Low-pressure hydrocephalus (LPH) is a condition whereby ventricles are enlarged and the individual experiences severe dementia, inability to walk, and incontinence - despite very low intracranial pressure (ICP). Low pressure hydrocephalus appears to be a more acute form of normal pressure hydrocephalus. If not diagnosed in a timely fashion, the individual runs the risk of remaining in the low pressure hydrocephalic state or LPHS. Shunt revisions, even when they are set to drain at a low ICP, are not always effective. The pressure in the brain does not get high enough to allow the cerebrospinal fluid to drain in a shunt system, therefore the shunt is open, but malfunctioning in LPH. In cases of LPH, chronic infarcts can also develop along the corona radiata in response to the tension in the brain as the ventricles increase in size. Certain causes of LPH include trauma, tumor, bleeding, inflammation of the lining of the brain, whole brain radiation, as well as other brain pathology that affects the compliance of the brain parenchyma. One treatment for the LPHS is an external ventricular drain (EVD) set at negative pressures. According to Pang & Altschuler et al., a controlled, steady, negative pressure siphoning with EVD, carefully monitored with partial computer tomography scans is a safe and effective way of treating LPH. In their experience, this approach helps restore the brain mantle. They caution against dropping or raising the pressure of the EVD too quickly as it increases risk and also destabilizes the ventricles. Getting the ventricles smaller, is the initial step, stabilising them is the second step before placing a shunt – which is the final step in therapy. Any variation from this formula can lead to an ineffective, yet patent shunt system, despite a low-pressure setting. Care should be taken with EVD therapy, as mismanagement of the EVD can lead to long-term permanent complications and brain injury.

The clinical presentation of hydrocephalus varies with chronicity. Acute dilatation of the ventricular system is more likely to manifest with the nonspecific signs and symptoms of increased intracranial pressure. By contrast chronic dilatation (especially in the elderly population) may have a more insidious onset presenting, for instance, with Hakim's triad (Adams triad).

Symptoms of increased intracranial pressure may include headaches, vomiting, nausea, papilledema, sleepiness or coma. Elevated intracranial pressure may result in uncal or tonsillar herniation, with resulting life-threatening brain stem compression.

Hakim's triad of gait instability, urinary incontinence and dementia is a relatively typical manifestation of the distinct entity normal pressure hydrocephalus (NPH). Focal neurological deficits may also occur, such as abducens nerve palsy and vertical gaze palsy (Parinaud syndrome due to compression of the quadrigeminal plate, where the neural centers coordinating the conjugated vertical eye movement are located). The symptoms depend on the cause of the blockage, the person's age, and how much brain tissue has been damaged by the swelling.

In infants with hydrocephalus, CSF builds up in the central nervous system, causing the fontanelle (soft spot) to bulge and the head to be larger than expected. Early symptoms may also include:

- Eyes that appear to gaze downward;

- Irritability;

- Seizures;

- Separated sutures;

- Sleepiness;

- Vomiting.

Symptoms that may occur in older children can include:

- Brief, shrill, high-pitched cry;

- Changes in personality, memory, or the ability to reason or think;

- Changes in facial appearance and eye spacing;

- Crossed eyes or uncontrolled eye movements;

- Difficulty feeding;

- Excessive sleepiness;

- Headache;

- Irritability, poor temper control;

- Loss of bladder control (urinary incontinence);

- Loss of coordination and trouble walking;

- Muscle spasticity (spasm);

- Slow growth (child 0–5 years);

- Slow or restricted movement;

- Vomiting.

Because hydrocephalus can injure the brain, thought and behavior may be adversely affected. Learning disabilities including short-term memory loss are common among those with hydrocephalus, who tend to score better on verbal IQ than on performance IQ, which is thought to reflect the distribution of nerve damage to the brain. However, the severity of hydrocephalus can differ considerably between individuals and some are of average or above-average intelligence. Someone with hydrocephalus may have coordination and visual problems, problems with coordination, or may be clumsy. They may reach puberty earlier than the average child (see precocious puberty). About one in four develops epilepsy.

Symptoms of IVH are similar to other intracerebral hemorrhages and include sudden onset of headache, nausea and vomiting, together with an alteration

of the mental state and/or level of consciousness. Focal neurological signs are either minimal or absent, but focal and/or generalized seizures may occur. Xanthochromia, yellow-tinged CSF, is the rule. Diagnosis can be confirmed by the presence of blood inside the ventricles on CT.

Intraventricular hemorrhage (IVH), also known as intraventricular bleeding, is a bleeding into the brain's ventricular system, where the cerebrospinal fluid is produced and circulates through towards the subarachnoid space. It can result from physical trauma or from hemorrhaging in stroke.

30% of intraventricular hemorrhage (IVH) are primary, confined to the ventricular system and typically caused by intraventricular trauma, aneurysm, vascular malformations, or tumors, particularly of the choroid plexus. However 70% of IVH are secondary in nature, resulting from an expansion of an existing intraparenchymal or subarachnoid hemorrhage. Intraventricular hemorrhage has been found to occur in 35% of moderate to severe traumatic brain injuries. Thus the hemorrhage usually does not occur without extensive associated damage, and so the outcome is rarely good.

This condition is acquired as a consequence of CNS infections, meningitis, brain tumors, head trauma, toxoplasmosis, intracranial hemorrhage (subarachnoid or intraparenchymal) and is usually painful.

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.

Brain herniation frequently presents with abnormal posturing a characteristic positioning of the limbs indicative of severe brain damage. These patients have a lowered level of consciousness, with Glasgow Coma Scores of three to five. One or both pupils may be dilated and fail to constrict in response to light. Vomiting can also occur due to compression of the vomiting center in the 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.

In "central herniation", the diencephalon and parts of the temporal lobes of both of the cerebral hemispheres are squeezed through a notch in the tentorium cerebelli. Transtentorial herniation can occur when the brain moves either up or down across the tentorium, called ascending and descending transtentorial herniation respectively; however descending herniation is much more common. Downward herniation can stretch branches of the basilar artery (pontine arteries), causing them to tear and bleed, known as a Duret hemorrhage. The result is usually fatal. Other symptoms of this type of herniation include small, dilated, fixed pupils with paralysis of upward eye movement giving the characteristic appearance of "sunset eyes". Also found in these patients, often as a terminal complication is the development of diabetes insipidus due to the compression of the pituitary stalk. Radiographically, downward herniation is characterized by obliteration of the suprasellar cistern from temporal lobe herniation into the tentorial hiatus with associated compression on the cerebral peduncles. Upwards herniation, on the other hand, can be radiographically characterized by obliteration of the quadrigeminal cistern. Intracranial hypotension syndrome has been known to mimic downwards transtentorial herniation.

Many of the signs and symptoms of aqueductal stenosis are similar to those of hydrocephalus. These typical symptoms include: headache, nausea and vomiting, cognitive difficulty, sleepiness, seizures, balance and gait disturbances, visual abnormalities, and incontinence.

- Headache may be a result of the raised intracranial pressure from the disrupted flow of CSF, and sometimes this symptom may come on suddenly as a “thunderclap headache”.

- In children, cognitive difficulty and developmental delay have been seen in a range of severities. Mild developmental delay is characterized by motor and neurological development that is no greater than 2 standard deviations below average for the age of the child, and moderate delay is characterized by greater than 2 standard deviations below. A child with severe delay may be unable to use spoken language or control movement or interact with others, and can behave abusively towards themselves.

- A patient's level of consciousness may also deteriorate with time, and this can lead to coma or death.

- The visual abnormalities previously mentioned include “upward gaze palsy”, where a person has difficulty looking up.

- Tremors have also been reported as a symptom, but are not as common as these previously mentioned.

Signs of aqueductal stenosis other than those mentioned in “Causes of stenosis” include detection of an enlarged lateral and third ventricle in conjunction with a smaller fourth ventricle. This variation in ventricle size is indicative of a blockage in the aqueduct because it lies between the third and fourth ventricles. Another sign of stenosis is deformation of the midbrain, which can be severe. This is caused by the pressure gradient formed from a blockage in the aqueduct.

It is not known what percentage of people with IIH will remit spontaneously, and what percentage will develop chronic disease.

IIH does not normally affect life expectancy. The major complications from IIH arise from untreated or treatment-resistant papilledema. In various case series, the long-term risk of ones vision being significantly affected by IIH is reported to lie anywhere between 10 and 25%.

The most common symptom of IIH is headache, which occurs in almost all (92–94%) cases. It is characteristically worse in the morning, generalized in character and throbbing in nature. It may be associated with nausea and vomiting. The headache can be made worse by any activity that further increases the intracranial pressure, such as coughing and sneezing. The pain may also be experienced in the neck and shoulders. Many have pulsatile tinnitus, a whooshing sensation in one or both ears (64–87%); this sound is synchronous with the pulse. Various other symptoms, such as numbness of the extremities, generalized weakness, loss of smell, and loss of coordination, are reported more rarely; none are specific for IIH. In children, numerous nonspecific signs and symptoms may be present.

The increased pressure leads to compression and traction of the cranial nerves, a group of nerves that arise from the brain stem and supply the face and neck. Most commonly, the abducens nerve (sixth nerve) is involved. This nerve supplies the muscle that pulls the eye outward. Those with sixth nerve palsy therefore experience horizontal double vision which is worse when looking towards the affected side. More rarely, the oculomotor nerve and trochlear nerve (third and fourth nerve palsy, respectively) are affected; both play a role in eye movements. The facial nerve (seventh cranial nerve) is affected occasionally –- the result is total or partial weakness of the muscles of facial expression on one or both sides of the face.

The increased pressure leads to papilledema, which is swelling of the optic disc, the spot where the optic nerve enters the eyeball. This occurs in practically all cases of IIH, but not everyone experiences symptoms from this. Those who do experience symptoms typically report "transient visual obscurations", episodes of difficulty seeing that occur in both eyes but not necessarily at the same time. Long-term untreated papilledema leads to visual loss, initially in the periphery but progressively towards the center of vision.

Physical examination of the nervous system is typically normal apart from the presence of papilledema, which is seen on examination of the eye with a small device called an ophthalmoscope or in more detail with a fundus camera. If there are cranial nerve abnormalities, these may be noticed on eye examination in the form of a squint (third, fourth, or sixth nerve palsy) or as facial nerve palsy. If the papilledema has been longstanding, visual fields may be constricted and visual acuity may be decreased. Visual field testing by automated (Humphrey) perimetry is recommended as other methods of testing may be less accurate. Longstanding papilledema leads to optic atrophy, in which the disc looks pale and visual loss tends to be advanced.

In cytotoxic edema, the blood–brain barrier remains intact but a disruption in cellular metabolism impairs functioning of the sodium and potassium pump in the glial cell membrane, leading to cellular retention of sodium and water. Swollen astrocytes occur in gray and white matter. Cytotoxic edema is seen with various toxins, including dinitrophenol, triethyltin, hexachlorophene, and isoniazid. It can occur in Reye's syndrome, severe hypothermia, early ischemia, encephalopathy, early stroke or hypoxia, cardiac arrest, and pseudotumor cerebri.

During an ischemic stroke, a lack of oxygen and glucose leads to a breakdown of the sodium-calcium pumps on brain cell membranes, which in turn results in a massive buildup of sodium and calcium intracellularly. This causes a rapid uptake of water and subsequent swelling of the cells. It is this swelling of the individual cells of the brain that is seen as the main distinguishing characteristic of cytotoxic edema, as opposed to vasogenic edema, wherein the influx of fluid is typically seen in the interstitial space rather than within the cells themselves. While not all patients who have experienced a stroke will develop a severe edema, those who do have a very poor prognosis.

In most instances, cytotoxic and vasogenic edema occur together. It is generally accepted that cytotoxic edema is dominant immediately following an injury or infarct, but gives way to a vasogenic edema that can persist for several days or longer. The use of specific MRI techniques has allowed for some differentiation between the two mechanisms and suggests that in the case of trauma, the cytotoxic response dominates

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)

NPH may exhibit a classic triad of clinical findings (known as the Adams triad or Hakim's triad) of urinary incontinence, gait disturbance, and dementia (commonly referred to as "wet, wacky and wobbly" or "weird walking water").

- Gait disturbance is typically the initial and most prominent symptom of the triad and may be progressive, due to expansion of the ventricular system, particularly at the level of the lateral ventricles, leading to traction on the corticospinal tract motor fibers descending to the lumbosacral spinal cord. The gait disturbance can be classified as mild (cautious gait or difficulty with tandem gait), marked (evident difficulty walking or considerable unstable gait) or severe (unaided gait not possible) In the early stages, most often this gait disturbance occurs in the form of unsteadiness and impaired balance, especially when encountering stairs and curbs. Weakness and tiredness of the legs may also be part of the complaint, although examination discloses no paresis or ataxia. Often a mobility aid is used for added stability, once the patient has reached the mild to marked stage. Such aids may include a quad cane or wheeled walker. The patient's gait at the marked stage will often show a decrease in step height and foot-floor clearance, as well as a decrease in walking speed. This style is often referred to as a magnetic gait, in which the feet appear to be stuck to the walking surface, and is considered the characteristic gait disturbance of NPH. The gait may begin to mimic a Parkinsonian gait, with short shuffling steps and stooped, forward-leaning posture, but there is no rigidity or tremor. An increased tendency to fall backwards is also seen, and a broad-based gait may be employed by the patient in order to increase their base of support and thereby their stability. In the very late stages, the patient can progress from an inability to walk, to an inability to stand, sit, rise from a chair or turn over in bed; this advanced stage is referred to as "hydrocephalic astasia-abasia".

- Dementia is predominantly frontal lobe in nature and of the subcortical type of dementia. It presents in the form of abulia, forgetfulness, inertia, inattention, decreased speed of complex information procession (also described as a dullness in thinking and actions), and disturbed manipulation of acquired knowledge, which is reflective of the loss of integrity of the frontal lobes. Memory problems are usually a component of the overall problem and have been predominant in some cases, which can lead to the misdiagnosis of Alzheimer's disease. However, in NPH there may be an obvious discrepancy between (often severely) impaired recall and intact or much less impaired recognition. The dementia is thought to result from traction on frontal and limbic fibers that also run in the periventricular region.

- Urinary incontinence appears late in the illness, and is found to be of the spastic hyperreflexic, increased-urgency type associated with decreased inhibition of bladder contractions and detrusor instability. In the most severe cases, bladder hyperreflexia is associated with a lack of concern for micturition due to the severe frontal lobe cognitive impairment. This is also known as "frontal lobe incontinence", where the patient becomes indifferent to their recurrent urinary symptoms.

Aqueductal stenosis is a narrowing of the aqueduct of Sylvius which blocks the flow of cerebrospinal fluid (CSF) in the ventricular system. Blockage of the aqueduct can lead to hydrocephalus, specifically as a common cause of congenital and/or obstructive hydrocephalus.

The aqueduct of Sylvius is the channel which connects the third ventricle to the fourth ventricle and is the narrowest part of the CSF pathway with a mean cross-sectional area of 0.5 mm in children and 0.8 mm in adults. Because of its small size, the aqueduct is the most likely place for a blockage of CSF in the ventricular system. This blockage causes ventricle volume to increase because the CSF cannot flow out of the ventricles and cannot be effectively absorbed by the surrounding tissue of the ventricles. Increased volume of the ventricles will result in higher pressure within the ventricles, and cause higher pressure in the cortex from it being pushed into the skull. A person may have aqueductal stenosis for years without any symptoms, and a head trauma, hemorrhage, or infection could suddenly invoke those symptoms and worsen the blockage.

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.

Normal pressure hydrocephalus (NPH), also termed Hakim's syndrome and symptomatic hydrocephalus, is a type of brain malfunction caused by expansion of the lateral cerebral ventricles and distortion of the fibers in the corona radiata. Its typical symptoms are urinary incontinence, dementia, and gait disturbance. CSF pressure is usually normal. Ventricles are chronically dilated.

The name “normal pressure” came out of a 1965 medical paper describing cases of hydrocephalus where the symptoms occurred in the presence of supposedly normal cerebrospinal-fluid pressure. The paper was published before continuous pressure-recording techniques were available. We now know that “normal pressure” is a misnomer.

The usual treatment is surgical installation of a ventriculoperitoneal shunt to drain excess CSF into the lining of the abdomen where the CSF will eventually be absorbed.

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.

Usually the cerebellum and brain stem are formed normally, although in some cases the cerebellum may also be absent. An infant with hydranencephaly may appear normal at birth or may have some distortion of the skull and upper facial features due to fluid pressure inside the skull. The infant's head size and spontaneous reflexes such as sucking, swallowing, crying, and moving the arms and legs may all seem normal, depending on the severity of the condition. However, after a few weeks the infant sometimes becomes irritable and has increased muscle tone (hypertonia). After several months of life, seizures and hydrocephalus may develop, if they did not exist at birth. Other symptoms may include visual impairment, lack of growth, deafness, blindness, spastic quadriparesis (paralysis), and intellectual deficits.

Some infants may have additional abnormalities at birth including seizures, myoclonus (involuntary sudden, rapid jerks), limited thermoregulation abilities, and respiratory problems.

Still other infants display no obvious symptoms at birth, going many months without a confirmed diagnosis of hydranencephaly. In some cases a severe hydrocephalus, or other cephalic condition, is misdiagnosed.

The blockage of cerebrospinal fluid (CSF) flow may also cause a syrinx to form, eventually leading to syringomyelia. Central cord symptoms such as hand weakness, dissociated sensory loss, and, in severe cases, paralysis may occur.

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.

Hydranencephaly or hydrancephaly is a condition in which the brain's cerebral hemispheres are absent to varying degrees and the remaining cranial cavity is filled with cerebrospinal fluid.

Hydranencephaly (or hydrancephaly) is a type of cephalic disorder.

These disorders are congenital conditions that derive from either damage to, or abnormal development of, the fetal nervous system in the earliest stages of development in utero. Cephalic is the medical term for “head” or “head end of body.” These conditions do not have any definitive identifiable cause factor; instead generally attributed to a variety of hereditary or genetic conditions, but also by environmental factors such as maternal infection, pharmaceutical intake, or even exposure to high levels of radiation.

This should not be confused with hydrocephalus, which is an accumulation of excess cerebrospinal fluid in the ventricles of the brain.

In hemihydranencephaly, only half of the cranial cavity is filled with fluid.

Patients with arachnoid cysts may never show symptoms, even in some cases where the cyst is large. Therefore, while the presence of symptoms may provoke further clinical investigation, symptoms independent of further data cannot—and should not—be interpreted as evidence of a cyst's existence, size, location, or potential functional impact on the patient.

Symptoms vary by the size and location of the cyst(s), though small cysts usually have no symptoms and are discovered only incidentally. On the other hand, a number of symptoms may result from large cysts:

- Cranial deformation or macrocephaly (enlargement of the head), particularly in children

- Cysts in the suprasellar region in children have presented as bobbing and nodding of the head called bobble-head doll syndrome.

- Cysts in the left middle cranial fossa have been associated with ADHD in a study on affected children.

- Headaches. A patient experiencing a headache does not necessarily have an arachnoid cyst.

- In a 2002 study involving 78 patients with a migraine or tension-type headache, CT scans showed abnormalities in over a third of the patients, though arachnoid cysts only accounted for 2.6% of patients in this study.

- A study found 18% of patients with intracranial arachnoid cysts had non-specific headaches. The cyst was in the temporal location in 75% of these cases.

- Seizures

- Hydrocephalus (excessive accumulation of cerebrospinal fluid)

- Increased intracranial pressure

- Developmental delay

- Behavioral changes

- Nausea

- Hemiparesis (weakness or paralysis on one side of the body)

- Ataxia (lack of muscle control)

- Musical hallucination

- Pre-senile dementia, a condition often associated with Alzheimer's disease

- In elderly patients (>80 years old) symptoms were similar to chronic subdural hematoma or normal pressure hydrocephalus:

- Dementia

- Urinary incontinence

- Hemiparesis

- Headache

- Seizures

Syringomyelia is a chronic progressive degenerative disorder characterized by a fluid-filled cyst located in the spinal cord. Its symptoms include pain, weakness, numbness, and stiffness in the back, shoulders, arms or legs. Other symptoms include headaches, the inability to feel changes in the temperature, sweating, sexual dysfunction, and loss of bowel and bladder control. It is usually seen in the cervical region but can extend into the medulla oblongata and pons or it can reach downward into the thoracic or lumbar segments. Syringomyelia is often associated with Chiari malformation type I and is commonly seen between the C-4 and C-6 levels. The exact development of syringomyelia is unknown but many theories suggest that the herniated tonsils in Chiari malformation type I form a "plug" which does not allow an outlet of CSF from the brain to the spinal canal. Syringomyelia is present in 25% of patients with Chiari malformation.