Intracranial Tumours Clinical Features

DISTURBED FUNCTION

Supratentorial - see higher cortical dysfunction, pages 105-113.

occipital lobe Visual field defect - homonymous hemianopia occipital lobe Visual field defect - homonymous hemianopia

frontal lobe Contralateral face, arm or leg weakness Expressive dysphasia

(dominant hemisphere) Personality change

- antisocial behaviour

- loss of inhibitions

- loss of initiative

- intellectual impairment -» profound dementia especially if the corpus callosum is involved temporal lobe Receptive dysphasia (dominant hemisphere) Visual field defect

- upper homonymous quadrantanopia

Supratentorial tumours may directly damage the I and II cranial nerves. Cavernous sinus compression or invasion may involve the 111—VI cranial nerves.

corpus callosum - dysconnection syndrome (page 113)

Apraxia

Word blindness parietal lobe Disturbed sensation

- localisation of touch

- two point discrimination

- passive movement

- astereognosis

- sensory inattention Visual field defect

- lower homonymous quadrantanopia

Right/left confusion Finger agnosia Acalculia Agraphia dominant hemisphere

Sensory or } non-dominant Motor neglect J hemisphere (e.g. dressing apraxia)

hypothalamus/pituitary Endocrine dysfunction.

Infratentorial midbrain/brain stem Cranial nerve lesions III—XII Long tract signs

- motor and sensory Deterioration of conscious level Tremor (red nucleus) Impaired eye movements Pupillary abnormalities Vomiting, hiccough (medulla)

cerebellum - see cerebellar

-dysfunction, pages 176-179 Ataxic gait Intention tremor Dysmetria Dysarthria Nystagmus n.b. Intrinsic brain stem tumours in contrast to extrinsic tumours are more likely to produce long tract (motor and sensory) signs early in the course of the disease.

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