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

In younger patients, vascular malformations, specifically AVMs and cavernous angiomas are more common causes for hemorrhage. In addition, venous malformations are associated with hemorrhage.

In the elderly population, amyloid angiopathy is associated with cerebral infarcts as well as hemorrhage in superficial locations, rather than deep white matter or basal ganglia. These are usually described as "lobar". These bleedings are not associated with systemic amyloidosis.

Hemorrhagic neoplasms are more complex, heterogeneous bleeds often with associated edema. These hemorrhages are related to tumor necrosis, vascular invasion and neovascularity. Glioblastomas are the most common primary malignancies to hemorrhage while thyroid, renal cell carcinoma, melanoma, and lung cancer are the most common causes of hemorrhage from metastatic disease.

Other causes of intraparenchymal hemorrhage include hemorrhagic transformation of infarction which is usually in a classic vascular distribution and is seen in approximately 24 to 48 hours following the ischemic event. This hemorrhage rarely extends into the ventricular system.

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.

The most common presentation of cerebrovascular diseases is an acute stroke, which occurs when blood supply to the brain is compromised. Symptoms of stroke are usually rapid in onset, and may include weakness of one side of the face or body, numbness on one side of the face or body, inability to produce or understand speech, vision changes, and balance difficulties. Hemorrhagic strokes can present with a very severe, sudden headache associated with vomiting, neck stiffness, and decreased consciousness. Symptoms vary depending on the location and the size of the area of involvement of the stroke. Edema, or swelling, of the brain may occur which increases intracranial pressure and may result in brain herniation. A stroke may result in coma or death if it involves key areas of the brain.

Other symptoms of cerebrovascular disease include migraines, seizures, epilepsy, or cognitive decline. However, cerebrovascular disease may go undetected for years until an acute stroke occurs. In addition, patients with some rare congenital cerebrovascular diseases may begin to have these symptoms in childhood.

Certain changes in morphology are associated with cerebral edema: the brain becomes soft and smooth and overfills the cranial vault, gyri (ridges) become flattened, sulci (grooves) become narrowed, and ventricular cavities become compressed.

Symptoms include nausea, vomiting, blurred vision, faintness, and in severe cases, seizures and coma. If brain herniation occurs, respiratory symptoms or respiratory arrest can also occur due to compression of the respiratory centers in the pons and medulla oblongata.

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.

Intracerebral hemorrhage (ICH), also known as cerebral bleed, is a type of intracranial bleed that occurs within the brain tissue or ventricles. Symptoms can include headache, one-sided weakness, vomiting, seizures, decreased level of consciousness, and neck stiffness. Often symptoms get worse over time. Fever is also common. In many cases bleeding is present in both the brain tissue and the ventricles.

Causes include brain trauma, aneurysms, arteriovenous malformations, and brain tumors. The largest risk factors for spontaneous bleeding are high blood pressure and amyloidosis. Other risk factors include alcoholism, low cholesterol, blood thinners, and cocaine use. Diagnosis is typically by CT scan. Other conditions that may present similarly include ischemic stroke.

Treatment should typically be carried out in an intensive care unit. Guidelines recommended decreasing the blood pressure to a systolic of less than 140 mmHg. Blood thinners should be reversed if possible and blood sugar kept in the normal range. Surgery to place a ventricular drain may be used to treat hydrocephalus but corticosteroids should not be used. Surgery to remove the blood is useful in certain cases.

Cerebral bleeding affects about 2.5 per 10,000 people each year. It occurs more often in males and older people. About 44% of those affected die within a month. A good outcome occurs in about 20% of those affected. Strokes were first divided into their two major types, bleeding and insufficient blood flow, in 1823.

Cerebrovascular disease includes a variety of medical conditions that affect the blood vessels of the brain and the cerebral circulation. Arteries supplying oxygen and nutrients to the brain are often damaged or deformed in these disorders. The most common presentation of cerebrovascular disease is an ischemic stroke or mini-stroke and sometimes a hemorrhagic stroke. Hypertension (high blood pressure) is the most important contributing risk factor for stroke and cerebrovascular diseases as it can change the structure of blood vessels and result in atherosclerosis. Atherosclerosis narrows blood vessels in the brain, resulting in decreased cerebral perfusion. Other risk factors that contribute to stroke include smoking and diabetes. Narrowed cerebral arteries can lead to ischemic stroke, but continually elevated blood pressure can also cause tearing of vessels, leading to a hemorrhagic stroke.

A stroke usually presents with an abrupt onset of a neurologic deficit - such as hemiplegia (one-sided weakness), numbness, aphasia (language impairment), or ataxia (loss of coordination) - attributable to a focal vascular lesion. The neurologic symptoms manifest within seconds because neurons need a continual supply of nutrients, including glucose and oxygen, that are provided by the blood. Therefore if blood supply to the brain is impeded, injury and energy failure is rapid.

Besides hypertension, there are also many less common causes of cerebrovascular disease, including those that are congenital or idiopathic and include CADASIL, aneurysms, amyloid angiopathy, arteriovenous malformations, fistulas, and arterial dissections. Many of these diseases can be asymptomatic until an acute event, such as a stroke, occurs. Cerebrovascular diseases can also present less commonly with headache or seizures. Any of these diseases can result in vascular dementia due to ischemic damage to the brain.

Cerebral edema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain.

Stroke presentations which are particularly suggestive of a watershed stroke include bilateral visual loss, stupor, and weakness of the proximal limbs, sparing the face, hands and feet.

Nine in ten people with sinus thrombosis have a headache; this tends to worsen over the period of several days, but may also develop suddenly (thunderclap headache). The headache may be the only symptom of cerebral venous sinus thrombosis. Many patients have symptoms of stroke: inability to move one or more limbs, weakness on one side of the face or difficulty speaking. This does not necessarily affect one side of the body as in the more common "arterial" stroke.

40% of people have seizures, although it is more common in women who develop sinus thrombosis peripartum (in the period before and after giving birth). These are mostly seizures affecting only one part of the body and unilateral (occurring on one side), but occasionally the seizures are generalised and rarely they lead to status epilepticus (persistent or recurrent seizure activity for a long period of time).

In the elderly, many of the aforementioned symptoms may not occur. Common symptoms in the elderly with this condition are otherwise unexplained changes in mental status and a depressed level of consciousness.

The pressure around the brain may rise, causing papilledema (swelling of the optic disc) which may be experienced as visual obscurations. In severely raised intracranial pressure, the level of consciousness is decreased, the blood pressure rises, the heart rate falls and the patient assumes an abnormal posture.

It is also possible to classify angiopathy by the associated condition:

- Diabetic angiopathy

- Congophilic angiopathy

A cerebral arteriovenous malformation (cerebral AVM, CAVM, cAVM) is an abnormal connection between the arteries and veins in the brain—specifically, an arteriovenous malformation in the cerebrum.

Watershed stroke symptoms are due to the reduced blood flow to all parts of the body, specifically the brain, thus leading to brain damage. Initial symptoms, as promoted by the American Stroke Association, are FAST (stroke), representing F = Facial weakness (droop), A = Arm weakness (drift), S = Speech difficulty (slur), and T = Time to act (priority of intervention).

All strokes are considered a medical emergency. Any one of these symptoms, whether seen alone or in combination, should be assumed to be stroke until proven otherwise. Emergency medical help should be sought IMMEDIATELY if any or all of these symptoms are seen or experienced. Early diagnosis and timely medical intervention can drastically reduce the severity of a stroke, limit damage to the brain, improve the chances of a full recovery and reduce recovery times massively.

After the initial stroke, other symptoms depend on the area of the brain affected. If one of the three central nervous system pathways is affected, symptoms can include numbness, reduced sensation, and hyperreflexia.

Most often, the side of the brain damaged results in body defects on the opposite side. Since the cranial nerves originate from the brainstem, damage to this area can lead to defects in the function of these nerves. Symptoms can include altered breathing, problems with balance, drooping of eyelids, and decreased sensation in the face.

Damage to the cerebral cortex may lead to aphasia or confusion and damage to the cerebellum may lead to lack of motor movement.

The symptoms of brain ischemia reflect the anatomical region undergoing blood and oxygen deprivation. Ischemia within the arteries branching from the internal carotid artery may result in symptoms such as blindness in one eye, weakness in one arm or leg, or weakness in one entire side of the body. Ischemia within the arteries branching from the vertebral arteries in the back of the brain may result in symptoms such as dizziness, vertigo, double vision, or weakness on both sides of the body . Other symptoms include difficulty speaking, slurred speech, and the loss of coordination. The symptoms of brain ischemia range from mild to severe. Further, symptoms can last from a few seconds to a few minutes or extended periods of time. If the brain becomes damaged irreversibly and infarction occurs, the symptoms may be permanent.

Similar to cerebral hypoxia, severe or prolonged brain ischemia will result in unconsciousness, brain damage or death, mediated by the ischemic cascade.

Multiple cerebral ischemic events may lead to subcortical ischemic depression, also known as vascular depression. This condition is most commonly seen in elderly depressed patients. Late onset depression is increasingly seen as a distinct sub-type of depression, and can be detected with an MRI.

The broad term, "stroke" can be divided into three categories: brain ischemia, subarachnoid hemorrhage and intracerebral hemorrhage. Brain ischemia can be further subdivided, by cause, into thrombotic, embolic, and hypoperfusion. Thrombotic and embolic are generally focal or multifocal in nature while hypoperfusion affects the brain globally.

Symptoms of AVM vary according to the location of the malformation. Roughly 88% of people with an AVM are asymptomatic; often the malformation is discovered as part of an autopsy or during treatment of an unrelated disorder (called in medicine an "incidental finding"); in rare cases, its expansion or a micro-bleed from an AVM in the brain can cause epilepsy, neurological deficit, or pain.

The most general symptoms of a cerebral AVM include headaches and epileptic seizures, with more specific symptoms occurring that normally depend on the location of the malformation and the individual. Such possible symptoms include:

- Difficulties with movement coordination, including muscle weakness and even paralysis;

- Vertigo (dizziness);

- Difficulties of speech (dysarthria) and communication, such as aphasia;

- Difficulties with everyday activities, such as apraxia;

- Abnormal sensations (numbness, tingling, or spontaneous pain);

- Memory and thought-related problems, such as confusion, dementia or hallucinations.

Cerebral AVMs may present themselves in a number of different ways:

- Bleeding (45% of cases)

- Acute onset of severe headache. May be described as the worst headache of the patient's life. Depending on the location of bleeding, may be associated with new fixed neurologic deficit. In unruptured brain AVMs, the risk of spontaneous bleeding may be as low as 1% per year. After a first rupture, the annual bleeding risk may increase to more than 5%.

- Seizure or brain seizure (46%) Depending on the place of the AVM, it can cause loss of vision in one place.

- Headache (34%)

- Progressive neurologic deficit (21%)

- May be caused by mass effect or venous dilatations. Presence and nature of the deficit depend on location of lesion and the draining veins.

- Pediatric patients

- Heart failure

- Macrocephaly

- Prominent scalp veins

There are two types of angiopathy: macroangiopathy and microangiopathy.

In macroangiopathy, atherosclerosis and a resultant blood clot forms on the large blood vessels, sticks to the vessel walls, and blocks the flow of blood. Macroangiopathy may cause other complications, such as ischemic heart disease, stroke and peripheral vascular disease which contributes to the diabetic foot ulcers and the risk of amputation.

In microangiopathy, the walls of the smaller blood vessels become so thick and weak that they bleed, leak protein, and slow the flow of blood through the body. The decrease of blood flow through stenosis or clot formation impairs the flow of oxygen to cells and biological tissues (called ischemia) and leads to cellular death (necrosis and gangrene, which in turn may require amputation). Thus, tissues which are very sensitive to oxygen levels, such as the retina, develop microangiopathy and may cause blindness (so-called proliferative diabetic retinopathy). Damage to nerve cells may cause peripheral neuropathy, and to kidney cells, diabetic nephropathy (Kimmelstiel-Wilson syndrome).

Cerebral atherosclerosis is a type of atherosclerosis where build-up of plaque in the blood vessels of the brain occurs. Some of the main components of the plaques are connective tissue, extracellular matrix, including collagen, proteoglycans, fibronectin, and elastic fibers; crystalline cholesterol, cholesteryl esters, and phospholipids; cells such as monocyte derived macrophages, T-lymphocytes, and smooth muscle cells. The plaque that builds up can lead to further complications such as stroke, as the plaque disrupts blood flow within the intracranial arterioles. This causes the downstream sections of the brain that would normally be supplied by the blocked artery to suffer from ischemia. Diagnosis of the disease is normally done through imaging technology such as angiograms or magnetic resonance imaging. The risk of cerebral atherosclerosis and its associated diseases appears to increase with increasing age; however there are numerous factors that can be controlled in attempt to lessen risk.

The most frequently observed problems, related to an AVM, are headaches and seizures, backaches, neckaches and eventual nausea, as the coagulated blood makes its way down to be dissolved in the individual's spinal fluid. It is supposed that 15% of the population, at detection, have no symptoms at all. Other common symptoms are a pulsing noise in the head, progressive weakness and numbness and vision changes as well as debilitating, excruciating pain.

In serious cases, the blood vessels rupture and there is bleeding within the brain (intracranial hemorrhage). Nevertheless, in more than half of patients with AVM, hemorrhage is the first symptom. Symptoms due to bleeding include loss of consciousness, sudden and severe headache, nausea, vomiting, incontinence, and blurred vision, amongst others. Impairments caused by local brain tissue damage on the bleed site are also possible, including seizure, one-sided weakness (hemiparesis), a loss of touch sensation on one side of the body and deficits in language processing (aphasia). Ruptured AVMs are responsible for considerable mortality and morbidity.

AVMs in certain critical locations may stop the circulation of the cerebrospinal fluid, causing accumulation of the fluid within the skull and giving rise to a clinical condition called hydrocephalus. A stiff neck can occur as the result of increased pressure within the skull and irritation of the meninges.

It is usually associated with amyloid beta.

However, there are other types:

- the "Icelandic type" is associated with Cystatin C

- the "British type" is associated with ITM2B

Research is currently being conducted to determine if there is a link between cerebral amyloid angiopathy and ingestion of excessive quantities of aluminum.

White softening is another form of cerebral softening. This type of softening occurs in areas that continue to be poorly perfused, with little to no blood flow. These are known as "pale" or "anemic infarcts" and are areas that contain dead neuronal tissue, which result in a softening of the cerebrum.

The diagnosis may be suspected on the basis of the symptoms, for example the combination of headache, signs of raised intracranial pressure and focal neurological abnormalities, or when alternative causes of headache and neurological abnormalities, such as a subarachnoid hemorrhage, have been excluded.

Arteriovenous malformation (AVM) is an abnormal connection between arteries and veins, bypassing the capillary system. This vascular anomaly is widely known because of its occurrence in the central nervous system (usually cerebral AVM), but can appear in any location. Although many AVMs are asymptomatic, they can cause intense pain or bleeding or lead to other serious medical problems.

AVMs are usually congenital and belong to the RASopathies.

The genetic transmission patterns of AVM, if any, are unknown. AVM is not generally thought to be an inherited disorder, unless in the context of a specific hereditary syndrome.

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.