Intracranial space occupying lesions

By- Jimmy jaskaran sunda

Intracranial space occupying lesions

Definition- any lesion occupying physical space within the cranial cavity.

- These lesions put pressure on the adjacent brain tissue and causing its damage

- Results in signs and symptoms due to - >dysfunction of the nearby structure- >raised intracranial pressure- > electrical disturbance - seizures

Classification of ICSOL

Traumatic –subdural haematoma,extradural haematoma.

Vascular- intracerebral haematoma. Infective –cerebral abscess,tuberculoma,

neurocysticercosis. Neoplastic

Clinical features of ICSOL

The clinical features of icsol are divided into following categories.

- s/s due to raised intracranial tension. - Localising signs- these are the signs which helps to detect the anatomical site of the lesion. - false localising signs- these are signs which do not have localising value.

s/s due to Increased intrcranial tension

Increased head size and /or papilledema- in infants there is separation of cranial sutures,wide fontanels and increased head circumference. Separation of the sutures compensates for increase in intracranial pressure.

MacEwen or crackpot sign- it indicates raised intracranial pressure after sutures have closed.Papilledema is unusual in infancy unless intracranial pressure is very high.

-Vomiting – unexplained projectile vomiting with or withoutheadache.It is due to the direct pressure on the medullary centre.-Headache –early morning headache is highly suspicious.-Diplopia and 6th nerve palsy- increased pressure displaces the brainstem downwards ,thus stretching the 6th nerve and results in paralysis of lateral gaze and diplopia.

Localising signs

Cranial nerve palsies- combined 6th & 7th nerve involvement may suggest a pontine lesion.Pseudobulbar palsy- it suggest 9th and 10th cranial nerve involvement. In this the patient loses control of facial muscles and has trouble chewing or speaking.

Head tilt- it is seen in superior oblique paralysis,cerebellar lesions and posterior fossa tumours

Ataxia –occurs in cerebellar,spinocerebellar tract,frontal lobe or thalmic lesions

Motor deficit- occurs in cerebral,brainstem & spinal cord lesions

-Seizures- cortical or subcortical lesion.-Decerebrate posturing- due to infratentorial lesions.

-Vision-impaired- vision with normal refraction should arouse suspicion of lesion near optic nerve, optic chiasma,optic radiation or cortical blindness.

Nystagmus - both irritative and destructive lesions of cerebellovestibular system may cause nystagmus.

-personality disturbances,inappropriate sphincter control and grasp response suggest localization of tumour near the frontal lobe.

Brain tumours

Brain tumours may be primary or secondary.The primary tumours may be malignant or

benign.benign tumours located near the vital area of brain may be life threatning.

Rapidly growing tumours represents earlier than the slow growing tumours as in case of slow growing tumours the various compensatory mechanisms prevents the raise in ICT and hence presents later in life .

Cerebellar tumours

Medulloblastoma- these are midline cerebellar tumours occurs in infancy.These are fast growing tumours.

-craniospinal spread along neuraxis is common and death occurs rapidly.

Clinical features /--truncal ataxia-early papilledema-tendency to walk with broad base-unsteadiness in sitting position

Astrocytoma -astrocytoma arise from astrocytes – star shaped cells that make up the supportive tissue of the brain.

Clinical features /--Nystegmus is observed on lateral gaze of the child the affected side.-Areflexia and hypotonia-Head is tilted to the side of the lesion to relieve the increased intracranial tension caused by herniation of tumour or cerebellar tonsils through foramen magnum.Treatment /-Complete surgical excision of the tumour - Chemotherapy with cisplatin,vincristine and tomustin.

Brainstem tumours Glioma of the brainstem/-The usual age of onset is later half of first

decade of life.-causes bilateral involvement of cranial

nerves .-cerebellar dysfunction is often present.-they carry worst prognosis. Most children

die within 18 months.Ependymomas of 4th ventricle/-Arise from the ependymal cells lining the ventricles of brain and centre of spinal cord.-flow of CSF is obstruted causing early rise

in ICT.

Supratentorial tumours Craniopharyngioma/-It is benign tumour arising from small nests of cells

near the pituitary stalk, occurs in sellar region near pituitary gland.

Clinical features/--s/s due to raisd ICT-symptoms due to pressure on optic tract-hemianopsia,unilateral visual field defects-growth failureEndocrine abnormalities like diabetes insipidus & delayed puberty.

Glioma of cerebral hemisphere/--Occurs during 1st and 2nd decade of life>clinical features /--seizures and hemiparesis-ataxia due to involvement of frontopontine cerebellar fibers.-vomiting,headache,papilledemaHypothelmic glioma/- These are rare tumours causing diencephalic syndrome.-children fails to thrive,the subcutaneous fat is lost and have sleep sleep and respiratory disturbance.Glioma of optic nerve/-c/f--visual disturbances ,squint,proptosis,exopthalmos and optic atropthy.

Inflamatory granulomasThese are most important causes of raised ICT and

partial seizures in childhood.Neurocysticercosis and tuberculoma are the

commenest granulomas.

Neurocysticercosis /-It is caused by larval stage of taenia solium.Pathogenesis-It is an infestation of CNS with larval

cyst ofpork tapeworm.Evolution occurs from a noattenuated

cyst to a ring with perilesional edema,to a disc lesion.which may

disappear,persist or even calcify.

CT of brain showing cyst with eccentric scolex and perilesional edema

Clinical features/--Parenchymal neurocysticercosis-seizures ,raised ICT,focal deficit & rarely meningeal signs-Intaventricular neurocysticercosis- features due to raised ICT,focal neurological deficit & hydrocephalous.-Spinal neurocysticercosis-presents with features of spinal cord compression .Diagnosis /-CT scan shows disc or ring like image with a hypodense centre .MRI is more useful than CT scan in doubtful cases.-ELISA -CSF may be examined for cells ,cysticercal antigens & PCRTreatment/--albendazole and praziquantel from 5 -28 days-corticosteroides-2-3days before initiating therapy for 5 days-anticonvalsants for 6-9 months but 2-3 yrs for calcified lesion

Tuberculoma/-Clinical presentation is similar to neurocysticercosis.There is a single or multiple ring enhansing lesions. Tuberculoma rings are usually large .The lesion often has a thick irregular wall and associated with severe perilesional edema.

Treatment/-antituberculous therapy is recommended for 1 year as for tubercular meningitis along with corticosteroides for initial 6-8 weeks.

Brain abscess-Brain abscess is an important differential diagnosis

among children with unexplained fever,altered

sensorium,elevated intracranial pressure,localizing neurological findings and

headache Predisposing factors – cyanotic heart

disease,immunosuppressed status,otitis media,sinusitis,mastoiditis,systemic sepsis and post traumatic.

Etiology- anaerobic organisms,streptococcus aureus,pneumococci,proteus and haemophilus influenzae are common infecting organisms

Clinical features/- -Features due to raise intracranial tension -Features suggesting toxemia-e.g fever ,chills & leukocytosis-Manifestation of intracranial suppuration such as irritability,drowsiness and meningeal irritation.-Focal neurological signs such as focal convulsions,cranial nerve palsies,aphasia,ataxia,visual field defects & neurological deficit.

- Diagnosis- is established by MRI or CT scan.

Management /-Investigation for the source of infection,treatment of precipitating cause ,management of raised ICT and symptoms.Cephalosporin,vancomycin and metronidazole are continued for 4-8 weeks.- Surgical drainage or excision of the abscess should be done in case of abscess of >2.5 c.m