Clinical manifestations of intraparenchymal hemorrhage are determined by the size and location of hemorrhage, but may include the following:

- Hypertension, fever, or cardiac arrhythmias

- Nuchal rigidity

- Subhyaloid retinal hemorrhages

- Altered level of consciousness

- Anisocoria, Nystagmus

- Focal neurological deficits

- Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopsia, aphasia, neglect, or apraxia

- Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion

- Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia

- Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion

- Brain stem - Tetraparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability

- Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness

Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately but can be delayed as much as 2 weeks. If the bleeds are large enough to put pressure on the brain, signs of increased ICP (intracranial pressure) or damage to part of the brain will be present.

Other signs and symptoms of subdural hematoma can include any combination of the following:

- A history of recent head injury

- Loss of consciousness or fluctuating levels of consciousness

- Irritability

- Seizures

- Pain

- Numbness

- Headache (either constant or fluctuating)

- Dizziness

- Disorientation

- Amnesia

- Weakness or lethargy

- Nausea or vomiting

- Loss of appetite

- Personality changes

- Inability to speak or slurred speech

- Ataxia, or difficulty walking

- Loss of muscle control

- Altered breathing patterns

- Hearing loss or hearing ringing (tinnitus)

- Blurred Vision

- Deviated gaze, or abnormal movement of the eyes.

Subdural hematomas are divided into acute, subacute, and chronic, depending on the speed of their onset. Acute subdural hematomas that are due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression.

Acute bleeds often develop after high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas. They are most severe if associated with cerebral contusions. Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the typically arterial bleeding of an epidural hemorrhage. Acute subdural bleeds have a high mortality rate, higher even than epidural hematomas and diffuse brain injuries, because the force (acceleration/deceleration) required to cause them causes other severe injuries as well. The mortality rate associated with acute subdural hematoma is around 60 to 80%.

Chronic subdural bleeds develop over a period of days to weeks, often after minor head trauma, though such a cause is not identifiable in 50% of patients. They may not be discovered until they present clinically months or years after a head injury. The bleeding from a chronic bleed is slow, probably from repeated minor bleeds, and usually stops by itself. Since these bleeds progress slowly, they present the chance of being stopped before they cause significant damage. Small chronic subdural hematomas, those less than a centimeter wide, have much better outcomes than acute subdural bleeds: in one study, only 22% of patients with chronic subdural bleeds had outcomes worse than "good" or "complete recovery". Chronic subdural hematomas are common in the elderly.

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.

Intraparenchymal hemorrhage (IPH) is one form of intracerebral bleeding in which there is bleeding within brain parenchyma. The other form is intraventricular hemorrhage (IVH).

Intraparenchymal hemorrhage accounts for approx. 8-13% of all strokes and results from a wide spectrum of disorders. It is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage, and therefore constitutes an immediate medical emergency. Intracerebral hemorrhages and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure (ICP) and potentially fatal herniation syndromes.

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.

Four grades are distinguished (by imaging or histology):

- grade I - hemorrhage is confined to the germinal matrix

- grade II - intraventricular hemorrhage without ventricular dilatation

- grade III - intraventricular hemorrhage with ventricular dilatation

- grade IV - intraventricular rupture and hemorrhage into the surrounding white matter

This may lead to various neurological sequelae including presentation with cerebral palsy, mental retardation and seizures.

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.

First symptoms may be subtle such as mild pain, flank tenderness, haematuria. Depending on blood loss, symptoms of hypovolemic shock may develop. Hematoma is usually contained in the retroperitoneum, allowing for a period of haemodynamic stability. Sometimes massive acute hemorrhage is seen when a hematoma ruptures Gerota's fascia and extends into the peritoneum. An ultrasound or CT scan can establish diagnosis, while lab tests may be inconclusive as changes of haematocrit or haemoglobin are not specific to the syndrome, while haematuria is not always present.

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.

If a Charcot–Bouchard aneurysm ruptures, it will lead to an intracerebral hemorrhage, which can cause hemorrhagic stroke, typically experienced as a sudden focal paralysis or loss of sensation.

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

Wunderlich syndrome is spontaneous, nontraumatic renal hemorrhage confined to the subcapsular and perirenal space. It may be the first manifestation of a renal angiomyolipoma (AML), or rupture of renal artery or intraparechymal aneurysm.

The primary symptom, hemorrhage, presents differently depending on the degree of injury, with the symptoms of major hemorrhage, shock, abdominal pain, and distention being clinically obvious. Minor hemorrhage often presents as upper left quadrant pain. Patients with unexplained left upper quadrant pain, particularly if there is evidence of hypovolemia or shock, are generally inquired regarding any recent trauma.

Charcot–Bouchard aneurysms (also known as miliary aneurysms or microaneurysms) are aneurysms of the brain vasculature which occur in small blood vessels (less than 300 micrometre diameter). Charcot–Bouchard aneurysms are most often located in the lenticulostriate vessels of the basal ganglia and are associated with chronic hypertension. Charcot–Bouchard aneurysms are a common cause of cerebral hemorrhage.

The main risk is intracranial hemorrhage. This risk is difficult to quantify since many patients with asymptomatic AVMs will never come to medical attention. Small AVMs tend to bleed more often than do larger ones, the opposite of cerebral aneurysms. If a rupture or bleeding incident occurs, the blood may penetrate either into the brain tissue (cerebral hemorrhage) or into the subarachnoid space, which is located between the sheaths (meninges) surrounding the brain (subarachnoid hemorrhage). Bleeding may also extend into the ventricular system (intraventricular hemorrhage). Cerebral hemorrhage appears to be most common.

One long-term study (mean follow up greater than 20 years) of over 150 symptomatic AVMs (either presenting with bleeding or seizures) found the risk of cerebral hemorrhage to be approximately 4% per year, slightly higher than the 2-3% seen in other studies. A simple, rough approximation of a patient's lifetime bleeding risk is 105 - (patient age in years), assuming a 3% bleed risk annually. For example, a healthy 30-year-old patient would have approximately a 75% lifetime risk of at least one bleeding event. Ruptured AVMs are a significant source or morbidity and mortality; post rupture, as many as 29% of patients will die, and only 55% will be able to live independently.

The primary concern in any splenic trauma is internal hemorrhage, though the exact amount of hemorrhage may be small or large, depending on the nature and degree of injury. Small or minor injuries often heal spontaneously, especially in children. Larger injuries hemorrhage extensively, often causing hemorrhagic shock. A splenic hematoma sometimes ruptures, usually in the first few days, although rupture can occur from hours to even months after injury.

If an aneurysm ruptures, blood leaks into the space around the brain. This is called a subarachnoid hemorrhage. Onset is usually sudden without prodrome, classically presenting as a "thunderclap headache" worse than previous headaches. Symptoms of a subarachnoid hemorrhage differ depending on the site and size of the aneurysm. Symptoms of a ruptured aneurysm can include:

- a sudden severe headache that can last from several hours to days

- nausea and vomiting

- drowsiness, confusion and/or loss of consciousness

- visual abnormalities

- meningism

Almost all aneurysms rupture at their apex. This leads to hemorrhage in the subarachnoid space and sometimes in brain parenchyma. Minor leakage from aneurysm may precede rupture, causing warning headaches. About 60% of patients die immediately after rupture. Larger aneurysms have a greater tendency to rupture, though most ruptured aneurysms are less than 10 mm in diameter.

The risk of a subarachnoid hemorrhage is greater with a saccular aneurysm than a fusiform aneurysm.

A ruptured microaneurysm may cause an intracerebral hemorrhage, presenting as a focal neurological deficit.

Rebleeding, hydrocephalus (the excessive accumulation of cerebrospinal fluid), vasospasm (spasm, or narrowing, of the blood vessels), or multiple aneurysms may also occur. The risk of rupture from a cerebral aneurysm varies according to the size of an aneurysm, with the risk rising as the aneurysm size increases.

If severe the child may develop jaundice, anemia or hypotension. In some cases it may be an indication of a linear skull fracture or be at risk of an infection leading to osteomyelitis or meningitis.

The swelling of a cephalohematoma takes weeks to resolve as the blood clot is slowly absorbed from the periphery towards the centre. In time the swelling hardens (calcification) leaving a relatively softer centre so that it appears as a 'depressed fracture'.

Cephalohematoma should be distinguished from another scalp bleeding called subgaleal hemorrhage (also called subaponeurotic hemorrhage), which is blood between the scalp and skull bone (above the periosteum) and is more extensive. It is more prone to complications, especially anemia and bruising.

Mortality of IIA is high, unruptured IIA are associated with a mortality reaching 30%, while ruptured IIA has a mortality of up to 80%. IIAs caused by fungal infections have a worse prognosis than those caused by bacterial infection.

Grey Turner's sign refers to bruising of the s, the part of the body between the last rib and the top of the hip. The bruising appears as a blue discoloration, and is a sign of retroperitoneal hemorrhage, or bleeding behind the peritoneum, which is a lining of the abdominal cavity. Grey Turner's sign takes 24–48 hours to develop, and can predict a severe attack of acute pancreatitis.

Grey Turner's sign may be accompanied by Cullen's sign. Both signs may be indicative of pancreatic necrosis with retroperitoneal or intraabdominal bleeding. Grey Turner's sign is named after British surgeon George Grey Turner.

The usual causes of a cephalohematoma are a prolonged second stage of labor or instrumental delivery, particularly forceps delivery. Ventouse application does not increase the incidence of cephalhematoma.

Causes include

- Acute pancreatitis, whereby methemalbumin formed from digested blood tracks subcutaneously around the abdomen from the inflamed pancreas.

- Pancreatic hemorrhage

- Retroperitoneal hemorrhage

- Blunt abdominal trauma

- Ruptured / hemorrhagic ectopic pregnancy.

- Spontaneous bleeding secondary to coagulopathy (congenital or acquired)

- Aortic rupture, from ruptured abdominal aortic aneurysm or other causes.