the midbrain, leading to haemorrhages and infarctions in the upper pons and midbrain. Damage to cranial nerves and circulation of CSF are added complications. The calcarine cortex on the medial aspect of the occipital lobe may be infarcted by posterior cerebral artery compression at the tentorium.
These secondary brain stem lesions are midline or paramedian haemorrhages or haemorrhagic necrosis placed centrally in the upper pons and midbrain.
References
1. Knight's Forensic Pathology, 3Ed, Bernard Knight and Pekka Sukko, Edward Arnold, 2004 London.
2. The Mechanism of Skull Fracture E. S. Gurdjian, M D., J. E. Webster, M.D. and H. R. Lissner, M.S.Radiology March 1950 54:3 313-339; 10.1148/54.3.313
No comments:
Post a Comment