Intracerebral bleeds are the second most common cause of stroke, accounting for 10% of hospital admissions for stroke. High blood pressure raises the risks of spontaneous intracerebral hemorrhage by two to six times. More common in adults than in children, intraparenchymal bleeds are usually due to penetrating head trauma, but can also be due to depressed skull fractures. Acceleration-deceleration trauma, rupture of an aneurysm or arteriovenous malformation (AVM), and bleeding within a tumor are additional causes. Amyloid angiopathy is a not uncommon cause of intracerebral hemorrhage in patients over the age of 55. A very small proportion is due to cerebral venous sinus thrombosis.

Risk factors for ICH include:

- Hypertension (high blood pressure)

- Diabetes mellitus

- Menopause

- Cigarette smoking

- Excessive alcohol consumption

- Severe migraine

Traumautic intracerebral hematomas are divided into acute and delayed. Acute intracerebral hematomas occur at the time of the injury while delayed intracerebral hematomas have been reported from as early as 6 hours post injury to as long as several weeks.

The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem. Intraparenchymal bleeds within the medulla oblongata are almost always fatal, because they cause damage to cranial nerve X, the vagus nerve, which plays an important role in blood circulation and breathing. This kind of hemorrhage can also occur in the cortex or subcortical areas, usually in the frontal or temporal lobes when due to head injury, and sometimes in the cerebellum.

For spontaneous ICH seen on CT scan, the death rate (mortality) is 34–50% by 30 days after the insult, and half of the deaths occur in the first 2 days. Even though the majority of deaths occurs in the first days after ICH, survivors have a long term excess mortality of 27% compared to the general population.

Intracranial hemorrhage is a serious medical emergency because the buildup of blood within the skull can lead to increases in intracranial pressure, which can crush delicate brain tissue or limit its blood supply. Severe increases in intracranial pressure (ICP) can cause brain herniation, in which parts of the brain are squeezed past structures in the skull.

Intracranial bleeding occurs when a blood vessel within the skull is ruptured or leaks. It can result from physical trauma (as occurs in head injury) or nontraumatic causes (as occurs in hemorrhagic stroke) such as a ruptured aneurysm. Anticoagulant therapy, as well as disorders with blood clotting can heighten the risk that an intracranial hemorrhage will occur.

Diabetes mellitus increases the risk of stroke by 2 to 3 times. While intensive blood sugar control has been shown to reduce small blood vessel complications such as kidney damage and damage to the retina of the eye it has not been shown to reduce large blood vessel complications such as stroke.

Nutrition, specifically the Mediterranean-style diet, has the potential for decreasing the risk of having a stroke by more than half. It does not appear that lowering levels of homocysteine with folic acid affects the risk of stroke.

Preventing or delaying premature birth is considered the most important step in decreasing the risk of PVL. Common methods for preventing a premature birth include self-care techniques (dietary and lifestyle decisions), bed rest, and prescribed anti-contraction medications. Avoiding premature birth allows the fetus to develop further, strengthening the systems affected during the development of PVL.

An emphasis on prenatal health and regular medical examinations of the mother can also notably decrease the risk of PVL. Prompt diagnosis and treatment of maternal infection during gestation reduces the likelihood of large inflammatory responses. Additionally, treatment of infection with steroids (especially in the 24–34 weeks of gestation) have been indicated in decreasing the risk of PVL.

It has also been suggested that avoiding maternal cocaine usage and any maternal-fetal blood flow alterations can decrease the risk of PVL. Episodes of hypotension or decreased blood flow to the infant can cause white matter damage.

Current clinical research ranges from studies aimed at understanding the progression and pathology of PVL to developing protocols for the prevention of PVL development. Many studies examine the trends in outcomes of individuals with PVL: a recent study by Hamrick, et al., considered the role of cystic periventricular leukomalacia (a particularly severe form of PVL, involving development of cysts) in the developmental outcome of the infant.

Other ongoing clinical studies are aimed at the prevention and treatment of PVL: clinical trials testing neuroprotectants, prevention of premature births, and examining potential medications for the attenuation of white matter damage are all currently supported by NIH funding.

Lymphocystis is a common viral disease of freshwater and saltwater fish. The viruses that cause this disease belong to the genus Lymphocystivirus of the family Iridoviridae.

Aquarists often come across this virus when their fish are stressed such as when put into a new environment and the virus is able to grow.

The fish starts growing small white pin-prick like growths on their fins or skin and this is often mistaken for Ich/Ick (Ichthyophthirius multifiliis) in the early stages. It soon clumps together to form a cauliflower-like growth on the skin, mouth, fins, and occasional gills. Lesions at the base of the dorsal fin are common among freshwater species of Central American origin, most notably Herichthys carpentis & inside the mouth of Herichthys cyanoguttatus & Geophagus steindachneri. On the tail fin of Koi, Carps, & US native sunfish (Lepomis sp.) On the side flanks of Walleye, Sauger & Flounder. On random head and/or tail areas of common goldfish, and oranda variants. This virus appears to present itself as a lesion(s) at differing locations depending on the species of fish being attacked, often complicating initial diagnosis.

Lymphocystis does show some host-specificity, i.e., each strain (or species) of lymphocystis can infect only its primary host fish, or some additional closely related, fish.

There is no known cure for this virus, though a privately owned fish research & breeding facility near Gainesville, Florida USA has reportedly been able to suppress the virus into remission using the human antiviral "Acyclovir" at the rate of 200 mg per 10 US gallons for 2 days. Otherwise, some aquarists recommend surgery to remove the affected area if it is very serious, followed by an antibiotic bath treatment to prevent a secondary bacterial infection of the open wounds.

Eventually the growths inhibit the fish's ability to swim, breathe or eat, and secondary bacterial infections usually kills the fish.

Usually the best cure is to simply give the fish a stress free life, a weekly bacteria treatment and the virus will slowly subside and the fins will repair themselves. This can take many months. Like most viral infections, even in humans, the first outbreaks are the most serious, whilst the immune system "learns" how to suppress it, the outbreaks become less severe over time assuming the organism survives the initial outbreaks.

All fish carry pathogens and parasites. Usually this is at some cost to the fish. If the cost is sufficiently high, then the impacts can be characterised as a disease. However disease in fish is not understood well. What is known about fish disease often relates to aquaria fish, and more recently, to farmed fish.

Disease is a prime agent affecting fish mortality, especially when fish are young. Fish can limit the impacts of pathogens and parasites with behavioural or biochemical means, and such fish have reproductive advantages. Interacting factors result in low grade infection becoming fatal diseases. In particular, things that causes stress, such as natural droughts or pollution or predators, can precipitate outbreak of disease.

Disease can also be particularly problematic when pathogens and parasites carried by introduced species affect native species. An introduced species may find invading easier if potential predators and competitors have been decimated by disease.

Pathogens which can cause fish diseases comprise:

- viral infections, such as esocid lymphosarcoma found in "Esox" species.

- bacterial infections, such as "Pseudomonas fluorescens" leading to fin rot and fish dropsy

- fungal infections

- water mould infections, such as "Saprolegnia" sp.

- metazoan parasites, such as copepods

- unicellular parasites, such as "Ichthyophthirius multifiliis" leading to ich

- Certain parasites like Helminths for example "Eustrongylides"

A phototoxic substance is a chemical compound which becomes toxic when exposed to light.

- Some medicines: tetracycline antibiotics, sulfonamides, amiodarone, quinolones

- Many cold pressed citrus essential oils such as bergamot oil

- Some plant juices: parsley, lime, and Heracleum mantegazzianum

- Others: psoralen

Phototoxicity, also called photoirritation, is a chemically induced skin irritation, requiring light, that does not involve the immune system. It is a type of photosensitivity.

The skin response resembles an exaggerated sunburn. The involved chemical may enter into the skin by topical administration or it may reach the skin via systemic circulation following ingestion or parenteral administration. The chemical needs to be "photoactive", which means that when it absorbs light, the absorbed energy produces molecular changes that cause toxicity. Many synthetic compounds, including drug substances like tetracyclines or fluoroquinolones, are known to cause these effects. Surface contact with some such chemicals causes photodermatitis; many plants cause phytophotodermatitis. Light-induced toxicity is a common phenomenon in humans; however, it also occurs in other animals.

Like humans and other animals, fish suffer from diseases and parasites. Fish defences against disease are specific and non-specific. Non-specific defences include skin and scales, as well as the mucus layer secreted by the epidermis that traps microorganisms and inhibits their growth. If pathogens breach these defences, fish can develop inflammatory responses that increase the flow of blood to infected areas and deliver white blood cells that attempt to destroy the pathogens.

Specific defences are specialised responses to particular pathogens recognised by the fish's body, that is adaptative immune responses. In recent years, vaccines have become widely used in aquaculture and ornamental fish, for example vaccines for furunculosis in farmed salmon and koi herpes virus in koi.

Some commercially important fish diseases are VHS, ich and whirling disease.

Poena cullei (from Latin 'penalty of the sack') under Roman law was a type of death penalty imposed on a subject who had been found guilty of parricide. The punishment consisted of being sewn up in a leather sack, sometimes with an assortment of live animals, and then being thrown into water. The punishment may have varied widely in its frequency and precise form during the Roman period. For example, the earliest fully documented case is from ca. 100 BCE, although scholars think the punishment may have developed about a century earlier (earlier than that, murderers, including parricides, would be handed over to the aggrieved family for punishment, rather than punishment being enacted by Roman state officials). Inclusion of live animals in the sack is only documented from Early Imperial times, and at the beginning, only snakes are mentioned. At the time of Emperor Hadrian (2nd century CE), the most well known form of the punishment was documented, where a cock, a dog, a monkey and a viper were inserted in the sack. However, at the time of Hadrian "poena cullei" was made into an optional form of punishment for parricides (the alternate being thrown to the beasts in the arena). During the 3rd century CE up to the accession of Emperor Constantine, "poena cullei" fell out of use; Constantine revived it, now with only serpents to be added in the sack. Well over 200 years later, Emperor Justinian reinstituted the punishment with the four animals, and "poena cullei" remained the statutory penalty for parricides within Byzantine law for the next 400 years, when it was replaced with the punishment for parricides to be burnt alive instead.

"Poena cullei" gained a revival of sorts in late medieval and early modern Germany, with late cases of being drowned in a sack along with live animals being documented from Saxony in the first half of the 18th century.

The "Wenxian Tongkao", written by Chinese historian Ma Duanlin (1245-1322), and the "History of Song" describe how the Byzantine emperor Michael VII Parapinakēs Caesar ("Mie li sha ling kai sa" 滅力沙靈改撒) of "Fu lin" (拂菻, i.e. Byzantium) sent an embassy to China's Song dynasty, arriving in November 1081, during the reign of Emperor Shenzong of Song (r. 1067-1085). The "History of Song" described the tributary gifts given by the Byzantine embassy as well as the products made in Byzantium. It also described forms of punishment in Byzantine law, such as caning, as well as the capital punishment of being stuffed into a "feather bag" and thrown into the sea. This description seems to correspond with the Romano-Byzantine punishment of "poena cullei".