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.

Subdural hematoma occurs when there is tearing of the bridging vein between the cerebral cortex and a draining venous sinus. At times they may be caused by arterial lacerations on the brain surface. Acute subdural hematomas are usually associated with cerebral cortex injury as well and hence the prognosis is not as good as extra dural hematomas. Clinical features depend on the site of injury and severity of injury. Patients may have a history of loss of consciousness but they recover and do not relapse. Clinical onset occurs over hours. A crescent shaped hemorrhage compressing the brain that does cross suture lines will be noted on CT of the head. Craniotomy and surgical evacuation is required if there is significant pressure effect on the brain.Complications include focal neurologic deficits depending on the site of hematoma and brain injury, increased intra cranial pressure leading to herniation of brain and ischemia due to reduced blood supply and seizures.

Epidural hematoma (EDH) is a rapidly accumulating hematoma between the dura mater and the cranium. These patients have a history of head trauma with loss of consciousness, then a lucid period, followed by loss of consciousness. Clinical onset occurs over minutes to hours. Many of these injuries are associated with lacerations of the middle meningeal artery. A "lenticular", or convex, lens-shaped extracerebral hemorrhage that does not cross suture lines will likely be visible on a CT scan of the head. Although death is a potential complication, the prognosis is good when this injury is recognized and treated.

As only 10 percent of people admitted to the emergency department with a thunderclap headache are having an SAH, other possible causes are usually considered simultaneously, such as meningitis, migraine, and cerebral venous sinus thrombosis. Intracerebral hemorrhage, in which bleeding occurs within the brain itself, is twice as common as SAH and is often misdiagnosed as the latter. It is not unusual for SAH to be initially misdiagnosed as a migraine or tension headache, which can lead to a delay in obtaining a CT scan. In a 2004 study, this occurred in 12 percent of all cases and was more likely in people who had smaller hemorrhages and no impairment in their mental status. The delay in diagnosis led to a worse outcome. In some people, the headache resolves by itself, and no other symptoms are present. This type of headache is referred to as "sentinel headache", because it is presumed to result from a small leak (a "warning leak") from an aneurysm. A sentinel headache still warrants investigations with CT scan and lumbar puncture, as further bleeding may occur in the subsequent three weeks.

The initial steps for evaluating a person with a suspected subarachnoid hemorrhage are obtaining a medical history and performing a physical examination. The diagnosis cannot, however, be made on clinical grounds alone and in general medical imaging and possibly a lumbar puncture is required to confirm or exclude bleeding.

A headache is called "thunderclap headache" if it is severe in character and reaches maximum severity within seconds to minutes of onset. In many cases, there are no other abnormalities, but the various causes of thunderclap headaches may lead to a number of neurological symptoms. The most important causes are subarachnoid hemorrhage, cerebral venous sinus thrombosis, and cervical artery dissection.

In subarachnoid hemorrhage, there may be syncope (transient loss of consciousness), seizures, meningism (neck pain and stiffness), visual symptoms, and vomiting. 50–70% of people with subarachnoid hemorrhage have an isolated headache without decreased level of consciousness. The headache typically persists for several days.

Cerebral venous sinus thrombosis, thrombosis of the veins of the brain, usually causes a headache that reflects raised intracranial pressure and is therefore made worse by anything that makes the pressure rise further, such as coughing. In 2–10% of cases, the headache is of thunderclap character. In most cases there are other neurological abnormalities, such as seizures and weakness of part of the body, but in 15–30% the headache is the only abnormality.

Carotid artery dissection and vertebral artery dissection (together cervical artery dissection), in which a tear forms inside the wall of the blood vessels that supply the brain, often causes pain on the affected side of the head or neck. The pain usually precedes other problems that are caused by impaired blood flow through the artery into the brain; these may include visual symptoms, weakness of part of the body, and other abnormalities depending on the vessel affected.

Thunderclap headaches can be caused by a number of primary conditions including:

- Subarachnoid hemorrhage (10–25% of all cases of thunderclap headache)

- Cerebral venous sinus thrombosis

- Cervical artery dissection

- Hypertensive emergency (severely raised blood pressure)

- Spontaneous intracranial hypotension (unexplained low cerebrospinal fluid pressure)

- Stroke (headache occurs in about 25% of strokes but usually not thunderclap character)

- Retroclival hematoma (hematoma behind the clivus in the skull, usually due to physical trauma but sometimes spontaneous)

- Pituitary apoplexy (infarction or hemorrhage of the pituitary gland)

- Colloid cyst of the third ventricle

- Meningitis (rarely features thunderclap headache)

- Reversible cerebral vasoconstriction syndrome (previously Call-Fleming syndrome, several subtypes)

- Primary cough headache, primary exertional headache, and primary sexual headache

- Primary thunderclap headache

Terson syndrome or Terson's syndrome is the occurrence of a vitreous hemorrhage of the human eye in association with subarachnoid hemorrhage. Vitreous hemorrhage of the eye can also occur in association with intracranial hemorrhage and elevated intracranial pressure (ICP). Intraocular hemorrhage can be a subretinal, retinal, preretinal, subhyaloidal, or intra-vitreal hemorrhage. Its likely cause is a rapid increase in ICP. The classic presentation is in the subhyaloidal space, which is beneath the posterior vitreous face and in front of the retina.

In subarachnoid hemorrhage, 13% of patients have Terson's syndrome, which is associated with more severe SAH (higher Hunt-Hess score, a marker of severity), and risk of death is significantly increased.

The first known report of the association was by the German ophthalmologist Moritz Litten in 1881. Still, French ophthalmologist Albert Terson's name is more commonly associated with the condition after a report by his hand from 1900.

The initial symptoms of pituitary apoplexy are related to the increased pressure in and around the pituitary gland. The most common symptom, in over 95% of cases, is a sudden-onset headache located behind the eyes or around the temples. It is often associated with nausea and vomiting. Occasionally, the presence of blood leads to irritation of the lining of the brain, which may cause neck rigidity and intolerance to bright light, as well as a decreased level of consciousness. This occurs in 24% of cases.

Pressure on the part of the optic nerve known as the chiasm, which is located above the gland, leads to loss of vision on the outer side of the visual field on both sides, as this corresponds to areas on the retinas supplied by these parts of the optic nerve; it is encountered in 75% of cases. Visual acuity is reduced in half, and over 60% have a visual field defect. The visual loss depends on which part of the nerve is affected. If the part of the nerve between the eye and the chiasm is compressed, the result is vision loss in one eye. If the part after the chiasm is affected, visual loss on one side of the visual field occurs.

Adjacent to the pituitary lies a part of the skull base known as the cavernous sinus. This contains a number of nerves that control the eye muscles. 70% of people with pituitary apoplexy experience double vision due to compression of one of the nerves. In half of these cases, the oculomotor nerve (the third cranial nerve), which controls a number of eye muscles, is affected. This leads to diagonal double vision and a dilated pupil. The fourth (trochlear) and sixth (abducens) cranial nerves are located in the same compartment and can cause diagonal or horizontal double vision, respectively. The oculomotor nerve is predominantly affected as it lies closest to the pituitary. The cavernous sinus also contains the carotid artery, which supplies blood to the brain; occasionally, compression of the artery can lead to one-sided weakness and other symptoms of stroke.

Pituitary apoplexy or pituitary tumor apoplexy is bleeding into or impaired blood supply of the pituitary gland at the base of the brain. This usually occurs in the presence of a tumor of the pituitary, although in 80% of cases this has not been diagnosed previously. The most common initial symptom is a sudden headache, often associated with a rapidly worsening visual field defect or double vision caused by compression of nerves surrounding the gland. This is followed in many cases by acute symptoms caused by lack of secretion of essential hormones, predominantly adrenal insufficiency.

The diagnosis is achieved with magnetic resonance imaging and blood tests. Treatment is by the timely correction of hormone deficiencies, and in many cases surgical decompression is required. Many people who have had a pituitary apoplexy develop pituitary hormone deficiencies and require long-term hormone supplementation. The first case of the disease was recorded in 1898.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by excessive unsuppressible release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. Unsuppressed ADH causes an unrelenting increase in solute-free water being returned by the tubules of the kidney to the venous circulation.

ADH is derived from a preprohormone precursor that is synthesized in cells in the hypothalamus and stored in vesicles in the posterior pituitary. "Appropriate" ADH secretion is regulated by osmoreceptors on the hypothalamic cells that synthesize and store ADH: plasma hypertonicity activates these receptors, ADH is released into the blood stream, the kidney increases solute-free water return to the circulation, and the hypertonicity is alleviated. "Inappropriate" ADH secretion causes a "unrelenting increase" in solute-free water ("free water") absorption by the kidneys, with two consequences. First, in the extracellular fluid (ECF) space, there is a dilution of blood solutes, causing hypoosmolality, including a low sodium concentration - hyponatremia. Then virtually simultaneously, in the intracellular space, cells swell, i.e. intracellular volume increases. Swelling of brain cells causes various neurological abnormalities which in severe or acute cases can result in convulsions, coma, and death.

The causes of SIADH are grouped into six categories: 1) central nervous system diseases that directly stimulate the hypothalamus, the site of control of ADH secretion; 2) various cancers that synthesize and secrete ectopic ADH; 3) various pulmonary diseases; 4) numerous (at least seventeen) drugs that chemically stimulate the hypothalamus; 5) inherited mutations that cause aquaporins always to be "turned on"; and 6) miscellaneous largely transient conditions.

Potential treatments of SIADH include restriction of fluid intake, correction of an identifiable reversible underlying cause, and/or medication which promotes solute-free water excretion by the kidney. The presence of cerebral edema may necessitate intravenous isotonic or hypertonic saline administration.

SIADH was originally described in 1957 in two people with small-cell carcinoma of the lung.

Antidiuretic hormone (ADH) is released from the posterior pituitary for a number of physiologic reasons. The majority of people with hyponatremia, other than those with excessive water intake (polydipsia) or renal salt wasting, will have elevated ADH as the cause of their hyponatremia. However, not every person with hyponatremia and elevated ADH has SIADH. One approach to a diagnosis is to divide ADH release into appropriate (not SIADH) or inappropriate (SIADH).

Appropriate ADH release can be a result of hypovolemia, a so-called osmotic trigger of ADH release. This may be true hypovolemia, as a result of dehydration with fluid losses replaced by free water. It can also be perceived hypovolemia, as in the conditions of congestive heart failure (CHF) and cirrhosis in which the kidneys perceive a lack of intravascular volume. The hyponatremia caused by appropriate ADH release (from the kidneys' perspective) in both CHF and cirrhosis have been shown to be an independent poor prognostic indicator of mortality.

Appropriate ADH release can also be a result of non-osmotic triggers. Symptoms such as nausea/vomiting and pain are significant causes of ADH release. The combination of osmotic and non-osmotic triggers of ADH release can adequately explain the hyponatremia in the majority of people who are hospitalized with acute illness and are found to have mild to moderate hyponatremia. SIADH is less common than appropriate release of ADH. While it should be considered in a differential, other causes should be considered as well.

Cerebral salt wasting syndrome (CSWS) also presents with hyponatremia, there are signs of dehydration for which reason the management is diametrically opposed to SIADH. Importantly CSWS can be associated with subarachnoid hemorrhage (SAH) which may require fluid supplementation rather than restriction to prevent brain damage.

Most cases of hyponatremia in children are caused by appropriate secretion of antidiuretic hormone rather than SIADH or another cause.