Intracranial Mass Lesions and Raised Intracranial Pressure Flashcards
What is a subdural haematoma?
Caused by bleeding from damaged bridging veins between cortex and venous sinuses.
Initial injury may be minor and often forgotten.
Most commonly secondary to trauma (e.g. old person/ alcoholic falling over).
What is the presentation of a subdural hematoma?
Headache
Classically conscious level fluctuates
Raised ICP
(Combination of falls, alcohol history, fluctuating episodes of consciousness and focal neurology = subdural haemorrhage. Always look out for “fluctuating consciousness in the question)
How is subdural haematoma treated?
Needs neurosurgical review.
Burr hole
What is an extradural haematoma?
Bleeding into the space between the dura mater and the skull.
Often caused by damage to the middle meningeal artery.
Often caused by acceleration-deceleration trauma or blow to the side of the head.
What are the clinical features of an extradural hematoma?
Features of raised ICP
Some patients exhibit lucid interval followed by rapid decrease in GCS
How can extradural and subdural haematomas be distinguished radiologically?
Extradural haematomas are limited by suture lines but not by venous sinuses
What are the causes of a subarachnoid haemorrhage?
85% are caused by a ruptured berry aneurysm.
Other causes include:
- AV malformations
- Trauma
- Tumours
What conditions are associated with berry aneurysms?
Adult polycystic kidney disease
Ehlers-Danlos syndrome
Coarctation of the aorta
How does an SAH present?
Abrupt onset of “first and worst” occipital headache.
Evidence of meningism
How is a suspected SAH investigated?
CT scan is first line, but is negative in 5% of patients (sensitivity of CT decreases with time).
LP is done after 12 hours (allowing time for xanthochromia to develop).
If CSF examination does not reveal any Hb breakdown products, but there remains high clinical suspicion then cerebral angiography is the next step.
What are the complications of SAH?
Rebleeding (30%)
Obstructive hydrocephalus
Vasospasm leading to cerebral ischaemia
ECG changes - typically deep symmetrical T wave inversion and prolonged QTc
How is SAH managed?
Neurosurgical opinion: no clear evidence over early surgical intervention against delayed intervention
Nimodipine (60mg/4h if BP allows) decreases the severity of the neurological deficit but does NOT influence risk of rebleeding (nimodipine was thought to decrease arterial vasospasm but recent studies suggest this is not the case)
What are intracranial venous sinus thromboses?
Clot in the dural venous sinuses.
Can cause cerebral infarction, much less common cf. arterial causes.
50% of patients have an isolated sagittal sinus thrombosis - the remainder have co-existant lateral sinus thromboses and cavernous sinus thromboses
What are the features of a dural venous sinus thrombosis?
Headache (may be sudden onset, thunderclap)
Nausea and vomiting
Papilloedema
Exact features depend on the sinus affected - e.g. lateral sinus thrombosis caused 6th and 7th nerve palsies
What are the features of a sagittal sinus thrombosis?
May present with seizures and hemiplegia
Parasagittal, biparietal or bifrontal haemorrhagic infarctions are sometimes seen
What are the features of a cavernous sinus thrombosis?
Usually multiple cranial nerve palsies - 3rd, 4th, and 6th nerve damage
Trigeminal involvement may lead to hyperaesthesia of upper face and eye pain
Central retinal veing thrombosis
Swollen eyelids
Other causes of cavernous sinus syndrome: local infection (e.g. sinusitis), neoplasia and trauma
What is idiopathic intracranial hypertension?
aka Pseudotumour cerebri
Condition classically seen in obese young women - obese young women with blurred vision and headaches think IIH!
What are the features of IIH?
Headache Blurred vision Papilloedema (usually present) Enlarged blind spot 6th nerve palsy may be present
What are the risk factors for IIH?
Obesity
Female sex
Pregnancy
Drugs (in this case it is NOT idiopathic): COC, steroids, tetracyclines, vitamin A
How is suspected IIH investigated and managed?
Ix:
1) CT scan
2) LP to measure opening pressure
3) Cerebral MRI with MR venography (to rule out dural venous sinus thrombosis)
Mx: Weight loss Drugs, e.g. acetazolamide Corticosteroids can be given Repeated LP Surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to decrease ICP
What is Von Hippel Lindau (VHL) disease?
Autosomal dominant condition predisposing to neoplasia. It is caused by an abnormality in the VHL gene on chromosome 3 (VHL has “3” letters).
Retinal and cerebellar haemangiomas are a key feature of VHL. Retinal haemangiomas are bilateral in 25% and can lead to vitreous haemorrhage.
What are the features of VHL?
Cerebellar haemangiomas (can secrete EPO that causes secondary polycythaemia)
Retinal haemangiomas: vitreous haemorrhage
Renal cysts (premalignant)
Phaeochromocytoma
Extra-renal cysts: epididymal, pancreatic, hepatic
Endolymphatic sac tumours
What is tuberous sclerosis?
Autosomal dominant condition and one of the phakomatoses (has neuro-cutaneous features).
These are best remembered using the adage - “Cigarettes and coffee with a rough stupid person with a butterfly on his nose whilst he is dancing”
- cigarettes (ash) - coffee (cafe-au-lait) - stupid (intellectual and developmental) - dancing (epilepsy)
What are the cutaneous features of tuberous sclerosis?
Depigmented ash leaf macules which fluoresce under Wood lamps
Roughened patches of skin over lumbar spine (Shagreen patches)
Adenoma sebaceum: butterfly distribution over nose
Fibromata beneath nails (subungal fibroma)
Cafe au lait spots may be seen
What are the neurological features of tuberous sclerosis?
Developmental delay
Epilepsy (infantile spasms or partial)
Intellectual impairment
What are some associations with tuberous sclerosis?
Retinal hamartomas: dense white area on retina (phakomata)
Rhabdomyomas of the heart
Gliomatous changes can occur in the brain later
Polycystic kidneys, renal angiomyolipomata
