Arachnoiditis is a chronic disorder with no known cure, and prognosis may be hard to determine because of an unclear correlation between the beginning of the disease and the appearance of symptoms. For many, arachnoiditis is a disabling disease that causes chronic pain and neurological deficits, and may also lead to other spinal cord conditions, such as syringomyelia.

The root cause of the condition is not entirely clear, and it appears to have multiple causes, including iatrogenic cause from misplaced epidural steroid injection therapy when accidentally administered intrathecally (inside the dura mater, the sac enveloping the arachnoid mater), or from contrast media used in myelography prior to the introduction of Metrizamide. Other noninfectious inflammatory processes include surgery, intrathecal hemorrhage, and the administration of anesthetics (e.g. chloroprocaine), and steroids (e.g. prednisolone, triamcinolone acetonide). A variety of other causes exist, including infectious, inflammatory, and neoplastic processes. Infectious causes include bacterial, viral, fungal, and parasitic agents. Prior spinal surgery has been documented as a cause of "arachnoiditis ossificans", as well as for the adhesive form. It can also be caused by long term pressure from either a severe disc herniation or spinal stenosis.

Generally, there are two forms of syringomyelia: congenital and acquired. (In addition, one form of the disorder involves the brainstem. The brainstem controls many of our vital functions, such as respiration and heartbeat. When syrinxes affect the brainstem, the condition is called syringobulbia.)

The first major form relates to an abnormality of the brain called an Arnold–Chiari malformation or Chiari Malformation. This is the most common cause of syringomyelia, where the anatomic abnormality, which may be due to a small posterior fossa, causes the lower part of the cerebellum to protrude from its normal location in the back of the head into the cervical or neck portion of the spinal canal. A syrinx may then develop in the cervical region of the spinal cord. Here, symptoms usually begin between the ages of 25 and 40 and may worsen with straining, called a valsalva maneuver, or any activity that causes cerebrospinal fluid pressure to fluctuate suddenly. Some patients, however, may have long periods of stability. Some patients with this form of the disorder also have hydrocephalus, in which cerebrospinal fluid accumulates in the skull, or a condition called arachnoiditis, in which a covering of the spinal cord—the arachnoid membrane—is inflamed.

Some cases of syringomyelia are familial, although this is rare.

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.

The exact cause of arachnoid cysts is not known. Researchers believe that most cases of arachnoid cysts are developmental malformations that arise from the unexplained splitting or tearing of the arachnoid membrane.

In some cases, arachnoid cysts occurring in the middle fossa are accompanied by underdevelopment (hypoplasia) or compression of the temporal lobe. The exact role that temporal lobe abnormalities play in the development of middle fossa arachnoid cysts is unknown.

There are some cases where hereditary disorders have been connected with arachnoid cysts.

Some complications of arachnoid cysts can occur when a cyst is damaged because of minor head trauma. Trauma can cause the fluid within a cyst to leak into other areas (e.g., subarachnoid space). Blood vessels on the surface of a cyst may tear and bleed into the cyst (intracystic hemorrhage), increasing its size. If a blood vessel bleeds on the outside of a cyst, a collection of blood (hematoma) may result. In the cases of intracystic hemorrhage and hematoma, the individual may have symptoms of increased pressure within the cranium and signs of compression of nearby nerve (neural) tissue.

Some scientists debate whether arachnoid cysts are a true congenite condition or if this should be separated from secondary cysts. A recent study shows differences in communication between the arachnoid cyst and the subarachnoid space by CT cisternography

. A comparison of arachnoid cyst fluid and CSF in a series of patients show differences in chemical composition.

Arachnoid cysts can also occur secondary to other disorders such as Marfan syndrome, arachnoiditis, or agenesis of the corpus callosum.

When Tarlov cysts are ruptured or drained they cause leakage of cerebrospinal fluid (CSF). Ruptures of Tarlov cysts have been reported associated with communicating aneurysms and from fracture in the proximity of the cysts. An undetected rupture can cause intracranial hypotension, including orthostatic neurological symptoms along with headache, nausea, and vomiting that improve when supine. The ruptured cysts can be patched either with a biosynthetic dural patch or using a blood patch to stem the flow of CSF.

Tarlov cysts are known to have the tendency to enlarge over time. The prominent theory that explains this phenomenon reasons the enlargement of the cysts is due to the cerebrospinal fluid being pushed into the cyst during systole pulsation, but unable to get out during the diastole phase, resulting in enlargement observed in clinical settings over time. Increased ICP from trauma or other injury, childbirth, and overextertion are thought to trigger enlargement along with inflammation and hemorrhagic infiltration. With the cysts often containing a valve like mechanism fluid becomes trapped, and the meningeal sac or nerve sheath grows in size. Some patients have been diagnosed for up to 20 years with little change in size, and those with small stable cysts may avoid much progression of symptoms. Those with generally larger sacral cysts pressed along the sacrum cause the sacrum to become eroded and thin.

Spinal arteriovenous malformations (AVMs, or angiomatous malformations) are congenital (from birth) abnormalities of blood vessels. Arteries that directly communicate with veins bypass the capillary network (which has not yet developed) and thus creates a shunt. AVMs appear as a mass of , dilated vessels. In regards to the spinal cord, they are usually located in the thoracolumbar region (between the thoracic and lumbar regions, 60% of the time), as opposed to the upper thoracic (20%) and cervical regions (approximately 15%). Cervical malformations arise from the anterior spinal artery and lie within the cord, whereas thoracolumbar malformations can be internal, external or encompass both areas of the cord.

Malformations can be recognised as part of an acute illness or gradual onset disease. In diseases such as subarachnoid hemorrhage, signs and symptoms include headache, neck stiffness and back and leg pain. Extradural, subdural and intramedullary hematomas are all signs of acute cord compression. Gradual onset diseases are more common (85-90% of all diseases leading to a diagnosis of malformation) and are usually due to an increased venous pressure. Other factors such as thrombosis or arachnoiditis can be involved. A bruit (unusual blood sounds) may be heard overlying the spinal arteriovenous malformation. Very occasionally, nevus (moles) or angiolipomas are found.

Myelography is used to confirm the diagnosis of AVMs and it shows 'snake-like' vessels on the cord's surface. If the myelogram is positive, angiography is required to show the extent of malformation and the exact site of the shunt. Magnetic resonance imaging (MRI) may show the appropriate area. If AVMs are left untreated, 50% of patients with gradual symptoms will be unable to walk within 3 years of onset. Operations can prevent progression and may improve any gait or incontinence.

Vascular myelopathy (vascular disease of the spinal cord) refers to an abnormality of the spinal cord in regard to its blood supply. The blood supply is complicated and supplied by two major vessel groups: the posterior spinal arteries and the anterior spinal arteries—of which the Artery of Adamkiewicz is the largest. Both the posterior and anterior spinal arteries run the entire length of the spinal cord and receive anastomotic (conjoined) vessels in many places. The anterior spinal artery has a less efficient supply of blood and is therefore more susceptible to vascular disease. Whilst atherosclerosis of spinal arteries is rare, necrosis (death of tissue) in the anterior artery can be caused by disease in vessels originating from the segmental arteries such as atheroma (arterial wall swelling) or aortic dissection (a tear in the aorta).

The median survival time of patients without treatment is four to six weeks. The best prognosis are seen from NM due to breast cancer with the median overall survival of no more than six months after diagnosis of NM. Death are generally due to progressive neurological dysfunction. Treatment is meant to stabilize neurological function and prolong survival. Neurological dysfunction usually cannot be fixed but progressive dysfunction can be halted and survival may be increased to four to six months.

Factors that lower survival:

Much of prognosis can be determined from the damage due to primary cancer. Negative hormone receptor status, poor performance status, more than 3 chemotherapy regimes, and high Cyfra 21-1 level at diagnosis, all indicates lower survival period of patients with NM. Cyfra 21-1 is a fragment of the cytokeratin 19 and may reflect the tumor burden within the CSF.

Neoplastic or malignant meningitis, also called meningitis carcinomatosa and leptomeningeal carcinomatosis, is the development of meningitis due to infiltration of the subarachnoid space by cancerous cells. Malignant cells come from primary cancer such as breast cancer or from a primary brain tumor like medulloblastoma. Neoplastic Meningitis (NM) was first reported in the 1870s with the most common cause being breast cancer, lung cancer, and malignant melanoma.

The incidence of adhesive capsulitis is approximately 3 percent in the general population. Occurrence is rare in children and people under 40 but peaks between 40 and 70 years of age. At least in its idiopathic form, the condition is much more common in women than in men (70% of patients are women aged 40–60). Frozen shoulder is more frequent in diabetic patients and is more severe and more protracted than in the non-diabetic population.

People with diabetes, stroke, lung disease, rheumatoid arthritis, or heart disease are at a higher risk for frozen shoulder. Injury or surgery to the shoulder or arm may cause blood flow damage or the capsule to tighten from reduced use during recovery. Adhesive capsulitis has been indicated as a possible adverse effect of some forms of highly active antiretroviral therapy (HAART). Cases have also been reported after breast and lung surgery.

A rotator cuff tear can be caused by the weakening of the rotator cuff tendons. This weakening can be caused by age or how often the rotator cuff is used. Adults over the age of 60 are more susceptible to a rotator cuff tear. According to a study in the Journal of Orthopaedic Surgery and Traumatology the frequency of rotator cuff tears can increase with age. The study shows the participants that were the ages of 70–90 years old had a rate of rotator cuff tears that were 1 to 5. The participants who were 90+ years old the frequency of a rotator cuff tear jumped to 1 to 3. This study shows that with an increase in age there is also an increase in the probability of a rotator cuff tear.

According to a study in the Journal of Orthopaedics the prevalence of a rotator cuff tear was considerably greater in males than in females within the ages of 50–60 years old, within the ages of 70–80 years old there wasn’t much difference in prevalence. The data of this study showed that the prevalence of a rotator cuff tear in the general population is 22.1% Yamamoto et al. performed a medical examination on 683 people whom live in a mountain village. The purpose of this study was to determine the prevalence of a rotator cuff tear among a population. Yamamoto found that among the mountain village population, rotator cuff tears were present in 20.7% of the village population. In both of these studies we see that the percentages of the prevalence of a rotator cuff tear are very close in number so these numbers show us the prevalence of rotator cuff tears in the general population.

In an autopsy study of rotator cuff tears, the incidence of partial tears was 28%, and of complete rupture 30%. Frequently, tears occurred on both sides and the frequency increased with age. The frequency was also higher in females. Other cadaver studies have noted intratendinous tears to be more frequent (7.2%) than bursal-sided (2.4%) or articular-sided tears (3.6%). However, clinically, articular-sided tears are found to be 2 to 3 times more common than bursal-sided tears and among a population of young athletes, articular-sided tears constituted 91% of all partial-thickness tears.

Dupuytren’s disease has a high recurrence rate, especially when a person has so called Dupuytren’s diathesis. The term diathesis relates to certain features of Dupuytren's disease and indicates an aggressive course of disease.

The presence of all new Dupuytren’s diathesis factors increases the risk of recurrent Dupuytren’s disease by 71% compared with a baseline risk of 23% in people lacking the factors. In another study the prognostic value of diathesis was evaluated. They concluded that presence of diathesis can predict recurrence and extension. A scoring system was made to evaluate the risk of recurrence and extension evaluating the following values: bilateral hand involvement, little finger surgery, early onset of disease, plantar fibrosis, knuckle pads and radial side involvement.

Minimally invasive therapies may precede higher recurrence rates. Recurrence lacks a consensus definition. Furthermore, different standards and measurements follow from the various definitions.

In those with calcific tendinitis of the shoulder high energy extracorporeal shock-wave therapy (which uses sound waves) can be useful. It is not useful in other types of tendinitis. This procedure may be known as .

Electroanalgesia, ice therapy, and heat offer symptomatic relief. The benefit of ultrasound in calcific tendinitis is debated; most studies are negative but a study by Ebenbichler et al. (1999) showed resolution of deposits and clinical improvement.

Improving the biomechanics of the shoulder will reduce the tension on the fault muscles allowing a decrease in symptoms. Improved biomechanics are thought to reduce the amount of calcification that occurs especially in the case on supraspinatus where it can be caused from repetitive compression against the acromion.

In 1997 Morrison et al.

published a study that reviewed the cases of 616 patients (636 shoulders) with impingement syndrome (painful arc of motion) to assess the outcome of non-surgical care. An attempt was made to exclude patients who were suspected of having additional shoulder conditions such as, full-thickness tears of the rotator cuff, degenerative arthritis of the acromioclavicular joint, instability of the glenohumeral joint, or adhesive capsulitis. All patients were managed with anti-inflammatory medication and a specific, supervised physical-therapy regimen. The patients were followed up from six months to over six years. They found that 67% (413 patients) of the patients improved, while 28% did not improve and went to surgical treatment. 5% did not improve and declined further treatment.

Of the 413 patients who improved, 74 had a recurrence of symptoms during the observation period and their symptoms responded to rest or after resumption of the exercise program.

The Morrison study shows that the outcome of impingement symptoms varies with patient characteristics. Younger patients ( 20 years or less) and patients between 41 and 60 years of age, fared better than those who were in the 21 to 40 years age group. This may be related to the peak incidence of work, job requirements, sports and hobby related activities, that may place greater demands on the shoulder. However, patients who were older than sixty years of age had the "poorest results". It is known that the rotator cuff and adjacent structures undergo degenerative changes with ageing.

The authors were unable to posit an explanation for the observation of the bimodal distribution of satisfactory results with regard to age. They concluded that it was "unclear why (those) who were twenty-one to forty years old had less satisfactory results". The poorer outcome for patients over 60 years old was thought to be potentially related to "undiagnosed full-thickness tears of the rotator cuff".

The literature on the pathophysiology of bursitis describes inflammation as the primary cause of symptoms. Inflammatory bursitis is usually the result of repetitive injury to the bursa.

In the subacromial bursa, this generally occurs due to microtrauma to adjacent structures, particularly the supraspinatus tendon. The inflammatory process causes synovial cells to multiply, increasing collagen formation and fluid production within the bursa and reduction in the outside layer of lubrication (Ishii et al., 1997).

Less frequently observed causes of subacromial bursitis include hemorrhagic conditions, crystal deposition and infection.

Many causes have been proposed in the medical literature for subacromial impingement syndrome. The bursa facilitates the motion of the rotator cuff beneath the arch, any disturbance of the relationship of the subacromial structures can lead to impingement. These factors can be broadly classified as intrinsic such as tendon degeneration, rotator cuff muscle weakness and overuse. Extrinsic factors include bone spurs from the acromion or AC joint, shoulder instability and neurologic problems arising outside of the shoulder.

"Adhesive capsulitis" (also known as "frozen shoulder") is a painful and disabling disorder of unclear cause in which the shoulder capsule, the connective tissue surrounding the glenohumeral joint of the shoulder, becomes inflamed and stiff, greatly restricting motion and causing chronic pain. Pain is usually constant, worse at night, and with cold weather. Certain movements or bumps can provoke episodes of tremendous pain and cramping. The condition is thought to be caused by injury or trauma to the area and may have an autoimmune component.

Risk factors for frozen shoulder include tonic seizures, diabetes mellitus, stroke, accidents, lung disease, connective tissue diseases, thyroid disease, and heart disease. Treatment may be painful and taxing and consists of physical therapy, occupational therapy, medication, massage therapy, hydrodilatation or surgery. A physician may also perform manipulation under anesthesia, which breaks up the adhesions and scar tissue in the joint to help restore some range of motion. Alternative treatments exist such as the Trigenics OAT Procedure, ART, and the OTZ method. But these can vary in efficacy depending on the type and severity of the frozen shoulder. Pain and inflammation can be controlled with analgesics and NSAIDs.

People who suffer from adhesive capsulitis usually experience severe pain and sleep deprivation for prolonged periods due to pain that gets worse when lying still and restricted movement/positions. The condition can lead to depression, problems in the neck and back, and severe weight loss due to long-term lack of deep sleep. People who suffer from adhesive capsulitis may have extreme difficulty concentrating, working, or performing daily life activities for extended periods of time. The condition tends to be self-limiting and usually resolves over time without surgery. Most people regain about 90% of shoulder motion over time.

In medicine, an enthesopathy refers to a disorder involving the attachment of a tendon or ligament to a bone. This site of attachment is known as the entheses.

If the condition is known to be inflammatory, it can more precisely be called an enthesitis.

Shoulder problems including pain, are one of the more common reasons for physician visits for musculoskeletal symptoms. The shoulder is the most movable joint in the body. However, it is an unstable joint because of the range of motion allowed. This instability increases the likelihood of joint injury, often leading to a degenerative process in which tissues break down and no longer function well.

Shoulder pain may be localized or may be referred to areas around the shoulder or down the arm. Other regions within the body (such as gallbladder, liver, or heart disease, or disease of the cervical spine of the neck) also may generate pain that the brain may interpret as arising from the shoulder.

The prognosis for non-ischemic cases of SBO is good with mortality rates of 3–5%, while prognosis for SBO with ischemia is fair with mortality rates as high as 30%.

Cases of SBO related to cancer are more complicated and require additional intervention to address the malignancy, recurrence, and metastasis, and thus are associated with poorer prognosis.

All cases of abdominal surgical intervention are associated with increased risk of future small-bowel obstructions. Statistics from U.S. healthcare report 18.1% re-admittance rate within 30 days for patients who undergo SBO surgery. More than 90% of patients also form adhesions after major abdominal surgery.

Common consequences of these adhesions include small-bowel obstruction, chronic abdominal pain, pelvic pain, and infertility.

Ankle sprains can occur through either sports or activities of daily living, and individuals can be at higher or lower risk depending on a variety of circumstances including their homeland, race, age, sex, or profession In addition, there are different types of ankle sprains such as eversion ankle sprains and inversion ankle sprains. Overall, the most common type of ankle sprain to occur is an inversion ankle sprain, where excessive plantar flexion and supination cause the anterior talofibular ligament to be affected. A study showed that for a population of Scandinavians, inversion ankle sprains accounted for 85% of all ankle sprains Most ankle sprains occur in more active people, such as athletes and regular exercisers.