Space-occupying Lesions

A space occupying lesion of the brain is usually due to malignancy but it can be caused by other pathology such as an abscess or a haematoma. Almost half of intracerebral tumours are primary but the rest have originated outside the CNS and are metastases.

The effect of the tumour may be local, due to focal brain damage and the presentation may give an indication of the location of the lesion but not its aetiology. There may be more general symptoms related to raised intracranial pressure or seizures, behavioural changes, or false localising signs. Large lesions in some regions, such as the frontal lobe, may be relatively silent whilst a small lesion in the dominant hemisphere may devastate speech.

A tumour may infiltrate and destroy important structures, it may obstruct the flow of CSF and cause hydrocephalus or it can induce angiogenesis (new blood vessels) and break down the blood brain barrier causing oedema.

Presenting features may include localising signs, generalized signs and false localising signs. A rapid onset of symptoms suggests a cerebrovascular lesion whilst a space occupying lesion will usually be more gradual. However, a space occupying lesion can mimic a stroke.

Many of these features may be due to raised intracranial pressure.

• Headache tends to be quite a late feature. It is usually severe and is the worst feature in half of patients. It resembles a tension headache in most cases and such "textbook" features as being worst in the morning and worse on bending or Valsalva manoeuvre are often absent.¹ A change in the pattern of headaches is a cause for concern. Headache is more common in posterior fossa tumours and rapidly growing tumours.² It may be a more important feature in children than in adults.
• Vomiting may occur. This may be without accompanying nausea.
• Nausea may be a feature
• A change in mental status or behavioural change is a cause for concern
• There may be weakness, ataxia or disturbance of gait
• Even deficits of speech or vision may be poorly localising signs
• There may be generalized convulsions

If there are generalised convulsions, try to get a good history. As described in the diagnosis of epilepsy, they may start with focal signs and then progress to a generalized convulsion as in Jacksonian epilepsy. The first features of the episode may be a good localising sign.

If raised intracranial pressure is suspected it is imperative to use the ophthalmoscope to look for papilloedema. This may be more marked in children than in adults.

If epilepsy starts in middle age or beyond, a space occupying lesion is one of the possible diagnoses that should be considered.

Many patients have headaches. Very few have brain tumours. A meticulous approach is required to identify those few.²

• The abducent nerve (cranial VI) has a long and tortuous intracranial path that makes it vulnerable. Abducent nerve palsy is not a useful localising sign. It supplies the lateral rectus muscle and its action is to move the eye laterally - as described in diplopia and cranial nerve lesions.
• Horner's syndrome is not a good localising lesion as the path of the sympathetic nerves is also long but as there is no chiasma (fibres don't cross the midline) it is a good lateralising sign. The lesion may also be outside the skull.
• If a headache is unilateral, this is often a good indicator of the side of the lesion.
• Cerebellar signs do not help to localize the lesion.

Cerebellum

Cerebellar ataxia is described rather more fully elsewhere. Space occupying lesions represent only a small part of the differential diagnosis.

• Ataxia may present as general clumsiness.
• Intention tremor is worst at the end of a movement and leads to past-pointing. Ask the patient to first touch his nose with his index finger, and then your index finger, held about 50cm away and back to his nose again. A positive sign is when he tends to point beyond your finger.
• Dysdiadochokinesis is tested by asking the patient to hold up his hands and rapidly pronate and supinate repetitively. Ask him to tap the back of his hand as fast as possible.
• Nystagmus may be seen.
• If truncal ataxia is worse when the eyes are closed, the lesion is in the dorsal columns, not the cerebellum.
• Cerebellar speech is described as staccato.
• Causes of cerebellar signs include acoustic neuroma, Friedreich's ataxia, stroke, haemangioma, tumours, multiple sclerosis, chronic alcohol excess and abscess.

Temporal lobe

Temporal lobe lesions often present with rather vague psychological problems.

• There may be depersonalisation, emotional changes, and disturbances of behaviour.
• There can be hallucinations of smell, taste, sound and sight. There may be Déja vu in which there is a feeling of familiarity as if the present has happened before.
• Dysphasia may be noted.
• Visual field defects involve the contralateral upper quadrant.
• There may be convulsions.
• Other psychological problems include forgetfulness, fugue (a disturbed state of consciousness in which the patient seems to perform acts in full awareness but upon recovery cannot recollect them), functional psychosis and fear or rage. There may be inappropriate sexual behaviour but the Kluver-Bucy syndrome is extremely rare.

Frontal lobe

• Frontal lobe tumours can cause anosmia. This is especially significant if it is unilateral.
• There may be a change in personality with the person becoming indecent, indiscreet or dishonest.
• Dysphasia can occur if Broca's area is involved.
• Hemiparesis or fits may affect the contralateral side.

Parietal lobe

Parietal lobe lesions can produce a very interesting neurological picture.

• There may be hemisensory loss.
• Decreased two-point discrimination.
• Astereognosis is the inability to recognize a familiar object placed in the hand.
• Extinction can be demonstrated by asking the patient to close his eyes and touch one side of his body. Ask him to point to where you touched. Repeat this but touching both sides simultaneously. He will acknowledge only one side.
• The patient may systematically ignore one side of his body, called sensory inattention. If you ask him to draw a clock face, he omits the half contralateral to the lesion.
• Dysphasia may occur.
• Gerstmann's syndrome can be congenital or acquired. The 4 components are:
  • Agraphia or dysgraphia
  • Acalculia or dyscalculia
  • Finger agnosia
  • Left-right disorientation

Occipital lobe

Visual field defects are discussed elsewhere. A lesion in front of the optic chiasma will affect just one eye. A lesion at the optic chiasma, such as a pituitary adenoma, will cause homonymous hemianopia. In the visual cortex, the hemianopia will cause contralateral visual field defects. A visual field defect from the eye or optic nerve will be seen as a black area but loss of the visual cortex often leads to ignoring the affected area.

Cerebellopontine angle

The commonest pathology here is an acoustic neuroma. Common features include:

• Ipsilateral deafness
• Tinnitus
• Nystagmus
• Reduced corneal reflex
• Facial and trigeminal nerve palsies
• Ipsilateral cerebellar signs

Corpus callosum

This is an interesting part of the brain that communicates between the two sides. Lesions usually cause severe rapid intellectual deterioration with focal signs of adjacent lobes. There may be signs of loss of communication between the lobes such as inability of the left hand to carry out verbal commands.

Midbrain

The following features suggest a midbrain lesion:

• Unequal pupils
• Inability to direct the eyes up or down
• Amnesia for recent events with confabulation
• Somnolence

If they are large they can cause homonymous hemianopia but the most obvious presenting features may be related to their endocrine effects.

• Routine blood tests will include FBC, U&E and LFTs. Na+ may be low due to inappropriate ADH secretion.
• Skull x-ray is usually unrewarding, but if the pineal gland is calcified, a shift may be seen.
• Imaging studies may include CT scan and MRI scan.³ Both are very good but MRI is better at delineating soft tissue.
• Biopsy of the lesion may be indicated.
• A known primary tumour may exist or it may be sought by chest x-ray or mammography.

Imaging may indicate the site of a lesion but usually it will not indicate the nature, including whether it is a tumour or an abscess.

Malignancy

• Metastases, gliomas, meningiomas, pituitary adenomas, and acoustic neuromas account for 95% of all brain tumours.
• In adults, two thirds of primary brain tumours are supratentorial, but in children, two thirds of brain tumours are infratentorial.
• Primary tumours include astrocytomas, glioblastoma multiforme, oligodendrogliomas and ependymomas. All have a 5 years survival rate of less than 50%. Cerebellar haemangioblastomas have a 40% survival at 20 years. Meningiomas have complete recovery if removed.
• Primary brain tumours do not usually metastasise.
• About 30% of brain tumours are metastatic and of these about 50% are multiple.
• About 15 to 20% of people with metastatic cancer develop cerebral metastases.
• The commonest primary is lung cancer followed by breast cancer, carcinoma of colon and malignant melanoma.

Other space occupying lesions

• A haematoma may follow trauma. Risk factors include old age and anticoagulation.
• Cerebral abscesses are uncommon but risk factors include COPD that may be a source of infection to the systemic circulation and a right to left shunt that permits infection to bypass the lungs that would normally filter it out. Cerebral abscesses are multiple in 25% of cases.
• Cerebral amoebiasis and cysticercosis are rare.
• Both infection and lymphomas of the CNS are more common with HIV infection.
• Granuloma and tuberculoma can occur.

Other causes of focal CNS signs

• Stroke
• Head injury
• Vasculitis including systemic lupus erythematosis, syphilis, polyarteritis nodosa and giant cell arteritis
• Multiple sclerosis
• Encephalitis
• Post-ictal (Todd's Palsy)

Management depends upon the cause of the lesion.

• If possible, especially with primary tumours, complete excision is the aim but this may be difficult due to infiltration and surrounding structures. They vary in radiosensitivity and response to chemotherapy.
• If the malignancy is metastatic,⁴ palliative care is usually required. This may include radiotherapy. However, surgery may be contemplated with up to 3 metastases.⁵
• Haematoma may need evacuation.
• Infectious lesions will usually need both evacuation and chemotherapy.

Other treatments may be required either as part of radical treatment or as palliative care.

• Dexamethasone can reduce cerebral oedema.⁵
• Mannitol may reduce raised intracranial pressure.
• Anticonvulsants may be required but should not be given prophylactically before fits occur.⁵
• Treat headache with codeine phosphate as it avoids the pupillary effect of opiates.