A Total Anterior Circulation Infarct (TACI) is a type of cerebral infarction affecting the entire anterior circulation supplying one side of the brain.

Total Anterior Circulation Stroke Syndrome (TACS) refers to the symptoms of a patient who clinically appears to have suffered from a total anterior circulation infarct, but who has not yet had any diagnostic imaging (e.g. CT Scan) to confirm the diagnosis.

It is diagnosed when it causes all 3 of the following symptoms:

- Higher dysfunction

- Dysphasia

- Visuospatial disturbances

- Decreased level of consciousness

- Homonymous hemianopia

- Motor and Sensory Defects (≥2/3 of face, arm, leg)

For more information, see stroke.

Each of the 5 classical lacunar syndromes has a relatively distinct symptom complex. Symptoms may occur suddenly, progressively, or in a fluctuating (e.g., the capsular warning syndrome) manner. Occasionally, cortical infarcts and intracranial hemorrhages can mimic lacunar infarcts, but true cortical infarct signs (aphasia, visuospatial neglect, gaze deviation, and visual field defects) are always absent. The 5 classic syndromes are as follows:

Partial Anterior Circulation Infarct (PACI) is a type of cerebral infarction affecting part of the anterior circulation supplying one side of the brain.

Partial Anterior Circulation Stroke Syndrome (PACS) refers to the symptoms of a patient who clinically appears to have suffered from a partial anterior circulation infarct, but who has not yet had any diagnostic imaging (e.g. CT Scan) to confirm the diagnosis.

It is diagnosed by any one of the following

- 2 out of 3 features of

- Higher dysfunction

- Dysphasia

- Visuospatial disturbances

- Homonymous hemianopia

- Motor and Sensory Defects (>2/3 of face, arm, leg)

- Higher dysfunction alone

- Partial Motor or Sensory Defect

If all of the above symptoms are present, a Total Anterior Circulation Infarct is more likely.

For more information, see stroke.

A silent lacunar infarction (SLI) is one type of silent stroke which usually shows no identifiable outward symptoms thus the term "silent". Individuals who suffer a SLI are often completely unaware they have suffered a stroke. This type of stroke often causes lesions in the surrounding brain tissue that are visibly detected via neuroimaging techniques such as MRI and computerized axial tomography (CT scan). Silent strokes, including silent lacunar infarctions, have been shown to be much more common than previously thought, with an estimated prevalence rate of eleven million per year in the United States. Approximately 10% of these silent strokes are silent lacunar infarctions. While dubbed "silent" due to the immediate lack of classic stroke symptoms, SLIs can cause damage to the surrounding brain tissue (lesions) and can affect various aspects of a persons mood, personality, and cognitive functioning. A SLI or any type of silent stroke places an individual at greater risk for future major stroke.

A Posterior Circulation Infarct (POCI) is a type of cerebral infarction affecting the posterior circulation supplying one side of the brain.

Posterior Circulation Stroke Syndrome (POCS) refers to the symptoms of a patient who clinically appears to have had a posterior circulation infarct, but who has not yet had any diagnostic imaging (e.g. CT Scan) to confirm the diagnosis.

It can cause the following symptoms:

- Cranial nerve palsy AND contralateral motor/sensory defect

- motor or sensory defect

- Eye movement problems (e.g.nystagmus)

- Cerebellar dysfunction

- Isolated homonymous hemianopia

It has also been associated with deafness.

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.

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.

Symptoms of cerebral infarction are determined by the parts of the brain affected. If the infarct is located in primary motor cortex, contralateral hemiparesis is said to occur. With brainstem localization, brainstem syndromes are typical: Wallenberg's syndrome, Weber's syndrome, Millard-Gubler syndrome, Benedikt syndrome or others.

Infarctions will result in weakness and loss of sensation on the opposite side of the body. Physical examination of the head area will reveal abnormal pupil dilation, light reaction and lack of eye movement on opposite side. If the infarction occurs on the left side brain, speech will be slurred. Reflexes may be aggravated as well.

Loss of consciousness, headache, and vomiting usually occur more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing the brain.

If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.

Cerebellar stroke syndrome is a condition in which the circulation to the cerebellum is impaired due to a lesion of the superior cerebellar artery, anterior inferior cerebellar artery or the posterior inferior cerebellar artery.

Cardinal signs include vertigo, headache, vomiting, and ataxia.

Cerebellar strokes account for only 2-3% of the 600 000 strokes that occur each year in the United States. They are far less common than strokes which occur in the cerebral hemispheres. In recent years mortality rates have decreased due to advancements in health care which include earlier diagnosis through MRI and CT scanning. Advancements have also been made which allow earlier management for common complications of cerebellar stroke such as brainstem compression and hydrocephalus.

Research is still needed in the area of cerebellar stroke management; however, it has been proposed that several factors may lead to poor outcomes in individuals who suffer from cerebellar stroke. These factors include:

1. Declining levels of consciousness

2. New signs of brainstem involvement

3. Progressing Hydrocephalus

4. Stroke to the midline of the cerebellum (a.k.a. the vermis)

If the area of the brain affected contains one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and the posterior column–medial lemniscus pathway, symptoms may include:

- hemiplegia and muscle weakness of the face

- numbness

- reduction in sensory or vibratory sensation

- initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), excessive reflexes, and obligatory synergies.

In most cases, the symptoms affect only one side of the body (unilateral). Depending on the part of the brain affected, the defect in the brain is "usually" on the opposite side of the body. However, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate a stroke.In addition to the above CNS pathways, the "brainstem" gives rise to most of the twelve cranial nerves. A brainstem stroke affecting the brainstem and brain, therefore, can produce symptoms relating to deficits in these cranial nerves:

- altered smell, taste, hearing, or vision (total or partial)

- drooping of eyelid (ptosis) and weakness of ocular muscles

- decreased reflexes: gag, swallow, pupil reactivity to light

- decreased sensation and muscle weakness of the face

- balance problems and nystagmus

- altered breathing and heart rate

- weakness in sternocleidomastoid muscle with inability to turn head to one side

- weakness in tongue (inability to stick out the tongue or move it from side to side)

If the "cerebral cortex" is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

- aphasia (difficulty with verbal expression, auditory comprehension, reading and writing; Broca's or Wernicke's area typically involved)

- dysarthria (motor speech disorder resulting from neurological injury)

- apraxia (altered voluntary movements)

- visual field defect

- memory deficits (involvement of temporal lobe)

- hemineglect (involvement of parietal lobe)

- disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)

- lack of insight of his or her, usually stroke-related, disability

If the "cerebellum" is involved, ataxia might be present and this includes:

- altered walking gait

- altered movement coordination

- vertigo and or disequilibrium

Vertigo, the sensation of spinning even while a person is still, is the most recognizable and quite often the sole symptom of decreased blood flow in the vertebrobasilar distribution. The vertigo due to VBI can be brought on by head turning, which could occlude the contralateral vertebral artery and result in decreased blood flow to the brain if the contralateral artery is occluded. When the vertigo is accompanied by double vision (diplopia), graying of vision, and blurred vision, patients often go to the optometrist or ophthalmologist. If the VBI progresses, there may be weakness of the quadriceps and, to the patient, this is felt as a buckling of the knees. The patient may suddenly become weak at the knee and crumple (often referred to as a “drop attack”). Such a fall can lead to significant head and orthopedic injury, especially in the elderly.

Transient ischemic attacks due to VBI will, by definition, have symptoms resolved within 24 hours. More often, however, the symptoms are very brief, lasting a few seconds to half an hour.

Reduced blood flow to the skin layers may result in mottling or uneven, patchy discoloration of the skin

There are various classification systems for a cerebral infarction.

- The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on the initial symptoms. Based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.

- The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation).

Brain ischemia is insufficient blood flow to the brain, and can be acute or chronic. Acute ischemic stroke is a neurologic emergency that may be reversible if treated rapidly. Chronic ischemia of the brain may result in a form of dementia called vascular dementia. A brief episode of ischemia affecting the brain is called a transient ischemic attack (TIA) often called a mini-stroke.

Vertebrobasilar insufficiency (VBI) or vertebral-basilar ischemia, also called beauty parlour syndrome (BPS), is a temporary set of symptoms due to decreased blood flow (ischemia) in the posterior circulation of the brain. The posterior circulation supplies blood to the medulla, cerebellum, pons, midbrain, thalamus, and occipital cortex (responsible for vision). Therefore, the symptoms due to VBI vary according to which portions of the brain experience significantly decreased blood flow (see image of brain ). In the United States, 25% of strokes and transient ischemic attacks occur in the vertebrobasilar distribution. These must be separated from strokes arising from the anterior circulation, which involves the carotid arteries.

A silent stroke is a stroke that does not have any outward symptoms associated with stroke, and the patient is typically unaware they have suffered a stroke. Despite not causing identifiable symptoms a silent stroke still causes damage to the brain, and places the patient at increased risk for both transient ischemic attack and major stroke in the future. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as MRI. The risk of silent stroke increases with age but may also affect younger adults. Women appear to be at increased risk for silent stroke, with hypertension and current cigarette smoking being amongst the predisposing factors.

These types of strokes include lacunar and other ischemic strokes and minor hemorrhages. They may also include leukoaraiosis (changes in the white matter of the brain): the white matter is more susceptible to vascular blockage due to reduced amount of blood vessels as compared to the cerebral cortex. These strokes are termed "silent" because they typically affect "silent" regions of the brain that do not cause a noticeable change in an afflicted person’s motor functions such as contralateral paralysis, slurred speech, pain, or an alteration in the sense of touch. A silent stroke typically affects regions of the brain associated with various thought processes, mood regulation and cognitive functions and is a leading cause of vascular cognitive impairment and may also lead to a loss of urinary bladder control.

In the Cardiovascular Health Study, a population study conducted among 3,660 adults over the age of 65. 31% showed evidence of silent stroke in neuroimaging studies utilizing MRI. These individuals were unaware they had suffered a stroke. It is estimated that silent strokes are five times more common than symptomatic stroke.

A silent stroke differs from a transient ischemic attack (TIA). In TIA symptoms of stroke are exhibited which may last from a few minutes to 24 hours before resolving. A TIA is a risk factor for having a major stroke and subsequent silent strokes in the future.

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.

Red softening is one of the three types of cerebral softening. As its name suggests, certain regions of cerebral softening result in a red color. This is due to a hemorrhagic infarct, in which blood flow is restored to an area of the brain that was previously restricted by an embolism. This is termed a "red infarct" or also known as red softening.

Upon autopsy of several subjects, Dr. Cornelio Fazio found that the most common areas of this type of softening occurred where there was a hemorrhage of the middle cerebral artery or the superior or deep branches to it. The subjects' softened area was not always near the arteries but where the capillaries perfused the brain tissue. The symptoms were similar to that of a stroke.

Amaurosis fugax (Latin "" meaning "fleeting", Greek "" meaning "darkening", "dark", or "obscure") is a painless temporary loss of vision in one or both eyes.

Children who have suffered silent strokes often have a variety of neuropsychological deficits. These deficits may include lowered I.Q., learning disabilities, and an inability to focus.

Silent strokes are the most common form of neurologic injury in children with sickle cell anemia, who may develop subtle neurocognitive deficits in the areas of attention and concentration, executive function, and visual-motor speed and coordination due to silent strokes which may not have been detected on physical examination.

Neurological causes include:

- Optic neuritis

- Compressive optic neuropathies

- Papilledema: "The underlying mechanism for visual obscurations in all of these patients appear to be transient ischemia of the optic nerve head consequent to increased tissue pressure. Axonal swelling, intraneural masses, and increased influx of interstitial fluid may all contribute to increases in tissue pressure in the optic nerve head. The consequent reduction in perfusion pressure renders the small, low-pressure vessels that supply the optic nerve head vulnerable to compromise. Brief fluctuations in intracranial or systemic blood pressure may then result in transient loss of function in the eyes." Generally, this transient visual loss is also associated with a headache and optic disk swelling.

- Multiple Sclerosis can cause amaurosis fugax due to a unilateral conduction block, which is a result of demyelination and inflammation of the optic nerve, and "...possibly by defects in synaptic transmission and putative circulating blocking factors."

- Migraine

- Pseudotumor cerebri

- Intracranial tumor

- Psychogenic

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.

Moyamoya disease is a disease in which certain arteries in the brain are constricted. Blood flow is blocked by the constriction, and also by blood clots (thrombosis).

A collateral circulation develops around the blocked vessels to compensate for the blockage, but the collateral vessels are small, weak, and prone to bleeding, aneurysm and thrombosis. On conventional X-ray angiography, these collateral vessels have the appearance of a "puff of smoke" (described as "もやもや (moyamoya)" in Japanese).

When Moyamoya is diagnosed by itself, with no underlying correlational conditions, it is diagnosed as Moyamoya disease. This is also the case when the arterial constriction and collateral circulation are bilateral. Moyamoya syndrome is unilateral arterial constriction, or occurs when one of the several specified conditions is also present. This may also be considered as Moyamoya being secondary to the primary condition.

Mainly, occlusion of the distal internal carotid artery occurs. On angiography, a "puff of smoke" appearance is seen, and the treatment of choice is surgical bypass.

Medial medullary syndrome, also known as inferior alternating syndrome, hypoglossal alternating hemiplegia, lower alternating hemiplegia, or Dejerine syndrome, is a type of alternating hemiplegia characterized by a set of clinical features resulting from occlusion of the anterior spinal artery. This results in the infarction of medial part of the medulla oblongata.