History and exam

Key diagnostic factors

common

Risk factors for gliomas include male sex; white ancestry; history of neurofibromatosis type 1, tuberous sclerosis, Li-Fraumeni syndrome, or Turcot's cancer syndrome; or history of exposure to ionising radiation.

Other diagnostic factors

common

Reported to occur in approximately 50% of patients presenting in the emergency department with a brain tumour.[25][31]

Reported to occur in approximately 60% of patients with brain tumours.[32][33]

Unilateral headache indicates the side of the lesion in approximately 80%.

Tends to be worse with coughing, with the Valsalva manoeuvre, or when the patient is supine.[20]

Reported to occur in approximately 50% of patients presenting in the emergency department with a brain tumour.[31]

Reported to occur in approximately 41% of patients presenting in the emergency department with a brain tumour.[31]

Reported to occur in approximately 37% of patients presenting in the emergency department with a brain tumour.[31]

Associated with cerebellar lesions.

Reported to occur in approximately 27% of patients presenting in the emergency department with a brain tumour.[31]

Associated with lesion in contralateral posterior frontal lobe or anywhere in the descending corticospinal tract.

Frequency ranges from 80% in patients with low-grade disease to 29% in patients with grade 4 astrocytoma.[25]

Associated with lesion in close relation to cerebral cortex. The type of seizure depends on the location of the tumour.

Reported to occur in approximately 23% of patients presenting in the emergency department with a brain tumour.[31]

May present as diplopia (cranial nerve palsy), visual field cut (cortical lesion in temporal, parietal, or occipital lobe), or loss of acuity (lesion in optic-hypothalamic region).

Reported to occur in approximately 21% of patients presenting in the emergency department with a brain tumour.[31]

Associated with lesion in dominant posterior temporal lobe or antero-lateral frontal lobe.

Reported to occur in approximately 12% of patients presenting in the emergency department with a brain tumour.[31]

Found in 37% to 58% of patients with left-sided tumours.[34]

Associated with lesion in dominant posterior temporal lobe or antero-lateral frontal lobe.

Reported to occur in approximately 19% of patients presenting in the emergency department with a brain tumour.[31]

Associated with lesion in contralateral anterior parietal lobe or ascending sensory pathway.

Reported to occur in approximately 37% of patients presenting in the emergency department with a brain tumour.[31]

Associated with lesion in contralateral posterior frontal lobe or anywhere in the descending corticospinal tract.

Reported to occur in approximately 20% of patients presenting in the emergency department with a brain tumour.[31]

May present as diplopia (cranial nerve palsy), visual field cut (cortical lesion in temporal, parietal, or occipital lobe), or loss of acuity (lesion in optic-hypothalamic region).

Reported to occur in approximately 26% of patients presenting in the emergency department with a brain tumour.[31]

Sixth (VI) nerve palsy as a consequence of intracranial hypertension or direct invasion of third (III), fourth (IV), or sixth (VI) cranial nerve nucleus by brainstem lesion.

Reported to occur in approximately 28% of patients presenting in the emergency department with a brain tumour.[31]

More common in patients with a posterior fossa tumour.

uncommon

Personality change has been reported in 16% to 34% of patients, and is associated with large and/or bilateral frontal lobe astrocytomas.[32]

Emotional lability is associated with large frontal lobe lesions.

Risk factors

weak

In the US, gliomas are more common in white people than in people of any other racial group.[3][4]

Glioma occurs more commonly in males than in females; glioblastoma incidence rate is 1.6-fold higher in men than in women.[3][4]

Approximately 15% of children with neurofibromatosis type 1 develop optic nerve pilocytic gliomas.[5] These tumours are usually diagnosed during childhood and rarely progress after diagnosis.[12]

Approximately 10% to 20% of people with tuberous sclerosis complex develop subependymal giant cell astrocytoma (thought to be unique to this syndrome).[13]

Associated with diffuse astrocytoma and glioblastoma.[14]

Associated with increased risk of developing glioblastoma. Relative risk of primary brain tumour is increased by a factor of 7.[15]

Associated with malignant glioma. The mechanism is related to radiation-induced DNA strand breaks and mutation.[9] Patients with a history of therapeutic radiation to the head are at increased risk of developing a glioblastoma later in life.[10][11]

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