Neurosurgery Extradural And Epidural Haematoma Notes

Neurosurgery

Neurosurgery Introduction

Head injuries derive their importance because of the fact that many patients who die or who are disabled belong to the younger age groups. Head injuries account for 1% of all deaths, one-fourth of deaths due to trauma and they are responsible for half of all deaths from road traffic accidents. The majority of the patients are young, adult males.

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Pathophysiology And Mechanism Of Head Injuries

Pathophysiology Classification:

1. Based on the clinical type:

1. Open
2. Closed

2. Based on type of injury:

1. Blunt injury—acceleration, deceleration
2. Missile injuries

• The term open head injury is used to denote a type of injury in which there is a fracture of the skull associated with tear of the dura and arachnoid, resulting in cerebrospinal fluid leak either to the external environment or into one of the potentially infective areas in the base of the skull, e.g. CSF rhinorrhoea or otorrhoea.
• A closed head injury is one where there is no such leakage. The advantage of this classification is that it helps the treating physician to recognise a group of patients who are likely to develop an infective complication following the head injury and he can initiate measures to prevent it.
• Blunt injuries, depending on the severity of impact, can result in an open or closed head injury. Missile injuries tend to result in an open head injury most often.
• The brain is protected by a bony box which has a vault and base of the skull. The base of skull in contrast to the vault is a rough terrain due to the various bony prominences, ridges and foramina.
• This factor is important in causing extensive brain damage to the brain in acceleration/deceleration type of injuries. In addition to the linear acceleration/ deceleration, rotational acceleration is also capable of producing damage to the brain as the brain swirls about inside the skull. Such injuries result in maximal damage at interfaces between structures of different densities such as grey matter–white matter junctions.

Pathophysiology Pathology:

The pathological changes due to trauma to the brain can be classified into primary and secondary.

1. Primary lesions:

• Diffuse axonal injury
• Shearing lesions
• Contusions and burst lobe

2. Secondary lesions:

• Swelling, haemorrhage
• Extradural haematoma
• Subdural, intracerebral haematoma
• Infection, SAH

1. Primary Lesions:

A few important primary lesions are discussed below.

• Diffuse neuronal damage is the most constant feature of blunt injuries. Immediately after an injury, no changes may be seen but changes begin after 14 hours of injury and maximum effects may last up to one week. Prolonged unconsciousness may follow injuries which produce only diffuse neuronal damage without any obvious macroscopic changes. Shearing lesions of the nerve fibres account for some severe injuries without any conspicuous changes to naked eye examination of the brain.
• Cerebral concussion: Alteration in consciousness without structural damage as a result of nonpenetrating traumatic brain injury. There might be loss of consciousness, confusion and amnesiThese are the features. Widespread degeneration of white matter occurs without much changes in the nervous system cortex or brainstem. These patients have spasticity in all four limbs after injury and when they regain consciousness, they are found to be severely demented.
• Contusion and burst lobe are the obvious naked eye changes seen after injuries and were thought to be the main injuries before diffuse neuronal damage and shearing lesions were describeContusions are seen on the summit of the gyri which get injured against the bone. The overlying pia is torn and the blood seeps into the subarachnoid space. A bleeding cortical vessel may result in the formation of the acute subdural haematoma or intracerebral haemorrhage. Brain oedema which develops surrounding the contusion and lacerations is the one that determines the outcome. Most often contusions are seen at the poles of the frontal and temporal lobes, under surface of frontal and temporal lobes, over corpus callosum, superior and anterior surfaces of cerebellum and anterior surface of brainstem.

2. Secondary Lesions:

• Brain swelling: This is a vague term applied to increase in brain bulk due to both oedema and venous congestion. It is aggravated by hypoxia or respiratory insufficiency which may be due to associated lung injury or obstruction to upper respiratory passages
• Sometimes such a swelling can lead to severe brain compression which is difficult to relieve since there is no single mass lesion.
• Intracranial haemorrhage: Extradural or subdural haemorrhages may develop as a clean-cut secondary event, even though bleeding may have started at the time of injury. These cause compression of brain, secondary rise in intracranial pressure and can cause death, if not detected and treated early.
• Infections: All open head injuries are liable to result in intracranial infection either as generalised meningitis or focal infection such as subdural empyema or brain abscess, osteomyelitis of skull.
• After closed head injuries, infection of a subpericranial blood clot may result in Pott’s puffy tumour. When infection supervenes on an already injured brain, it may retard the recovery or may even lead to death. Hence, it becomes mandatory to treat all infections vigorously.

Cause of Death in Head Injuries:

• It is instructive to consider the pathological findings in fatal cases and to speculate the deaths which might have been preventeFor example, earlier many deaths which had occurred as a result of aggravation of brain swelling due to hypoxia could have been prevented by ventilation and anti-oedema measures. It should be emphasised that the role of the treating physician is to anticipate and take appropriate measures to prevent the patient from succumbing to the secondary injuries (damages— seizures, hypoxia). In extensive primary damage to the brain, apart from supportive treatment, one may have to wait and hope.
• Extensive injury to vital areas such as diencephalon, or patients with diffuse damage are not likely to survive. These are patients who are unconscious from the time of injury with bilateral, dilated, fixed pupils, flaccidity in all 4 limbs and autonomic disturbances.
• Sometimes a head injury associated with extensive injuries to chest, abdomen or the limbs by their sheer severity can cause death.
• Intracranial complications such as haematomas, brain swelling, infection, and extracranial complications such as chest injury/metabolic abnormalities, if recognised and treated early, can go a long way in saving the life of the patients.

Intracranial Haematoma

• Most of the head injuries are mild or minor and irrespective of how they are managed, the patient recovers on his own. All those who are unconscious, even if briefly, run the risk of respiratory obstruction. Some of the so-called trivially injured run the risk of developing an intracranial haematomHence, all head injuries must be taken seriously. A complicated head injury is one where any of the secondary pathological changes may occur and threaten the life of the patient. An uncomplicated head injury is one where no such events occur. However, it could be a severe one where the unconsciousness is prolonged.
• These haematomas could develop in any one of the planes intracranially. Extradural (epidural), subdural, intracerebral haematoma, or a haemorrhagic contusion.
• The clinical presentations of these haematomas are due to either an increase in the intracranial pressure or due to signs of cerebral compression. In the case of acute subdural haematoma or intracerebral haematoma, the clinical picture and the outcome of treatment are also dependent on associated brain damage, age of the patient, time of presentation and GCS at presentation.

Extradural And Epidural Haematoma

• The clot collects between the dura and the inner table of skull. A majority of them occur in the middle cranial fossa, since injury to middle meningeal vessels (vein and artery) is the commonest cause.
• However, about 20–25% of the extradural haematomas can occur in the frontal, parietal regions, at the vertex or in the posterior fossInjuries to the dural venous sinuses or a large diploic venous channel are the other causes for the formation of a haematomDepending upon the source of bleeding, the haematoma could collect rapidly (hyperacute type) or slowly over a period of a few hours to a few days and present as a chronic calcified lesion. 60–80% of these patients have an associated fracture of the skull bone and only a few of them may present with classical symptoms with lucid interval. In the remaining patients, the initial picture can vary from an unconscious state to a fully conscious person with or without a history of post-traumatic amnesiWith the widespread availability and use of CT scan, the diagnosis has become much simpler nowadays. However, a few clinical features are worth mentioning.

1. Deteriorating Consciousness Level:

• This is one of the hallmarks for the diagnosis of intracranial haematomThe term ‘lucid interval’ is used when a patient recovers from an initial period of unconscious state. Though in earlier days, this was said to be associated with intracranial haematomas, it can occur in other conditions such as brain oedema, multiple contusions. To assess the consciousness level properly, instead of using vaguely defined terms such as semiconscious, obtunded, etthe ‘Glasgow Coma Score’ is widely used, to avoid observer errors in the observation of such patients.
• Restlessness in a previously quiet patient indicates increasing intracranial pressure, which again needs to be investigateAt the earliest appearance of focal neuronal deficit, the patient has to be taken up for exploratory burr holes.
• Progressive neurological deficit indicates cerebral compression and the manifestation may depend on the area of the brain affected.

2. Pupillary Abnormalities:

• These are to be considered as a late manifestation. It is due to pressure by the herniating uncus of the temporal lobe on the ipsilateral third nerve at the tentorial hiatus. In the early stages due to irritation of the nerve, there is a sluggish response to the light source. This is called early third nerve and is associated with neurological obtundation, bradycardia and constriction. Since it is a transient phenomenon, the early constriction goes unnoticed most of time.
• The patients are often detected in the next stage, i.e. pupillary dilatation, caused by paralysis of pupilloconstrictor fibres in the third nerve. However, if the cerebral compression is unrelieved, this may go onto bilateral. Pupillary dilatation is due to ischaemia of the third nerve nucleus at the midbrain which is caused by pressure on the posterior cerebral artery. These series of pupillary changes have been termed Hutchinsonian pupils. The dilated pupil has a definite localising value in that if an exploratory burr hole has been decided upon, it should be done on the side of the initially dilated pupil.

3. Autonomic Disturbances:

Bradycardia though said to be a definite sign, is a late and not an early sign. Initially, there may be a rise in the pulse rate (tachycardia) which may progress to bradycardia, when the systolic blood pressure increases. At times there may be a rise in the diastolic pressure also. These changes occur due to changes in the cerebral blood flow as a consequence of increased intracranial pressure. Respirations become deep and slow rate (bradypnoea) and later patients may develop CheyneStokes ventilation due to brainstem ischaemia.

4. Non-Localising Signs:

Kernonhan’s notch—contralateral pupillary dilatation 6th nerve and 8th nerve palsy in posterior fossa lesions and CVJ anomalies.

• Local scalp swelling is seen in more than half of the cases. Thus, examination of the head for any such swelling becomes important.
• Some of these patients may have a stiff neck either due to increased intracranial pressure or due to associated injury to neck muscles. Mild fever may, at times, occur and this sometimes confuses the observer. In such a case, the patients must be investigated with a definitive investigation like CT scan. If much time is not available, one should not hesitate to proceed to exploratory burr holes or a ‘trauma craniotomy flap’ has to be employed to rule out a haematom
• Local scalp swelling is seen in more than half of the cases. Thus, examination of the head for any such swelling becomes important.
• Some of these patients may have a stiff neck either due to increased intracranial pressure or due to associated injury to neck muscles. Mild fever may, at times, occur and this sometimes confuses the observer. In such a case, the patients must be investigated with a definitive investigation like CT scan. If much time is not available, one should not hesitate to proceed to exploratory burr holes or a ‘trauma craniotomy flap’ has to be employed to rule out a haematom

As has been pointed out earlier, the advent of CT scan of the head has made the diagnosis easier and more specifiHowever, it should be emphasised that in the absence of CT scan, if adequate clinical features point out to the possibility of an intracranial haematoma, the patient must be taken up immediately for an exploratory surgery rather than wait and allow him to develop irreversible brainstem damage. Since 60–80% of patients with an intracranial haematoma have a skull bone fracture, irrespective of his consciousness level has to be observed for at least 24–48 hours. Occasionally, one may have to resort to old investigations such as angiography not only to establish the haematoma but also to rule out associated vascular anomalies.

Treatment Of Head Injuries In General

1. Resuscitation and Support

1. Admission is indicated when
   1. Definite history of unconsciousness
   2. Fracture temporal bone
   3. A person who cannot be attended by the doctors immediately, i.e. no medical facilities nearby
   4. Post-traumatic seizures—the patient should be admitted.
2. Casualty reception:
   1. Airway:
      • Mouth gag—to prevent tongue from falling backwards.
      • Endotracheal intubation with positive pressure ventilation. Hypoxia is an important cause of cerebral oedema which worsens the level of consciousness.
   2. General assessment of patient:
      • To rule out abdominal injuries such as splenic rupture.
      • Haemothorax—may need an intercostal tube.
      • Long bone fractures
   3. General assessment of the degree of shock by pulse, blood pressure monitoring and treatment.
   4. Neurological assessment by Glasgow Coma Scale:
      • The total score is 15; minimum score is 3. Any patient who has a coma score of 8 or less than 8 is said to be in coma.

2. Care of the Unconscious:

1. Ryle’s tube aspiration or feeding (in the absence of skull base fractures)
2. Care of the eyes—padding
3. Catheter for drainage of urine
4. Change of position to avoid bedsores.
5. Intubation for elective ventilation/airway protection

3. Surgical Treatment for Extradural Haematoma:

Immediate surgery for removal of haematoma and relief of cerebral compression is a must. Extradural haematoma, in particular, is a neurosurgical emergency and patient survival will depend upon the speed with which the compression is relieveIt is not an exaggeration to state that even if decompression has to be done with unsterile instruments, at the bedside it may be worth the effort. In every neurosurgeon’s career, at least one such situation might have occurred and a live patient may justify the means employeOnce consciousness is lost, pupils are dilated and decerebrate rigidity and periodic breathing develop, it may be only a few minutes that may be available to save the life of the patient and one should not wait and waste time. In the case of extradural haematoma, the outcome is dependent on the size of the haematoma and the stage in which the patient was taken up for surgery. In the case of acute subdural and intracerebral haematoma, it depends on associated brain damage. If the associated brain damage is very severe, patients succumbs to the brain damage.

Acute Subdural Haematoma:

Impact damage is more as compared to epidural haematomThere is associated underlying brain injury Symptoms are due to compression of underlying brain with midline shift, in addition to parenchymal brain injury.

Acute Subdural Haematoma Causes

• Parenchymal laceration bleed
• Torn cortical bridging vessel
• May occur in people who are on anticoagulant therapy.
• Mortality—50–90%
• Outcome is better, if surgery is done within 4 hours.

Chronic Subdural Haematoma

• Common in old people.
• In the elderly, the distance between the dura and the brain increases because of the shrinkage of the brain. Even a minor trauma can tear the cortical veins resulting in collection of blood.
• Bleeding is never progressive and the blood in the subdural space slowly forms membranes and the inflammatory cytokines cause seepage of fluid into this potential space causing increase in ICP and symptoms compress the brain causing features of raised intracranial pressure (ICP).

Chronic Subdural Haematoma Clinical Features:

• Elderly patients with history of minor trauma
• Bilateral headache, mental apathy
• Slowness, confusion—later alteration in the level of consciousness may progress to unconsciousness
• Waxing and waning of the level of consciousness is seen in some patients. If such a history is elicited, one should always suspect chronic subdural haematoma.
• Unilateral weakness (contralateral), alterations in speech, seizures.

Chronic Subdural Haematoma Diagnosis:

CT scan or, if feasible, MRI scan are the ideal investigations (cerebral angiography had been used and is still being used in some centres where access to the latest imaging facilities are not available).

Chronic Subdural Haematoma Treatment:

• Burr hole and drainage of the haematoma usually under local anaesthesia or occasionally under general anaesthesia is often the practised mode of treatment.
• At times, the patient may need two or more burr holes to ensure adequate evacuation.
• If the brain fails to expand and obliterate the cavity, especially in older people or in persons with a very thick inner membrane, a large craniotomy and wide excision of the subdural membrane has to be carried out to remove the constricting effect.
• Adequate bedrest and plenty of fluid administration are also important postoperative measures.
• Ideally, 2 burr holes and a posterior wick drain is placed for 24 hours, with 3 days of bed rest and adequate hydration.

Raised Intracranial Pressure

Normal ICP is 8–12 mmHg.

Measures to Reduce the Raised ICP:

Aim is to keep ICP 20 mmHg

• Head and elevation up to 30°
• Hyperventilation
• Sedation—with or without muscle relaxant
• Use of diuretics—furosemide, mannitol
• Thermoregulation
• Use of barbiturates—thiopentone—reduces brain metabolic rate
• Maintaining fluid and electrolyte balance
• Seizure control
• Steroids in severe head injury are associated with increased mortality and should not be use(On the contrary, they are used for reducing vasogenic oedema secondary to tumours).

Fracture Skull

Anterior Fossa Fracture:

1. Fracture cribriform plate can result in CSF rhinorrhoe
2. Fracture may extend to the orbit—subconjunctival haemorrhage.
3. Olfactory nerve involvement—partial anosmi
4. Optic nerve may be contused or fracture may involve the optic foramen resulting in partial or total loss of vision.
5. Rarely, 3rd nerve palsy gives rise to dilated pupil. Traumatic mydriasis
6. Raccoon eyes

Middle Cranial Fossa Fracture:

1. Epistaxis due to fracture venous/sphenoid sinuses.
2. CSF from the ear: Blood mixes with CSF and so, does not clot.
3. 7th nerve palsy.
4. Rarely 6th and 8th nerves are also involved.
5. Battle sign: Discolouration of skin and haemosinus within the mastoid air cells.

Posterior Cranial Fossa Fracture:

1. Extravasation of blood in the suboccipital region causing boggy swelling in the nape of the neck.
2. 9th, 10th, and 11th cranial nerves may be involved.
3. Battle sign: Discolouration of skin and collection of blood occur in the region of mastoid process.

CSF Rhinorrhoea

• There should be a communication between the intradural cavity (subarachnoid space) and the nose.
• It indicates tear of the dura mainly in the basal region and a fracture involving paranasal sinuses—frontal, ethmoidal or sphenoidal.
• There is always an injury to a small portion of the brain. It (the portion of brain) plugs the tear, preventing the dura from healing. Thus, the rhinorrhoea persists for many days.
• This leads to complication, i.e. infection and meningitis.
• Two types:
  • Traumatic: It can be iatrogenic following surgery or can be post-traumatic (62 to 80%).
  • Nontraumatic spontaneous: It can be due to high pressure (hydrocephalus) or congenital.
• Confirmation of CSF rhinorrhoea is on the bedside by following clinical signs.
  • Ring sign: Onto linen, ring of blood with 1 layer ring of clear fluiHalo or target sign.
  • Reservoir sign: Gush of CSF in certain position of the head.
• β₂ transferrin is the most accurate method.
• CSF may be collected and fluid glucose can be assessed to differentiate from nasal discharge.

CSF Rhinorrhoea Treatment:

• Acetazolamide 250 mg three times a day.
• Lumbar drainage can be done in the absence of raised ICP.
• Prophylactic antibiotics.
• If the rhinorrhoea persists, repair of the dural defect alone, (or) at times with a shunt procedure will be needed.
• Conservative management may be tried for up to 2 weeks before resorting to anterior cranial fossa floor repair.

Pott’S Puffy Tumour

• This is a subperiosteal infection usually caused by osteomyelitis of the underlying skull.
• It is common in the frontal region and the frontal bone is commonly involved.
• The cause of infection is through frontal sinusitis.
• Another common cause of infection of a subpericranial haematoma following needle aspiration.
• It can also follow chronic suppurative otitis media.
• Pus collects in the subpericranial space and extradural plane, which communicate with each other (dumbbell-type abscess).
• It causes a boggy swelling in the frontal region and tenderness over the scalp.
• Pitting oedema over the scalp is conclusively called Pott’s puffy tumour.
• Severe headache, vomiting and blurring of vision should clinch the diagnosis.

Pott’S Puffy Tumour Treatment:

1. CT scan to confirm the diagnosis.
2. A burr hole and aspiration of pus can be done followed by 6–8 weeks of antibiotics.
3. In chronic cases, the wall of the abscess may have to be removeThe associated osteomyelitic skull bone requires a radical removal under cover of antibiotics.

Hydrocephalus

Hydrocephalus Definition:

This is a condition that occurs due to disturbances of CSF flow and imbalance between CSF production and absorption resulting in the accumulation of CSF and dilatation of ventricles.

Hydrocephalus CSF Production:

CSF is mainly produced by the choroid plexus of lateral ventricles by an active autoregulated process.

Daily production: 450 ml—total volume is 150 ml.

CSF Circulation:

CSF leaves the 4th ventricle by foramen of Luschka and Magendie to circulate over the convexity where it is finally absorbed over arachnoid granulations.

Aetiopathology:

Hydrocephalus occurs due to two reasons:

• If there is an overproduction of CSF or CSF circulation.
• If there is decreased absorption.
  • Overproduction: True overproduction is rare and occurs in cases of choroid plexus papilloma
  • Decreased absorption: Failure of CSF absorption is much more common due to infection and haemorrhage.
  • Other causes are: Structural abnormality occurring in CSF pathway—tumour, and congenital malformation such as aqueduct stenosis.

Hydrocephalus Types:

1. Communicating: Due to obstruction in sub-arachnoid space.
2. Noncommunicating: Due to obstruction in ventricular system. Obstructive hydrocephalus.

Hydrocephalus Clinical Features:

1. Infantile Hydrocephalus:

• Difficulty in delivery of large head
• Craniofacial disproportion
• Increase in head circumference more than 2 cm/ month
• Scalp is thin, shiny and prominent veins
• Fontanelles: Bulging and tense especially on crying
• Sutures: Open, excessive irritability.
• Macewen’s sign—cracked pot sound on percussing over dilated ventricles.
• Inability to retain feeds, mental retardation, delayed milestones, hypothalamic disturbances.
• Sunset sign: Weakness of upward gaze palsy.

2. Childhood/Adult Hydrocephalus:

• By this time, fontanelles have closed.
• Features of increased intracranial pressure: Headache, nausea, vomiting.
• Irritability, indifference, apathy, drowsiness.
• Blurring of vision is not the sign of papilloedema.
• Blindness is due to ophthalmoplegia.
• Bradycardia, systemic hypertension, altered respiratory rate is due to distortion of brainstem. Untreated cases also develop unilateral or bilateral abducens palsy or upward gaze palsy.

Hydrocephalus Treatment:

Aim:

1. To decrease CSF production by using pharmacological agents:

• Acetazolamide
• Furosemide
• Isosorbide
• Glycerol

2. Direct removal of cause of obstruction.

3. Diversion of CSF to another viscus for reabsorption by means of various shunt procedures.

Shunts

Ventriculoperitoneal shunt and ventriculoatrial shunt

Tumours

Eight percent of all primary cancers arise in the CNS. In adults, it constitutes the sixth largest group of cancers and in children the CNS is the commonest site for solid tumours.

Presenting Feature:

1. Progressive neurological deficit: In up to two-thirds of the patients, a focal motor weakness is the most common presentation. This deficit arises from the direct neuronal damage or are due to compression on brain or cranial nerves by the tumour. Sudden change may be due to haemorrhage into a preexisting tumour.

2. Headache: It occurs in over 50% of patients caused by raised intracranial pressure (ICP). Only 10% patients have the classic presentation of headache with early morning worsening, associated with nausea and a temporary relief by vomiting.

3. Generalised or focal seizures occur in 25%. Focal seizures may help to localise the site of a tumour. A high index of suspicion is required for patients past the second decade with recent-onset epilepsy.

4. Other presentations include visual disturbances, visual field defects, mental changes, etdepending on the site of tumour.

Tumours Investigations:

1. CT scan: The best initial investigation. This shows where the tumour alters the attenuation of the X-ray beam as it passes through the brain. It also shows distortion of the ventricular system or obliteration of the pattern of the sulci.
2. MRI: Often gives extra information and may eventually supersede CT completely. It is the investigation of choice for imaging the posterior fossa and the spine as it can ‘see through’ bone.
3. X-rays are only of anecdotal interest picking up incidental calcifications or erosion of parts of the skull. Newer imaging modalities including SPECT and PET scans are increasingly being used in higher centres.
4. DSA/CT angio/MR angio when indicated to assess and visualize the vascularity of the tumour or to plan interventional procedures.

Specific Types Of Brain Tumours

Gliomas:

• Astrocytoma
• Oligodendroglioma
• Mixed tumours

Astrocytoma: WHO Classification

Grade 1: Pilocytic

Grade 2: Diffuse

Grade 3: Anaplastic

Grade 4: Glioblastoma multiforme

• This is the most common primary brain tumour arising from the supporting glial cells and diffusely infiltrates brain tissue early on.
• Two grading systems are available: WHO and St Anne/Mayo. Grade 1 and Grade 2 (low-grade) tumours are slow growing and compatible with good quality survival. Grades 3 and 4 are rapidly growing. Grade 4 tumours are also called glioblastoma multiforme are highly radio and chemoresistant with median survival of only 12 months even with optimal treatment. Even low grade astrocytomas may evolve over time into secondary glioblastomas.

Glioblastoma Multiforme:

• Most common in 5th and 6th decades.
• Treatment includes surgery to confirm the diagnosis and achieve a macroscopic excision, followed by a high dose (60 gy) of irradiation.
• Chemotherapy wafers impregnated with carmustine must be inserted GLIADIL wafers.

Oligodendroglioma:

• This type of glioma is usually a slow-growing tumour and over half arise in the frontal lobes.
• There may be a history of epilepsy or even focal neurological signs of many years’ duration.
• They may show calcification, both microscopically and macroscopically.

Ependymoma:

• These glial tumours arise from cells that line the ventricles of the brain and the central canal of the spinal cord.
• They are most common in the fourth ventricle in children and young adults where they block CSF flow and often present with hydrocephalus. In adults, they are considered as a differential for intramedullary lower spinal cord lesion.

Embryonal Tumours:

• Primitive neuroectodermal tumours (PNETs) are a group of highly malignant tumours of which the cerebellar PNET or medulloblastoma is the archetype.
• Commonest in children and young adults. It may originate from primitive cell nests which have undergone malignant transformation. Medulloblastoma is the most common brain tumour in children.
• The patient presents with truncal ataxia, headache, vomiting and sometimes diplopiAll PNETs are prone to spread within the CNS producing ‘sugarcoating metastasis’ which are best seen on MRI of the spine.

Schwannoma (Neurilemmoma):

• Peripheral neurons get their myelin sheaths from Schwann cells. Occasionally, these form slow growing benign tumours on cranial or spinal nerves.
• The cranial nerve most affected is the vestibular division of the 8th cranial nerve and the tumour is then usually called acoustic neuromNewer terminology is vestibular schwannom
• It causes progressive deafness, hydrocephalus and ataxiIt is slow growing. Less often it may involve the trigeminal or the vagus nerve.
• Often associated with NF2, especially in bilateral acoustic tumours and multiple meningiomas.
• Commonest presentation: Unilateral or bilateral progressive deafness (sensorineural hearing loss— SNHL) with tinnitus and vertigo.

Meningioma:

• Eighty percent are supratentorial.
• These tumours arise from the arachnoid layer of the meninges and the arachnoid villi. They are commonest over the falx and the convexity of the skull but rarely may also arise from the skull base (especially from the sphenoid wing and olfactory groove) or inside the lateral ventricle.
• Commonest in middle-aged women and may occur at the site of a previous radiation fielMost are benign and slowly growing. Signs occur based on the site of tumour
• They tend to provoke endosteal hypertrophy or exostosis of the overlying skull and is still occasionally detected on an incidental skull film or even by palpation of the skull. Patient with neurofibromatosis type 2 often have multiple meningiomas. Rarely, they are malignant.
• Paediatric meningiomas tend to be atypical in location.
• Recurrence depends on the extent of resection (SIMPSON’s grading of excision).

Pituitary Tumours:

• 10–15% of all intracranial tumours
• The majority are benign adenoma
• Prolactinoma—30%
• Nonfunctioning adenoma—20%
• GH secreting adenoma—15%
• ACTH secreting adenoma—10%.
• May produce mass effect—bitemporal hemianopia or cranial nerve dysfunction.
• Endocrine dysfunction such as galactorrhoea, primary/secondary amenorrhoea, Cushing’s syndrome, acromegaly.
• Pituitary apoplexy—results in sudden onset of headache, visual loss, ophthalmoplegia and altered conscious level. Caused by haemorrhagic infarction of a pituitary tumour.

Other Tumours:

They are pineal region tumours, pituitary adenomas, craniopharyngiomas, choroid plexus tumours, etc.

Metastases:

One-fourth of all cancer patients have intracerebral metastases at the time of death. Common primary sites include the bronchus (50%), breast (15%), and melanoma (10%).

Tumours Treatment

They can be divided into medical and surgical lines of treatment.

1. Medical
   • Acutely raised intracranial pressure (ICP) is treated with IV mannitol 0.5–1 g/kg body weight.
   • Hydrocephalus can be relieved using a CSF diversion system (closed external ventricular drainage or a ventriculoperitoneal shunt).
   • Seizures are treated with lorazepam and phenytoin commonly and maintained on phenytoin.
   • Corticosteroids, especially dexamethasone 4 mg qid is given to reduce symptoms of raised ICP, which may make surgery easier.
2. Surgery:
   • This is the mainstay of treatment. The aim of surgery is to obtain a complete tumour excision without producing a neurological deficit.
   • This is not always possible due to the site of the tumour, in which case compromises must be made and a debulking procedure is done.
   • Any residual tissue may be observed or treated with adjuvant radiotherapy.
   • Stereotactic guided surgery is now a well-established concept in brain surgery allowing more targeted treatment of the lesion with minimal surrounding damage.
3. Radiotherapy: Intracranial tumours are relatively radioresistant, and radiotherapy is primarily a palliative treatment.
4. Chemotherapy: No definite benefit of chemotherapy for the treatment of brain tumours. Temozolomide is a promising new drug for the treatment of brain tumours.

Tumours Outcome:

• Surgery offers good prospects for the treatment of benign brain tumours such as meningioma or pituitary adenoma, but outcome of treatment of malignant tumours is still poor.

Trigeminal Neuralgia

• Superior cerebellar artery or multiple sclerosis plaque can cause this condition.
• Severe episodic lancinating facial pain occurring in the distribution of V cranial nerve.
• Vascular compression of the nerve near the root entry zone, multiple sclerosis may be causative factors.
• Investigation—MRI.

Tumours Treatment:

• Carbamazepine or gabapentin.
• 75% will not respond to medical treatment.
• Surgery: Refractory cases
  1. Percutaneous glycerol injection, radiofrequency ablation, thermocoagulation, balloon compression, local nerve block.
  2. Microvascular decompression via craniotomy.
  3. Stereotactic radiosurgery.

Brainstem Death

Irreversible loss of consciousness, loss of brainstem reflexes and apnoea.

Diagnosis of brainstem death is done in three stages:

1. Identification of the cause of irreversible coma.
2. Exclusion of reversible causes of coma.
3. Clinical demonstration of absence of brainstem reflexes.

Brainstem Reflexes:

• Pupillary reaction to light, corneal reflexes, vestibular ocular reflex, cough reflex, gag reflex, motor response to pain.
• Apnoea test—apnoea despite a CO2 increase to >6.65 kPa or 50 mmHg.
• All reflexes must be absent and are tested independently twice by 2 doctors.

Ct Scans Of Head Injuries

Neurosurgery Multiple-Choice Questions

Question 1. The following is not the feature of the Glasgow Coma Scale:

1. Eyes opening
2. Motor response
3. Verbal response
4. Sensory response

Answer: 4. Sensory response

Question 2. Closed head injuries include the following:

1. Head injury with fractured skull
2. Head injury with a black eye
3. Head injury with facial nerve palsy
4. Head injury with CSF rhinorrhoea

Answer: 4. Head injury with CSF rhinorrhoea

Question 3. Which of the following is included under secondary lesions following head injury?

1. Diffuse neuronal damage
2. Contusions
3. Lacerations
4. Swelling

Answer: 4. Swelling

Question 4. Post-traumatic amnesia is a feature of:

1. Raised intracranial tension
2. Fall from a height
3. Fracture skull
4. Cerebral concussion

Answer: 4. Cerebral concussion

Question 5. Which is an important cause of brain swelling following head injury?

1. Infection
2. Oedema
3. Acidosis
4. Bleeding

Answer: 2. Oedema

Question 6. The cause of extradural haematoma is bleeding from:

1. Venous sinuses
2. Cavernous sinus bleeding
3. Basal veins bleeding
4. Middle meningeal vessels bleeding

Answer: 4. Middle meningeal vessels bleeding

Question 7. Lucid interval is typically seen in:

1. Extradural haematoma
2. Acute subdural haematoma
3. Chronic subdural haematoma
4. Pontine haematoma

Answer: 1. Extradural haematoma

Question 8. Which nerve is paralysed after herniation of temporal lobe in extradural haematoma?

1. Oculomotor nerve
2. Ophthalmic nerve
3. Trigeminal nerve
4. Facial nerve

Answer: 2. Ophthalmic nerve

Question 9. Pupillary dilatation following head injury is due to ischaemia of the third nerve caused by:

1. Middle cerebral artery
2. Posterior cerebral artery
3. Inferior cerebral artery
4. Anterior cerebral artery

Answer: 2. Posterior cerebral artery

Question 10. The following are definite indications for admission in a head injury patient except:

1. Fracture skull
2. CSF rhinorrhoea
3. History of unconsciousness
4. Scalp bleeding

Answer: 4. History of unconsciousness