Synostosis of the superior radio-ulnar joint is a rare congenital condition, in which the hinge movements at the elbow are free, but supination is impossible; an attempt may be made by operation to form a new joint.

Volkmann's ischaemic contracture of the muscles of the forearm, resulting in the production of claw-hand, is described in Volume I., p. 415.

Deformities of the Forearm and Hand.—The radius may be absent completely or in part, frequently in combination with other malformations. The most evident result is a deviation of the hand to the radial side—one variety of club-hand. The forearm is shortened, the ulna thickened and often bent, and the thumb and its metacarpal bone are often absent, so that the usefulness of the hand and arm is greatly impaired (Fig. 171). For this condition Bardenheuer devised an operation which consists in splitting the lower end of the ulna longitudinally and inserting the proximal bones of the carpus into the cleft.

Congenital deficiency of the ulna is extremely rare.

Intra-uterine amputation by constriction of amniotic bands sometimes occurs (Figs. 168, 169).



Drop Wrist from Anterior Poliomyelitis.—In this condition the capacity of extending the fingers is deficient or absent. Recovery can be confidently predicted if, on still further flexing the fingers, they can be voluntarily extended towards the point from which they are flexed (Tubby and Jones). Considerable improvement may result from fixing the hand by means of a splint in the attitude of dorsal flexion. The splint is removed at frequent intervals to allow of massage and other treatment being carried out, and it has usually to be worn for a period of one to two years. In some cases recourse should be had to arthrodesis.



In spastic paralysis the most pronounced deformity is flexion of the forearm and pronation and flexion of the hand (Fig. 166). Gradual extension at the wrist may be brought about by the use of a malleable splint, in which the angle is gradually increased, over a period of at least twelve months. Failing success by this method, operation may be had recourse to, and this consists in lengthening of tendons, and tendon transplantation. Tubby has devised an operation for converting the pronator radii teres into a supinator, and Robert Jones another in which the flexors of the carpus are made to take the place of the extensors. "These operations, combined if necessary with elongation of the flexors of the fingers, pave the way for diminution of the angle of flexion at the elbow, lessening of the pronator spasm, increase of the supinating power, reduction of the carpal flexion, and addition to the extensor power at the wrist" (Tubby and Jones).

Congenital Club-hand.—This rare deformity corresponds to congenital club-foot, and probably arises in the same way. The hand and fingers are rigidly flexed to the ulnar or radial side, so that the patient is incapable of moving them. Treatment is carried out on the same lines as for club-foot.

A deformity resembling this, acquired club-hand, is brought about when the growth of either of the bones of the forearm has been arrested as a result of disease or of traumatic separation of its lower epiphysis. The hand deviates to the side on which the growth has been arrested—manus valga or vara. The treatment consists in resecting a portion of the longer bone.



Madelung's Deformity of the Wrist.—In 1878, Madelung called attention to a deformity also called sub-luxation of the hand, in which the lower articular surface of the radius is rotated so that it looks towards the palm; there is palmar displacement of the carpus, and the lower end of the ulna projects on the dorsum. The cause of the condition is obscure, but it is met with chiefly in young women with slack ligaments, whose laborious occupation or athletic pursuits subject the hand and wrist to long-continued or repeated strain. It is as frequently unilateral as bilateral and may recur in successive generations. There is a good deal of pain, the grasping power of the hand is impaired, and dorsiflexion is considerably restricted. The deformity disappears on forcible traction, but at once reappears when the traction is removed. A wristlet of poroplastic or leather extending from the mid-forearm to the knuckles is moulded to the limb in the corrected position, and is taken off at intervals for massage and exercises.

When operative treatment is called for, it takes the form of osteotomy of the radius and ulna about an inch or more above their articular surfaces.

Congenital dislocation of the wrist is rare.

Deformities of the Fingers.—Various forms of congenital dislocation of the fingers are met with, but they are of little clinical importance, as they interfere but slightly with the usefulness of the digit affected.

Congenital lateral deviation of the phalanges is more unsightly than disabling; it is met with chiefly in the thumb, in which the terminal phalanx deviates to the radial or to the ulnar side in extension; the deviation disappears on flexion.

Congenital contraction of the fingers is comparatively common. It is an inherited deformity, and is often met with in several members of the same family. It most frequently affects the little or the ring and little fingers (Fig. 172), and is usually bilateral. The second and third phalanges are flexed towards the palm; the first phalanx is dorsiflexed, this being the reverse of what is observed in Dupuytren's contraction. Duncan Fitzwilliams suggests that it should be called "hook-finger," and that it is probably due to imperfect development of the anterior ligament of the first inter-phalangeal joint. He has observed it in association with laxity of the ligaments of the other joints of the body.



The affection is usually disregarded in infancy and childhood as being of no importance. In young children, the deformity is corrected by wearing a light splint fixed with strips of plaster, or a piece of whalebone or steel inside the finger of a glove. In older children, the finger may be straightened by subcutaneous division of the ligament over the palmar aspect of the base of the middle phalanx, or failing this by lengthening the flexor tendons and resecting a wedge from the dorsal aspect of the first phalanx close to the inter-phalangeal joint.

Dupuytren's Contraction.—This is an acquired deformity resulting from contraction of the palmar fascia and its digital prolongations (Fig. 173). It is rare in childhood and youth, but is common after middle life, especially in men. It is often hereditary, and is said to occur in those who are liable to gout and to arthritis deformans. While it is met with in the working-classes and attributed to the pressure of some hard object on the palm of the hand—such as a hammer or shovel or whip—its greater frequency in those who do no manual work, and the fact that it is very often bilateral, indicate that the constitutional factor is the more important in its causation.



In the initial stage there is a localised induration in the palm opposite the metacarpo-phalangeal joint, and the skin over it is puckered and closely adherent to the underlying fascia. After a variable interval, the finger is gradually and progressively flexed at the metacarpo-phalangeal joint. The ring finger is usually the first to be affected, less often the fifth, although both are commonly involved. It is rarest of all in the index. The flexion may be confined to the metacarpo-phalangeal joint, or the middle and distal phalanges may also be flexed; and as the deformity becomes more pronounced, the nail of the affected finger may come into contact with the skin of the palm. Dissections show that the flexion of the finger is the result of a chronic interstitial overgrowth or fibrositis and subsequent contraction of the palmar fascia and of its prolongations on to the sides of the fingers. The digital processes of the fascia are thickened and shortened, and come to stand out like the string of a bow. The adipose tissue in the skin of the palm disappears, and the skin and fascia thus brought into contact become fused. The tendons and their sheaths are not implicated; they are found lying deeply in the concavity of the curve of the flexed digit. There is no pain, but the grasp of the hand is interfered with, the patient is unable to wear an ordinary glove, and he may be incapacitated from following his occupation.

The condition is easily diagnosed from congenital contraction by the fact that in the latter the proximal phalanx is dorsiflexed.

Treatment.—When seen in the initial stage, contraction may be prevented by passive movements of the finger and by massage of the indurated fascia; we have observed cases in which these measures have held the malady in check for many years, but when flexion has already occurred, they are useless, and according to the social position, habits, or occupation of the patient, the condition is left alone or the deformity is corrected by operation.

Adam's operation consists in multiple subcutaneous division of the contracted fascia in the palm and of its prolongations on to the finger; in addition to dividing the fascia, the tenotomy knife should be used also to separate the skin from the fascia. The finger is then forcibly extended, and a well-padded splint secured to the hand and forearm. The skin on the palmar aspect opposite the first inter-phalangeal joint may give way when the finger is extended; should this occur, the resulting gap may be covered by a skin graft.

After healing has occurred, massage and movements must be persevered with, and a splint (Fig. 174) worn at night, as there is an inveterate tendency to recurrence of the contraction. In view of this tendency there is much to be said in favour of the radical operation which consists in removal of the fascia by open dissection. Owing to the long time required for healing and the sensitiveness of the scar, the results of excision of the fascia are sometimes disappointing. Greig has obtained good results by resecting the head of the metacarpal bone. When the little finger is completely flexed towards the palm it may be amputated, as it is always in the way.



Supernumerary Fingers (Polydactylism).—These may coexist with supernumerary toes, and the condition is often met with in several members of the same family. Sometimes the extra finger is represented by a mere skin appendage, the nature of which may only be indicated by the presence of a rudimentary nail; sometimes it contains bone representing one or more phalanges, or it may be fully formed (Fig. 175). In the majority of cases the superfluous finger should be removed.



Congenital Deficiencies in the Number of Fingers.—One or more fingers may be absent, such deficiency being often associated with imperfect development of the radius or ulna; or they may be represented by short rounded stumps, which are ascribed to the strangulation of the digits by amniotic bands in utero—the so-called intra-uterine amputation.

Webbing of Fingers (Syndactylism).—Congenital webbing or fusion of the fingers may be associated with polydactylism or with congenital hypertrophy, and, like other digital deformities, may affect several members of the same family. The degree of fusion ranges from a web of skin joining the fingers to a fusion of the bones, the latter being well seen in skiagrams. If an operation is decided upon, it should not be performed until the age of five or six years. In the simplest cases it is only necessary to divide the web and to unite the cut edges of skin along each finger by sutures, a skin graft being inserted into the angle between the fingers. An operation in which the skin is dissected up in the form of flaps may be required, but it should not be lightly entered upon, as in young children it has been known to be followed by gangrene of one or more of the digits.

Congenital Hypertrophy of the Fingers.—This is a form of local giantism affecting one or more digits, and involving all the tissues. The finger is usually of abnormal size at birth, and continues to grow more rapidly than the others, and it may also come to deviate from its normal axis. Such a finger should be trimmed down or removed, to permit of the use of the other digits.

Trigger Finger (Fig. 176).—This is an acquired condition in which movement of a finger or thumb, either in flexion or extension, is arrested, and is only completed with the assistance of the other hand. The obstacle to movement is usually overcome with a jerk or snap suggesting a resemblance to the trigger of a gun or the blade of a clasp-knife. The commonest cause is a disproportion between the size of the tendon and its sheath, such as may result from a localised thickening of the tendon. Recovery usually takes place under massage and passive movements. Failing this, the thickened portion of the tendon is pared down to its normal size; if it is the sheath of the tendon that is narrow, it is laid freely open.



Drop or mallet finger is described on p. 121.



CHAPTER XI

THE SCALP

Surgical Anatomy—Injuries: Contusion; Haematoma; Cephal-haematoma; Wounds; Avulsion—Diseases: Infective conditions; Cystic and solid tumours; Air-containing swellings; Vascular tumours.

Surgical Anatomy.—The skin of the scalp is intimately united to the epicranial aponeurosis by a network of firm fibrous tissue containing some granular fat, and representing the subcutaneous connective tissue. These three layers constitute the scalp proper, and they are so closely connected as to form a single structure which can be moved to a certain extent by the action of the epicranius muscle. The epicranius (occipito-frontalis) muscle with its aponeurosis extends from the superciliary ridge in front to the superior nuchal (curved) line of the occipital bone behind, and laterally to the level of the zygoma where it blends with the temporal fascia. Between the scalp proper and the pericranium is a quantity of loose areolar tissue, in the meshes of which extravasated blood or inflammatory products can rapidly spread over a wide area. Blood extravasated under the pericranium is limited by the attachments of this membrane at the sutures.

The blood supply of the frontal region is derived from the internal carotid arteries through their supra-orbital branches; the remainder of the scalp is supplied from the external carotids through their temporal, posterior auricular and occipital branches. The vessels, which run in the subcutaneous tissue, superficial to the epicranial aponeurosis, anastomose freely with one another and across the middle line. The main branches run towards the vertex, and incisions should, as far as possible, be directed parallel with them.

The venous return is through the frontal, temporal, and occipital veins. These have free communications, through the emissary veins, with the intra-cranial sinuses, and by these routes infective conditions of the scalp may readily be transmitted to the interior of the skull. The most important of the emissary veins are: the mastoid, condyloid, and occipital, passing to the transverse (lateral) sinus; the parietal, which enters the superior sagittal (longitudinal) sinus; and a branch from the nose which traverses the foramen caecum and enters the anterior end of the superior sagittal sinus.

The supra-trochlear, supra-orbital and auriculo-temporal branches of the trigeminal nerve, together with the greater and lesser occipital nerves, supply the scalp with sensation, while the muscles are supplied from the facial nerve.

The lymph vessels pass to the parotid, occipital, mastoid, and submaxillary groups of glands, the different areas of drainage being ill-defined.

INJURIES OF THE SCALP

Subcutaneous Injuries.—In simple contusion of the superficial layers, owing to the density of the tissues, the blood effused is small in quantity and remains confined to the area directly injured, which is firm and tender to the touch, swollen and discoloured. The disappearance of the swelling may be hastened by elastic pressure and massage.

Haematoma of the scalp results when lacerated vessels bleed into the sub-aponeurotic space. Owing to the laxity of the connective tissue in this area, the effused blood tends to diffuse itself widely, and, according to the position assumed by the patient, gravitates to the region of the eyebrow, the occiput, or the zygoma. When a large artery is torn the swelling may pulsate. A haematoma of the scalp may readily be mistaken for a depressed fracture of the skull, owing to the fact that the margins of the effusion are often raised and of a firm resistant character. A differential diagnosis can usually be made by observing that the swelling is on a higher level than the rest of the skull; that the raised margin can to a large extent be dispersed by making firm, steady pressure over it with the finger; and that, on doing so, the smooth and intact surface of the skull can be recognised. When a fracture exists, the finger sinks into the depression and the irregular edge of the bone can be felt. In doubtful cases, if cerebral symptoms are present, an exploratory incision should be made.

Even a large haematoma is usually completely absorbed, but the dispersion of the clot may be hastened by massage and elastic pressure. Any excoriation or wound of the skin must be disinfected.

Sometimes a blood-cyst, consisting of a connective-tissue capsule filled with a yellowish-red fluid, remains, and may require to be emptied with a hollow needle.

These effusions are to be distinguished from the cephal-haematoma, in which the blood collects between the pericranium and the bone. This is oftenest seen in newly born children as a result of pressure on the head during delivery, and is characterised by its limitation to one particular bone—usually the parietal—the further spread of the blood being checked by the attachment of the pericranium at the sutures. Occasionally a permanent thickening of the edges of the bone remains after the absorption of the extravasated blood. This condition is to be diagnosed from traumatic cephal-hydrocele (p. 390).

Wounds of the Scalp.—So long as a scalp wound, however extensive, is kept free from infection, it involves comparatively little risk, but the introduction of organisms to even the most trivial wound is fraught with danger, on account of the ease and rapidity with which the infection may spread along the emissary veins to the meninges and intra-cranial sinuses.

The deeper the wound, the greater is the risk. If the epicranial aponeurosis is divided, the "dangerous area" between it and the pericranium is opened, and if infection occurs, it may lead to widespread suppuration. Should the wound extend through the pericranium, infection is more liable to spread to the bone and to the cranial contents.

The usual varieties of wounds—incised, punctured, contused, and lacerated—are met with in the scalp, and they vary in degree from a simple superficial cut to complete avulsion. For medico-legal purposes it is important to bear in mind that a scalp wound produced by the stroke of a blunt weapon, such as a stick or baton, may closely simulate a wound made with a cutting instrument.

On account of the density of the integument and its close connection with the aponeurosis, scalp wounds do not gape unless the epicranial aponeurosis is widely divided. This facilitates union in incised wounds, but interferes with drainage in the long narrow tracts which result from punctures, and which are so liable to be infected and to implicate the sub-aponeurotic space, the pericranium, or even the bone. It also favours the inclusion in the wound of a foreign body, such as the broken point of a knife, or a piece of glass. The bleeding from scalp wounds is often profuse and difficult to control, because the vessels, fixed as they are in the dense subcutaneous tissue, cannot retract and contract so as to bring about the natural arrest of haemorrhage, and it is difficult to apply forceps or ligatures to their cut ends, suture ligatures are more efficient. On account of the free arterial anastomosis in the deeper layers of the integument, large flaps of scalp will survive when replaced, even if badly bruised and torn, and it is never advisable to cut away any un-infected portion of the scalp, however badly it may be lacerated or however narrow may be the pedicle which unites it to the head.

Gun-shot wounds of the scalp are usually associated with damage to the skull and brain. A spent shot, however, may pierce the scalp, and then, glancing off the bone, lodge in the soft parts.

Complete Avulsion.—In women, the scalp is sometimes torn from the cranium as a result of the hair being caught in revolving machinery. The portion removed, as a rule, consists of integument and aponeurosis with portions of muscle attached. In a few cases the pericranium also has been torn away. So long as any attachment to the intact scalp remains, the parts should be replaced, and, if asepsis is maintained, a satisfactory result may be hoped for. When the scalp is entirely separated, recourse must be had to skin-grafting.

Treatment of recent Scalp Wounds.—To ensure asepsis, the hair should be shaved from the area around the wound, and the part then purified. Gross dirt ground into the edges of lacerated wounds is best removed by paring with scissors. Undermined flaps must be further opened up and drained—by counter-openings if necessary. When there is reason to suspect their presence, foreign bodies should be sought for. Bleeding is arrested by forci-pressure or by ligature; when, as is often the case, these measures fail, the haemorrhage may be controlled by passing a needle threaded with catgut through the scalp so as to include the bleeding vessel. The wound is stitched with horse-hair or silk, and, except in very small and superficial wounds, it is best to allow for drainage. With the use of iodine as a disinfectant, it is often advantageous to dispense with dressings altogether.

Complications of Scalp Wounds.—The most common complications are those due to infection, which not only aggravates the local condition, but is apt to lead to spreading cellulitis, osteomyelitis, meningitis, or inflammation of the intra-cranial sinuses. These dangerous sequelae are liable to follow infection of any scalp wound, but more especially such as implicate the sub-aponeurotic area, or the pericranium. In the integument, a small localised abscess, attended with pain and oedema of surrounding parts, may form. Pus forming under the aponeurosis is liable to spread widely, pointing above the eyebrow, in the occipital region, or in the line of the zygoma. Suppuration under the pericranium tends to be limited by the inter-sutural attachments of the membrane. Necrosis of the outer table, or even of the whole thickness of the skull, may follow, although it is by no means uncommon for large denuded areas of bone to retain their vitality.

The onset of infection is indicated by restlessness, throbbing pain and heat in the wound, a feeling of chilliness or the occurrence of a rigor, and tension of the stitches from oedema of the surrounding tissues. The oedema often extends to the eyelids and face; a puffiness of the eyelids, indeed, is not infrequently the first evidence of the occurrence of infection in the wound.

Treatment.—When suppuration ensues, the stitches should be removed, the wound opened up and purified with eusol, and packed. A dressing of ichthyol and glycerine should be employed for a few days.

Erysipelas of the scalp may originate even in wounds so trivial as to be almost invisible, or from suppurative processes in the region of the frontal sinuses or nasal fossae. It tends to be limited by the attachments of deep fasciae, and seldom spreads to the cheek or neck. Symptoms of cerebral complications, in the form of delirium or coma, and of meningitis may supervene. Cellulitis beneath the aponeurosis from mixed infection is a dangerous complication.

DISEASES OF THE SCALP

Infective Conditions.—It is not uncommon for localised abscesses to occur in the subcutaneous cellular tissue in delicate children, and such collections are not infrequently associated with pediculi, impetigo, or chronic dermatitis. They develop slowly and painlessly, and are only covered by a thin, bluish pellicle of skin. It is not improbable that they result from a mixed infection by pyogenic and tuberculous organisms. As a rule they heal quickly after incision and drainage, but when they are allowed to burst, tedious superficial ulcers may form. Localised abscesses may also form in connection with disease of the cranial bones. Suppuration following upon injuries has already been referred to.

Boils and carbuncles are not common on the hairy part of the scalp. Lupus rarely originates on the scalp, although it may spread thither from the face. Syphilitic lesions are common and present the same characters as elsewhere. Gummata may develop in the soft parts, but more commonly they take origin in the pericranium or bone. Eczema capitis is of surgical importance only in so far as it often forms the starting-point of infection of lymph glands by pyogenic and other organisms.

Cystic and Solid Tumours.—A great variety of swellings is met with in the scalp.

Sebaceous cysts or wens are of frequent occurrence, and have been described in Volume I.

A dermoid cyst is most commonly situated over the position of the anterior fontanelle, in the region of the occipital protuberance, or at the lateral angle of the orbit. As it frequently lies in a gap in the skull, it may be connected by a pedicle with the dura mater, and is liable to be mistaken for a meningocele.



Serous cysts are occasionally found in the occipital region, and are believed to be meningoceles that have become shut off from the interior of the skull before birth.

Adenomas originating in the sebaceous or sweat glands are sometimes multiple, of a purplish colour, and the skin covering them is thin and glistening. They show a tendency to ulcerate and fungate, giving rise to a foetid discharge, and may be mistaken for epithelioma; they are also liable to become the seat of epithelioma. They are treated by excision.

Large, flat papillomas or warts may be single or multiple; they are of slow growth, and as they may also become the starting-point of epithelioma, they should be removed.



The plexiform neuroma forms a loose soft tumour situated in the course of one or more branches of the trigeminal nerve, especially the supra-orbital branch. In its most aggravated form the tumour hangs over the face or neck in large pendulous masses, and is described as a pachydermatocele (V. Mott).

A sarcoma usually has its origin in the bones of the skull, and only implicates the scalp secondarily.

Epithelioma of the scalp may originate in relation to a wart, an ulcerated wen or sebaceous adenoma, or the cicatrix of a burn. It may affect comparatively young persons, may spread over a wide area, or pass deeply and involve the bone. Free and early removal is indicated.

Rodent cancer may originate on the scalp, but usually spreads thither from the face.

In operating for extensive tumours of the scalp the haemorrhage is sometimes formidable. It may be controlled by an elastic tourniquet applied horizontally round the head, or if, on account of the position of the tumour or from other causes, this is not practicable, by ligation or temporary clamping of the external carotid on one or on both sides.

Air-containing Swellings—Pneumatocele Capitis.—Cases have been recorded in which, as a result of pathological or traumatic perforations of the mastoid, and less frequently of the frontal cells, air has passed under the pericranium and given rise to a tense rounded tumour, resonant on percussion, and capable of being emptied by firm pressure. Such swellings exhibit neither pulsation nor fluctuation; and as they are painless, and give rise to almost no inconvenience, they do not call for treatment.

Emphysema of the scalp may follow fractures implicating any of the air sinuses of the skull, the air infiltrating the loose cellular tissue between the pericranium and the aponeurosis, and on palpation yielding a characteristic crepitation. It usually disappears in a few days.

Vascular Tumours.—Naevi on the scalp present the same features as elsewhere. If placed over one of the fontanelles, a naevus may derive pulsation from the brain, and so simulate a meningocele.

Cirsoid aneurysm is usually met with in the course of the temporal artery, and may involve the greater part of the scalp. Large, distended, tortuous, bluish vessels pulsating synchronously with the heart are seen and felt. They can be emptied by pressure, but fill up again at once on removal of the pressure. The patient complains of dizziness, headache, and a persistent rushing sound in the head. Ulceration of the skin over the dilated vessels, leading to fatal haemorrhage, may take place.

They may be treated by excision, after division and ligation of the larger vessels entering the swelling; or the dilated vessels may be cut across at several points and both ends ligated. Krogius recommends the introduction of a series of subcutaneous ligatures so as to surround the whole periphery of the pulsating tumour, and interrupt the blood flow. Ligation of the main afferent vessels, or of the external or common carotid, has been followed by recurrence, owing to the free anastomatic circulation in the scalp. In some cases electrolysis has yielded good results.

Traumatic aneurysm of the temporal artery was comparatively common in the days when the practice of bleeding from this vessel was in vogue, but it is seldom met with now.

Arterio-venous aneurysm may also occur in the course of the temporal artery, as a result of injury, and is best treated by complete extirpation of the segments of the vessels implicated.



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.