INTRACRANIAL TUMOUR :- Majority of intracranial tumours, are metastatic in origin. The tumours may be benign or malignant. Cysts and abscess though not tumours yet clinically they behave as tumours.
CLASSIFICATION OF INTRACRANIAL TUMOUR
The main varieties are as follows:
(i) Tumour of brain substance-Glioma 50%, Glioblastoma, Astrocytoma, Ependymoma, Medulloblastoma, Oligodendroglioma, Microglioma, etc.
(ii) Tumour arising from the meninges, Meningioma (20%), Fibroblastoma, Reticulum cell sarcoma.
(iii) Tumour arising from the nerve sheath 10% Neurofibroma
(iv) Secondary carcinoma and sarcoma 20% usually from lungs; breast, kidney, prostate, stomach, thyroid, etc.
(v) Tumours arising from blood vessels-Angioma.
(vi) Tumour arising from the hypophysis or its stalk, e.g., Craniopharyngioma, Pituitary adenoma.
(vii) Infective granuloma.
(viii) Parasitic and other cysts (colloid cyst) may also behave as tunour.
In children tumours of posterior fossa, e.g.,gliomas, medulloblastomas and in adults supratentorial tumours– glioblastomas, meningiomas are common.
Onset is gradual
Age : All ages.
Symptoms may be divided into two groups
(a) Symptoms due to local involvement of cerebral structures.
(b) Symptoms of increased intracranial tension.
Features of Local Involvement
These vary according to the type, site of affection, rate of growth of tumour, etc. Tumours which grow very slowly or are encapsulated do not produce symptoms early. Malignant tumours produce symptoms comparatively early and progressive increment of symptoms develop. Site of tumour is also important. A small tumour in the vicinity of brain stem will produce symptoms early, while a quite large tumour in frontal area does not. Haemorrhage inside a tumour will produce acute episodes simulating a stroke. Symptoms are aggravated when considerable oedema develops surrounding a tumour.
Local irritation to the cerebral cortex gives rise to Jacksonian epilepsy which is a helpful localising sign. Vascular tumours are difficult to diagnose. In some of them vascular murmur may be heard over the skull. According to the involvement of different anatomical areas of the cerebral cortex different syndromes are observed. These are given below
This gives rise to progressive dementia, loss of cerebration, memory and intelligence. There is loss of social sense and personality changes. Patient is careless about the dress and forgets the social bindings. Generalised convulsion, grasp reflex, anosmia, aphasia are seen. When the site is pre-frontal area, pyramidal tract is involved and hemiparesis may develop.
This may produce spatial disorientation, apraxia, agnosia, sensory inattention or perceptual rivalry, receptive aphasia, homonymous hemianopia, sensory type of Jacksonian epilepsy, cortical type of sensory loss, contralateral hemiparesis, hyper-reflexia, astereognosis. Hyperpathia and spontaneous pain called Thalamic pain may develop. All these disturbances occur contralaterally.Lesion of the left angular zyrus may cause Gerstmann’s syndrome (combination of alexia, agraphia, acalculia, right-left confusion and finger agnosia). When left submarginal zyrus is involved ideational apraxia may be present. Anosognosia (denial, neglect or rejection of paralysed limb) is present when there is lesion of the non-dominant hemisphere. With right-sided lesion constructional apraxia and dressing apraxia may also develop. Contralateral homonymous field defect or lower quadrantanopia may develop….| INTRACRANIAL TUMOUR
Visual hallucinations, visual disturbances (contralateral homonymous field defect), dreamy states, (deja vu/Jamais vu) automatic behaviour, temporary upsets of memory, inability to learn new things, aphasia, psychomotor type of convulsive seizure are observed. Tumour of the uncinate area may result in seizures with olfactory or gustatory hallucinations, motor features, e.g., sucking or smacking of lips, loss of external awareness without loss of consciousness, etc. There may be auditory illusions and hallucinations. In left-sided lesion there may be dysnomia and receptive aphasia while right-sided lesion may give rise to inability to perceive musical notes and melodies. Loss of personality is also seen. Emotional changes, depersonalisation, behaviour changes, micropsia, macropria etc may also develop.
Crude visual hallucinations and seizure (e.g., flashing of light), characteristic crossed homonymous hemianopia sparing the macular area, headache and papilloedema are seen. In left- sided or bilateral lesion there is visual agnosia both for colour and objects but in unilateral lesion visual hallucination may be seen. In bilateral occipital lobe involvement cortical blindness may develop with presence of light reflex.
There may be colour blindness, inability to identify familiar face (prosopagnosia), inability to integrate and interpret a composite scene but not to its unit component (simultagnosia) and failure to turn the eyes of a particular point in space in spite of preservation of spontaneous and reflex eye movement (Balint’s syndrome). There may be denial of blindness or field defect (Anton’s syndrome).
Loss of equilibrium, in-coordination,early development of headache and pepilloedema are seen. When vermis is involved there may be marked ataxia of trunk and when cerbellar hemispheres are affected the limbs will show hypotonia, incoordination, ataxia and ataxic gait.
Ataxia incoordination, multiple cranial nerve palsy, nystagmus ataxia UMN and sensory loss in one or both sides. Tumour in intrinsic will produse symptoms lately.
FEATURES OF INCREASED INTRACRANIAL TENSION
Patient may express it to be a mere fullness of the head or to a type of agonising pain. This may be intermittent or continuous. Often if appears in the early morning or during recumbency or stooping forwards. It is rarely localised or may be altogether absent.
Two-thirds of all patients will have this symptom. This is projectile in type and occurs at the height of headache. It is not preceded by nausea.
This is very important of all general manifestations. It depends on the degree of intracranial pressure referred to intracranial vessels. The whole margin of the optic disc is blurred, it becomes pinkish in colour, venous engorgement is also seen.
Lasting papilloedema gives rise to secondary optic atrophy. Vision may or may not be disturbed but subtentorial growths may give rise to more intense and early papilloedema.
Headache, vomiting, papilloedema are three classic triad of increased intracranial tension. In lesions of the posterior fossa and with lesions above the tentorium cerebelli these features are very well-pronounced.
Mental deterioration, drowsiness and loss of vivacity
There is delayed cerebration. Insomnia is rare and drowsiness gradually increases resulting in coma.
Pulse and Respiration
Bradycardia even to an extent of 40 beats per minute may develop. Respiration tends to be slow and shallow and there may be Cheyne-Stoke’s type of respiration.
It is a peculiar symptom in some cases which is difficult to explain.
May also be seen.
False Localising signs
These signs when present will not indicate the site of mass effect
(a) Bilateral 6th nerve palsy.
(b) Unilateral 3rd nerve palsy.
(c) Hemiparesis on the same side.
(d) Bilateral or unilateral extensor plantar response.
- X-ray of the skull may show erosion of the posterior clinoid processes, internal auditory meatus or apex of the petrous part of the temporal bone. There may be lateral shift of the pineal body, sometimes intracerebral calcification and evidence of increased intracranial tension.
- X-ray of chest, barium X-ray of the G.I. tract, urogram and bone X-ray should be taken to find out the primary source, if any
- Cerebral angiography either carotid or vertebral, may sometimes be helpful. It may show stretching of vessels or displacement due to tumour or may indicate whether the tumour is vascular or avascular. Avascular mass is indicative of haematoma, abscess etc. Aneurysm is definitely diagnosed by angiography.
4. Pneumoencephalography : By this the expanding lesion, if any, can be demonstrated. Ventricular chambers can be well-visualised. It is contraindicated in presence of papilloedema or tumour. This is rarely required now-a-days.
5. Ventriculography : This may be of help in some rare cases.
6. Electroencephalography EEG abnormality may be seen in some cases but from this, the nature of the tumour whether vascular, neoplastic, benign or malignant cannot be known.
7. Echoencephalography may show lateral shift.
8. Cerebroscintigraphy is also helpful to localise the tumour.
9. CSF may be taken by LP or cisternal puncture. If there is marked papilloedema LP is contraindicated. The protein level may be high in cases of auditory neurofibroma and meningioma. There may be pleocytosis in cerebral abscess.
10. CT scan: This is the commonest investigation done in such cases now-a-days. It can locate the mass lesion but cannot tell its basic pathology. The characteristic appearance of meningioma is practically diagnostic by CT scan.
11. MRI scan is also helpful and can be done in specialized centres. It is more helpful for tumours of the posterior fossa and brain stem where CT scan is also helpful. MRI with gadolinium enhancement is very much helpful now-a-days as it can precisely locate the anatomical site, its shape, size, extent of damage, or whether there is any mass effect or oedema.
12. Technetium brain scan is also helpful.
TREATMENT OF INTRACRANIAL TUMOUR
The only effective treatment is surgical excision but it is not possible in all cases. In some cases radiotherapy may be helpful. Meningioma, acoustic neurinoma glioblastoma, astrocytorma, meduloblastoma, ependymoma, oligoden- droglioma, cerebellar tumour, haemangioblastoma, pinealoma, craniopharyngioma require surgery. Primary cerebral lymphoma, Pinealoma, meduloblastoma, etc. may require radiation and/or chemotherapy.
Palliative treatment includes lowering of intracranial tension by IV Mannitol or oral IV Glycerine. Steroids may be useful to reduce cerebral oedema. To relieve headache and pain, Aspirin may be used. Chemotheraphy particularly nitroso ureas and semustine may be useful. Convulsion may be treated with antiepileptic drugs.