Intracranial tumours, infection and aneurysms

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This chapter provides a brief overview of three important neurosurgical conditions: intracranial tumours, cerebral aneurysms and intracranial infection. A brief description of each of these pathologies will be given and the principles of treatment will be discussed.

Brain tumours

Brain tumours are responsible for approximately 2% of all cancer deaths. However, central nervous system (CNS) tumours comprise the most common group of solid tumours in young patients, accounting for 20% of all paediatric neoplasms.

The general brain tumour classification is related to cell or origin, and is shown in General classifications of brain tumours. Table 49, “Incidence of common cerebral tumours (%)” shows the approximate distribution of the more common brain tumours, some of which will be described in this chapter.

Table 49. Incidence of common cerebral tumours (%)
Tumour  % Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.
Neuroepithelial 52
Astrocytoma 44
(all grades including glioblastoma)
Ependymoma 3
Oligodendroglioma 2
Medulloblastoma 3
Metastatic 15
Meningioma 15
Pituitary 8
Acoustic neuroma 8


Epidemiological studies have not indicated any particular factor, either chemical or traumatic, that causes brain tumours in humans. There is no genetic predisposition to brain tumours, but many specific chromosome abnormalities involving chromosomes 10, 13, 17 and 22 have been noted in a wide range of CNS tumours.

At present there is considerable conjecture regarding the role of trauma, electromagnetic radiation and organic solvents in the development of brain tumours, but as yet there is no convincing evidence to implicate.

Molecular biology techniques have enabled the identification of a variety of alterations in the genome of the tumour cell, including those of brain tumours. Tumour suppressor genes are normally present in the genome, and act as a ‘brake’ on cell transformation. Mutations in the p53 tumour suppressor gene are the most common gene abnormality found in tumours to date, and have been shown to occur in both astrocytomas and meningiomas.

Cerebral glioma

Gliomas comprise the majority of cerebral tumours and arise from neuroglial cells. There are four distinct types of glial cells: astrocytes, oligodendroglia, ependymal cells and neuroglial precursors. Each of these gives rise to tumours with different biological and anatomical characteristics.


The most common gliomas arise from the astrocyte cells, which comprise the majority of intraparenchymal cells of the brain. The tumours arising from the astrocytes range from the relatively benign to the highly malignant. The term malignant for brain tumours differs from its usage for systemic tumours, in that intrinsic brain tumours very rarely metastasise (except for medulloblastoma and ependymoma), and the term malignant refers to the aggressive biological characteristics and poor prognosis.

There are many classifications of brain tumours in general and gliomas in particular. The World Health Organization classification of cerebral gliomas recognises four grades. Grade 1 is assigned to the pilocytic astrocytoma, an uncommon tumour that is very slowly growing and biologically distinct from the diffuse astrocytomas, which are classified as astrocytoma (WHO grade II), anaplastic astrocytoma (WHO grade III), and glioblastoma multiforme (WHO grade IV) and comprise over 50% of the astrocytoma tumours.


The hallmark of the pathology of cerebral gliomas is invasion of the tumour cells into the adjacent normal brain. Although in certain areas the margin of the tumour may seem to be macroscopically well defined from the brain, there are always microscopic nests of tumour cells extending well out into the brain. The histological appearance of the tumour varies with the tumour grade, with increasing cellular atypia, mitoses, endothelial and adventitial cell proliferation and necrosis with increasing grade of the tumour.


The presenting features of all intracranial tumours can be classified under:

  • raised intracranial pressure
  • focal neurological signs
  • epilepsy.

The duration of the symptoms and the progression evolution of the clinical presentation will depend on the grade of the tumour (i.e. the rate of growth). A patient presenting with a low-grade astrocytoma (grade I or II) may have a history of seizures extending over many years antedating the development of progressive neurological signs and raised intracranial pressure. Patients with the more common higher grade tumour present with a shorter history, and glioblastoma multiforme is characterised by a short illness of weeks or a few months.

Raised intracranial pressure is due to the tumour mass, surrounding cerebral oedema and hydrocephalus due to blockage of cerebrospinal fluid (CSF) pathways. The main clinical features of raised intracranial pressure are headaches, nausea and vomiting, drowsiness and papilloedema.

Headache associated with increased intracranial pressure is usually worse on waking in the morning and is relieved by vomiting. Intracranial pressure increases during sleep, probably from vascular dilatation due to carbon dioxide retention.

Nausea and vomiting are usually worse in the morning.

Drowsiness is the most important clinical feature of raised intracranial pressure. It is the portent of rapid neurological deterioration.

Papilloedema is the definitive sign of raised intracranial pressure. The early features of increased pressure on the optic nerve head are those of dilatation or failure of normal pulsations of retinal veins. As the intracranial pressure rises, the nerve head becomes more swollen and the disc margins become blurred on fundoscopic examination. Flame-shaped haemorrhages develop, particularly around the disc margins and along the vessels.

Sixth nerve palsy, causing diplopia, may result in raised intracranial pressure owing to stretching of the sixth cranial nerve by cordal displacement of the brainstem. This is a so-called ‘false localising sign’.

Focal neurological signs are common in patients presenting with cerebral gliomas, and the nature of the deficit will depend on the position of the tumour.

Patients presenting with tumours involving the frontal lobes frequently may have pseudo-psychiatric problems with personality change and mood disorders. Limb paresis results from interference of the pyramidal tracts, either at a cortical or subcortical level, and field defects are associated with tumours of the temporal, occipital or parietal lobes. Dysphasia, either expressive or receptive, is a particularly distressing symptom in patients involving the relevant areas of dominant hemisphere.


Computed tomographic (CT) scanning and magnetic resonance imaging (MRI) of the brain are the essential radiological investigations and an accurate diagnosis can be made in nearly all tumours.

Low-grade gliomas show decreased density on CT scanning and the T1-weighted MRI, with minimal surrounding oedema and no enhancement with contrast (Low-grade glioma with decreased density on T1-weighted magnetic resonance image.). Calcification may be present. High-grade gliomas are usually large and enhance vividly following intravenous injection of contrast material and have extensive surrounding oedema (Low-grade glioma with decreased density on T1-weighted magnetic resonance image.).

Low-grade glioma with decreased density on T1-weighted magnetic resonance image.

High-grade glioma (glioblastoma multiforme) showing vivid enhancement after intravenous injection of contrast material.

Magnetic resonance imaging, particularly when used with gadolinium contrast enhancement, improves the visualisation of cerebral gliomas. Gadolinium enhancement is more likely to occur in high-grade tumours.


Following the presumptive diagnosis of a glioma, the management involves

  • surgery
  • radiotherapy
  • other adjuvant treatments.

Surgery: The aim of surgery is to

  • make a definitive diagnosis
  • reduce the tumour mass to relieve the symptoms of raised intracranial pressure
  • reduce the tumour mass as a precursor to adjuvant treatments.

Radiotherapy: Post-operative radiation therapy is often used as an adjunct to surgery in the treatment of high-grade gliomas as it has been shown to double the median survival from high-grade gliomas to 37 weeks.


At present there is no satisfactory treatment for cerebral glioma. The median survival following surgery for the high-grade glioma (glioblastoma multiforme) is approximately 17 weeks, and when radiotherapy is used as an adjunct, the median survival is approximately 37 weeks. Chemotherapy for high-grade gliomas has been disappointing and the best results for surgery, radiation therapy and chemotherapy consistently show a median survival time of less than 1 year.


Oligodendroglioma are much less common than the astrocytoma group, being responsible for approximately 5% of all gliomas.

Oligodendrogliomas have the same spectrum of histological appearance as astrocytomas but, as distinct from the astrocytoma series, are more likely to be slow growing. Calcium deposits are found in 90% of the tumours (Oligodendroglioma that is highly calcified.).

Oligodendroglioma that is highly calcified.

The clinical presentation is essentially the same as for the astrocyte group, but as these tumours are more likely to be slow growing, epilepsy is more common.

The principles of treatment are the same as for the astrocytoma group. Surgery is necessary to make a definitive diagnosis and debulking the tumour will relieve the features of raised intracranial pressure as well as reducing the tumour burden for adjuvant therapies. Radiotherapy is probably helpful in reducing the rate of growth of any remnant tumour. Unlike the astrocytoma group, chemotherapy has been shown to be of some use in helping to control those tumours with an oligodendroglial component, especially those tumours with loss of heterozygosity on chromosome 1p or 19q.

Metastatic tumours

Metastatic tumours are responsible for 15% of brain tumours in clinical series, but up to 30% of brain tumours reported by pathologists. Approximately 30% of deaths are due to cancer and 20% of these will have intracranial metastatic deposits at autopsy. The metastatic tumours most commonly originate from

  • carcinoma of the lung
  • carcinoma of the breast
  • metastatic melanoma
  • carcinoma of the kidney
  • gastrointestinal carcinoma.

In 15% of cases a primary origin is never found. Most metastatic tumours are multiple and one-third are solitary. In about half of the solitary tumours, systemic spread is not apparent. The incidence of tumours in the cerebrum relative to the cerebellum is 8 to 1. Metastatic tumours are often surrounded by intense cerebral oedema.

Clinical presentation

The interval between diagnosis of the primary cancer and cerebral metastasis varies considerably. In general, secondary tumours from carcinoma of the lung present relatively soon after the initial diagnosis, with a median interval of 5 months. Although cerebral metastases may present within a few months of the initial diagnosis of malignant melanoma or carcinoma of the breast, some patients may live many years before an intracranial tumour appears.

The presenting clinical features for cerebral metastasis are similar to those described for other tumours:

  • raised intracranial pressure
  • focal neurological signs
  • epilepsy.

Radiological investigations

A CT scan or MRI will diagnose metastatic tumour and show whether or not the deposits are solitary or multiple. Most metastatic tumours are isodense on un-enhanced scan and they enhance vividly after intravenous contrast material. Magnetic resonance image following gadolinium contrast may demonstrate small metastatic tumours often not visible on a CT scan (Multiple metastatic tumours.).

Multiple metastatic tumours.


Steroid medication will control cerebral oedema and should be commenced immediately if there is raised intracranial pressure.

Surgery to remove the metastasis is indicated if:

  • there is a solitary metastasis in a surgically accessible position
  • there is no systemic spread.

Removal of a solitary secondary is preferable especially if the primary site of origin has been, or will be, controlled. Excision of a single metastasis will provide excellent symptomatic relief and consequently may be indicated even if the primary site cannot be treated satisfactorily.

Radiotherapy, together with steroid medication to control cerebral oedema is used to treat patients with multiple cerebral metastases and may be advisable following excision of a single metastasis. More recently, stereotactic radiosurgery, which uses a highly focussed beam of radiation, has been used to treat single and multiple cerebral metastases if the tumour size is less than 3 cm in diameter.


The 1-year median survival for patients having had a surgical excision of a solitary metastatic deposit is:

  • 50% for patients with carcinoma of the breast
  • 30% for patients with carcinoma of the lung
  • 30% for patients with melanoma
  • 50% for patients in whom the source of metastatic tumour is undetermined.

Paediatric brain tumours

Intracranial tumours are the most common form of solid tumours in childhood, with 60% of tumours occurring below the tentorium cerebelli. The most common supratentorial tumours are astrocytomas, followed by anaplastic astrocytomas and glioblastoma multiforme.

Posterior fossa paediatric tumours

Sixty per cent of paediatric brain tumours occur in the posterior fossa. The relative incidence of tumours is:

  • cerebellar astrocytoma 30%
  • medulloblastoma (infratentorial primary neuroectodermal tumour) 30%
  • ependymoma 20%
  • brainstem glioma 10%
  • miscellaneous 10% (choroid plexus papilloma, haemangioblastoma, epidermoid, dermoid, chordoma).

Clinical presentation

The presenting clinical features of posterior fossa neoplasms in children are related to:

  • raised intracranial pressure
  • focal neurological signs.

Raised intracranial pressure is the most common presenting feature. It is due to hydrocephalus caused by obstruction of the fourth ventricle and is manifest by headaches, vomiting, diplopia and papilloedema. The raised intracranial pressure may result in a strasbismus causing diplopia due to stretching of one or both of the sixth (abducens) cranial nerves (a false localising sign).


Focal neurological signs are due to the tumour invading or compressing the cerebellum, the brainstem and cranial nerves. Truncal and gait ataxia result particularly from midline cerebellar involvement. Horizontal gaze paretic nystagmus often occurs in tumours around the fourth ventricle. Vertical nystagmus is indicative of brainstem involvement. Disturbance of bulbar function, such as difficulty in swallowing, with nasal regurgitation of fluid, dysarthria and impaired palatal or pharyngeal reflexes result from brainstem involvement. Compression or tumour invasion of the pyramidal tracts may result in hemiparesis or sensory disturbance.


Computed tomography scan and MRI will confirm the position of the tumour and whether there is hydrocephalus ((A) Posterior fossa cystic astrocytoma with small tumour nodule and large cyst. (B) Enhancing midline posterior fossa tumour (medulloblastoma).).

(A) Posterior fossa cystic astrocytoma with small tumour nodule and large cyst. (B) Enhancing midline posterior fossa tumour (medulloblastoma).


The treatment of posterior fossa tumours involves surgery, radiotherapy and chemotherapy.

A CSF shunt may need to be performed to control raised intracranial pressure due to hydrocephalus. The CSF diversion can be achieved with either an external drain or ventriculoperitoneal shunt. The shunt will provide immediate and controlled relief of intracranial hypertension and the subsequent posterior fossa operation can be performed as a planned elective procedure. A criticism of pre-operative ventriculoperitoneal shunt is that it may promote the metastatic spread of these tumours.

In general, the treatment of medulloblastoma and ependymoma involves surgery to excise the tumour, followed by radiation therapy, which may be to the whole neuraxis as the tumour may spread throughout the CNS, followed by chemotherapy. The 5-year survival of these tumours is approximately 40%. Many cerebellar astrocytoma tumours have a small single nodule surrounded by a large cyst. These tumours can often be cured by excision of the nodule alone, and adjuvant therapy is not necessary. In contrast, the treatment of brainstem glioma usually involves only a biopsy of the tumour to confirm the diagnosis, possibly followed by radiotherapy and/or chemotherapy. These tumours usually cause death within 24 months of diagnosis, although some patients with low-grade tumours will live longer.

Benign brain tumours

The most common benign brain tumours are:

  • meningioma
  • acoustic neuroma
  • haemangioblastoma
  • dermoid and epidermoid tumours
  • colloid cysts
  • pituitary tumours
  • craniopharyngioma.


Meningiomas are the most common of the benign brain tumours and constitute about 15% of all intracranial tumours, being about one-third the number of gliomas. Although they may occur at any age, they reach their peak incidence in middle age and are very uncommon in children.

Unlike gliomas, where the classification system is based on the histological appearance of the tumours, meningiomas are usually classified according to the position of origin rather than histology. The reason for this is that, in general, the biological activity of the tumour, the presenting features, the treatment and prognosis all relate more to the site of the tumour than the histology (Table 50, “Position of intracranial meningioma (%)”).

Table 50. Position of intracranial meningioma (%)
Position  % Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.
Parasagittal and falx 25
Convexity 20
Sphenoidal wing 20
Olfactory groove 12
Suprasellar 12
Posterior fossa 9
Ventricle 1.5
Optic sheath 0.5

Meningiomas present with features of:

  • raised intracranial pressure
  • focal neurological signs
  • epilepsy.

The position of the tumour (Classical positions of meningiomas.) will determine the features of the clinical presentation. The tumours often grow slowly and there is frequently a long history, often of many years, of symptoms prior to diagnosis.

Classical positions of meningiomas.

Parasagittal tumours often arise in the middle third of the vault, and the patient may present with focal epilepsy and paresis, usually affecting the opposite leg and foot, as the motor cortex on the medial aspect of the posterior frontal lobe is affected. Urinary incontinence is occasionally a symptom for a large frontal tumour, especially if it is bilateral.

Convexity tumours often grow around the position of the coronal suture. Patients present with raised intracranial pressure, and more posterior tumours will cause focal neurological symptoms and epilepsy.

An inner sphenoidal wing meningioma will cause compression of the adjacent optic nerve and patients may present with a history of uniocular visual failure.

Olfactory groove meningioma will cause anosmia, initially unilateral and later bilateral. The presenting features may include symptoms of raised intracranial pressure.

Suprasellar tumours arise from the tuberculum sellae and will cause visual failure with a bitemporal hemianopia.

Posterior fossa tumours may arise from the cerebellar convexity or from the cerebellopontine angle or clivus.


Computed tomography scan and MRI show tumours that enhance vividly following intravenous contrast ((A) Axial magnetic resonance image (MRI) and (B) coronal MRI showing meningioma with vivid contrast enhancement arising from floor of anterior carnial fossa (olfactory groove) and growing into superior frontal lobes.). Hyperostosis of the cranial vault may occur at the site of attachment of the tumour, and these bony changes may often be seen on plain skull X-ray.

(A) Axial magnetic resonance image (MRI) and (B) coronal MRI showing meningioma with vivid contrast enhancement arising from floor of anterior carnial fossa (olfactory groove) and growing into superior frontal lobes.


The treatment of meningiomas is total surgical excision including obliteration of the dural attachment. Although this objective is often possible, there are some situations where complete excision is not possible because of the position of the tumour. Surgery may be preceded by embolisation of the main vascular supply of the tumour.

Acoustic neuroma

Acoustic schwannomas arise from the eighth cranial nerve and account for 8% of intracranial tumours. The tumours are schwannomas, with their origin from the vestibular component of the eighth cranial nerve near the internal auditory meatus.

Clinical presentation

The clinical presentation of an acoustic schwannoma will depend on the size of the tumour at the time of diagnosis. The earliest symptoms are associated with eighth nerve involvement. Tinnitus and unilateral partial or complete sensory neural hearing loss are the earliest features. With extension into the cerebellopontine angle, the tumour will compress the cerebellum, resulting in ataxia and compression of the pyramidal tracts due to a large tumour causing brainstem compression, which will cause a contralateral hemiparesis. A very large tumour will cause obstructive hydrocephalus.

Radiological investigations

Computed tomography scan or MRI will show an enhancing tumour in the cerebellopontine angle with extension into the internal auditory meatus that will be widened, indicating the tumour has arisen from the eighth cranial nerve (Acoustic neuroma showing extension to tumour into internal auditory canal.). Small tumours within the internal auditory meatus are best diagnosed using MRI following gadolinium enhancement.

Acoustic neuroma showing extension to tumour into internal auditory canal.

The treatment of a large acoustic neuroma is surgical. Stereotactic radiosurgery has been advocated by some for small tumours (<2 cm diameter), although as yet its efficacy is not definitely proven in controlling the growth of the tumour and there is an increased incidence of fifth cranial nerve morbidity following radiosurgery. Intracanalicular, or very small tumours in the elderly, may be just observed and treatment advised only if there is evidence of tumour growth.

Colloid cyst of third ventricle

A colloid cyst of the third ventricle is situated in the anterior part of the ventricle and applied to the roof just behind the foramen Munro. As the cyst grows it causes bilateral obstruction to the foramena of Munro resulting in raised intracranial pressure from hydrocephalus.

Radiological investigations include MRI and CT scan, which show a round tumour in the anterior third ventricle that usually enhances following intravenous contrast (Colloid cyst of third ventricle.). The treatment is surgical excision.

Colloid cyst of third ventricle.

Pituitary tumours

Pituitary tumours account for 8–10% of all intracranial tumours.


Historically, three main types of pituitary tumours were defined by their cytoplasmic staining characteristics; chromophobic, acidophilic and basophilic. The development of immunoperoxidase techniques and electron microscopy have provided a more refined classification of pituitary adenomas based on the specific hormone produced. This classification is shown in Table 51, “Classification of pituitary adenomas”. The tumours can be further classified via their size with microadenomas (being tumours <1 cm diameter) and macroadenomas (>1 cm) being either confined to the sella or with extrasellar extension (Large pituitary tumour with marked suprasellar extension causing compression of the optic chiasma.).

Table 51. Classification of pituitary adenomas
Hormone secreted Percentage of tumours Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.
Prolactin 40
Growth hormone 20
Null cell (no hormone) 20
Prolactin and growth hormone 5
FSH/LH 1–2
Acidophil stem cell (no hormone) 1–2
Large pituitary tumour with marked suprasellar extension causing compression of the optic chiasma.

Clinical presentation

The presenting clinical features of pituitary tumours are due to:

  • the size of the tumour
  • endocrine disturbance.

Headache occurs principally in patients with acromegaly and is uncommon in other types of pituitary tumours.


Suprasellar extension of the pituitary tumour causes compression of the optic chiasm resulting in bitemporal hemianopia. Optic atrophy will be evident in patients with long-standing compression of the chiasm. Extension of the tumour into the cavernous sinus may cause compression of the third, fourth or sixth cranial nerves.


Endocrine disturbance is due to either hypopituitism or excess secretion of a particular pituitary hormone.

Hypopituitism results from failure of the hormone secreted by the adenohypophysis. The endocrine secretions are not equally depressed, but there is a selective failure, and the order of susceptibility is as follows: growth hormone, gonadotrophin, corticotrophin, thyroid stimulating hormone. Hypopituitarism initially results in vague symptoms including lack of energy, undue fatiguability, muscle weakness and anorexia, and when prolonged or severe will cause low blood pressure. Clinical hypothyroidism is manifest by physical and mental sluggishness and a preference for warmth. When the hypopituitarism is severe episodic confusion occurs and the patient will become drowsy.

Pituitary apoplexy results from sudden spontaneous haemorrhage into the pituitary tumour. It is characterised by sudden severe headache followed by transient and more prolonged loss of consciousness, with features of neck stiffness or vomiting and photophobia.

Prolactinoma: Prolactin-secreting tumours may be a microadenoma or a macroadenoma. The patients with microadenomas are usually women who present with infertility associated with amenorrhoea and galactorrhoea. These tumours can usually be treated with a dopamine agonist such as bromocryptine. Very large macroadenomas may occur in males who present with features of hypopituitarism and visual failure due to suprasella extension.

Acromegaly results from growth hormone-secreting pituitary adenomas. Clinical features include bone and soft tissue changes as evidenced by an enlarged supraciliary ridge, enlarged frontal sinuses and increased mandibular size, which will cause the chin to project (prognathism). The hands and feet enlarge, the skin becomes coarse and greasy and sweats profusely. The voice becomes hoarse and gruff. Systemic problems include hypertension, cardiac hypertrophy and diabetes.

Cushing's disease is due to ACTH producing pituitary adenomas. Over 80% of the tumours are microadenomas. The onset is often insidious and the disease may affect children or adults. Severe obesity occurs, the skin is tense and painful and purple striae appear around the trunk. Fat is deposited, particularly on the face (moonface), neck, cervicodorsal junction (buffalo hump) and trunk. The skin becomes a purple colour due to vasodilatation and stasis. Spontaneous bruising is common. The skin is greasy, acne is common and facial hair excessive. Osteoporosis predisposes to spontaneous fractures and there is wasting of the muscles. Glucose tolerance is impaired and hypertension occurs. Laboratory investigations are vital to confirm the diagnosis.


The treatment of patients with pituitary tumours depends on whether the patient has presented with features of endocrine disturbance or problems related to compression of adjacent neural structures.

Surgical excision will be used as the primary method of treatment for:

  • large tumours causing compression of adjacent neural structures, particularly the visual pathways
  • growth hormone-secreting tumours causing acromegaly
  • ACTH-secreting tumours causing Cushing's disease
  • the occasional treatment of a prolactin-secreting adenoma when the medical treatment using bromocryptine is not tolerated.

Most tumours can be excised via the trans-sphenoidal approach to the pituitary fossa. Post-operative radiotherapy may be indicated if there has been a subtotal excision of the tumour or if the post-operative endocrine studies demonstrate residual excessive hormone secretion.

Subarachnoid haemorrhage and cerebral aneurysm

The sudden onset of a severe headache in a patient should be regarded as subarachnoid haemorrhage until proven otherwise. The most common cause of subarachnoid haemorrhage in adults is rupture of a berry aneurysm. Subarachnoid haemorrhage in children is much less common than in the adult population, and the most common paediatric cause is rupture of an arteriovenous malformation. Cerebral aneurysm as a cause of subarachnoid haemorrhage becomes more frequent than arteriovenous malformation in patients over the age of 20 years.

Subarachnoid haemorrhage

Clinical presentation


The sudden onset of a severe headache of a type not previously experienced by the patient is the hallmark of subarachnoid haemorrhage. A relatively small leak from an aneurysm may result in a minor headache, sometimes referred to as a ‘sentinel headache’, and this may be the warning episode of a subsequent major haemorrhage from the aneurysm.


Most patients have some deterioration of their conscious state following subarachnoid haemorrhage. This varies from only slight change, when the haemorrhage has been minor, to apoplectic death resulting from massive haemorrhage.


Blood in the subarachnoid CSF will cause the features of meningismus (headache, neck stiffness, photophobia and fever or vomiting).


Focal neurological signs may occur in subarachnoid haemorrhage due to concombinant intracerebral haemorrhage, the local pressure effects on the aneurysm (such as a third cranial nerve palsy resulting from pressure from a posterior communicating artery aneurysm) itself or cerebral vasospasm.

Clinical assessment

The major differential diagnosis of subarachnoid haemorrhage is meningitis, although a minor haemorrhage is often misdiagnosed as migraine. Confirmation of the clinical diagnosis of subarachnoid haemorrhage should be undertaken as soon as possible by CT scanning (Diffuse blood in the basal cisterns confirming the diagnosis of subarachnoid haemorrhage.). If there is any doubt that subarachnoid blood is present on the CT scan, as may occur following more minor haemorrhages, a lumbar puncture is essential. The presence of xanthochromia (yellow staining) in the CSF will confirm subarachnoid haemorrhage.

Diffuse blood in the basal cisterns confirming the diagnosis of subarachnoid haemorrhage.

Cerebral angiography ((A) Cerebral aneurysm on angiogram. (B) Arteriovenous malformation.) will confirm the cause of the subarachnoid haemorrhage and will determine the subsequent treatment.

(A) Cerebral aneurysm on angiogram. (B) Arteriovenous malformation.

Cerebral aneurysm

Cerebral aneurysms are the most common cause of subarachnoid haemorrhage in the adult population. The great majority of aneurysms arise at branch points of two vessels and are situated mainly on the Circle of Willis; about 85% on the anterior half of the circle and 15% in the posterior circulation (Position of cerebral aneurysm). Aneurysms occur in more than one position in approximately 15% of cases.


Management of patients following rupture of a cerebral aneurysm is determined by three factors:

  • severity of the initial haemorrhage
  • re-bleeding of the aneurysm
  • cerebral vasospasm.

About 30% of all patients suffering a subarachnoid haemorrhage from a ruptured aneurysm either have an apoplectic death or are deeply comatose as a result of the initial haemorrhage. Re-bleeding occurs in about 50% of patients within 6 weeks and 25% of patients within 2 weeks of the initial haemorrhage. The only certain way to prevent the aneurysm re-bleeding is to occlude it from the circulation. Cerebral vasospasm occurs in 50% of patients following subarachnoid haemorrhage and in 25% it results in serious neurological complications. Clinical vasospasm is treated using hypertension and volume expansion, and consequently the treatment is most effective if the aneurysm has been occluded.

Surgery - endovascular occlusion

Although in the past surgery has often been delayed for fear that it might exacerbate cerebral vasospasm, the current treatment of cerebral aneurysm is immediate obliteration of the aneurysm by either surgery or an endovascular technique. Surgery is not performed on patients who are comatose or have features of decerebrate posturing unless the CT scan shows a large intracerebral haematoma resulting from the ruptured aneurysm that needs to be evacuated, or hydrocephalus as a cause of the poor neurological state. Evacuation of intracerebral haematoma or drainage of the hydrocephalus should be performed urgently, and the aneurysm occluded.

The surgical procedure involves a craniotomy with occlusion of the neck of the aneurysm. Endovascular techniques, using detachable coils, have been shown to have an increasing role in the treatment of cerebral aneurysms, particularly for posterior fossa (basilar tip) aneurysms. Most centres treating aneurysms utilise endovascular coiling in over 50% of cases.

Intracranial infection

Although infections involving the nervous system may present in many ways and involve a large variety of pathogens, the most common infections involving the neurosurgeon are acute bacterial meningitis and cerebral abscess.


Bacterial meningitis is a serious life-threatening infection of the meninges. Most of the common organisms that cause bacterial meningitis are related to the patient's age and to the presence and nature of any underlying predisposing disease. Table 52, “Common organisms causing primary bacterial meningitis related to age” shows the common organisms causing bacterial meningitis related to age.

Table 52. Common organisms causing primary bacterial meningitis related to age
Age Organism Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.
Neonate (0–4 weeks) Group B streptococcus, Escherichia coli
4–12 weeks Group B streptococcus, Streptococcus pneumoniae, Salmonella, Haemophilus influenzae, Listeria monocytogenes
3 months–5 years Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitidis
Over 5 years and adults Streptococcus pneumoniae, Neisseria meningitidis

The bacteria reach the meninges and CSF by three main routes:

  • haematogenous spread from extracranial foci of infection
  • retrograde spread via infected thrombi within emissary veins from infections adjacent to the CNS such as sinusitis, otitis or mastoiditis
  • direct spread into the subarachnoid space such as from osteomyelitis of the skull and infected paranasal sinuses.

Clinical presentation

Bacterial meningitis is usually an acute illness with rapid progression of the clinical signs. The major presenting features are:

  • high fever
  • meningismus including headache, neck stiffness, photophobia and vomiting.

Although patients are usually alert at the commencement of the illness, they will frequently become drowsy and confused.

In infants, neonates, the elderly and the immunocompromised, the presentation of bacterial meningitis may be different. Neck stiffness and fever are often absent and the presentation includes listlessness and irritabilty in the young and confusion or obtundation in the elderly. A careful search must be made for a skin rash. Meningococcal infection frequently has a coexisting petechial rash, which occurs less frequently in other bacterial or viral infections. The original source of the infection, for example sinusitis, bacterial endocarditis, otitis media or mastoiditis may be evident and many patients have evidence of pharyngitis - bacterial meningitis sometimes follows another respiratory tract infection.

The diagnosis is made by CSF examination obtained by lumbar puncture, which should be performed immediately once the diagnosis is suspected. If the patient is drowsy, has other signs of raised intracranial pressure or if there are focal neurological signs, an urgent CT scan must be performed prior to lumbar puncture to exclude an intracranial space-occupying lesion.

The CSF features in a lumbar puncture are:

  • raised cell count, predominantly a polymorphonuclear leucocytosis
  • protein level greater than 0.8 g/L
  • glucose level less than 2 mmol/L
  • positive Gram stain in more than 70%.

Other tests that should be performed on the CSF include examination for Cryptococcus neoformans and for Mycobacterium tuberculosis. Other investigations should include blood cultures and radiological investigations to detect the source of the infection; chest X-ray, CT scan or skull X-ray for sinusitis.

The differential diagnoses include:

  • other types of meningitis (viral, fungal, carcinomatosis)
  • subdural empyema (patients are drowsy, with focal neurological signs, and usually have seizures)
  • subarachnoid haemorrhage
  • viral encephalitis.


High-dose intravenous antibiotic therapy should be commenced immediately, and the selection of the antibiotic depends on the initial expectation of the most likely organism involved, taking into account the age of the patient, source of infection, CSF microbiology studies and the antibiotic that has best penetration to CSF.

There are many antibiotic regimes, but if there is no obvious site of infection initial therapy should commence immediately as follows:

  • Neonates (under months) - cefotaxime or ceftriaxone plus benzoyl penicillin or amoxy/ampicillin
  • Three months to 15 years - cefotaxime or ceftriaxone
  • 15 years to adults - benzyl penicillin + cefotaxime/ ceftriaxone
  • Add vancomycin if Gram-positive streptococci are seen and there is any suspicion of intermediate and/or resistant Streptococcus pneumoniae.

When the organism has been identified, the most appropriate antibiotic should be used, depending on sensitivites and the ability of the antibiotic to penetrate into the CSF.

The usual specific antimicrobial therapy following identification of the organism is:

  • Pneumococcus or meningococcus - Benzyl penicillin (child: 60 mg/kg up to 1.8-2.4 g intravenously 4 hourly). If the patient is sensitive to penicillin use cefotaxime (child: 15 mg/kg 6 hourly or ceftriaxone 100 mg/kg daily). About half the patients with meningococcal meningitis have petechiae or purpura. Subclinical or clinical disseminated intravascular coagulation often accompanies meningococcaemia and may progress to haemorrhage infarction of the adrenal glands, renal cortical necrosis, pulmonary vascular thrombosis, shock and death. The antibiotic therapy must be accompanied by intensive medical supportive therapy.
  • Haemophilus influenzae - amoxy/ampicillin if organism is susceptible. If the patient is allergic or organism-resistant use cefotaxime or ceftriaxone.
  • Listeria - benzyl penicillin or amoxy/ampicillin plus trimethoprim and sulfamethoxazole
  • Hospital-acquired meningitis - vancomycin plus cefotaxime, ceftriaxone or meropenem

Complications of bacterial meningitis

Complications are more likely to occur if treatment is not commenced immediately. The major complications are:

  • Cerebral oedema
  • Seizures
  • Hydrocephalus - communicating hydrocephalus. This may occur early in the disease or as a late manifestation
  • Subdural effusion - particularly in children. Most resolve spontaneously but some may require drainage
  • Subdural empyaema. A rare complication that usually requires drainage
  • Brain abscess - occurs as a rare complication of meningitis.

Brain abscess

Cerebral abscess may result from:

  • haematogenous spread from a known septic site or occult focus
  • direct spread from an infected paranasal or mastoid sinus
  • trauma causing a penetrating wound.

Metastatic brain abscesses arising from haematogenous dissemination of infection are frequently multiple and develop at the junction of white and grey matter. Most common sites of infection include skin pustules, chronic pulmonary infection (bronchiectasis), diverticulitis, osteomyelitis and bacterial endocarditis. The site of origin of haematogenous spread is unknown in approximately 25% of patients.

Direct spread from paranasal sinuses, mastoid air cells or the middle ear are the most common pathogenic mechanisms in many series. Infection from the paranasal sinuses spread either into the frontal or temporal lobe and the abscesses are usually single and located superficially. Frontal sinusitis may cause an abscess in the frontal lobe. Middle ear infection may spread into the temporal lobe and uncommonly the cerebellum.


Table 53, “Cerebral abscess: pathogenesis and principal organisms” details the pathogenesis and principal organisms in cerebral abscess. Streptococci are isolated from approximately 80% of brain abscesses. The most common single species is the alpha haemolytic carboxyphilic Streptococcus milleri, whose major habitat is the alimentary tract including the mouth and dental plaque. Otogenic abscesses usually yield mixed flora including Bacteroides, various Streptococci and members of the Enterobacteriaceae. Staphylococcus aureus is often the pathogen in abscesses resulting from trauma.

Table 53. Cerebral abscess: pathogenesis and principal organisms
History Site of infection Predominant organism Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.
Sinusitis - frontal Frontal lobe Aerobic streptococci
Streptococcus milleri
Haemophilus species
Mastoiditis, otitis Temporal lobe Mixed flora
Aerobic and anaerobic streptococci
Bacteroides fragilis
Haemophilus species
Haematogenous, cryptogenic Brain Aerobic streptococci
Anaerobic streptococci
Trauma Brain Staphylococcus aureus

Presenting features

Presenting features include:

  • an intracranial mass (raised intracranial pressure, focal neurological signs, epilepsy)
  • systemic toxicity (fever and malaise in 60% of cases)
  • clinical features of the underlying source of infection (sinusitis, bacterial endocarditis, diverticulitis).


A CT scan and MRI (Cerebral abscess - a ring enhancing mass. Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.) show a ring enhancing mass often surrounded by considerable oedema.

Cerebral abscess - a ring enhancing mass. Reproduced with permission from Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.


The principles of treatment are:

  • identify the bacterial organism
  • institute antibiotic therapy
  • drain or excise the abscess.

A specimen of pus is essential for accurate identification of the organism. Antibiotic therapy should be commenced as soon as the pus has been obtained. The initial choice of antibiotic, before culture results are available, will depend on the probable cause of the brain abscess and the Gram stain. The therapy will be refined once the organism is known. Anticonvulsant medication should be commenced as there is an incidence of seizures of 30–50%.

The abscess may need to be treated by either single or repeat aspiration. Surgical excision of the abscess may be necessary if there is persistent re-accumulation of the pus, or if a fibrous capsule develops that fails to collapse despite repeat aspirations. A cerebellar abscess requires excision.

Further reading

Colli BC, Carlotti CG, Machado HR, Assirati JA. Intracranial bacterial infections. Neurosurg Quart. 1999;9:258–284.

Dorsch NWC, King MT. A review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage. J Clin Neurosci. 1994;1:19–26.

Kaye AH. Essential Neurosurgery. 3rd ed. Oxford: Blackwells; 2005.

Kaye AH, Black PMcL. Operative Neurosurgery. Edinburgh: Churchill Livingstone; 1999.

Kaye AH, Laws ER. Brain Tumors. 2nd ed. Edinburgh: Churchill Livingstone; 2001.

Stephanov S. Surgical treatment of brain abscess. Neurosurgery. 1988;22:724–730.

International Subarachnoid Aneurysm Trial (ISAT) of Neurosurgical Clipping vs Endovascular Coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. Lancet. 2002;360:1267–1273.

Weir B. Unruptured intracranial aneurysms: a review. J Neurosurg. 1996;3–42.
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