Many patients with unruptured IIA may have no symptoms. In patients who do have symptoms these are often related to rupture of the aneurysm and to its cause. Rupture of an IIA results in subarachnoid hemorrhage, symptoms of which include headache, dizziness, seizures, altered mental status and focal neurological deficits.

In contrast to other cerebral aneurysms, large aneurysm size does not increase the chance of rupture. Small IIAs

tend to have high rupture rates, while larger IIAs more commonly cause symptoms due to pressure on the surrounding brain tissue.

An infectious intracranial aneurysm (IIA, also called mycotic aneurysm) is a cerebral aneurysm that is caused by infection of the cerebral arterial wall.

Abdominal aneurysms are usually asymptomatic, but rarely can cause lower back pain or lower limb ischemia

If an aneurysm ruptures, blood leaks into the space around the brain. This is called a subarachnoid hemorrhage. Onset is usually sudden without prodrome, classically presenting as a "thunderclap headache" worse than previous headaches. Symptoms of a subarachnoid hemorrhage differ depending on the site and size of the aneurysm. Symptoms of a ruptured aneurysm can include:

- a sudden severe headache that can last from several hours to days

- nausea and vomiting

- drowsiness, confusion and/or loss of consciousness

- visual abnormalities

- meningism

Almost all aneurysms rupture at their apex. This leads to hemorrhage in the subarachnoid space and sometimes in brain parenchyma. Minor leakage from aneurysm may precede rupture, causing warning headaches. About 60% of patients die immediately after rupture. Larger aneurysms have a greater tendency to rupture, though most ruptured aneurysms are less than 10 mm in diameter.

The risk of a subarachnoid hemorrhage is greater with a saccular aneurysm than a fusiform aneurysm.

A small, unchanging aneurysm will produce few, if any, symptoms. Before a larger aneurysm ruptures, the individual may experience such symptoms as a sudden and unusually severe headache, nausea, vision impairment, vomiting, and loss of consciousness, or the individual may experience no symptoms at all.

Symptoms can occur when the aneurysm pushes on a structure in the brain. Symptoms will depend on whether an aneurysm has ruptured or not. There may be no symptoms present at all until the aneurysm ruptures. For an aneurysm that has not ruptured the following symptoms can occur:

- Fatigue

- Loss of perception

- Loss of balance

- Speech problems

- Double vision

For a ruptured aneurysm, symptoms of a subarachnoid hemorrhage may present:

- Severe headaches

- Loss of vision

- Double vision

- Neck pain or stiffness

- Pain above or behind the eyes

Head pain occurs in 50–75% of all cases of vertebral artery dissection. It tends to be located at the back of the head, either on the affected side or in the middle, and develops gradually. It is either dull or pressure-like in character or throbbing. About half of those with VAD consider the headache distinct, while the remainder have had a similar headache before. It is suspected that VAD with headache as the only symptom is fairly common; 8% of all cases of vertebral and carotid dissection are diagnosed on the basis of pain alone.

Obstruction of blood flow through the affected vessel may lead to dysfunction of part of the brain supplied by the artery. This happens in 77–96% of cases. This may be temporary ("transient ischemic attack") in 10–16% of cases, but many (67–85% of cases) end up with a permanent deficit or a stroke. The vertebral artery supplies the part of the brain that lies in the posterior fossa of the skull, and this type of stroke is therefore called a posterior circulation infarct. Problems may include difficulty speaking or swallowing (lateral medullary syndrome); this occurs in less than a fifth of cases and occurs due to dysfunction of the brainstem. Others may experience unsteadiness or lack of coordination due to involvement of the cerebellum, and still others may develop visual loss (on one side of the visual field) due to involvement of the visual cortex in the occipital lobe. In the event of involvement of the sympathetic tracts in the brainstem, a partial Horner's syndrome may develop; this is the combination of a drooping eyelid, constricted pupil, and an apparently sunken eye on one side of the face.

If the dissection of the artery extends to the part of the artery that lies inside the skull, subarachnoid hemorrhage may occur (1% of cases). This arises due to rupture of the artery and accumulation of blood in the subarachnoid space. It may be characterized by a different, usually severe headache; it may also cause a range of additional neurological symptoms.

13–16% of all people with vertebral or carotid dissection have dissection in another cervical artery. It is therefore possible for the symptoms to occur on both sides, or for symptoms of carotid artery dissection to occur at the same time as those of vertebral artery dissection. Some give a figure of multiple vessel dissection as high as 30%.

If a Charcot–Bouchard aneurysm ruptures, it will lead to an intracerebral hemorrhage, which can cause hemorrhagic stroke, typically experienced as a sudden focal paralysis or loss of sensation.

Inflammatory Aortic Aneurysms occur typically in a younger population compared to the typical Abdominal Aortic Aneurysm group. Risk of rupture for the IAA group, due to thinning of anuerysm walls, are also rare due to inflammation and fibrosis

Unruptured inflammatory AAAs are usually symptomatic:

- abdominal or back pain (70 to 80%)

- abdominal tenderness

- fever

- weight loss

- elevated erythrocyte sedimentation rate (90%)

An infected aneurysm (also known as mycotic aneurysm or microbial arteritis) is an aneurysm arising from bacterial infection of the arterial wall. It can be a common complication of the hematogenous spread of bacterial infection.

William Osler first used the term "mycotic aneurysm" in 1885 to describe a mushroom-shaped aneurysm in a patient with subacute bacterial endocarditis. This may create considerable confusion, since "mycotic" is typically used to define fungal infections. However, mycotic aneurysm is still used for all extracardiac or intracardiac aneurysms caused by infections, except for syphilitic aortitis.

The term "infected aneurysm," proposed by Jarrett and associates is more appropriate, since few infections involve fungi. According to some authors, a more accurate term might have been endovascular infection or infective vasculitis, because mycotic aneurysms are not due to a fungal organism.

Mycotic aneurysms account for 2.6% of aortic aneurysms. For the clinician, early diagnosis is the cornerstone of effective treatment. Without medical or surgical management, catastrophic hemorrhage or uncontrolled sepsis may occur. However, symptomatology is frequently nonspecific during the early stages, so a high index of suspicion is required to make the diagnosis.

Intracranial mycotic aneurysms (ICMAs) complicate about 2% to 3% of infective endocarditis (IE) cases, although as many as 15% to 29% of patients with IE have neurologic symptoms.

Charcot–Bouchard aneurysms (also known as miliary aneurysms or microaneurysms) are aneurysms of the brain vasculature which occur in small blood vessels (less than 300 micrometre diameter). Charcot–Bouchard aneurysms are most often located in the lenticulostriate vessels of the basal ganglia and are associated with chronic hypertension. Charcot–Bouchard aneurysms are a common cause of cerebral hemorrhage.

Vertebral artery dissection is one of the two types of dissection of the arteries in the neck. The other type, carotid artery dissection, involves the carotid arteries. Vertebral artery dissection is further classified as being either traumatic (caused by mechanical trauma to the neck) or spontaneous, and it may also be classified by the part of the artery involved: extracranial (the part outside the skull) and intracranial (the part inside the skull).

Subdural hematomas are divided into acute, subacute, and chronic, depending on the speed of their onset. Acute subdural hematomas that are due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression.

Acute bleeds often develop after high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas. They are most severe if associated with cerebral contusions. Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the typically arterial bleeding of an epidural hemorrhage. Acute subdural bleeds have a high mortality rate, higher even than epidural hematomas and diffuse brain injuries, because the force (acceleration/deceleration) required to cause them causes other severe injuries as well. The mortality rate associated with acute subdural hematoma is around 60 to 80%.

Chronic subdural bleeds develop over a period of days to weeks, often after minor head trauma, though such a cause is not identifiable in 50% of patients. They may not be discovered until they present clinically months or years after a head injury. The bleeding from a chronic bleed is slow, probably from repeated minor bleeds, and usually stops by itself. Since these bleeds progress slowly, they present the chance of being stopped before they cause significant damage. Small chronic subdural hematomas, those less than a centimeter wide, have much better outcomes than acute subdural bleeds: in one study, only 22% of patients with chronic subdural bleeds had outcomes worse than "good" or "complete recovery". Chronic subdural hematomas are common in the elderly.

Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately but can be delayed as much as 2 weeks. If the bleeds are large enough to put pressure on the brain, signs of increased ICP (intracranial pressure) or damage to part of the brain will be present.

Other signs and symptoms of subdural hematoma can include any combination of the following:

- A history of recent head injury

- Loss of consciousness or fluctuating levels of consciousness

- Irritability

- Seizures

- Pain

- Numbness

- Headache (either constant or fluctuating)

- Dizziness

- Disorientation

- Amnesia

- Weakness or lethargy

- Nausea or vomiting

- Loss of appetite

- Personality changes

- Inability to speak or slurred speech

- Ataxia, or difficulty walking

- Loss of muscle control

- Altered breathing patterns

- Hearing loss or hearing ringing (tinnitus)

- Blurred Vision

- Deviated gaze, or abnormal movement of the eyes.

The classic symptom of subarachnoid hemorrhage is thunderclap headache (a headache described as "like being kicked in the head", or the "worst ever", developing over seconds to minutes). This headache often pulsates towards the occiput (the back of the head). About one-third of people have no symptoms apart from the characteristic headache, and about one in ten people who seek medical care with this symptom are later diagnosed with a subarachnoid hemorrhage. Vomiting may be present, and 1 in 14 have seizures. Confusion, decreased level of consciousness or coma may be present, as may neck stiffness and other signs of meningism.

Neck stiffness usually presents six hours after initial onset of SAH. Isolated dilation of a pupil and loss of the pupillary light reflex may reflect brain herniation as a result of rising intracranial pressure (pressure inside the skull). Intraocular hemorrhage (bleeding into the eyeball) may occur in response to the raised pressure: subhyaloid hemorrhage (bleeding under the hyaloid membrane, which envelops the vitreous body of the eye) and vitreous hemorrhage may be visible on fundoscopy. This is known as Terson syndrome (occurring in 3–13 percent of cases) and is more common in more severe SAH.

Oculomotor nerve abnormalities (affected eye looking downward and outward and inability to lift the eyelid on the same side) or (loss of movement) may indicate bleeding from the posterior communicating artery. Seizures are more common if the hemorrhage is from an aneurysm; it is otherwise difficult to predict the site and origin of the hemorrhage from the symptoms. SAH in a person known to have seizures is often diagnostic of a cerebral arteriovenous malformation.

The combination of intracerebral hemorrhage and raised intracranial pressure (if present) leads to a "sympathetic surge", i.e. over-activation of the sympathetic system. This is thought to occur through two mechanisms, a direct effect on the medulla that leads to activation of the descending sympathetic nervous system and a local release of inflammatory mediators that circulate to the peripheral circulation where they activate the sympathetic system. As a consequence of the sympathetic surge there is a sudden increase in blood pressure; mediated by increased contractility of the ventricle and increased vasoconstriction leading to increased systemic vascular resistance. The consequences of this sympathetic surge can be sudden, severe, and are frequently life-threatening. The high plasma concentrations of adrenaline also may cause cardiac arrhythmias (irregularities in the heart rate and rhythm), electrocardiographic changes (in 27 percent of cases) and cardiac arrest (in 3 percent of cases) may occur rapidly after the onset of hemorrhage. A further consequence of this process is neurogenic pulmonary edema where a process of increased pressure within the pulmonary circulation causes leaking of fluid from the pulmonary capillaries into the air spaces, the alveoli, of the lung.

Subarachnoid hemorrhage may also occur in people who have had a head injury. Symptoms may include headache, decreased level of consciousness and hemiparesis (weakness of one side of the body). SAH is a frequent occurrence in traumatic brain injury, and carries a poor prognosis if it is associated with deterioration in the level of consciousness.

While thunderclap headache is the characteristic symptom of subarachnoid hemorrhage, less than 10% of those with concerning symptoms have SAH on investigations. A number of other causes may need to be considered.

The clinical presentation of CST can be varied. Both acute, fulminant disease and indolent, subacute presentations have been reported in the literature.

The most common signs of CST are related to anatomical structures affected within the cavernous sinus, notably cranial nerves III-VI, as well as symptoms resulting from impaired venous drainage from the orbit and eye.

Classic presentations are abrupt onset of unilateral periorbital edema, headache, photophobia, and bulging of the eye (proptosis).

Other common signs and symptoms include:

Ptosis, chemosis, cranial nerve palsies (III, IV, V, VI). Sixth nerve palsy is the most common. Sensory deficits of the ophthalmic and maxillary branch of the fifth nerve are common. Periorbital sensory loss and impaired corneal reflex may be noted. Papilledema, retinal hemorrhages, and decreased visual acuity and blindness may occur from venous congestion within the retina. Fever, tachycardia and sepsis may be present. Headache with nuchal rigidity may occur. Pupil may be dilated and sluggishly reactive. Infection can spread to contralateral cavernous sinus within 24–48 hours of initial presentation.

Inflammatory aortic aneurysm (IAA), also known as Inflammatory abdominal aortic aneurysm (IAAA), is a type of abdominal aortic aneurysm (AAA) where the walls of the aneurysm become thick and inflamed. Similar to AAA, IAA occurs in the abdominal region. IAA is closely associated and believed to be a response to and extensive peri-anuerysmal fibrosis, which is the formation of excess fibrous connective tissue in an organ or tissue in a reparative or reactive process IAA accounts for 5-10% of aortic aneurysms. IAA is occurs mainly in a population that is on average younger by 10 years than most AAA patients. Some common symptoms of IAA may include back pain, abdominal tenderness, fevers, weight loss or elevated Erythrocyte sedimentation rate (ESR) levels. Corticosteroids and other immunosuppressive drugs have been found to decrease symptoms and the degree of peri-aortic inflammation and fibrosis

Intracranial hemorrhage (ICH), also known as intracranial bleed, is bleeding within the skull. It includes intracerebral bleeds (intraventricular bleeds and intraparenchymal bleeds), subarachnoid bleeds, epidural bleeds, and subdural bleeds.

Intracerebral bleeding affects 2.5 per 10,000 people each year.

Fever, headache, and neurological problems, while classic, only occur in 20% of people with brain abscess.

The famous triad of fever, headache and focal neurologic findings are highly suggestive of brain abscess. These symptoms are caused by a combination of increased intracranial pressure due to a space-occupying lesion (headache, vomiting, confusion, coma), infection (fever, fatigue etc.) and focal neurologic brain tissue damage (hemiparesis, aphasia etc.).

The most frequent presenting symptoms are headache, drowsiness, confusion, seizures, hemiparesis or speech difficulties together with fever with a rapidly progressive course. Headache is characteristically worse at night and in the morning, as the intracranial pressure naturally increases when in the supine position. This elevation similarly stimulates the medullary vomiting center and area postrema, leading to morning vomiting.

Other symptoms and findings depend largely on the specific location of the abscess in the brain. An abscess in the cerebellum, for instance, may cause additional complaints as a result of brain stem compression and hydrocephalus. Neurological examination may reveal a stiff neck in occasional cases (erroneously suggesting meningitis).

Patients with intraparenchymal bleeds have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed. Other symptoms include those that indicate a rise in intracranial pressure caused by a large mass putting pressure on the brain.

Intracerebral hemorrhages are often misdiagnosed as subarachnoid hemorrhages due to the similarity in symptoms and signs. A severe headache followed by vomiting is one of the more common symptoms of intracerebral hemorrhage. Another common symptom is a patient can collapse. Some people may experience continuous bleeding from the ear. Some patients may also go into a coma before the bleed is noticed.

Rasmussen's aneurysm is a pulmonary artery aneurysm adjacent or within a tuberculous cavity. It occurs in up to 5% of patients with such lesions. It may lead to rupture and haemorrhage. It is named after Fritz Valdemar Rasmussen. It is quoted as the cause of hemoptysis in tuberculosis patients.

While the "classic" terminology relates the lesion to cavitary tuberculosis, the term is now used for the anatomic aneurysm associated with other destructive lung lesions. Even when the pulmonary aneurysm is present, the actual bronchial bleeding may be from the bronchial artery, rather than from the pulmonary artery.

Cavernous sinus thrombosis (CST) is the formation of a blood clot within the cavernous sinus, a cavity at the base of the brain which drains deoxygenated blood from the brain back to the heart. The cause is usually from a spreading infection in the nose, sinuses, ears, or teeth. "Staphylococcus aureus" and "Streptococcus" are often the associated bacteria. Cavernous sinus thrombosis symptoms include: decrease or loss of vision, chemosis, exophthalmos (bulging eyes), headaches, and paralysis of the cranial nerves which course through the cavernous sinus. This infection is life-threatening and requires immediate treatment, which usually includes antibiotics and sometimes surgical drainage.

A cirsoid aneurysm is the dilation of a group of blood vessels due to congenital malformations with AV (arterio venous) shunting. Cirsoid means resembling a varix.

Sometimes, a minor traumatic episode, such as a fall or bump on the head, can lead to the formation of a cirsoid aneurysm. Often these are trivial traumatic episodes

Cirsoid aneurysm, in general, is a hemangioma of an artery. It most commonly occurs over the head, usually the superficial temporal artery and also its branches. It can also occur in places where medium vessels lie over bones without much intervening tissues between them and the skin.

The superficial temporal artery is the most commonly involved artery.

Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space — the area between the arachnoid membrane and the pia mater surrounding the brain. Symptoms may include a severe headache of rapid onset, vomiting, decreased level of consciousness, fever, and sometimes seizures. Neck stiffness or neck pain are also relatively common. In about a quarter of people a small bleed with resolving symptoms occurs within a month of a larger bleed.

SAH may occur as a result of a head injury or spontaneously, usually from a ruptured cerebral aneurysm. Risk factors for spontaneous cases included high blood pressure, smoking, family history, alcoholism, and cocaine use. Generally, the diagnosis can be determined by a CT scan of the head if done within six hours. Occasionally a lumbar puncture is also required. After confirmation further tests are usually performed to determine the underlying cause.

Treatment is by prompt neurosurgery or radiologically guided interventions. Medications such as labetalol may be required to lower the blood pressure until repair can occur. Efforts to treat fevers are also recommended. Nimodipine, a calcium channel blocker, is frequently used to prevent vasospasm. Routine use medications to prevent further seizures is of unclear benefit. Nearly half of people with a SAH due to an underlying aneurysm die within 30 days and about a third who survive have ongoing problems. 10–15 percent die before reaching a hospital.

Spontaneous SAH occurs in about one per 10,000 people per year. Females are more commonly affected than males. While it becomes more common with age, about 50% of people present under 55 years old. It is a form of stroke and comprises about 5 percent of all strokes. Surgery for aneurysms was introduced in the 1930s. Since the 1990s many aneurysms are treated by a less invasive procedure called "coiling", which is carried out through a large blood vessel.

Clinical manifestations of intraparenchymal hemorrhage are determined by the size and location of hemorrhage, but may include the following:

- Hypertension, fever, or cardiac arrhythmias

- Nuchal rigidity

- Subhyaloid retinal hemorrhages

- Altered level of consciousness

- Anisocoria, Nystagmus

- Focal neurological deficits

- Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopsia, aphasia, neglect, or apraxia

- Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion

- Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia

- Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion

- Brain stem - Tetraparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability

- Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness