Most people who develop SCSFLS feel the sudden onset of a severe and acute headache. It is a headache usually made worse by standing, typically becoming prominent throughout the day, with the pain becoming less severe when lying down. Orthostatic headaches can become chronic and disabling to the point of incapacitation. Some patients with SCSFLS will develop headaches that begin in the afternoon. This is known as "second-half-of-the-day headache". This may be an initial presentation of a spontaneous CSF leak or appear after treatment such as an epidural patch, and likely indicates a slow CSF leak.

Apart from headache, about 50% of patients experience neck pain or stiffness, nausea, and vomiting. Other symptoms include dizziness and vertigo, facial numbness or weakness, unusually blurry or double vision, neuralgia, fatigue, or a metallic taste in the mouth. Leaking CSF can sometimes be felt or observed as a discharge from the nose or ear.

Lack of CSF pressure and volume can allow the brain to sag and descend through the foramen magnum (large opening) of the occipital bone, at the base of the skull. The lower portion of the brain is believed to stretch or impact one or more cranial nerve complexes, thereby causing a variety of sensory symptoms. Nerves that can be affected and their related symptoms are detailed in the table at right.

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.

SCSFLS is classified into two main types, cranial leaks and spinal leaks. The vast majority of leaks are spinal. Cranial leaks occur in the head. In some of these cases, CSF can be seen dripping out of the nose, or ear. Spinal leaks occur when one or more holes form in the dura along the spinal cord. Both cranial and spinal spontaneous CSF leaks cause neurological symptoms as well as spontaneous intracranial hypotension, diminished volume and pressure of the cranium. While referred to as "intracranial hypotension", the intracranial pressure may be normal, with the underlying issue instead being low-volume CSF. For this reason SCSFLS is referred to as "CSF hypovolemia" as opposed to "CSF hypotension".

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.

Posterior spinal artery syndrome is much rarer than its anterior counterpart as the white matter structures that are present are much less vulnerable to ischemia since they have a better blood supply. When posterior spinal artery syndrome does occur, dorsal columns are damaged and ischemia may spread into the posterior horns. Clinically the syndrome presents as a loss of tendon reflexes and loss of joint position sense

Transient ischemic attacks (TIAs) rarely affect the spinal cord and usually affect the brain; however, cases have been documented in these areas. Spinal ateriovenous malformations are the main cause and are represented later in this article. However, TIAs can result from emboli in calcific aortic disease and aortic coarctation.

3 affected domains of neurological function:

- Cerebral hemisphere (15%)

- Cranial Nerves (35%)

- Spinal cord and roots (60%)

Signs reported

- headache

- mental status change

- confusion

- cognitive impairment

- seizures

- hemiparesis

- gait instability

Other symptoms that are less common are dementia, autonomic dysfunction, cranial nerve abnormalities, spinal symptoms such as limb weakness and paresthesia, and bowel and bladder dysfunction. Diplopia is the most common symptom of cranial nerve dysfunction. Trigeminal sensory or motor loss, cochlear dysfunction, and optic neuropathy are also common findings. Spinal signs and symptoms include weakness, dermatomal or segmental sensory loss, and pain in the neck, back, or following radicular patterns.

Typical symptoms of PRES, listed according to prevalence, include: altered mental status (encephalopathy), seizure, and headache. Less commonly there may be visual disturbances, focal neurologic signs, and status epilepticus.

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

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.

Arachnoid cysts can be found on the brain or on the spine. Intracranial arachnoid cysts usually occur adjacent to the arachnoidal cistern. Spinal arachnoid cysts may be extradural, intradural, or perineural and tend to present with signs and symptoms indicative of a radiculopathy.

Arachnoid cysts may also be classified as primary (congenital) or secondary (acquired) and have been reported in humans, cats, and dogs.

Arachnoid cysts can be relatively or present with symptoms; for this reason, diagnosis is often delayed.

The diagnosis is typically made clinically with magnetic resonance imaging of the brain often revealing hyperintensities on "T"-weighed imaging. Three patterns have been described: superior frontal sulcus, dominant parieto-occipital, and holohemispheric watershed.

Epidural hematoma is when bleeding occurs between the tough outer membrane covering the brain and the skull. Often there is loss of consciousness following a head injury, a brief regaining of consciousness, and then loss of consciousness again. Other symptoms may include headache, confusion, vomiting, and an inability to move parts of the body. Complications may include seizures.

The cause is typically head injury that results in a break of the temporal bone and bleeding from the middle meningeal artery. Occasionally it can occur as a result of a bleeding disorder or blood vessel malformation. Diagnosis is typically by a CT scan or MRI. When this condition occurs in the spine it is known as a spinal epidural hematoma.

Treatment in generally by urgent surgery in the form of a craniotomy or burr hole. Without treatment death typically results. The condition occurs in one to four percent of head injuries. Typically it occurs in young adults. Males are more often affected than females.

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.

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.

Epidural, subdural, and subarachnoid hemorrhages are extra-axial bleeds, occurring outside of the brain tissue, while intra-axial hemorrhages, including intraparenchymal and intraventricular hemorrhages, occur within it.

Epidural hematomas may present with a lucid period immediately following the trauma and a delay before symptoms become evident. After the epidural hematoma begins collecting, it starts to compress intracranial structures which may impinge on the CN III. This can be seen in the physical exam as a fixed and dilated pupil on the side of the injury. The eye will be positioned down and out, due to unopposed CN IV and CN VI innervation.

Other manifestations will include weakness of the extremities on the opposite side as the lesion (except in rare cases), due to compression of the crossed pyramid pathways, and a loss of visual field opposite to the side of the lesion, due to compression of the posterior cerebral artery on the side of the lesion.

The most feared event that takes place is tonsillar herniation which could result in respiratory arrest since the medullary structures are compromised. The trigeminal nerve (CN V) may be involved late in the process as the pons becomes compressed, but this is not a significant clinical presentation, since by that time the patient may already be dead. In the case of epidural hematoma in the posterior cranial fossa, the herniation is tonsillar and causes the Cushing's triad: hypertension, bradycardia, and irregular respiration.

Epidural bleeding is rapid because it is usually from arteries, which are high pressure. Epidural bleeds from arteries can grow until they reach their peak size at six to eight hours post injury, spilling from 25 to 75 cubic centimeters of blood into the intracranial space. As the hematoma expands, it strips the dura from the inside of the skull, causing an intense headache. Epidural bleeds can become large and raise intracranial pressure, causing the brain to shift, lose blood supply, or be crushed against the skull. Larger hematomas cause more damage. Epidural bleeds can quickly expand and compress the brain stem, causing unconsciousness, abnormal posturing, and abnormal pupil responses to light.

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.

Symptoms suggestive of cord compression are back pain, a dermatome of increased sensation, paralysis of limbs below the level of compression, decreased sensation below the level of compression, urinary and fecal incontinence and/or urinary retention. Lhermitte's sign (intermittent shooting electrical sensation) and hyperreflexia may be present.

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.

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.

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.

On cardiotocography (CTG), umbilical cord compression can present with variable decelerations in fetal heart rate.

Diagnosis is by X-rays but preferably magnetic resonance imaging (MRI) of the whole spine. The most common causes of cord compression are tumors, but abscesses and granulomas (e.g. in tuberculosis) are equally capable of producing the syndrome. Tumors that commonly cause cord compression are lung cancer (non-small cell type), breast cancer, prostate cancer, renal cell carcinoma, thyroid cancer, lymphoma and multiple myeloma.

Umbilical cord compression is the obstruction of blood flow through the umbilical cord secondary to pressure from an external object or misalignment of the cord itself. Cord compression happens in about one in 10 deliveries.

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