Aneurysms relatively rarely produce symptoms without first rupturing. This may because they have grown very large, sufficent to act as a mass in the brain producing headaches as would a brain tumour. Alternatively pulsation in the dome of the aneurysm may act upon adjacent structures producing symptoms. Some typical examples are described below.
Occasionally an aneurysm will present by irritating one of the nerves that control movements of the eye. Irritation of one particular nerve - the oculomotor nerve- generates particular concern that an aneurysm of the internal carotid artery is enlarging and at-risk of rupture.
The oculomotor nerve may be affected in isolation by superior cerebellar artery and baasilar trunk aneurysms as well. If the oculomotor nerve is affected in concert with the other nerves controlling the globe of the eye- the trochlear and abducens nerves- then the aneurysm is most likely to be located in the skull base (see below under Cavernous Sinus Syndromes.)
The oculomotor nerve also contains fibres that constrict the pupil. In most cases where an aneurysm is pressing on the nerve these fibres malfunction and the pupil enlarges. In general it will be accomapnied by pain behind the affected eye. The aneurysm has not ruptured but it is believed these symptoms reflect a sudden change in its morphology and portend rupture. It requires distinction from similar clinical syndromes produced by mini-strokes affecting the brainstem.
A painful oculomotor nerve palsy is considered a neurosurgical emergency. The prognosis for recovery of the nerve depends on how on how complete the injury is before treatment. The aneurysm may be made secure by surgical clipping or endovascular treatment.
Other conflicts with cranial nerves are rare but are known to occur e.g.: visual loss as a result of compression of the optic nerve and facial pain resulting from trigeminal nerve compression.
Approximately 10% of unruptured aneurysms are discovered when after an episode of cerebral ischaemia, a stroke having occurred or after a transient ischaemic attack (TIA). By definition in the latter any neurological deficit will have recovered within twenty-four hours.
Rarely the unruptured aneurysm is located proximal to the area affected by stroke and implicated by the presence of thrombus within its walls. Theoretically such thrombus may bbe propagated distally in the vessel causing neurological symptoms. Medication to prevent the aggregation of platelets in blood is considered in such circumstances and the best know of such medicines is aspirin. There is naturally reservation that the administration of a drug that effectively reduces blood's ability to clot might be dangerous in the presence of an aneurysm. In fact there is no compelling evidence that aspirin increases the risk that an aneurysm would bleed. In fact there is some evidence that patients on aspirin are less likely to form aneurysms which subsequently rupture. Were an aneurysm to rupture however it is possible that the effect of aspirin could compound the injury done by bleeding.
The development of blood clot within an aneurysm may be ominous. It may form part of a process that enlarges the aneurysm over time. Chemicals originating in the blood clot are theorised to have an inflammatory effect on the wall of the aneurysm potentially weakening it. Thrombosis is a relatively common finding in giant (>25mm) aneurysms, being found in approximately 50%. Thrombosis within the aneurysm dome will sometimes trigger swelling the brain around the aneurysm resulting in headache, seizures or focal neurological symptoms. A similar reaction is occasionally seen after otherwise successful treatment of aneurysms with flow-diverting stents designed to promote thrombosis.
The development of symptoms that might point to thrombosis of a known aneurysm include, but are not limited to:
The cavernous sinuses are bony enclosures in the base of the skull that transmit the internal carotid arteries as they enter the cranial cavity to supplu blood to he brain. They also contain trabeculated venous spaces that communicate the veins of the brain with the veins of the head and neck. In their walls intimately assosciated with the arteries run the oculomotor, abducent, trochlear and trigeminal which control the movement of the eyes and sensation from the face.
Aneurysms may develp on the internal carotid artery within the cavernous sinus. They are usually at low risk of causing subarachnoid haemorrhage when confined within the sinus. Occasionally they may expand or thrombose triggering facial pain,and double vision. This type of pain, altered sensation in the face, constriction of the pupil and double vision is termed cavernous syndrome.
Rupture of a cavernous aneurysm is a rare cause of direct carotid-cavernous fistula creating an abnomrsal communication between the artery and the veins of the orbit and face. Other causes of such direct fistulas include trauma and as a complication of surgery. An indirect carotico-cavernous fistula develops when abnormal channels develop between the external (to a lesser extent) the internal carotid circulation and the venous spaces in the cavernous sinus. This probably occurs in response to venous thrombosis in the region.
Intractable pain or deterioration of vision are indications for treatment. Sometimes symptoms will subside as the swelling around the thrombosis settles down.