CHAPTER XII

THE CRANIUM AND ITS CONTENTS

Anatomy and physiology--Cerebral localisation--Lumbar puncture. HEAD INJURIES--Concussion--Cerebral irritation--Compression--Contusion and laceration of the brain, and traumatic intra-cranial haemorrhage: _Middle meningeal haemorrhage_; _Haemorrhage from internal carotid and venous sinuses_--Intra-cranial haemorrhage of the newly born. Cerebral oedema--Wounds of brain--After-effects of head injuries--Traumatic epilepsy and insanity--Infective complications.

#Anatomy and Physiology.#--The _Cranium_ is irregularly ovoid in shape, and its floor is broken up by various projections to form three separate fossae--anterior, middle, and posterior--in which rest respectively the frontal, the temporal, and the occipital lobes of the brain; the cerebellum, pons, and medulla oblongata also occupy the posterior fossa.

The _outer_ table is the most elastic layer of the calvarium, and it varies greatly in thickness in different skulls and in different parts of the same skull. It is nourished chiefly from the pericranium which is firmly bound down along the lines of the sutures. The _inner_ or vibreous table is thin and fragile, and its smooth internal surface is grooved by the middle meningeal and other arteries of the dura mater, and by the large venous sinuses. The intermediate layer--the _diploe_--is highly vascular, branches of the meningeal vessels anastomosing freely in its open porous substance with branches derived from the pericranial vessels. Some of its veins open into the external veins, and others into the intra-cranial sinuses, and they communicate with the emissary veins as these pass through the bone, which explains the spread of infective processes from the structures outside the skull to those within. The possibility of withdrawing blood from the interior of the skull by leeching, bleeding, or cupping depends on the existence of the emissary veins.

_The Membranes of the Brain._--The _dura mater_ is a fibro-serous membrane, the outer, fibrous layer constituting the endosteum of the skull, the inner, serous layer forming one of the coverings of the brain. Between the fibrous layer and the bone the meningeal vessels ramify; and along certain lines the two layers split to form channels in which run the cranial venous sinuses. Inside the dura, and separated from it by a narrow space--the _sub-dural space_--lies the _arachno-pial membrane_, consisting of an outer (_arachnoid_) layer which envelops the brain but does not pass into the sulci, and a highly vascular inner layer--the _pia mater_--which closely invests the brain and lines its entire surface.

The space between these layers--the _sub-arachnoid space_--is traversed by a network of fine fibrous strands, in the meshes of which the cerebro-spinal fluid circulates. Each nerve-trunk as it leaves the skull or spinal canal carries with it a prolongation of each of these membranes and their intervening spaces. The membranes gradually become lost in the fibrous sheaths of the nerves, and the sub-dural and sub-arachnoid spaces become continuous with the lymph spaces of the nerves.

The _cerebro-spinal fluid_ is secreted by the choroid plexuses and fills the cerebral ventricles, the central canal of the cord, the sub-dural and sub-arachnoid spaces, and the sheaths of the intra-cerebral blood vessels. At the base of the brain, particularly in the posterior fossa, the sub-arachnoid space is wider than elsewhere, forming "cisterns" filled with cerebro-spinal fluid which supports the cerebral structures. Through the foramen of Magendie in the roof of the fourth ventricle the sub-arachnoid fluid of the cranial cavity communicates with that of the vertebral canal.

Although it differs in its chemical constitution from true lymph, the cerebro-spinal fluid seems to functionate as lymph, in addition to acting as a lubricating agent, and playing a part in regulating the vascular supply of the brain. In cases of cerebral haemorrhage, abscess, tumour, or depressed fracture, room is made up to a certain point for the extraneous matter by displacement of cerebro-spinal fluid.

_Vascular supply._--The free anastomosis between the vessels entering into the formation of the circulus arteriosus (circle of Willis) ensures an abundant supply of blood to the brain. The larger arteries run in the sub-arachnoid space and give off branches which ramify in the pia mater before entering the cerebral substance. Within the brain, each artery being more or less terminal, there is no free anastomosis between adjacent vessels, with the result that if any individual artery is obstructed the vitality of the area supplied by it is seriously impaired. The venous arrangements are also peculiar in that the veins are thin-walled and valveless, and open into the rigid, incompressible sinuses which run between the layers of the dura mater. Most of the blood passes to the internal jugular vein, and any increase in the pressure of this vessel is immediately transmitted back to the cerebral veins. As the blood vessels project into a rigid case filled with incompressible material, and as the total _volume_ of blood in the brain is constant (Munro and Kelly), any alteration in the supply of blood to the cerebral tissue must be due to an increased _velocity_ of flow, and this in turn depends upon changes in the aortic and vena cava pressure. Thus, if the aortic pressure rises, more blood will enter the cerebral vessels and will move along more rapidly; while if the pressure in the vena cava rises there is obstruction to the passage of blood in the arteries and diminished velocity of flow. The ebb and flow of cerebro-spinal fluid in and out of the spinal canal may also help to control the pressure.

#Nerve Elements.#--The nervous system is composed of a multitude of units, called _neurones_, each neurone consisting of a nucleated cell, with branching protoplasmic processes or _dendrites_ and one _axis-cylinder_ or _axon_. The nutrition of an axis cylinder depends on its continuity with a living cell. If the cell dies, the axis cylinder degenerates. If the axis cylinder is severed at any point, it degenerates beyond that point, and the nucleus of the nerve-cell disintegrates--chromatolysis.

The axis cylinder of one cell ends in a number of fine filaments which arborise around another nerve-cell, thus bringing it into physiological, if not anatomical, relationship with the first cell. The termination is called a cell-station or _synapsis_. In this way the various sections of the nervous system are kept in association with one another and with the rest of the body.

_Motor Functions and Mechanism._--The nerve centres, which together make up the motor area, and govern the voluntary muscular movements of the body, are situated in the grey matter of the praecentral or ascending frontal gyrus, and of the frontal aspect of the central sulcus (fissure of Rolando). The upper limit of the motor area reaches on to the mesial aspect of the paracentral lobule, and the lower limit stops short of the lateral cerebral fissure (fissure of Sylvius) (Fig. 179).

Each group of muscles has its own regulating centre, the size of the area representing any group depending upon the character and complexity of the movements performed by the muscles, rather than upon the amount of muscular tissue that is governed by the centre--for example, the centre for the mouth, tongue, and vocal cords is larger than that for the muscles of the trunk.

The motor centres have been localised on the surface of the brain with approximate accuracy. For example, above the superior genu of the praecentral gyrus, the centres governing the hip, knee, and toes are grouped; opposite the genu are the centres for the movements of the trunk; between the superior and middle genua lie the centres for the upper extremity; opposite the middle genu, those for the neck, and below it, those for the face, jaws, and tongue, pharynx and larynx.

#The Motor Tracts.#--It is now generally accepted that there are two paths by which motor impulses pass from the brain: one--the _rubro-spinal tract_--which controls the more elemental movements of the body, such as standing, walking, breathing, etc.; the other--the _pyramidal tract_--developed later in the evolution of the nervous system, and concerned with the finer and more skilled movements.

The pyramidal tract is the more important clinically. From the pyramidal cells in the cortex of the Rolandic area, the axis cylinders pass through the centrum ovale towards the base of the brain. They converge at the internal capsule, and pass through the anterior two-thirds of its posterior limb (Figs. 180 and 195). The fibres for the eyes, face, and tongue lie farthest forward, and next in order from before backward, those for the arm and the leg.

From the internal capsule, the motor fibres pass as the _pyramidal tract_ through the crusta of each crus cerebri, the pons and the medulla oblongata. Throughout this part of its course, numerous axons leave the tract, and enter the mid-brain, pons, and medulla in which lie the nuclei of the motor cranial nerves.

At the _decussation of the pyramids_ in the lower third of the medulla, the main mass of the motor fibres crosses the middle line, and enters the lateral column of the spinal cord as the _crossed pyramidal tract_. The remaining fibres pass down as the _direct pyramidal tract_, and decussate in the cord near their termination.

The fibres forming the second path pass through the red nucleus in the cerebral peduncle (crus cerebri) and thence by way of the rubro-spinal tract in the lateral column of the cord.

The existence of this double motor path explains how after a hemiplegic stroke in which the pyramidal tract is destroyed while the rubro-spinal tract escapes, the patient is able to perform such primitive movements as are involved in walking or standing, while he is unable to carry out finer movements that require higher education.

The pyramidal and rubro-spinal tracts, in addition to conveying motor impulses, convey impulses that influence muscle tonus and the deep reflexes. The pyramidal tract conveys impulses that inhibit muscle tonus, while the rubro-spinal tract is the path by which excitatory impulses travel. When the inhibitory influences are cut off, as in a lesion of the internal capsule, the paralysed muscles become spastic, and the deep reflexes are exaggerated. When the excitatory impulses are also lost, as in a total transverse lesion of the cord, the paralysed muscles are flaccid and the deep reflexes disappear. In destructive lesions of the lower neurones, the muscles are always flaccid.

The axons passing from the cerebral cortex terminate at different levels in the cord by breaking up into dendrites which arborise around the cells on the grey matter of the posterior horns--this system of cells, axons, and dendritic processes forming an _upper neurone_. From this synapsis the _lower neurone_ proceeds, its axons travelling to the anterior horn and arborising around the motor cells. The axis cylinders pass out in the anterior nerve roots to the spinal nerves and are continued in them to their distribution in voluntary muscles.

If the continuity of any group of these lower neurones is interrupted, not only do the nerve fibres degenerate, but the nutrition of the muscles supplied by them is interfered with and they rapidly degenerate and waste, and after an interval show the reaction of degeneration. In addition, the reflex arc is disturbed, and reflexes are lost. As these changes do not occur in lesions of the upper neurones, an appreciation of the differences enables us to distinguish between lesions implicating the upper and the lower neurones.

#Sensory Functions and Mechanism.#--Three kinds of sensory impulses pass from the periphery to the brain; (1) deep, or muscular sensibility, (2) protopathic sensibility, and (3) epicritic sensibility.

_Deep sensibility_ includes the recognition of (_a_) deep pressure, say by the blunt end of a pencil; (_b_) the position of a joint on passive movement (joint sense); (_c_) active muscular contraction (kinesthetic sense). The fibres that convey these impulses to the spinal cord pass in the afferent nerves from the muscles, tendons, and bones, and so long as these nerves are intact these sensations are retained, even if the surface of the skin is quite anaesthetic.

_Protopathic sensibility_ is of a lower order than epicritic. It consists in the recognition of painful cutaneous stimuli and of extreme degrees of heat and cold. The fibres concerned are non-medullated and regenerate comparatively quickly after injury, so that protopathic sensibility is regained before epicritic.

_Epicritic sensibility_ is the most highly specialised and permits of the recognition of light touch, _e.g._, with a wisp of cotton wool, of fine differences of temperature, and of discriminating as separate the points of a pair of compasses 2 cm. apart. These sensations are carried by medullated nerve fibres, and are slow to return after injury to the nerves.

The sensory nerve fibres conveying these different impulses pass to the ganglionic cells of the posterior nerve roots. From each of these cells a process passes into the cord and bifurcates into an ascending and a descending branch. In the cord the fibres rearrange themselves and pass to the brain by a double path. Those that convey sensations of pain and of temperature pass by the spino-thalamic route by way of the tract of Gowers and the fillet to the optic thalamus; those that are concerned with the muscular sense, the joint sense, and tactile discrimination pass up the posterior columns in the tracts of Goll and Burdach to the nuclei gracilis and cuneatus in the medulla, whence they pass to the optic thalamus.

From the cell station in the optic thalamus the fibres proceed to the _cortical sensory centres_, that for tactile sensation being situated in the post-central (ascending parietal) gyrus; that for muscular and stereognostic sense lying probably in the adjacent portions of the parietal lobe.

In a unilateral lesion of the cord, pain and the temperature sense may be disturbed in one limb, and motor power and tactile sensibility in the other, as the fibres that convey impressions of pain, and those that subserve the discrimination of temperature, pass up and decussate in the cord a few segments above their point of entrance.

#Effects of Lesions of the Motor and Sensory Mechanisms.#--Lesions of the _motor mechanism_ differ in their fundamental characters according as they affect the upper or the lower neurones. The signs also vary according as the affected area is _destroyed_ or merely _irritated_, say by the pressure of a tumour. Irritative lesions in general produce muscular spasms or convulsions, while destructive lesions cause paralysis. The essential differences in the effects of destructive lesions of upper and lower neurones may be indicated thus:--

_Upper Neurone Lesion._ _Lower Neurone Lesion._

Spastic paralysis of voluntary Flaccid paralysis of voluntary muscles. muscles. No marked wasting of paralysed Marked wasting of paralysed muscles. muscles. No reaction of degeneration. Reaction of degeneration. Exaggeration of reflexes. Loss of reflexes.

Irritative lesions of the sensory mechanism cause numbness and tingling (paraesthesia); more extensive paralytic lesions produce anaesthesia, astereognosis, loss of muscle sense, loss of pain, or inability to distinguish temperature, according to the tracts that are affected.

_Lesions of the Upper Motor Neurone_ may occur in any part of its course. _Localised lesions of the motor cortex_ of an irritative kind, for example, a patch of meningitis, a tumour, meningeal haemorrhage, or a spicule of bone, produce spasms in those groups of muscles on the opposite side of the body that are supplied by the centres implicated--Jacksonian epilepsy. The cortical discharge may overflow into neighbouring centres and cause more widespread convulsive movements, or, if strong and long-continued, may even lead to general convulsions. Consciousness is usually lost before the whole of one side becomes implicated in the spasms; always before they spread to the opposite side. Contracture may occur in the muscles affected after the spasms cease.

If an area of the cortex is destroyed by the lesion, paralysis is produced of the corresponding muscles on the opposite side of the body. At first the paralysed muscles are flaccid, but spasticity soon develops. In some cortical lesions, for reasons not yet understood, the paralysis remains of the flaccid type. The seat and extent of the paralysis depend upon the area of the cortex destroyed. In rare cases the whole motor area is destroyed--_cortical hemiplegia_; more generally the lesion affects one or more groups of muscles, and occasionally all the muscles of one limb are paralysed--_cortical monoplegia_. Lesions are often both irritative and destructive, and lead to paralysis of one or more groups of muscles associated with spasms and convulsions of the muscles governed by neighbouring areas of the cortex. Irritation or destruction of the sensory centres may also exist, giving rise to areas of paraesthesia and anaesthesia.

Lesions in the _centrum ovale_, which destroy the fibres proceeding from the overlying cortex, produce a corresponding spastic paralysis on the opposite side of the body. No irritative phenomena are associated with such a sub-cortical lesion.

Lesions in the region of the _internal capsule_ often produce complete spastic hemiplegia of the opposite side of the body. When the posterior part of the capsule is involved, there are, in addition, hemianaesthesia and hemianopia, and sometimes disturbances of hearing, smell, and taste.

A lesion of the _crus_ may in like manner produce spastic hemiplegia and hemianaesthesia of the opposite side, often associated with a lower neurone paralysis of the third and fourth nerves of the same side (crossed paralysis). The optic tract, which crosses the crus, may also be affected, and hemianopia result.

Lesions of the _corpora quadrigemina_ cause interference with the reaction of the pupil, disturbance of the functions of the oculo-motor nerve and of mastication, ataxia, and inco-ordination of the movements of the limbs.

The symptoms produced by lesions of the _pons and medulla_ vary according to the position of the lesion. If it is unilateral, there may be spastic hemiplegia and hemianaesthesia of the opposite side; if it is situated in the lower part of the pons or in the medulla, there is often also a lower neurone paralysis of one or more of the cranial nerves on the same side as the lesion (crossed paralysis). Paralysis of the external rectus of one eye and of the internal rectus of the other (conjugate paralysis) is frequently found in pontine, and in cortical and internal capsule lesions.

_Cerebellar_ lesions are associated with special symptoms. In ataxia, there is inco-ordination of muscular movements, especially of the coarse movements, such as walking. The gait becomes irregular and staggering, with a tendency to fall, sometimes to the side on which the lesion is situated, sometimes to the opposite side. In patients who cannot walk, ataxia may be tested by ordering repeated pronation and supination of the forearm. Paresis or asthenia may be found in the trunk muscles, or evidenced by weakness of the grip, or drooping of the head to one side. Changes in muscle tone may arise and lead to exaggerated or decreased reflexes, often varying from day to day. Vertigo and nystagmus may also be present, in addition to occipital headache and tenderness on percussion. When one lateral lobe is implicated, the symptoms are referred to the same side; when the median lobe is involved, they are bilateral, and there may be retraction of the neck with extension of the legs, probably as the result of the associated internal hydrocephalus.

A unilateral lesion of the _spinal cord_ causes a lower neurone paralysis of the muscles supplied from the cord at the level of the lesion, with spastic paralysis of the muscles of the same side of the body supplied from a lower level of the cord. The sensory symptoms are variable. Typically there is some anaesthesia in the structures supplied from the damaged section of the cord--incomplete owing to the overlapping by other sensory nerves. Just above the lesion there is irritation of spinal nerves, and hyperaesthesia and pain referred to their distribution. On the same side below the lesion, there is a loss of epicritic, stereognostic and deep sensibility, and on the opposite side below the lesion, loss of the sense of pain and the discrimination between heat and cold. Ordinary tactile sensibility, which is governed by a double path, may or may not be lost on either side below the lesion.

#Other Special Centres.#--The cortical centres for _vision_ lie on the median surfaces of the occipital lobes in the neighbourhood of the calcarine fissure. Each half-vision centre--for there is one in each occipital lobe--receives the fibres from the same side of both retinae. Destruction of one half-vision centre produces the condition known as _homonymous hemianopia_, in which the medial (nasal) half of one visual field and the lateral (temporal) half of the other is affected, so that there is an inability to see objects situated on the side opposite to the lesion.

_Auditory impulses_ are received in the posterior part of the superior temporal convolution.

_Aphasia._--The use of language, spoken or written, as a means of expression depends upon the co-ordination of four different centres: the visual, the auditory, the graphic, and the articulatory. These are situated in different parts of the brain and are connected by sub-cortical association tracts, the main pathway of which lies in the vicinity of the upper end of the fissure of Sylvius. Marie has proved that aphasia results from lesions in this area.

The _olfactory_ and _gustatory_ centres are situated in the uncus close to the pituitary fossa.

Lesions of the frontal cortex anterior to the motor centres, even if extensive, may produce few or no symptoms, and in consequence this region has been called a "silent" area. Occasionally there results a change in temperament or intelligence, and the region is on this account supposed to be concerned with the higher psychical functions. There is evidence that the pre-frontal cortex has a centre for the conscious initiation of movements, and that lesions produce "apraxia," _i.e._, inability to perform, or clumsiness in voluntarily performing fine movements such as touching the nose with the finger, though such movements may be perfectly carried out unintentionally. This centre is probably situated in the superior and middle left frontal convolutions in right-handed people. The fibres from the centre to the right motor area cross in the anterior part of the corpus callosum.

#Cerebral Localisation.#--The various parts of the brain can be localised in relation to the surface by various methods. That devised by Professor Chiene has been found reliable.

#Relation of Cerebral Centres to the Surface.#--Numerous attempts have been made to formulate rules for locating the different parts of the brain in relation to the surface of the head. The method devised by Chiene is free from many of the difficulties and fallacies common to most other methods, inasmuch as the results obtained do not depend upon making definite measurements in inches, or determining particular angles. Certain fixed and easily recognised bony landmarks--the glabella, the external occipital protuberance, the lateral angular process, and the root of the zygoma--are taken, and connected by lines, which are further subdivided--_always being bisected_. Figs. 179 and 181 explain the method. The head being shaved, a line (GO) is drawn along the vertex from the glabella (G) to the external occipital protuberance (O). This line is bisected in M, which constitutes the "mid-point." The posterior half of the line MO is bisected in T, constituting the "three-quarters point," and the posterior half TO is bisected in S--"the seven-eighths point." The lateral angular process (E) is next connected to the root of the zygoma (P) by a line EP, and the root of the zygoma with the seven-eighths point by PS; the line EPS thus forms the base line. The lateral angular process is now joined to the three-quarters point by ET. The two segments of the base line EP and PS are bisected in N and R respectively, and these points connected with the mid-point (M) by lines NM and RM. These lines cut off a part of ET--AB, which is now bisected in C, and from C the line CD is drawn parallel to AM.

In this way practically all the points of the brain which are wanted for operative purposes may be mapped out. Thus the quadrilateral space MDCA contains the Rolandic area. MA represents the praecentral sulcus, and if it be trisected in K and L, these points will correspond to the origins of the superior and inferior frontal sulci. The pentagon ABRPN corresponds to the temporal lobe. The apex of the temporal lobe extends a little in front of N. The supra-marginal convolution lies in the triangle HBC. The angular gyrus is at B. A is over the anterior branch of the middle meningeal artery, and the bifurcation of the lateral or Sylvian fissure; AC follows the horizontal limb of the lateral fissure. The transverse or lateral sinus at its highest point touches the line PS at R (Fig. 181).

The _fissure of Rolando_ or _central sulcus_ may be marked out by taking a point half an inch behind the mid-point (M) (Fig. 181), and drawing a line downwards and forwards for a distance of about three and a half inches, at an angle of 67.5 deg. with the line GO. The angle of 67.5 deg. can be readily determined by folding a square piece of paper on itself so as to make a triangle. The angle at the fold equals 45 deg.. By folding the paper again upon itself in the same direction, the right angle of the paper is divided into four angles of 22.5 deg. each. Three of these angles taken together make up the 67.5 deg.. If the straight edge of the paper be placed along the sagittal suture with the angle of folding over the upper end of the fissure of Rolando, the folded edge falls over the line of the fissure (Chiene).

LUMBAR PUNCTURE

Quincke, in 1891, first suggested the withdrawal of cerebro-spinal fluid from the theca in the lumbar region, as a means of relieving excessive intra-cranial tension in tuberculous meningitis, and to obtain specimens of the fluid for diagnostic purposes. The scope of the procedure, both as a therapeutic and as a diagnostic measure, has since been widely extended.

_Technique._--The puncture may be made with the patient either lying on his left side, the spine being fully flexed by approximating the knees and shoulders; or sitting on the table with the knees drawn up and the body bent forward. The upper edge of the fourth lumbar spine is identified by drawing a horizontal line across the back at the level of the highest part of the iliac crests (Fig. 183). The space between the fourth and fifth lumbar vertebrae being the widest, is that usually selected. The skin having been purified, an exploring needle, about three inches long, is introduced about half an inch below the fourth lumbar spine in the middle line, and passed for about two inches in a direction forwards and slightly upwards. The needle usually encounters some resistance as it pierces the interspinous ligament, and then enters the sub-arachnoid space. If bone is struck, the needle should be withdrawn and introduced at a different level. If the cerebro-spinal fluid does not escape at once, a stylet should be passed through the needle to clear it of blood-clot or shreds of tissue. When the intra-thecal tension is normal, the fluid trickles away drop by drop, but if it is increased, as, for example, in meningitis, intra-cranial tumour, hydrocephalus, or uraemia, it may escape in a jet.

The _normal cerebro-spinal fluid_ is clear and colourless, has a specific gravity of 1004-1008, and contains a trace of serum globulin and albumose, some chlorides, and a substance which reduces Fehling's solution. Microscopically, it may contain some large endothelial cells and a few lymphocytes, or may be entirely devoid of cells. It does not contain the antitoxins and opsonins which are normally found in the plasma and lymph, hence the liability to infective meningitis after injuries and operations on the central nervous system. With a view to diminishing these risks, hexamine, which is excreted into the cerebro-spinal fluid, is administered for its antiseptic properties in cases of head injury and before intra-cranial operations.

_Diagnostic Puncture._--Examination of the fluid withdrawn has proved useful in diagnosis in cases of intra-cranial and intra-spinal haemorrhage, in various forms of meningitis, in cerebral abscess, and in some cases of cerebral tumour.

The first few drops should be discarded, as they may be stained with blood from the puncture, and about 5 c.c. collected in each of two sterile tubes. To determine whether blood in the fluid is due to the puncture or to a pre-existing intra-cranial or intra-thecal haemorrhage, the fluid should be centrifugalised; in the former case the supernatant fluid is clear and limpid, in the latter it retains a yellow tinge. In extra-dural haemorrhage there is no blood in the cerebro-spinal fluid.

In acute meningitis the fluid is turbid, and contains an excess of albumin. Organisms also are present, such as the diplococcus intracellularis in acute cerebro-spinal meningitis; staphylococci, streptococci, and pneumococci, particularly in the intra-cranial complications of middle ear disease. In all cases of acute microbic infection, and especially in the suppurative forms, polynuclear leucocytes are found in the fluid; while in chronic affections, such as tubercle and syphilis, there is an excess of lymphocytes (Purves Stewart). The detection of the tubercle bacillus is confirmatory of a diagnosis of tuberculous meningitis, but, as it is often difficult to find, its absence does not negative this diagnosis. In tuberculous meningitis the clot which forms floats in the centre of the fluid, and is translucent, grey, and flaky; in the pyogenic forms it is yellow, and sticks to the side of the vessel.

In a few cases of malignant tumour of the spinal cord and its membranes, characteristic cells have been found in the fluid after centrifugalising.

In uraemia there is a diminution of chlorides, and an increase of phosphates and sulphates.

The Wasserman test is sometimes positive in the cerebro-spinal fluid, when it is negative in the blood.

_Therapeutic Puncture._--In certain cases of cerebral tumour, and of tuberculous meningitis associated with an excessive quantity of fluid in the arachno-pial space, temporary relief of such symptoms of increased intra-cranial tension as headache, vertigo, blindness, or coma, has followed the withdrawal of from 30 to 40 c.cm. of the fluid. Terrier and others have found this measure useful in relieving pain in the head, delirium, and even coma, in cases of basal fracture. Carriere has found it beneficial in some cases of uraemia. The quantity withdrawn must not exceed 40 c.cm., lest the ventricles be emptied and pressure be exerted directly on the basal ganglia (Tuffier). In a number of cases sudden death has followed the withdrawal of cerebro-spinal fluid.

This route is sometimes selected for the induction of spinal anaesthesia, and for the injection of antitoxin in cases of tetanus.

HEAD INJURIES

The brain is protected from injury by moderate degrees of violence applied to the head, by the dense and mobile scalp, the dome-like shape of the skull, the elasticity of its outer table and the buffer-like sutural membrane between the numerous bones of which it is composed, and the various internal osseous projections with the membranes attached to them, all of which tend to diminish vibrations and to disperse forces so that they expend themselves before they reach the brain. Further protection is provided by the water-bed of cerebro-spinal fluid, and by the external buttresses formed by the zygomatic arch and the thick muscular pads related to it, as well as by the mobility of the skull upon the spine.

In all cases of head injury, the questions that dominate the whole clinical outlook are, whether the brain is directly damaged or not, and whether it is likely to become the seat of infection.

It is impossible to consider separately in their clinical aspects injuries of the cranium and injuries of the brain. It seldom happens that one is seriously damaged without the other suffering to a greater or less extent. Sometimes the skull suffers comparatively little, while the brain is severely damaged, but it is rare for a serious injury to the bone to be unaccompanied by definite brain lesions. In any case it is the damage to the brain, however slight, that gives to the injury its clinical importance. It is an old and a true saying that "no injury of the head is so trivial as to be despised or so serious as to be despaired of." Injuries at first sight apparently slight may prove fatal from haemorrhage or infection; on the other hand, recovery has followed injuries of great severity--for example, the famous "American crowbar case," in which a bar of iron three and a half feet long and one and a half inches thick passed through the head, and yet the patient recovered.

It is convenient to consider the injuries of the brain before those of the skull.

TRAUMATIC LESIONS OF THE BRAIN

It is probable that in all cases of injury to the head in which a patient loses consciousness, there is some definite damage to the cerebral tissue. This takes the form of a greater or less degree of contusion or laceration, and the lesions are usually most severe and dangerous when the skull is fractured and fragments are driven in upon the brain, but they may exist--indeed they may be very extensive--in the absence of fracture.

Several degrees are recognised.

(1) Numerous minute _petechial haemorrhages_ may be found widely scattered throughout the brain substance, as a result of a diffused blow on the head, which has shaken up the brain and caused symptoms of cerebral shock or "concussion." We have found, on microscopic examination in such cases, in addition to these small extravasations, collections of colloid bodies, patches of miliary sclerosis, and chromatolysis and vacuolation of nerve-cells.[3]

[3] Miles, _Laboratory Reports, Royal College of Physicians, Edinburgh_, vol. iv.

(2) In more severe cases there are often several _visible areas of extravasation_, most commonly in the grey matter of the cortex (Fig. 184). These foci vary in size from a split-pea to a hazel-nut, and consist of a dark central zone of extravasated blood, surrounded by an area of "red softening" of the brain matter, beyond which are numerous minute capillary haemorrhages. These intra-cerebral lesions may be accompanied by an effusion of blood into the meshes of the arachno-pial membrane, and they may occur either at the part of the head struck, or at the opposite pole of the axis of percussion--the so-called point of _contre-coup_. The symptoms vary with the size and site of the extravasations. It is probable that the phenomena of "cerebral irritation" are to be explained by the occurrence of such haemorrhages widely scattered through the cerebral cortex. Effusions into the cortical motor areas give rise to irritation or paralysis of the muscles governed by the affected centres. Different forms of aphasia and interference with vision or with hearing follow implication of the centres governing these functions. In the pre-frontal and in the lower temporal convolutions no special symptoms seem to follow. When the haemorrhages are extensive and numerous, symptoms of compression may ensue, and these are aggravated when oedema of the brain is superadded.

Localised haemorrhages also occur, although less frequently, in the crura cerebri, the pons, the floor of the fourth ventricle, and the cerebellum. In these situations they usually prove fatal by causing rapidly advancing coma and interference with the respiratory and cardiac centres. The temperature immediately rises to 106 deg. or even 108 deg. F., and a modified form of Cheyne-Stokes respiration is present.

(3) Still more gross lesions, in the form of distinct _lacerations_, are comparatively common at the tips of the frontal, temporal, and occipital lobes, on the surface of the cerebellum, and at the base of the brain. These are usually associated with symptoms of compression in its most typical form, and as a rule prove fatal. The grey matter is torn, and extensive effusion of blood takes place into the brain substance, and on the surface, filling up the sulci, and distending the arachno-pial space (Fig. 184). In a compound fracture, brain matter may be extruded through the opening in the skull.

(4) The extravasated blood may burst _into the lateral ventricles_, in which case the pulse becomes small and rapid--130, 160, or even 170. The respiration also is rapid--45 to 60--and greatly embarrassed, and the temperature suddenly rises to 103 deg. or 104 deg. F., and continues to rise till death ensues.

(5) _Traumatic Oedema._--It is not uncommon for a diffuse oedematous infiltration of the brain substance or of the arachno-pial membrane to take place in the vicinity of the injured portion of brain. This serous exude, on account of the natural adhesions of the arachno-pia, usually remains limited to the damaged area, but it may become generalised.

_Mechanism._--The explanation of these widespread haemorrhages is to be found, according to Duret, in the disturbance of the cerebro-spinal fluid which accompanies a severe blow on the head. This fluid not only surrounds the brain, but it also fills the ventricles, and permeates its substance in every direction in the peri-vascular and perilymphatic spaces. As the brain tissue is incompressible, if an area of the skull is momentarily depressed by a localised blow, space is provided for it by displacement of a quantity of cerebro-spinal fluid, which sets up a fluid wave, and this by hydrostatic pressure increases the tension of the fluid throughout the entire brain. Vessels may be lacerated at any point, either by the flow of this wave or during the ebb which follows the recoil. Hence it is that the lesion is not always at the seat of impact, but may be at the opposite side of the skull or at other remote points.

_Repair._--As the disintegrated brain matter is replaced by cicatricial tissue, neither the nerve cells nor the fibres being regenerated, the loss of function of the parts destroyed is usually permanent. A localised extravasation of blood may become encapsulated, and constitute a "haemorrhagic cyst." We have experimentally confirmed Duret's observations and agree with his conclusions.

CLINICAL MANIFESTATIONS OF INJURIES TO THE BRAIN

For convenience, the clinical manifestations of cerebral injury are usually described under the terms "concussion," "cerebral irritation," and "compression," but no precise pathological significance attaches to these terms, they are essentially clinical. As the conditions so described do not occur as independent entities and may overlap or merge into one another their differentiation is more or less arbitrary, and cases are frequently met with that do not run the course characteristic of any of these groups.

#Concussion of the Brain or Cerebral Shock.#--The symptoms associated with concussion of the brain are to all intents and purposes those of surgical shock (Volume I., p. 250), the activity of the vital centres being disturbed by violence acting directly upon the brain tissue instead of by impulses transmitted to it by way of the afferent nerves. Various theories have been put forward to account for the depression of the vital functions in concussion. According to Duret, with whose views we agree, the wave of cerebro-spinal fluid set in motion by the impact of the blow on the skull, passes, both in the ventricles and in the sub-arachnoid space, towards the base, where it impinges upon the pons and medulla, stimulating the restiform bodies and so inducing a fall in the blood pressure and a profound anaemia of the brain. The disturbance of the cerebro-spinal fluid may at the same time produce the microscopic lesions in the brain tissues described on p. 341.

The symptoms of shock may be the only evidence of injury, or they may be superadded to those of fracture of the skull, or laceration of the brain.

The _clinical features_ vary according to the severity of the violence. In the slightest cases the patient does not lose consciousness, but merely feels giddy, faint, and dazed for a few seconds. His mind is confused, but he rapidly recovers, and, perhaps after vomiting, feels quite well again, save for a slight shakiness in his limbs.

In more severe cases, immediately on receiving the blow the patient falls to the ground unconscious. Sometimes he suffers from a general tetanic seizure associated with arrest of respiration, which is usually of short duration and is frequently overlooked, but may prove fatal. The pulse is slow, small, and feeble, and is sometimes irregular in force and frequency. The respirations are short, shallow, slow, and frequently sighing in character. The temperature falls to 97 deg. F., or even lower. The skin is cold and pallid and covered with clammy sweat, and the features are pinched and pale.

In uncomplicated cases the pupils are usually equal, moderately dilated, and react sluggishly to light. The patient can be partially roused by shouting or by other forms of external stimulation, but he soon subsides again into a lethargic condition. Although voluntary movement and the deep reflexes are abolished, there is no true muscular paralysis.

After a period, varying from a few minutes to several hours, he rallies, the first evidence often being vomiting, which is usually repeated. Sometimes reaction is ushered in by a mild epileptiform seizure. He then turns on his side, the face becomes flushed, and gradually the symptoms pass off and consciousness returns. The temperature rises to 99 deg. or 100 deg. F., and in some cases remains elevated for a few days. In most cases it falls again to 97 deg. or 97.5 deg., and remains persistently subnormal for one or two weeks. During reaction the pulse becomes quick and bounding, but after a few hours it again becomes slow, and usually remains abnormally slow (40 to 60) for ten or fourteen days. There is sometimes a tendency to constipation, and for the bladder to become distended, although he has no difficulty in passing water. Very commonly the patient complains of pain in the head for some days after the return of consciousness. Children often sleep a great deal during the first few days, but sometimes they are very fretful.

In cases complicated by gross brain lesions the symptoms of concussion may imperceptibly merge into those of compression or there may be a "lucid interval" of some hours duration.

_After-Effects of Concussion._--The majority of patients recover completely. A number complain for a time of headache, languor, muscular weakness, and incapacity for sustained effort--_traumatic neurasthenia_. Sometimes there is a condition of mental instability, the patient is easily excited, and is unduly affected by alcohol or other stimulants. Occasionally there is permanent mental impairment. It is not uncommon to find that the patient has entirely forgotten the circumstances of the injury and of the events which immediately preceded it. In some instances the memory is permanently impaired. On the other hand, it has occurred that a patient, after concussion, has recovered his memory of a foreign language long since forgotten.

As it is never possible to determine the precise extent of the damage to the brain, the immediate prognosis, even in the mildest cases of concussion, should always be guarded. If the patient has been actually unconscious, the condition should be looked upon as a serious one, and treated accordingly.

_Treatment._--The immediate treatment is the same as that of shock. Absolute rest and quietness are called for. When the symptoms begin to pass off, the head should be raised on pillows to prevent congestion and to diminish the risk of bleeding from damaged blood vessels in the brain. The value of applying an ice-bag or Leiter's tubes with a view to arresting haemorrhage inside the skull, is more than doubtful. Lumbar puncture, venesection, or the application of leeches over the temple or behind the ear may be employed with benefit. The use of small doses of atropin and ergotin was recommended by von Bergmann. The bowels should be thoroughly opened by calomel, croton oil, or Henry's solution, and a light milk diet given. The patient is kept in a shaded room, and should be confined to bed for from fourteen to twenty-one days. It is often difficult to convince the patient of the necessity for such prolonged confinement, but the responsibility for curtailing it must rest upon him or his friends. Reading, conversation, and argument must be avoided to ensure absolute rest to the brain.

#Cerebral Irritation.#--In some cases of injury to the head--particularly of the anterior part and the parietal region--as the symptoms of concussion are passing off, the patient begins to exhibit a peculiar train of symptoms, which was graphically described by Erichsen under the name of cerebral irritation. "The attitude of the patient is peculiar, and most characteristic: he lies on one side and is curled up in a state of general flexion. The body is bent forwards and the knees are drawn up on the abdomen, the legs bent, the arms flexed, and the hands drawn in. He does not lie motionless, but is restless, and often, when irritated, tosses himself about. But, however restless he may be, he never stretches himself out nor assumes the supine position, but invariably maintains an attitude of flexion. The eyelids are firmly closed, and he resists violently every effort made to open them; if this be effected, the pupils will be found to be contracted. The surface is pale and cool, or even cold. The pulse is small, feeble, and slow, seldom above 70. The sphincters are not usually affected, and the patient will pass urine when the bladder requires to be emptied; there may, however, though rarely, be retention.

"The mental state is equally peculiar. Irritability of mind is the prevailing characteristic. The patient is unconscious, takes no heed of what passes, unless called to in a loud tone of voice, when he shows signs of irritability of temper or frowns, turns away hastily, mutters indistinctly, and grinds his teeth. It appears as if the temper, as much as or more than the intellect, were affected in this condition. He sleeps without stertor.

"After a period varying from one to three weeks, the pulse improves in tone, the temperature of the body increases, the tendency to flexion subsides, and the patient lies stretched out. Irritability gives place to fatuity; there is less manifestation of temper, but more weakness of mind. Recovery is slow, but though delayed, may at length be perfect...."

The _treatment_ consists in keeping the patient quiet, in a darkened room, on much the same lines as for concussion.

#Compression of the Brain.#--This term is used clinically to denote the train of symptoms which follows a marked increase of the intra-cranial tension produced by such causes as haemorrhage, oedema, the accumulation of inflammatory exudate, or the growth of tumours within the skull. The only pathological idea the term conveys is that there is more inside the skull than it can conveniently hold.

_Clinical Features._--The following description refers to compression due to haemorrhage within the skull as a result of injury. In a majority of such cases, the symptoms of compression supervene on those of concussion; in certain conditions, notably haemorrhage from the middle meningeal artery, there is an interval, during which the patient regains complete consciousness, in others the symptoms of concussion gradually and imperceptibly merge into those of compression. The rapidity of onset of the symptoms and their course and duration vary widely according to the nature and extent of the brain lesion. Death may occur in a few hours, or recovery may take place after the patient has been unconscious for several weeks.

The first symptoms are of an irritative character--dull pain in the head, restlessness, and hyper-sensitiveness to external stimuli. The face is suffused, and the pupils at first are usually contracted. The temperature falls to 97 deg., or even to 95 deg. F. Vomiting is not infrequent.

As the pressure increases, paralytic symptoms ensue. The patient gradually loses consciousness, and passes into a condition of coma. The face is cyanosed, and the distension of the veins of the eyelids furnishes an index of the severity of the intra-cranial venous stasis (Cushing). The pulse becomes slow, full, and bounding. The respiration is slow and deep, and eventually stertorous or snoring in character from paralysis of the soft palate, and the lips and cheeks are puffed out from paralysis of the muscles of these parts. The temperature, which at first falls to 97 deg. or even 95 deg. F., in the course of three or four hours usually rises (100.5 deg. or 102.5 deg. F.). If the temperature reaches 104 deg. F., or higher, the condition usually proves fatal. Sometimes it rises as high as 106 deg. or 108 deg. F.--_cerebral hyperpyrexia_ (Fig. 185). Retention of urine from paralysis of the bladder, and involuntary defecation from paralysis of the sphincter ani, are common.

During the progress of the symptoms there is frequently evidence of direct pressure upon definite cortical centres or cranial nerves, giving rise to _focal symptoms_. Particular groups of muscles on the side opposite to the lesion may first show spasmodic jerkings or spasms (unilateral monospasm), and later the same groups become paralysed (monoplegia). The paralysis frequently affects the whole of one side of the body (hemiplegia) and the oculo-motor nerve is often paralysed at the same time.

The pupils vary so widely in different cases that their condition does not form a reliable diagnostic sign. Perhaps it is most common for the pupil on the same side as the lesion to be contracted at first and later to become fully dilated, while that on the opposite side remains moderately dilated. As a rule, they are irresponsive to light. Ophthalmoscopic examination shows swelling of the disc, and the vessels of the papilla are distended and tortuous.

In cases which go on to a fatal termination, the coma deepens and the muscular and sensory paralyses become general and complete. The vital centres in the medulla oblongata gradually become involved, and death results from paralysis of the respiratory centre. The fatal issue is often hastened by the onset of hypostatic pneumonia. Not infrequently a modified type of Cheyne-Stokes respiration is observed for some time before death ensues.

A similar train of symptoms may ensue in cases of head injury as a result of _pyogenic infection_ having given rise to meningitis or abscess with accumulation of inflammatory exudate.

_Pathology._--When any addition is made to the bulk of matter inside the cranial cavity, room is gained in the first instance by the displacement into the vertebral canal of a certain amount of cerebro-spinal fluid. The capacity of the spinal sheath, however, is limited, and as soon as the tension oversteps a certain point, the pressure comes to bear injuriously on the cerebral capillaries, disturbing the circulation, and so interfering with the nutrition of the brain tissue. As the intra-cranial tension still further increases, the pressure gradually comes to affect the cerebral tissue itself, and so the extreme symptoms of compression are produced. The vagus and vaso-motor centres are irritated, and this causes slowing of the pulse, contraction of the small arteries, and increase of the arterial tension which tends to maintain an adequate circulation in the vital centres in the medulla. The Cheyne-Stokes respiration is due to rhythmical variations in the arterial tension: during the period of fall the centres become anaemic and the respiration fails; during the rise the medulla is again supplied with blood, and breathing is resumed (Eyster).

The parts of the brain directly pressed upon become anaemic, while the other parts become congested, and the nutrition of the whole brain is thus seriously interfered with. Different parts of the brain and cord show varying powers of resistance to this circulatory disturbance. The cortex is the least resistant part, and next in order follow the corona radiata, the grey matter of the spinal cord, the pons, and, last, the medulla oblongata. Hence it is that the respiratory and cardiac centres hold out longest.

_Depressed Bone as a Cause of Compression._--It is more than doubtful whether a depressed portion of bone is of itself capable of inducing symptoms of compression of the brain. When such symptoms accompany depressed fracture, they are to be attributed either to associated haemorrhage, or to interference with the circulation and consequent oedema which the displaced bone produces. Fragments of bone may, however, aggravate the symptoms by irritating the cerebral tissue on which they impinge.

_Foreign Bodies._--The role of foreign bodies, such as bullets, in the production of compression symptoms is similar to that of depressed bone. That foreign bodies of themselves are not a cause of compression seems evident from the fact that it is not uncommon for them to become permanently embedded in the brain substance without inducing any symptoms. Not only have bullets, the points of sharp instruments, and other substances remained embedded in the brain for years without doing harm, but in many cases the patients have continued to occupy important and responsible positions in life.

_Differential Diagnosis._--It not infrequently happens that a patient is found in an insensible condition under circumstances which give no clue to the cause of his unconsciousness. He is usually removed to the nearest hospital, and the house-surgeon under whose charge he comes must exercise the greatest care and discretion in dealing with him. In attempting to arrive at the cause of the condition, numerous possibilities have to be borne in mind, but it is often impossible to make a definite diagnosis. The chief of these causes are trauma, apoplexy or cerebral embolism, epileptic coma, alcohol and opium poisoning, uraemic and diabetic coma, sunstroke, and exposure to cold. The commonest error is to mistake a case of cerebral compression for one of drunkenness. It is scarcely necessary to say that a man who smells of alcohol is not necessarily intoxicated; the drink may have been given with the object of reviving him. It may be that one or other of the above-named conditions has caused the patient to fall, and in his fall he has incidentally sustained an injury to the head, which, however, is in no way responsible for his unconsciousness. Whenever there is the least doubt, therefore, the patient should be admitted to hospital.

In the first instance, careful search should be made for any sign of injury, especially on the head. The discovery of a severe scalp wound or of a fracture of the skull, in association with the symptoms of concussion or compression, will in most cases raise the presumption that the unconsciousness is due to some traumatic intra-cranial lesion. Examination of the fluid withdrawn by lumbar puncture may furnish useful information (p. 338).

In the absence of evidence of a head injury, the stomach should be washed out and its contents examined to see if any narcotic poison is present. The urine also should be drawn off and examined for albumin and sugar.

In haemorrhage due to the rupture of diseased cerebral arteries (apoplexy), or to embolism, the symptoms are essentially those of compression, and, in the absence of a definite history of injury to the head, it is seldom possible to arrive at an accurate diagnosis as to the cause of the condition. The history that the patient has previously had "an apoplectic shock," and the fact that he is up in years and shows signs of arterial degeneration and of cardiac hypertrophy which would favour such haemorrhage, are presumptive evidence that the lesion is not traumatic.

If a history is forthcoming that the patient is an epileptic, there is a strong presumption that the symptoms are those of _epileptic coma_.

In _alcoholic poisoning_ the examination of the stomach contents will furnish evidence. The patient is not completely unconscious, nor is he paralysed; the pupils are usually contracted, but react; and the temperature is often markedly subnormal. Improvement soon takes place after the stomach has been emptied.

In _opium poisoning_ the general condition of the patient is much the same as in poisoning by alcohol. The pupils, however, are markedly contracted, and do not react to light. When the poison has been taken in the form of laudanum, this may be recognised by its odour.

In the _coma_ of _uraemia_ or of _diabetes_ there is no true paralysis, nor is there stertor. The urine contains albumin or sugar, and there may be oedema of the feet and legs.

_Prognosis._--The prognosis depends so much on the nature and extent of the injury to the brain that it is impossible to formulate any general statements with regard to it. It may be said, however, that the symptoms which indicate a bad prognosis are immediate rise of temperature, particularly if it goes above 104 deg. F., the early onset of muscular rigidity, extreme and persistent contraction of the pupils, with loss of the reflex to light, conjugate deviation of the eyes, and the early appearance of bed-sores.

In the majority of cases compression ends fatally in from two to seven days. On the other hand, recovery may ensue after the stuporous condition has lasted for several weeks.

The _treatment_ of compression is considered with the different lesions which cause it; the principle in all cases being to remove, if possible, the cause of the increased pressure within the skull.

#Traumatic Oedema.#--In practice, cases are frequently met with, particularly in children, that do not conform to the classical description of either concussion, cerebral irritation, or compression. The injury may be followed by a varying degree of concussion which soon passes off but leaves the patient in a listless, drowsy state that may persist for days or even for weeks. The cerebration is disturbed, so that while the patient is not unconscious, he is apathetic and has lost his bearings and fails to recognise where or with whom he is. He complains of headache, there is tenderness on percussion over the skull, the knee jerks are diminished or absent, but there is no motor paralysis. In some cases there are localised jerkings, in others generalised convulsive attacks during which the patient becomes deeply cyanosed. The condition differs from compression due to middle meningeal haemorrhage in that it is less severe and is not steadily progressive.

When the symptoms are localised, the condition is probably due to oedematous infiltration of the injured portion of brain; when generalised, to increased intra-cranial tension from serous effusion into the arachno-pial space.

The _treatment_ consists in diminishing the intra-cranial tension by purgation, leeches, bleeding, or lumbar puncture, or if life is threatened, by opening the skull over the seat of injury, or failing evidence of this, by a decompression operation in the temporal region.

INTRA-CRANIAL HAEMORRHAGE

Apart from the haemorrhage that accompanies laceration of brain tissue, bleeding may occur inside the skull, either from arteries or from veins. The effused blood may collect either between the dura mater and the bone (_extra-dural haemorrhage_), or inside the dura (_intra-dural haemorrhage_).

#Middle Meningeal Haemorrhage.#--The commonest cause of extra-dural haemorrhage is laceration of the middle meningeal artery. This artery--a branch of the internal maxillary--after entering the skull through the foramen spinosum, crosses the anterior inferior angle of the parietal bone, and divides into an anterior and a posterior branch which supply the meninges and calvaria (Fig. 186). Either branch may be injured in association with fractures, or from incised, punctured, or gun-shot wounds. The vessel may be ruptured without the skull being fractured, and sometimes it is the artery on the side opposite to the seat of the blow that is torn. The most common situations for rupture are at the anterior inferior angle of the parietal bone, in which case the anterior branch is torn (90 to 95 per cent.); and on the inner aspect of the temporal bone, where the posterior branch is torn (5 to 10 per cent.).

It is probable that the size of the haemorrhage depends on the nature, extent, and severity of the injury to the head. The recoil of the skull after the blow separates the dura from the bone, and if the meningeal artery is lacerated or punctured, blood is effused into the space thus formed (Fig. 187). A localised blow therefore results in a small area of separation and a correspondingly small clot; while a diffuse blow is followed by more extensive lesions. It is believed that, once the dura is partly separated, the force of the blood poured out from the lacerated artery is--on the principle of the hydraulic press--sufficient to continue the separation.

_Clinical Features._--The typical characteristics of middle meningeal haemorrhage are met with only when the bleeding takes place between the dura and the bone. Under these conditions the symptoms of concussion are usually most prominent at first, and those of compression only ensue after a varying interval, during which the patient as a rule regains consciousness. In some cases, indeed, he is able to continue his work, or to walk home or to hospital, before any evidence of intra-cranial mischief manifests itself. This "lucid interval" helps to distinguish the symptoms due to middle meningeal haemorrhage from those of laceration of the brain substance, as in the latter the symptoms of concussion merge directly into those of compression. Lumbar puncture may aid in the differential diagnosis between extra-and intra-dural haemorrhage, as blood is present in the fluid withdrawn in the latter, but not in the former.

A few hours after the accident the patient experiences severe pain in the head, and he usually vomits repeatedly. For a time he is restless and noisy, but gradually becomes drowsy, and the stupor increases more or less rapidly until coma supervenes. The pulse usually becomes slow and full. The respiration is rapid (30 to 50), and becomes greatly embarrassed and stertorous. The temperature progressively rises, and before death may reach 106 deg. F., or even higher. Monoplegia, usually beginning in the face or arm on the side opposite to the lesion, gradually comes on, and is followed by hemiplegia, from pressure on the motor areas, underlying the clot. The condition of the pupils is so variable as to have no diagnostic value; but if both are widely dilated and irresponsive to light, the prognosis is grave. Death usually ensues in from twenty-four to forty-eight hours, unless the pressure within the skull is relieved by operation; even after removal of the clot death may ensue if the brain has been lacerated, or if there is haemorrhage at the base.

When the haemorrhage takes place from the anterior branch, the clot tends to spread towards the base, and may press upon the cavernous sinus, causing congestion and protrusion of the eye, with paralysis of the oculo-motor nerve and wide dilatation of the pupil.

In some cases of middle meningeal haemorrhage there is no gross injury to the brain; the area underlying the clot is merely compressed and emptied of blood, and, on being exposed, the brain is found flattened, or even deeply indented by the blood-clot, and it does not pulsate. If the clot is removed, the brain may regain its normal contour and its pulsation return. The mortality is over 50 per cent.

If the fracture is compound, the blood can escape, and therefore the pressure symptoms are less evident or may be entirely absent.

It is a fact of some medico-legal importance that haemorrhage from the middle meningeal may not take place till some days, or even weeks, after an injury, which at the time was only attended with symptoms of concussion. This condition is known as _traumatic apoplexy_.

_Treatment._--Immediate operation is imperatively called for, not only to arrest the haemorrhage and remove the clot, but also to ward off the oedema of the brain, which is often responsible for the fatal issue. When there is no external wound, the point at which the skull is to be opened is determined by the symptoms; for example, paralysis of the arm and face on one side indicates trephining over the centres governing these parts on the side opposite to the paralysis.

If the bleeding cannot otherwise be arrested it may be necessary to ligate the external carotid artery. It has been suggested by J. B. Murphy that, when the patient is seen while the symptoms of compression are coming on, instead of trephining, the haemorrhage from the meningeal vessels should be arrested by applying a ligature to the external carotid, under local anaesthesia.

Injury to the #internal carotid# artery within the skull may result from penetrating wounds, or may be associated with a fracture of the base. It is almost invariably fatal. In some cases a communication is established between the artery and the cavernous sinus, and an arterio-venous aneurysm is thus produced. Ligation of the internal carotid in the neck or of the common carotid is the only feasible treatment.

Injuries of the #venous sinuses# may occur apart from gross lesions of the skull, but as a rule they accompany fractures and penetrating wounds. The transverse (lateral), superior sagittal (longitudinal), and cavernous sinuses are those most frequently damaged. On account of the low pressure in the sinuses, spontaneous arrest of extra-dural haemorrhage usually takes place, and recovery ensues. In some cases, however, the amount of blood extravasated is sufficient to cause compression. If the dura mater is torn, and the blood passes into the sub-arachnoid space, it may spread over the whole surface of the brain. Sometimes the bleeding only commences after a depressed fracture has been elevated.

In the presence of an open wound, the venous source of the bleeding is recognised by the dark colour of the blood and the continuous character of the stream. It may be arrested by pressure with gauze pads or by packing a strand of catgut into the sinus (Lister), or, if this fails, by grasping the sinus with forceps and leaving these in position for twenty-four or forty-eight hours. A small puncture in the outer wall of the sinus may be closed with sutures. Signs of increasing compression call for trephining and opening of the dura if this is necessary to admit of the clot being removed.

#Intra-cranial Haemorrhage in the Newly-Born.#--An extravasation of blood into the arachno-pial space frequently occurs during birth. The observations of Cushing seem to show that this is usually due to tearing of the delicate cerebral veins which pass from the cortex to the superior sagittal sinus, from the strain put upon them by the overlapping of the parietal bones, in the moulding of the head. It may sometimes be due to an excessive degree of asphyxia during birth. The extravasation is usually most marked over the central area of the cortex near the middle line, and it is often bilateral.

This condition is most frequently met with in a first-born child--and more often in boys than in girls--the labour having been prolonged and difficult, and the presentation abnormal. There is usually a history that the infant was deeply cyanosed when born, and that there was difficulty in getting it to breathe. As a rule, there is no external evidence of trauma. The anterior fontanelle is tense and does not pulsate, the pulse is slow, and for several days the child appears to have difficulty in sucking and swallowing, and is abnormally still. In the course of a few days definite symptoms of localised pressure appear. It is noticed that one leg or arm, or one side of the body is not moved, or both sides may be affected; when the paralysis is bilateral, the absence of movement is more liable to be overlooked. The infant may suffer from convulsions; there may be paralysis of certain of the ocular muscles, and inequality of the pupils; sometimes there is blindness. Persistent rigidity of the limbs, with turning of the thumbs towards the palm, is present in some cases. Lumbar puncture may reveal the presence of blood corpuscles in the cerebro-spinal fluid, and increase in the tension of the fluid.

If untreated, the condition is usually followed by the development of spastic paralysis of one or more limbs, on one or on both sides of the body (Little's disease), by blindness, deafness, and varying degrees of mental deficiency, or by Jacksonian epilepsy.

_Treatment._--To obviate these after-effects the clot may be removed by raising an osteo-plastic flap, including nearly the whole of the parietal bone. The operation should be undertaken within the first week or two, and great care must be taken to keep up the body-warmth, and to prevent undue loss of blood. It may be necessary to operate on both sides, an interval being allowed to elapse between the two operations.

For the immediate relief of increased intra-cranial tension, the daily withdrawal of 10-12 c.c. of cerebro-spinal fluid by lumbar punctures may be employed, or a sub-temporal decompression operation may be performed.

WOUNDS OF THE BRAIN

#Wounds of the Brain.#--_Incised_ wounds of the brain usually result from sabre-cuts, hatchet blows, or circular saws. A portion of the scalp and cranium may be raised along with a slice of brain matter, and in some cases the whole flap is severed. The extent of the injury, the conditions under which it is received, and the liability to infection, render such wounds extremely dangerous.

_Punctured wounds_ may be inflicted on the vault by stabs with a knife or dagger, or by other sharp objects, such as the spike of a railing. More frequently a pointed instrument, such as a fencing foil, the end of an umbrella, or a knitting needle, is thrust through the orbit into the base of the brain. Occasionally the base of the skull has been perforated through the roof of the pharynx, for example, by the stem of a tobacco-pipe. All such wounds are of necessity compound, and the risk of infection is considerable, particularly if the penetrating object is broken and a portion remains embedded within the skull. The infective complications of such injuries are described later.

_Bullet wounds_ have many features in common with punctured wounds. There is more contusion of the brain substance, disintegrated brain matter is usually found in the wound of entrance, and the bullet often carries in with it pieces of bone, cloth, or wad, thus adding to the risk of infection.

Aseptic foreign bodies, especially bullets, may remain embedded in the brain without producing symptoms.

The _treatment_ of punctured wounds consists in enlarging the wounds in the soft parts, trephining the skull, and removing any foreign body that may be in it, purifying the track, and establishing drainage.

AFTER-EFFECTS OF HEAD INJURIES

Various after-effects may follow injuries of the head. Thus, for example, _chronic interstitial changes_ (sclerosis) may spread from an area of cicatrisation in the brain; or _softening_ may ensue, either in the form of pale areas of necrosis (white softening) or of haemorrhagic patches (red softening). The symptoms vary with the area implicated. _Adhesions_ between the brain and its membranes may produce severe headache and attacks of vertigo, especially on the patient making sudden exertion.

After a head injury, the patient's whole mental attitude is sometimes changed, so that he becomes irritable, unstable, and incapacitated for brain-work--_traumatic neurasthenia_. In some cases self-control is lost, and alcoholic and drug habits are developed.

#Traumatic epilepsy# may ensue as a result of some circumscribed cortical lesion, such as a spicule of bone projecting into the cortex, the presence of adhesions between the membranes and the brain, a cicatrix in the brain tissue leading to sclerosis or a haemorrhagic cyst in the membranes or cerebral tissue.

The convulsive attacks are of the Jacksonian type, beginning in one particular group of muscles and spreading to neighbouring groups till all the muscles of the body may be affected. The convulsions may begin soon after the injury, for example, when the cause is a fragment of bone irritating the cortex; in other cases it may be several years before they make their appearance. The onset is usually sudden, and the "signal symptom"--for example, jerking of the thumb, conjugate deviation of the eyes, or motor aphasia--indicates the seat of the lesion. At first the attacks only recur at intervals of, it may be weeks or months, but as time goes on they become more and more frequent, until there may be as many as forty or fifty in a day. Sometimes the patient loses consciousness during the fit; sometimes he remains partly conscious. In course of time the same degenerative changes as occur in other forms of epilepsy ensue: certain groups of muscles may become paralysed; the patient may pass into a state of idiocy, or into what is known as the "status epilepticus," in which the fits succeed one another without remission, the breathing becomes stertorous, the temperature rising, the pulse becoming very rapid; finally coma supervenes, and the patient dies.

_Treatment._--The administration of bromides is only palliative. Operation is indicated only when the "signal symptom" indicates a limited and accessible portion of the brain as the seat of the lesion, or when there is a depression of the skull or other definite evidence of cranial injury. The more recent the injury the better is the prospect, as secondary changes are less likely to have taken place, and the peculiarly irritable state of the brain--sometimes referred to as the "epileptic habit"--has not developed. The operation consists in opening the skull freely, and removing any discoverable cause of irritation--depressed bone, thickened and adherent membranes, a cyst, or sclerosed patch of cortex; it may be necessary to interpose a layer of tissue, a flap of fascia lata, for example, between the bone and the cortex of the brain. The point at which the skull is opened is determined by the seat of the injury and the focal brain symptoms.

The return of fits within a few days of the operation does not necessarily mean failure, as they often pass off again. Complete and permanent cure is not common, but the number and severity of the attacks are usually so far diminished that life is rendered bearable.

#Traumatic insanity# may follow injury to any part of the brain, and it may come on either immediately or after an interval. It may or may not be associated with epilepsy. Any form of insanity may occur, either as a direct result of the trauma, or from the resistance of the brain being lowered by the injury in a patient predisposed to insanity. When insanity follows as a direct consequence of injury, the organic lesion is usually a superficial one, and the disturbance of brain function is generally due to reflex irritation of the dura mater (Duret). These facts possibly explain the immediate improvement which occasionally follows the opening of the skull at the point of injury and removal of the exciting cause. Cases occurring within a few days of the injury usually recover within a month or two. The later the condition is in developing the less obvious is the relationship between the trauma and the insanity, and therefore the worse is the prognosis.

_Meningitis_, _sinus thrombosis_, and _cerebral abscess_ may follow upon any form of head injury attended with infection. The clinical features--save for the history of a trauma--correspond so closely with those of the same conditions occurring apart from injury, that they are most conveniently considered together (p. 374).