The British Journal of Surgery Vol. 63 : No. 3 : March 1976 Br. J. Surg. Vol. 63 (1976) 169-172 Temporal lobe swelling : a common treatable complication of head injury R . S. M A U R I C E - W I L L I A M S * SUMMARY Four cases are described ofjocal contusion and swelling of the temporal lobe after head injury, giving rise to acute cerebral compression. The clinical features, pathology and treatment of this condition are discussed. It is suggested that this occurrence may be a common treatable complication of closed head injuries which may easily be overlooked, with fatal results, if exploratory cranial surgery is undertaken without preliminary cerebral angiography. CONTUSION of the pole of the temporal lobe with subsequent considerable focal brain swelling is a complication of closed head injury which is known to most neurosurgeons but is unfamiliar to many of the general and orthopaedic surgeons who undertake the primary care of head injuries in this country. Four instances of this syndrome treated by a single surgeon within a short period of time are described. It is argued that it may be a commoner occurrence than is supposed and that early diagnosis and definitive treatment may make the difference between a good functional recovery and death. Case reports Case 1 : A 45-year-old deaf and dumb woman was knocked down while crossing a road. On arrival a t hospital she was found to have a left occipital scalp laceration but no other external injuries. She was irritable and confused but had no focal neurological signs. A skull X-ray showed a linear left parietal fracture. Over the next 12 hours her conscious level deteriorated and she began to show decerebrate extension of the left arm to noxious stimulation. The right pupil was now larger than the left and reacted sluggishly to light. By the time that carotid angiography was commenced 3 hours later, she had a fixed dilated right pupil and bilateral decerebrate rigidity in all four limbs. A right carotid angiogram showed an avascular swelling in the right temporal region with marked elevation of the middle cerebral vessels, and shift of the midline structures to the left (Fig. 1 ) . At operation the right temporal region was exposed by turning scalp and bone flaps, the temporal bone beneath the lower edge of the bone flap being nibbled away to remove the outer wall of the middle fossa. No extradural or subdural blood was found, but the brain was noted to be extremely tense, 14 despite the administration of 120 g of intravenous mannitol during the previous hour. The right temporal lobe, which was soft and necrotic, with multiple subpial and intracerebral haemorrhages, was widely debrided until the remaining brain was slack and pulsating. The dura was left open, covered with loose Gelfoam sheeting. The bone flap was not replaced. The patient was discharged 21 days later, after an uneventful postoperative recovery. Three months later she was able to run her household without difficulty and n o intellectual or neurological deficit was apparent. Her skull defect was slack, and, being roofed over by the temporalis muscle, it did not present a cosmetic deformity. Case 2 : A 55-year-old housewife was knocked down by a lorry. O n admission to St Leonard’s Hospital, London, she was unconscious, but when roused made symmetrical purposeful limb movements. Her pupils were normal. She was bleeding from the right ear but had no other external injury. A skull X-ray showed a linear right temporal fracture. She was given dexamethasone 4 mg every 6 hours, but 3 days later, when it had become clear that her conscious level had declined, she was admitted to the Neurosurgical Unit of St Bartholomew’s Hospital. By now, she responded to pain with feeble purposeful movements of the left arm only. Her eyes were deviated to the left, but the pupillary sizes and responses were normal. She had a right upper and lower facial weakness. Bilateral carotid angiography showed marked swelling of the left temporal lobe with shift of the midline vessels to the right. No abnormality was apparent on the right side. The left temporal region was exposed by turning down flaps of the scalp and temporalis muscle and nibbling away the whole outer wall of the middle fossa, to leave a bone defect of 7.5 x 3.5 cm. The dura was widely opened and a large quantity of blood clot and macerated brain was expelled under high pressure. The contused temporal lobe was further debrided until the brain was slack. Part of the expelled blood clot was subdural and part intracerebral. The dura was left open, the dural defect being covered with Surgicel. Postoperative recovery was complicated by bronchopneumonia requiring a temporary tracheostomy, but a month after operation the patient was alert and continent without any facial o r limb weakness. However, she showed a total motor and receptive aphasia, and a t follow-up 3 months later this aphasia had not recovered significantly and it seems likely that she will require hospitalization indefinitely. Case 3 : A 30-year-old woman was knocked down by a car. On admission to hospital she was semiconscious and irritable and made good symmetrical purposeful limb movements. * Department of Neurosurgery, St Bartholomew’s Hospital, London. 169 R. S. Maurice-Williams a b Fig. 1. Case 1. Right carotid angiogram. a, Lateral view showing elevation of the middle cerebral vessels (arrow). b, Anteroposterior view showing elevation and stretching of the middle cerebral vessels by the swollen temporal lobe, and displacement of the anterior cerebral artery across the midline. There was bruising around the right eye and at the left occiput. Her pupils were normal. A skull X-ray showed a linear left occipital fracture. Over the next few hours she became drowsier, and 6 hours after the accident she rapidly developed a complete right third nerve palsy, with wide pupillary ditatation and complete ptosis. Over the next hour, multiple retinal haemorrhages appeared, more on the right fundus than on the left. Eight hours after the accident she was deeply unconscious, making only feeble non-purposeful flexion movements of the arms in response to deep pain. Breathing was now shallow and irregular. She was given 50 g of mannitol intravenously. A right carotid angiogram showed a massive avascular swelling of the right temporal lobe with shift of the midline vessels to the left. There was a small extracerebral collection. The outer wall of the middle fossa was removed, having been exposed by turning down scalp and muscle flaps. Despite the previous intravenous mannitol, the dura was very tense, and when it was opened, blood clot and macerated brain were expelled with some force. The temporal pole was contused, and beneath the temporal lobe was a layer of subdural clot. Both this and necrotic temporal lobe tissue were removed until the brain was slack and pulsating. When dkbridement had been carried out, it could be seen that several of the superficial veins of the temporal lobe had thrombosed over the contused area. The dura was left widely open, being closed over by the temporalis muscle which was resutured in position. Postoperative recovery was rapid. She had a post-traumatic amnesia of 2 weeks. Her right third nerve palsy recovered almost completely over a 6-week period. Five months after her injury she had returned to work as a secretary and was able to d o this and run her household without disability. No intellectual or personality changes were apparent and the only neurological deficit was a slightly enlarged pupil with a slow response to light on the right side. Case 4: A 32-year-old woman was thrown through the window of a car in which she had been a front seat passenger. On arrival at hospital she was deeply unconscious. A short while later she showed signs of regaining consciousness and thrashed around with her limbs, but then lapsed once more into an unresponsive state. An acute extradural haemorrhage was suspected as the skull X-ray had shown a linear fracture of 170 the right squamous temporal hone, crossing the line of the middle meningeal artery. She was transferred to the neurosurgical unit, and by the time that she had arrived her conscious level had once more lightened and she was found to respond t o deep pain with symmetrical purposeful limb movements. The left pupil responded briskly to light, but the right pupil could not be seen because of a large peri-orbital haematoma which extended into the right temporal fossa. There was bleeding from the right ear and a scalp laceration to the right of the vertex, but no apparent injury elsewhere in the body, although a chest X-ray showed an avulsion of the neck and transverse process of the right first rib. In view o f her fluctuating conscious level and the right temporal scalp haematoma, it was decided to explore the temporal fracture. Although this overlay the middle meningeal artery, the artery had not torn and there was no extradural haematoma. A 3-cm diameter craniectomy was performed, to reveal a tense blue dura. O n incising the dura, subdural clot was expelled under high pressure. Residual clot was removed, together with a small quantity of contused underlying cortex. The dura was left open. Twelve hours later her neurological state had not improved. She had now developed upper airway obstruction and a leftsided pneumothorax. The pneumothorax was drained and a tracheostomy performed. Afterwards her neurological status had clearly worsened. Stimulation produced non-purposeful arm flexion only. Her pupils were mid-sized (the right one slightly larger), fixed to light and the oculocephalic reflexes were absent. Carotid angiography showed bilateral temporal lobe swelling, much greater on the right side, the midline vessels being shifted to the left. Twenty-four hours after the accident she was taken back to the operating theatre. The right temporal craniectomy was enlarged to remove the whole outer wall of the middle fossa. The temporal lobe was very tense, soft and necrotic. The greater part was removed until the brain was slack. Once more the dura was left open. For 5 days she was hyperventilated to reduce cerebral swelling. She developed a right-sided pneumothorax requiring drainage. For a while she had a right hemiparesis and a complete right internal and external opbthalmoplegia, but her condition gradually improved. Unfortunately, her recovery was retarded by a fall from bed at the convalescent hospital Temporal lobe swelling which caused a cervical fracture dislocation and her readmission to the neurosurgical unit. Twelve months after the accident she has returned home and is rapidly improving. She is continent and well orientated without any neurological deficit, but her personality is lethargic and irritable since her head injury. However, these mental changes are recovering and it is anticipated that she will eventually be able to return to an independent existence. A lumbar air encephalogram performed 1 I weeks after the injury to exclude a post-traumatic communicating hydrocephalus showed no evidence of this, but did show a cystic expansion of the temporal horn of the right lateral ventricle, which was presumably due to the adjacent excision of cerebral tissue (Fig. 2). Discussion One of the main principles of the treatment of closed head injuries is the early detection and treatment of complications which lead to cerebral compression. The occurrence of extradural and subdural haemorrhage and of diffuse cerebral oedema is well known. The same cannot be said of the occurrence described here. It is not discussed in any of the standard undergraduate or postgraduate surgical texts and it is not dealt with, other than incidentally, either in Rowbotham’s (1964) classic work on head injuries or in a recent English textbook of neurosurgery (Northfield, 1973), although a fuller account is given in Lewin’s The Management of Head Injuries (1966). It is clear why the temporal pole is more liable than other regions of the brain to develop local contusional necrosis and swelling after a head injury. The front of the temporal lobe is flung forwards against the sharp edge of the lesser wing of the sphenoid and sustains an extensive abrasion. In addition, rupture of the bridging veins from the temporal pole to the sphenoparietal sinus will cause subdural and subpial bleeding, together with infarction of adjacent brain. It may be that a spreading traumatic cortical venous thrombosis occurs which extends this zone of infarction and oedema (Maurice-Williams, 1974), and in this connection it is of interest that in Case 3 thrombosed superficial veins were clearly seen adjacent to and over the contused area. Clinically, temporal lobe contusion might be expected to be indistinguishable from an extradural haemorrhage from a torn middle meningeal artery. In both there is a rapidly expanding mass in the middle cranial fossa occurring a short interval after injury. In the cases described here the interval from injury to symptoms of cerebral compression ranged from 8 hours to 3 days. However, temporal lobe swelling would probably only occur after a fairly severe injury which could abrade the brain surface and rupture veins. This was so in the cases described here, where the shortest period of post-traumatic amnesia (probably the most satisfactory index of the severity of a closed head injury) was 10 days. Most middle fossa extradural haematomas are associated with an overlying vault fracture (McKissock et al., 1960), but althoughall4of the present cases had skull fractures, in only 1 case was the fracture in the ipsilateral squamous temporal bone. With a rapid swelling of the temporal lobe, it might be expected that the classic sequence of ipsilateral third nerve palsy, a crossed hemiparesis Fig. 2. Case 4. Lumbar air encephalogram 11 weeks after injury showing expansion of the right temporal h o r n (arrow) secondary to cerebral debridement. and then the medullary vasomotor response of bradycardia and hypertension, would be commonplace, but this is not SO. Only 2 cases developed pupillary dilatation on the side of the lesion and only one showed a crossed hemiparesis. None showed a cerebral vasomotor response. It has recently been pointed out that many patients with a supratentorial mass who cone do not exhibit a lateralized uncal herniation with an oculomotor palsy, but a central downward shift of the brain stem, with a deterioration in conscious level followed by symmetrical pupillary changes and the appearance of non-purposeful limb movements (Plum and Posner, 1972). The rate of deterioration in these cases was rapid, and all had reached a n advanced stage of cerebral compression by the time of operation. It seems clear that without surgery all 4 patients would have died. A full dose of an intravenous dehydrating agent (2 cases) and of steroids (1 case) had failed to control the intracranial tension by the time of surgery. Despite this, 2 of the patients have returned to their normal lives without any disability and a third will probably do so in time. The remaining patient is likely to stay permanently disabled by a global dysphasia following excision of the contused temporal lobe of the dominant hemisphere. Effective treatment must depend on a clear preoperative diagnosis, and for this carotid angiography is essential. This will show an avascular swelling of the temporal region, with elevation and stretching of the Sylvian vessels and displacement of midline vessels to the opposite side. There may be a coexisting small subdural haematoma over the temporal lobe, showing as a displacement of cortical vessels away from the inner table. Exploratory burr holes as the initial investigation will impose not only a possible dangerous delay but also other hazards. Evacuation of a small subdural haemorrhage arising from the contused area may lead the surgeon to suppose that everything possible has been done. Burr holes will only permit one to say that the intracranial pressure is raised, not 171 R. S. Maurice-Williams Fig. 3. Case 4. Skull X-ray showing the extent of the bone defect (arrow) after operation. part of the temporal lobe) and providing an external decompression by removing the outer bony wall of the middle fossa and leaving the dura widely open. This bone defect may be fashioned either by a formal bone flap or by nibbling away the squamous temporal bone after the temporalis muscle has been either turnep downwards or split vertically. An eventual bone defect of about 6 x 4 cm is likely to be needed (Figs. 3 , 4). The dural defect may be covered over with cellulose sheeting, and after repositioning of the temporalis muscle to cover it the skull defect does not constitute a cosmetic problem and needs no future repair. How common a problem of a closed head injury is temporal lobe swelling? The 4 cases described here presented in a single neurosurgical unit within a 12month period. During this time, 1 1 other cases of acute or subacute traumatic cerebral compression required surgery, comprising 1 extradural and 10 subdural haematomas. This suggests that temporal lobe swelling might be a fairly frequent occurrence which is not being diagnosed because many cases are being subjected to exploratory burr holes without preliminary angiography. In the patients who die the true state of affairs may not be obvious at postmortem, as the cerebral oedema may become more widespread as a terminal event, and a small coexisting subdural collection might be erroneously interpreted as the significant pathology. Acknowledgements I would like to thank Mr R. Campbell Connolly, Surgeon-in-charge, Department of Neurosurgery, St Bartholomew’s Hospital, for permission to report these cases, and Miss Susan Perkins for her secretarial assistance. References Fig. 4. The hatched area of the skull shows the extent of bone removal usually necessary for adequate debridement and decompression of the temporal lobe. whether it is due to general brain swelling or a focal lesion, and by themselves they will not provide any decompression. These points are illustrated by Case 4, where an initial evacuation of a small subdural haematoma provided neither diagnosis nor effective treatment. Treatment consists of providing an internal decompression of the brain by removing devitalized necrotic and haemorrhagic cerebral tissue (generally the greater 172 (1966) The Management of Head Injuries. London, Bailliere, Tindall & Cassell. MCKISSOCK w., TAYLOR J. c . , BLOOM w . H. and TILL K. (1960) Extradural haematoma : observations on 125 cases. Lancet 2, 167-172. MAURICE-WILLIAMS R. s. (1974) Post-traumatic progressive cortical thrombophlebitis. Br. Med. J. 3, 24. NORTHFIELD D. W. C. (1973) The Surgery of the Central Nervous System. Oxford, Blackwell. PLUM F. and POSNER J. B. (1972) The Diagnosis of Stupor and Coma. Philadelphia, Davis. ROWBOTHAM G . F. (1964) Acute Injuries of the Head, 3rd ed. Edinburgh, Livingstone. LEWIN w .