Neurosurgery

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CHAPTER 18 Neurosurgery

Head injuries

In the UK, head injuries account for annual attendance rates at A&E departments of almost 1 million people. Head injuries account for nine deaths per 100 000 population and in young males, account for 15–20% of all deaths. Some 20% of all patients attending A&E departments with head injuries are admitted, and over 25% of these have alcohol-related head injuries. More than 50% of all patients admitted with head injuries are discharged within 24 h. Head injuries, therefore, cause a considerable workload and bed occupancy. It is therefore necessary to have a protocol to decide which patients need admission and which patients need further investigation.

It is recommended that all patients are monitored using the Glasgow Coma Scale after initial resuscitation (→ Table 4.1, in Ch. 4). In all cases, the diagnosis and initial treatment of serious extracranial injuries takes priority over investigations of head injury, or transfer to a neurosurgical unit.

Criteria for hospital admission after recent head injury

The presence of one or more of the following:

• Confusion or any other depression of the level of consciousness at the time of examination

• Skull fracture

• Neurological signs; persistent or worsening headache or vomiting

• Signs suggesting skull base fracture, e.g. haemotympanum, panda eyes, Battle’s sign

• Difficulty in assessing the patient, e.g. alcohol, the young, epilepsy

• Other medical conditions, e.g. haemophilia

• The patient’s social conditions or lack of responsible adult/relative if discharged.

• Post-traumatic amnesia with full recovery is not an indication for admission

• Many patients who appear fully orientated are not. Strict assessment of orientation is necessary prior to discharge

• Patients sent home should be given written instructions about possible complications and appropriate action

• Minor head injury with amnesia or unconsciousness usually causes post-concussion symptoms, which can cause significant morbidity, particularly if not explained to the patient.

Skull radiography after recent head injury

CT scan is the preferred option. A skull radiograph images the skull but provides no information about the brain and therefore is of little use. All patients suffering a significant head injury should have a CT scan, which in most cases will identify any skull fracture.

Simple scalp laceration is not a criterion for skull radiography if the history can exclude a significant impact.

Types of brain injury

Primary

This is the damage caused as an immediate result of trauma. It results in contusions, lacerations or diffuse brain damage. Treatment cannot reverse primary brain injury.

Secondary

This develops as a result of complications such as intracranial bleeding, cerebral hypoxia, cerebral oedema and infection. The prevention, recognition and treatment of these secondary complications is the mainstay of treatment of the patient with head injuries.

Assess the level of consciousness as this is the most significant factor after head injury. Use GCS (→ Table 4.1) and check pupillary reactions. Pupillary changes may indicate brain swelling or compression. Pressure on a cerebral hemisphere causes the third nerve on that side to be stretched over the edge of the tentorium. The resultant paralysis of the nerve allows unopposed action of the dilator pupillae under the control of the sympathetic nervous system and the pupils dilate. There is also loss of light reaction of the pupil on the affected side. If compression continues, the contralateral third nerve is compressed and the opposite pupil also dilates and is fixed to light. Bilateral fixed dilated pupils in a patient with a head injury are a grave prognostic sign and recovery is rare. Pupillary changes are always late signs (‘undertaker signs’), and are always preceded by an alteration in conscious level caused by raised intracranial pressure. Direct blows to the eyes can cause dilated pupils in patients without severe brain injury.

CT and MRI brain scanning

Computerized tomography (CT) and magnetic resonance imaging (MRI) provide very rapid and highly accurate detail of the brain. CT also provides excellent bone detail and should be performed if a significant brain injury is suspected. Resuscitation must always precede any form of imaging, however sophisticated. MRI is not at present necessary for management of acute head injury but may provide important prognostic data. A cervical spine X-ray or CT scan of the cervical spine is mandatory for all significant head injuries and must include C7/T1.

Skull fractures

A skull fracture is an indication for hospital admission. Patients with skull fractures are more likely to suffer secondary brain damage. Skull fractures are classified as closed, i.e. the skin over the underlying fracture is intact, or open (compound) where the skin overlying the fracture is broken, or the fracture connects with an air sinus or the external auditory canal.

They may be further classified as follows:

Linear, stellate or comminuted non-depressed

These fractures are serious if they cross major vascular channels, e.g. the groove for the middle meningeal artery.

Depressed fracture

A portion of the vault of the skull is depressed inwards. Surgery may be required to elevate the fracture.

Compound comminuted fractures with damage to the underlying brain

These are treated by removing all bony fragments, debridement and closure. Failure to remove all bony fragments may lead to development of cerebral abscess. They are associated with epilepsy.

Fractures of the base of the skull

They usually involve the anterior or middle cranial fossa. Those affecting the anterior fossa may cause nasal bleeding, periorbital haematoma, subconjunctival haemorrhage, CSF rhinorrhoea and cranial nerve injuries (I–V). Middle cranial fossa fractures involving the petrous temporal bone may cause bleeding from the ear, CSF otorrhoea, bruising over the ear and over the mastoid, and cranial nerve injuries (VII and VIII).

Summary

The emphasis in the management of head injuries is on damage to the underlying structures rather than on any skull fracture per se. CT scanning is the investigation of choice for patients with head injury and no patient with a significant head injury should be admitted to a hospital A&E department that does not have immediate 24-hour access to CT scanning.

Management of CSF leakage

It may be difficult to distinguish bleeding from blood mixed with CSF. Place a drop of the blood-stained discharge on a clean white gauze. If CSF is present there will be a spreading yellowish ring around a central stain of blood (halo sign). CSF leakage implies that the dura and arachnoid are torn and therefore there is a potential pathway allowing infection to spread to the meninges and brain. The head of the bed should be elevated 30°. The patient should be advised not to blow their nose. In many cases, the leakage settles spontaneously but all CSF leaks should be referred for a neurosurgical opinion. Where CSF rhinorrhoea occurs do not pass a nasogastric tube. Do not pack the nose or ears.

Intracranial bleeding

This may be extradural, subdural (acute or chronic) and intracerebral. Subarachnoid haemorrhage commonly follows trauma.

Extradural

This results from bleeding between the bone and the dura. It is most likely to occur when a fracture occurs in the temporal region crossing the middle meningeal artery. It may occasionally occur without a fracture. Usually low-speed injury.

Symptoms and signs

History of head injury (may be relatively minor). Temporary concussion. Recovery (‘lucid interval’), then increasing headache, decreased conscious level, coma. There may be no lucid period or the patient may have the signs when admitted unconscious. Falling pulse rate. Rising BP. Reduced and irregular respiration. Dilated ipsilateral pupil. Contralateral hemiparesis or focal fits. May be boggy swelling overlying the site of the fracture as extradural blood may track through the fracture and into the subcutaneous tissues.

Investigations

CT scan. This should always be done immediately, before surgery is contemplated.

Treatment

This is a true emergency and requires neurosurgical assistance. If none is immediately available and the patient’s condition is critical despite resuscitation, i.v. mannitol should be given and ventilation commenced. A burr hole should be made over the suspected site of clot. Enlarge the hole with bone-nibbling forceps. Gently evacuate the clot. Clip or diathermy the bleeding vessel.

Subdural

Acute

This results from tearing of small bridging veins that bleed into the subdural space and is usually associated with a lacerated brain resulting from high-speed injuries. The haematoma spreads over a large area. The patient usually has marked brain injury at the outset and is comatose but the condition deteriorates further. Can rarely be caused by a ruptured aneurysm, which can cause the patient’s collapse and a secondary head injury. The history of the event should distinguish from primary trauma.

Symptoms and signs

Severe head injury. May be rapid deterioration. Signs of raised ICP. Localizing signs. Pupillary inequality.

Investigations

CT scan.

Treatment

Craniotomy. Evacuation of clot. Recovery depends on degree of underlying brain damage.

Chronic

Usually in the elderly. Brain shrinkage makes the bridging veins between cortex and venous sinuses vulnerable. May have only been a trivial and forgotten head injury. It may occur weeks or months after the injury, presenting with neurological signs, headache or coma, confusion or personality change. A brain tumour may be suspected in the differential diagnosis. There may be fluctuating level of consciousness.

Investigations

CT scan.

Treatment

Evacuation of clot via burr holes and short course of dexamethasone. Reaccumulation may occur.

Intracerebral

This occurs as a result of primary brain injury but may expand causing secondary brain damage. It may extend into the ventricles. A discrete haematoma may require craniotomy if the patient’s condition deteriorates. Always consider other primary causes for the intracerebral haematoma causing collapse and secondary head injury.

Complications

Meningitis

Organisms enter via compound skull fractures. Prophylactic antibiotics should be used for all compound fractures. Current prophylaxis includes cefuroxime given for a minimum of 1 week. It is not necessary for the drug to cross the blood–brain barrier if given for prophylaxis but it is necessary for it to cross the blood–brain barrier if given for specific treatment of meningitis.

Cerebral hypoxia

This is a major and preventable cause of secondary brain injury. Respiratory failure after head injury may be peripheral or central. Peripheral causes include upper airway obstruction, e.g. tongue; vomit; chest injuries; pneumothorax; pneumonitis; shock lung. Central causes include primary brainstem injury or depressant drugs, e.g. alcohol. Hypertension may also contribute.

Management of head injuries

Always consider – is this only a head injury or was it caused by something else, e.g. myocardial infarction, fit, intracranial bleed? A good history is vital.

Minor

The most important question is: does the patient need a CT scan and/or admission? The patient should be monitored for 24 h. The majority of complications will occur during this time. If no problems occur after 24 h, the patient can be discharged into the care of a responsible adult. Patients should be given an information sheet detailing symptoms and signs for which they should be on the look-out, with instructions to return to the hospital should any of these symptoms occur. They should be advised about post-concussional symptoms and be referred to a head injury clinic for further management.

Observations during admission

The primary observations are the GCS (→ Table 4.1). In addition pulse, BP, respiratory rate and pupillary size and reaction are monitored. These are carried out by the nursing staff on the ward, the frequency depending on the severity of the symptoms. Hourly observations are usually the norm. Signs of deterioration include falling coma score, falling pulse rate, raised BP, reduced or irregular respirations, dilatation of the pupils, loss of light reflex and asymmetrical pupils. An alteration of conscious level occurs before signs of brainstem compression.

Major

Does the patient need a neurosurgical referral? If the patient deteriorates rapidly and an extradural is suspected, burr holes may be required, but if appropriately diagnosed, it is usually preferable to transfer the patient immediately to a neurosurgical unit. In many patients with head injury, no surgical intervention is warranted. These patients may be in a coma with diffuse cerebral injury and oedema and may require ventilation. Other injuries may be present. Intensive care will be required. The following may be required in management:

• Monitoring of vital signs and neurological status

• Assisted ventilation

• i.v. fluids and nasogastric aspiration

• Avoidance of fluid overload

• Maintain electrolyte balance, avoid hyponatraemia (which exacerbates cerebral oedema)

• Control raised ICP, e.g. i.v. mannitol (osmotic effect reduces cerebral oedema); furosemide; controlled ventilation assists management of cerebral oedema; dexamethasone is not effective in head injuries in the control of cerebral oedema.

Other complications of head injury

Epilepsy

Post-traumatic epilepsy may occur, particularly after prolonged post-traumatic amnesia, depressed fractures and intracerebral haematoma. It is associated with cortical damage and subsequent scarring. Long-term anticonvulsive therapy is usually required. Prophylactic anticonvulsants are given to patients in high-risk categories although efficacy is uncertain.

Post-concussion syndrome

Headache, dizziness, fatigue and poor memory are common after head injury. Loss of ability to concentrate and a labile emotional state are often sequelae. Management includes reassurance and symptomatic treatment. Often strong reassurance is necessary to explain that the condition is usually self-limiting within a few weeks or months. In most patients, symptoms cease within 12 months. Imipramine may be helpful. Strong codeine-based analgesics should be avoided. Failing to recognize and treat the syndrome can cause significant morbidity and psychiatric disturbance (depression). This may be helped by cognitive behavioural therapy.

Brain death

Regrettably, some patients do not recover from head injury and are dependent on life-support systems. The brainstem death criteria were drawn up to allow a way of determining which patients had sustained irreversible brain damage so that they were not kept on life-support systems to no avail and to the distress of relatives and the nursing staff. The diagnosis of brain death depends on the demonstration of permanent and irreversible destruction of brainstem function.

There are prerequisites for the diagnosis of brainstem death:

• The patient must not be medicated with any CNS depressant drugs or neuromuscular blocking agents

• The core temperature must be above 35°C

• There should be no metabolic disturbance

• The cause of the brain damage must be known.

The following tests reflecting brainstem reflexes must then be carried out by two doctors, on two occasions. Both doctors must have been registered for at least 5 years and be of consultant or senior registrar grade. They must be completely independent of any organ transplant team.

• No pupillary response to light – direct or consensual – this reflex involves cranial nerves II and III

• Absent corneal reflex – normally would result in blinking – this reflex involves cranial nerves V and VII

• No motor response in the cranial nerve distribution to stimuli in any somatic area – e.g. supraorbital or nail bed pressure leading to a grimace

• No gag reflex – back of throat is stimulated with a catheter – this reflex tests cranial nerves IX and X

• No cough reflex – no response to bronchial stimulation with a suction catheter – this reflex tests cranial nerves IX and X

• No vestibulo-ocular reflex – head is flexed to 30° and 50 mL of ice cold water is injected over 1 min into each external auditory meatus. There should be no eye movements – this reflex tests cranial nerves III, VI and VIII

• Apnoea test – the patient is pre-oxygenated with 100% O₂ for 10 min. PaCO₂ is allowed to rise to 5 kPa (before testing); the patient is disconnected from the ventilator and O₂ insufflated at 6 L per min via a tracheal catheter. PaCO₂ is allowed to rise to 6.5 kPa. At this point, there should be no respiratory effort.

There is no set time period recommended between the two sets of tests but 6–24 h is usual. Once two sets of brainstem death criteria are satisfied, the decision to discontinue ventilation is made. The official time of death is that of the timing of the first set of tests. The possibility of a patient becoming an organ donor should be discussed sensitively with the next of kin. Many relatives gain some consolation out of the death of their loved ones, knowing that their organs are giving life to others.

Management of raised intracranial pressure (ICP)

Causes Head injury, meningoencephalitis, haemorrhage (extradural, subdural, subarachnoid, intracerebral), tumour, infection, hydrocephalus.

Symptoms and signs

Headache, drowsiness, vomiting, fits, irritability, listlessness, slowing pulse, rising BP. Irregular respiration. As the pressure increases the cerebral hemisphere is pushed through the tentorial hiatus alongside the brainstem. The third nerve is compressed against the edge of the tentorium and the brainstem is compressed by the herniating cerebral hemisphere – symptoms and signs: deepening coma, irregular slow breathing progressing to Cheyne–Stokes respiration and apnoea. Pressure on the third nerve causes ipsilateral and then bilateral pupillary dilatation. Eventually, the patient exhibits the decerebrate posture.

A sixth nerve palsy may be an early false localizing sign. The long intracranial course of this nerve makes it susceptible to stretching.

Investigations

• CT scan

• Cerebral angiography.

Lumbar puncture should not be carried out in the presence of raised ICP. If the spinal CSF pressure is reduced by removing CSF, the high ICP may force the brainstem and cerebellar tonsils through the foramen magnum (coning) with fatal results.

Cerebral tumours

These may be broadly classified as glial and non-glial depending on the cell of origin (→ Table 18.1).

TABLE 18.1 Classification of cerebral tumours

Primary
Glial (gliomas)	Astrocytoma
	Medulloblastoma
	Ependymomas
	Oligodendrogliomas
Non-glial	Meningiomas
	Acoustic neuroma
	Pituitary tumours
Secondary	Lung
	Breast
	Kidney
	Melanoma

Symptoms and signs

• General, e.g. confusion, dementia, and epilepsy

• Raised ICP, e.g. drowsiness, headache, vomiting

• Focal signs, e.g. weakness, sensory disturbance

• Epilepsy.

Symptoms vary depending upon the site of tumour. A full neurological examination should be carried out. Papilloedema is uncommon (about 15%). Symptoms occur alone or in combination.

Investigations

• MRI

• CT scan

• Angiography

• CXR to exclude primary

• Burr hole

• Biopsy.

Types of cerebral tumour

Astrocytoma

The peak incidence of astrocytoma is in early middle age. They vary in malignancy and some are slow growing. All are infiltrative. Most malignant astrocytomas are radio-resistant and survival overall is usually less than 5 years. Surgical cure is usually impossible as they extend into deep structures. In children, the tumour is often well-differentiated and cystic, and occurs in the cerebellum. This type is histologically benign and may often be completely excised with potential cure.

Glioblastoma multiforme

This is the most malignant brain tumour. It is rapidly growing and usually occurs between 40 and 60 years. It is rarely removable surgically and is radio-resistant. Most patients are dead within a year of diagnosis.

Medulloblastoma

This is the commonest glioma of childhood. It occurs in the first decade of life arising in the roof of the fourth ventricle and infiltrates into the cerebellum. It may cause obstructive hydrocephalus. Spread is by the CSF and it may seed on the spinal cord. Radical removal is followed by radiotherapy. Chemotherapy may be required.

Ependymomas

Those arising from the choroid plexus of the ventricles may be totally removable. Those arising from the ventricular walls are difficult to remove. The more malignant forms may seed via the subarachnoid space. Craniospinal irradiation is required and gives good results.

Oligodendrogliomas

These occur in the cerebral hemispheres and are slow growing. Treatment is by tumour debulking and radiotherapy. Most patients are dead within 5 years of diagnosis. Relatively few survive 10 years or more.

Meningiomas

Meningiomas arise from arachnoid cells. They usually occur in females in the 40–60 age group. They compress the cerebral cortex early in their growth and therefore fits may be an early sign. They may rarely cause osteoblastic change in the overlying bone, giving rise to exostosis producing a palpable lump over the vault of the skull. Common sites include parasagittal, along the falx; sphenoid – lesser wing; and olfactory groove. They are usually slow growing and do not invade brain tissue but compress it. Small tumours are usually curable by surgical excision. Even with subtotal excision for large tumours the prognosis is good. They may respond to hormonal therapy.

Acoustic neuroma

This arises from Schwann cells of the nerve sheath of the VIIIth cranial nerve at the internal auditory meatus. As the tumour grows it expands the internal auditory canal and extends into the cerebellopontine angle compressing the pons, cerebellum, and adjacent cranial nerves. It may be a feature of von Recklinghausen’s disease.

Symptoms and signs

An acoustic neuroma should always be considered in a patient with unilateral sensorineural deafness, especially with tinnitus. Occurs in those aged 30–60. Facial weakness with unilateral taste loss is a later manifestation. The corneal reflexes are lost relatively early when the trigeminal nerve is stretched by the tumour. Dysphagia, hoarseness and dysarthria may arise owing to involvement of nerves IX, X, XII. Ultimately cerebellar signs and features of raised ICP may occur, but these are now a rare occurrence.

Investigations

• CT

• MRI.

Treatment

Surgical excision. Most can be completely removed with cure. Early diagnosis ensures preservation of facial nerve function and occasionally hearing. Stereotactic radio-surgery may be used, particularly for small tumours <3 cm.

Pituitary tumours

These cause symptoms due to their endocrine capacity or due to their effects on the optic chiasma.

Secretory tumours (e.g. prolactinoma) Many tumours contain a mixture of secretory cells. Presentation is influenced by the hormonal production and size of the tumour. These tumours are usually small.

Non-secretory tumour Null cell adenomas – usually grow to a larger size and present because of local effects.

Symptoms and signs

These depend on whether the symptoms are due to the endocrine capacity or local pressure effects. Bitemporal hemianopia results from compression of the optic chiasma. Compression of secretory cells by non-secretory tumours may result in hypopituitarism. Symptoms include reduced libido, infertility, amenorrhoea, myxoedema, depression, loss of sex characteristics and hypoadrenalism. In children, growth arrest may occur. Hormonally active tumours may result in the following:

• Overproduction of growth hormone: before fusion of the epiphyses this will cause gigantism; in adult life, acromegaly results

• Hyperprolactinaemia: this is characterized by amenorrhoea, infertility, galactorrhoea and impotence

• Cushing’s disease (→ Ch. 11).

Investigations

• MRI

• CT is contraindicated if MRI available because of radiation of optic chiasma

• Visual field assessment

• Hormonal analysis

• Skull radiograph is never the primary investigation but a pituitary tumour may be discovered incidentally on a skull radiograph (expansion of sella turcica).

Treatment

Surgery or medical therapy in selected cases. Tumour removal may be carried out by the transnasal route. Some pituitary tumours are radio-sensitive and radiotherapy may be used as an adjunct to surgery or rarely as primary therapy in those with large tumours or in poor general health. Radiotherapy may be administered by external beam or stereotactic radio-surgery. Hormonally responsive tumours, e.g. prolactinoma, acromegaly, can be treated with hormonal antagonists.

Craniopharyngioma

This a cystic benign tumour arising in a remnant of Rathke’s pouch. It may present in childhood or adult life. Symptoms are those of hypopituitarism due to compression, visual defects or raised ICP. The treatment of choice is radical excision but this may be difficult because of their size.

Intracranial vascular lesions

These include:

• Aneurysms of the circle of Willis at the base of the brain. Most of these are acquired, the remainder being congenital.

• Angiomas that may occur in any part of the CNS. AV malformations may be associated with these.

Aneurysms

The majority are acquired as a consequence of cerebrovascular disease. Most patients are smokers. Mycotic aneurysms are very rare. Some are associated with polycystic kidney disease, Ehlers–Danlos syndrome, coarctation of the aorta and Type III collagen deficiency. Hypertension is a contributory factor.

Symptoms and signs

The classic history is one of sudden severe headache with nausea, vomiting, collapse and often coma. Death may occur within minutes in major bleeds. With less serious bleeding, there may be photophobia, and neck stiffness. Isolated cranial nerve palsy may occur, e.g. third nerve. A sudden onset of headache, particularly accompanied by vomiting, requires further investigation with CT scan in all patients.

Investigations

• CT scan (may miss small bleeds)

• LP (only if the diagnosis is in doubt and the patient is conscious without focal neurological signs); if positive, carry out urgent cerebral angiography.

Treatment

Early consultation with a neurosurgeon. If the patient is conscious with little neurological deficit, angiography is undertaken with a view to endovascular coiling or surgery. Surgery involves an intracranial approach to the aneurysm with clipping of the neck of the aneurysm with a non-magnetic metal clip. Occasionally, angiography fails to show an aneurysm, possibly indicating that thrombosis has taken place in the aneurysm. Such cases may be treated conservatively and often do well. The majority of aneurysms are now coiled. Surgery is reserved for those where coiling is considered inappropriate.

Prognosis

Some 25% of patients die without regaining consciousness; 5% bleed again within 3 weeks of the initial haemorrhage, and in rebleeding, the mortality is high. After 6 weeks, the chances of a rebleed are about 10% per annum, without treatment.

Hydrocephalus

This may be divided into two types:

Non-communicating or obstructive. In this type the CSF cannot escape from the brain through the cerebral aqueduct and ventricular dilatation alone occurs. The aqueduct may be blocked by congenital stenosis, Arnold–Chiari malformation (downward herniation of the fourth ventricle and cerebellar tonsils), infection or tumour.

Communicating. The ventricles communicate with a subarachnoid space and the CSF can escape within the brain but absorption via the arachnoid villae is prevented. This may result from meningitis, intraventricular haemorrhage in premature infants or malignant deposits on the meninges.

Clinically, hydrocephalus may be divided into two groups, congenital and acquired.

Congenital

The commonest causes are stenosis of the aqueduct of Sylvius, stenosis of the foramina of Magendie and Lushka, and Arnold–Chiari malformation.

Symptoms and signs

Developmental delay. Abnormal skull enlargement. Frontal bossing. Prominent scalp veins. ‘Setting sun’ sign (eyeballs displace downwards). ‘Crackpot’ sign on percussion of skull. Diffuse transillumination of the skull only if the hydrocephalus is very gross. Bulging fontanelles that fail to close at the appropriate time. Later, there may be epilepsy and profound mental impairment. Associated congenital deformities may occur, especially spina bifida.

Investigations

• USS if fontanelles open

• CT/MRI: ventricular dilatation and may confirm cause.

Treatment

In some infants, natural arrest of the condition occurs. A shunting procedure is usually required to direct the CSF to an absorptive area. In obstructive hydrocephalus, the CSF is shunted from the ventricles into the peritoneal cavity. The shunt incorporates a unidirectional valve set at a specific opening pressure.

Spinal tumours

Spinal tumours are classified in Table 18.2.

TABLE 18.2 Classification of spinal tumours

Extradural	Secondary spinal deposits are most common
Extradural	Primary bone tumours, e.g. osteoblastoma and myeloma
Intradural–extramedullary	Meningioma
Intradural–extramedullary	Neurofibroma
Intramedullary	Rare and include astrocytomas and ependymomas