External Compression Headache is caused by any type of headwear. This includes headwear that places pressure on the head — including tight hats, helmets, headbands, headphones and goggles. It is not known why some people are more sensitive than others to this type of pressure. External compression headaches can affect anyone who uses headwear. The headaches are more common among people who have migraines. It is believed to affect about four percent of the population. It is also referred to as "swim goggle headache".

These headaches can be brought on by such innocuous sources as wearing a halter top (presses against the neck), earplugs (presses against the jaw and inner ear), or wearing even a tiny hair clip (compresses the scalp). There is no known preventative treatment except to avoid the offending trigger. However, once symptoms arise and the trigger is removed, "Triptan"-type migraine treatment is effective.

ATN is usually attributed to inflammation or demyelination, with increased sensitivity of the trigeminal nerve. These effects are believed to be caused by infection, demyelinating diseases, or compression of the trigeminal nerve (by an impinging vein or artery, a tumor, or arteriovenous malformation) and are often confused with dental problems. An interesting aspect is that this form affects both men and women equally and can occur at any age, unlike typical trigeminal neuralgia, which is seen most commonly in women. Though TN and ATN most often present in the fifth decade, cases have been documented as early as infancy.

Atypical trigeminal neuralgia (ATN), or type 2 trigeminal neuralgia, is a form of trigeminal neuralgia, a disorder of the fifth cranial nerve. This form of nerve pain is difficult to diagnose, as it is rare and the symptoms overlap with several other disorders. The symptoms can occur in addition to having migraine headache, or can be mistaken for migraine alone, or dental problems such as temporomandibular joint disorder or musculoskeletal issues. ATN can have a wide range of symptoms and the pain can fluctuate in intensity from mild aching to a crushing or burning sensation, and also to the extreme pain experienced with the more common trigeminal neuralgia.

Nerve compression syndrome or compression neuropathy, also known as entrapment neuropathy, is a medical condition caused by direct pressure on a nerve. It is known colloquially as a "trapped nerve", though this may also refer to nerve root compression (by a herniated disc, for example). Its symptoms include pain, tingling, numbness and muscle weakness. The symptoms affect just one particular part of the body, depending on which nerve is affected. Nerve conduction studies help to confirm the diagnosis. In some cases, surgery may help to relieve the pressure on the nerve but this does not always relieve all the symptoms. Nerve injury by a single episode of physical trauma is in one sense a compression neuropathy but is not usually included under this heading.

A nerve may be compressed by prolonged or repeated external force, such as sitting with one's arm over the back of a chair (radial nerve), frequently resting one's elbows on a table (ulnar nerve), or an ill-fitting cast or brace on the leg (peroneal nerve). Part of the patient's body can cause the compression and the term "entrapment neuropathy" is used particularly in this situation. The offending structure may be a well-defined lesion such as a tumour (for example a lipoma, neurofibroma or metastasis), a ganglion cyst or a haematoma. Alternatively, there may be expansion of the tissues around a nerve in a space where there is little room for this to occur, as is often the case in carpal tunnel syndrome. This may be due to weight gain or peripheral oedema (especially in pregnancy), or to a specific condition such as acromegaly, hypothyroidism or scleroderma and psoriasis.

Some conditions cause nerves to be particularly susceptible to compression. These include diabetes, in which the blood supply to the nerves is already compromised, rendering the nerve more sensitive to minor degrees of compression. The genetic condition HNPP is a much rarer cause.

A 1994 community-based study indicated that two out of every 100,000 people suffered from SCSFLS, while a 2004 emergency room-based study indicated five per 100,000. SCSFLS generally affects the young and middle aged; the average age for onset is 42.3 years, but onset can range from ages 22 to 61. In an 11-year study women were found to be twice as likely to be affected as men.

Studies have shown that SCSFLS runs in families and it is suspected that genetic similarity in families includes weakness in the dura mater, which leads to SCSFLS. Large scale population-based studies have not yet been conducted. While a majority of SCSFLS cases continue to be undiagnosed or misdiagnosed, an actual increase in occurrence is unlikely.

Final outcomes for people with SCSFLS remain poorly studied. Symptoms may resolve in as little as two weeks, or persist for months. Less commonly, patients may suffer from unremitting symptoms for many years. People with chronic SCSFLS may be disabled and unable to work. Recurrent CSF leak at an alternate site after recent repair is common.

Perioperative PION patients have a higher prevalence of cardiovascular risk factors than in the general population. Documented cardiovascular risks in people affected by perioperative PION include high blood pressure, diabetes mellitus, high levels of cholesterol in the blood, tobacco use, abnormal heart rhythms, stroke, and obesity. Men are also noted to be at higher risk, which is in accordance with the trend, as men are at higher risk of cardiovascular disease. These cardiovascular risks all interfere with adequate blood flow, and also may suggest a contributory role of defective vascular autoregulation.

There are many causes of TOS. The most frequent cause is trauma, either sudden (as in a clavicle fracture caused by a car accident), or repetitive (as in a legal secretary who works with his/her hands, wrists, and arms at a fast paced desk station with non-ergonomic posture for many years). TOS is also found in certain occupations involving lots of lifting of the arms and repetitive use of the wrists and arms.

One cause of arterial compression is trauma, and a recent case involving fracture of the clavicle has been reported.

The two groups of people most likely to develop TOS are those suffering from neck injuries due to traffic accidents and those who use computers in non-ergonomic postures for extended periods of time. TOS is frequently a repetitive stress injury (RSI) caused by certain types of work environments. Other groups which may develop TOS are athletes who frequently raise their arms above the head (such as swimmers, volleyball players, dancers, badminton players, baseball pitchers, and weightlifters), rock climbers, electricians who work long hours with their hands above their heads, and some musicians.

Many cases resolve within 1–2 weeks of controlling blood pressure and eliminating the inciting factor. However some cases may persist with permanent neurologic impairment in the form of visual changes and seizures among others. Though uncommon, death may occur with progressive swelling of the brain (cerebral edema), compression of the brainstem, increased intracranial pressure, or a bleed in the brain (intracerebral hemorrhage). PRES may recur in about 5-10% of cases; this occurs more commonly in cases precipitated by hypertension as opposed to other factors (medications, etc.).

Neurapraxia is most commonly observed in athletes involved in collision sports, such as American football. Athletes participating in collision sports most often suffer from cervical cord neurapraxia, also known as transient neurapraxia. Cervical cord neurapraxia is the result of a severe collision in which a blow to the crown of the athlete’s head forcefully extends or compresses the neck. Numbness, stinging, and/or weakness in the arms, legs or both, distinguish cervical cord neurapraxia. Typical episodes of transient nuerapraxia only last a few seconds and symptoms dissipate entirely. Though the severity of the injury can range, transient neurapraxia does not lead to permanent paralysis of the affected muscles. Subsequent spinal cord injury after an episode of cervical cord neurapraxia has not been observed. However, athletes who experience an episode of transient cervical neurapraxia face an approximately 50% chance of a repeat episode if they continue to participate in collision sports.

The number cases of PRES that occur each year is not known. It may be somewhat more common in females.

As illustrated by the risk factors above, perioperative hypoxia is a multifactorial problem. Amidst these risk factors it may be difficult to pinpoint the optic nerve’s threshold for cell death, and the exact contribution of each factor.

Low blood pressure and anemia are cited as perioperative complications in nearly all reports of PION, which suggests a causal relationship. However, while low blood pressure and anemia are relatively common in the perioperative setting, PION is exceedingly rare. Spine and cardiac bypass surgeries have the highest estimated incidences of PION, 0.028% and 0.018% respectively, and this is still extremely low. This evidence suggests that optic nerve injury in PION patients is caused by more than just anemia and low blood pressure.

Evidence suggests that the multifactorial origin of perioperative PION involves the risks discussed above and perhaps other unknown factors. Current review articles of PION propose that vascular autoregulatory dysfunction and anatomic variation are under-investigated subjects that may contribute to patient-specific susceptibility.

10-15% of intracranial AV malformations are DAVFs. There is a higher preponderance in females (61-66%), and typically patients are in their fourth or fifth generation of life. DAVFs are rarer in children.

Neurapraxia is a disorder of the peripheral nervous system in which there is a temporary loss of motor and sensory function due to blockage of nerve conduction, usually lasting an average of six to eight weeks before full recovery. Neurapraxia is derived from the word apraxia, meaning “loss or impairment of the ability to execute complex coordinated movements without muscular or sensory impairment”.

This condition is typically caused by a blunt neural injury due to external blows or shock-like injuries to muscle fibers and skeletal nerve fibers, which leads to repeated or prolonged pressure buildup on the nerve. As a result of this pressure, ischemia occurs, a neural lesion results, and the human body naturally responds with edema extending in all directions from the source of the pressure. This lesion causes a complete or partial action potential conduction block over a segment of a nerve fiber and thus a reduction or loss of function in parts of the neural connection downstream from the lesion, leading to muscle weakness.

Neurapraxia results in temporary damage to the myelin sheath but leaves the nerve intact and is an impermanent condition; thus, Wallerian degeneration does not occur in neurapraxia. In order for the condition to be considered neurapraxia, according to the Seddon classification system of peripheral nerve injury, there must be a complete and relatively rapid recovery of motor and sensory function once nerve conduction has been restored; otherwise, the injury would be classified as axonotmesis or neurotmesis. Thus, neurapraxia is the mildest classification of peripheral nerve injury.

Neurapraxia is very common in professional athletes, especially American football players, and is a condition that can and should be treated by a physician.

Dexamethasone (a potent glucocorticoid) in doses of 16 mg/day may reduce edema around the lesion and protect the cord from injury. It may be given orally or intravenously for this indication.

Surgery is indicated in localised compression as long as there is some hope of regaining function. It is also occasionally indicated in patients with little hope of regaining function but with uncontrolled pain. Postoperative radiation is delivered within 2–3 weeks of surgical decompression. Emergency radiation therapy (usually 20 Gray in 5 fractions, 30 Gray in 10 fractions or 8 Gray in 1 fraction) is the mainstay of treatment for malignant spinal cord compression. It is very effective as pain control and local disease control. Some tumours are highly sensitive to chemotherapy (e.g. lymphomas, small-cell lung cancer) and may be treated with chemotherapy alone.

Once complete paralysis has been present for more than about 24 hours before treatment, the chances of useful recovery are greatly diminished, although slow recovery, sometimes months after radiotherapy, is well recognised.

The median survival of patients with metastatic spinal cord compression is about 12 weeks, reflecting the generally advanced nature of the underlying malignant disease.

TOS can be attributed to one or more of the following factors:

- Congenital abnormalities are frequently found in persons with TOS. These include cervical rib, prolonged transverse process, and muscular abnormalities (e.g., in the scalenus anterior muscle, a sickle-shaped scalenus medius) or fibrous connective tissue anomalies.

- Trauma (e.g., whiplash injuries) or repetitive strain is frequently implicated.

- Rarer acquired causes include tumors, hyperostosis, and osteomyelitis

Arachnoid cysts are seen in up to 1.1% of the population with a gender distribution of 2:1 male:female Only 20% of these have symptoms, usually from secondary hydrocephalus.

A study that looked at 2,536 healthy young males found a prevalence of 1.7% (95% CI 1.2 to 2.3%). Only a small percentage of the detected abnormalities require urgent medical attention.

There are few studies of the long-term outcomes of patients treated for MALS. According to Duncan, the largest and more relevant late outcomes data come from a study of 51 patients who underwent open surgical treatment for MALS, 44 of whom were available for long-term follow-up at an average of nine years following therapy. The investigators reported that among patients who underwent celiac artery decompression and revascularization, 75% remained asymptomatic at follow-up. In this study, predictors of favorable outcome included:

- Age from 40 to 60 years

- Lack of psychiatric condition or alcohol use

- Abdominal pain that was worse after meals

- Weight loss greater than 20 lb (9.1 kg)

The most common causes in young children are birth trauma and a type of cancer called neuroblastoma. The cause of about a third of cases in children is unknown.

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.

Most arachnoid cysts are asymptomatic, and do not require treatment. Where complications are present, leaving arachnoid cysts untreated, may cause permanent severe neurological damage due to the progressive expansion of the cyst(s) or hemorrhage (bleeding). However, with treatment most individuals with symptomatic arachnoid cysts do well.

More specific prognoses are listed below:

- Patients with impaired preoperative cognition had postoperative improvement after surgical decompression of the cyst.

- Surgery can resolve psychiatric manifestations in selected cases.

A 2014 meta-analysis of three small trials evaluating probiotics showed a slight improvement in management of chronic idiopathic constipation, but well-designed studies are necessary to know the true efficacy of probiotics in treating this condition.

Children with functional constipation often claim to lack the sensation of the urge to defecate, and may be conditioned to avoid doing so due to a previous painful experience. One retrospective study showed that these children did indeed have the urge to defecate using colonic manometry, and suggested behavioral modification as a treatment for functional constipation.

Complications are likely to result in cases of excess blood loss or punctures to certain organs, possibly leading to shock. Swelling and bruising may result, more so in high-impact injuries. Pain in the affected areas may differ where severity of impact increases its likelihood and may radiate if symptoms are aggravated when one moves around.

According to a review of 51 studies from 21 countries, the average incidence of subarachnoid hemorrhage is 9.1 per 100,000 annually. Studies from Japan and Finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not entirely understood. South and Central America, in contrast, have a rate of 4.2 per 100,000 on average.

Although the group of people at risk for SAH is younger than the population usually affected by stroke, the risk still increases with age. Young people are much less likely than middle-age people (risk ratio 0.1, or 10 percent) to have a subarachnoid hemorrhage. The risk continues to rise with age and is 60 percent higher in the very elderly (over 85) than in those between 45 and 55. Risk of SAH is about 25 percent higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from the menopause, such as a decrease in estrogen levels.

Genetics may play a role in a person's disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid hemorrhage. However, lifestyle factors are more important in determining overall risk. These risk factors are smoking, hypertension (high blood pressure), and excessive alcohol consumption. Having smoked in the past confers a doubled risk of SAH compared to those who have never smoked. Some protection of uncertain significance is conferred by caucasian ethnicity, hormone replacement therapy, and diabetes mellitus. There is likely an inverse relationship between total serum cholesterol and the risk of non-traumatic SAH, though confirmation of this association is hindered by a lack of studies. Approximately 4 percent of aneurysmal bleeds occur after sexual intercourse and 10 percent of people with SAH are bending over or lifting heavy objects at the onset of their symptoms.

Overall, about 1 percent of all people have one or more cerebral aneurysms. Most of these, however, are small and unlikely to rupture.