Cobb syndrome is a rare congenital disorder characterized by visible skin lesions with underlying spinal angiomas or arteriovenous malformations (AVMs). The skin lesions of Cobb syndrome typically are present as port wine stains or angiomas, but reports exist of angiokeratomas, angiolipomas, and lymphangioma circumscriptum. The intraspinal lesions may be angiomas or AVMs and occur at levels of the spinal cord corresponding to the affected skin dermatomes. They may in turn produce spinal cord dysfunction and weakness or paralysis.

The disorder was first described by Berenbruch in 1890, but became widely known only after Cobb's report in 1915. Cobb syndrome is thought to be more common in males and have no racial predilection, but only a few dozen cases are known. It is believed to be due to a sporadic mutation, since parents of affected children usually have no evidence of the disease.

The age range of patients with OPLL is from 32 to 81 years (mean = 53), with a male predominance. Prevalence is higher in those of Japanese or Asian ancestry (2-3.5%) and rarer in other racial groups (0.16%). Schizophrenia patients in Japan may have as high as 20% incidence.

Most patients suffer from only mild symptoms. Symptoms typically last approximately 13 months. Of patients without myelopathy at initial presentation, only 29% of them will develop myelopathy within 30 years.

Stimmler syndrome is a rare autosomal recessive congenital disorder first described by Stimmler et al. in 1970. It is characterized by dwarfism, diabetes, a small head, and high levels of alanine in the urine.

The disease is present at birth, but clinical manifestations are often not seen until later in life. Patients typically experience the sudden onset of pain, numbness, or weakness in their extremities as children or young adults. These symptoms may remit or remain stable and often can be localized below a specific dermatome. Symptoms tend to worsen over time either by discrete steps or continuously. Early development of weakness may portend a more aggressive course. Less commonly, weakness or bowel and bladder dysfunction may be presenting symptoms.

The major debility from Cobb syndrome is the onset of weakness, paresis, sensory loss, and loss of bowel and bladder control. A possible complication if treatment is delayed is Foix-Alajouanine disease or subacute necrotic myelopathy due to thrombosis in the spinal angioma.

Cutaneous lesions may be distributed anywhere in the dermatome, from midline back to abdomen. Midline back lesions may be associated with spina bifida. The cutaneous lesion may be very faint and may be more pronounced when the patient performs a Valsalva maneuver which increases abdominal pressure and causes preferential filling of the cutaneous angioma. Neurological examination will reveal weakness or paralysis and numbness or decreased sensation with a sharp upper cutoff.

Symptoms for the disease include microcephaly, a low birth weight, dwarfism, small teeth, and diabetes. The symptoms of Stimmler syndrome are closely related to a disease studied by Haworth et al. in 1967 as well as Leigh subacute necrotizing encephalopathy with lactic acidosis

Surfer's myelopathy is a rare nontraumatic paraparesis. It is a spinal cord injury caused by hyperextension of the back. When the back is hyperextended, a blood vessel leading to the spine can become kinked, depriving the spinal cord of oxygen

The condition gets its name because the phenomenon is most often seen in those surfing for the first time, but it can be caused by any activity in which the back is hyperextended (yoga, pilates, etc). In some cases the paralysis is permanent. As of 2007 there were 9 recorded cases. A case series of 19 novice surfers with nontraumatic myelopathy was published in 2012, with all patients' MRI scans showing hyperintensity from the lower thoracic spinal cord to the conus medullaris. An additional study of 23 cases was published in 2013.

The exact cause of the condition is unknown. There is most evidence to support vascular infarction and ischemic necrosis of salivary gland lobules as a mechanism for the condition. Experimentally, local anaesthetic injections and tying of the arteries is reported to trigger the development of tissue changes similar to NS in lab rats. Factors which are thought to cause this ischemia are listed below, however sometimes there is no evident predisposing factor or initiating event.

- Trauma e.g. during intubation, or surgical procedures

- Local anesthetic injection

- Smoking

- Alcohol

- Diabetes mellitus

- Vascular disease, (e.g. arteriosclerosis)

- Pressure from a dental prosthesis

- Allergy

- Bulimia

- Infection

- Ionizing radiation

This syndrome has two forms, A and B, referred to as Morquio A and Morquio B syndrome or MPA IVA and MPS IVB. The two forms are distinguished by the gene product involved; A involves a malfunction in the GALNS gene product (galactosamine-6 sulfatase), while B involves a malfunction of the GLB1 gene product (beta-galactosidase).

The treatment for Morquio syndrome consists of prenatal identification and of enzyme replacement therapy. On 12 February 2014, the US Food and Drug Administration approved the drug elosulfase alfa (Vimizim) for treating the disease.

Most people with mild to moderate symptoms do not get worse. While many improve in the short term after surgery this improvement decreases somewhat with time. A number of factors present before surgery are able to predict the outcome after surgery, with people with depression, cardiovascular disease and scoliosis doing in general worse while those with more severe stenosis beforehand and better overall health doing better.

The natural evolution of disc disease and degeneration leads to stiffening of the intervertebral joint. This leads to osteophyte formation—a bony overgrowth about the joint. This process is called spondylosis, and is part of the normal aging of the spine. This has been seen in studies of normal and diseased spines. Degenerative changes begin to occur without symptoms as early as age 25–30 years. It is not uncommon for people to experience at least one severe case of low back pain by the age of 35 years. This can be expected to improve and become less prevalent as the individual develops osteophyte formation around the discs.

In the US workers' compensation system, once the threshold of two major spinal surgeries is reached, the vast majority of workers will never return to any form of gainful employment. Beyond two spinal surgeries, any more are likely to make the patient worse, not better.

"Primary" Central Nervous System (CNS) vasculitis is said to be present if there is no underlying cause. The exact mechanism of the primary disease is unknown, but the fundamental mechanism of all vasculitides is auto-immune. Other possible causes of cerebral vasculitis are infections, systemic auto-immune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis, medications and drugs (amphetamine, cocaine and heroin), some forms of cancer (lymphomas, leukemia and lung cancer) and other forms of systemic vasculitis such as granulomatosis with polyangiitis, polyarteritis nodosa or Behçet's disease. It may imitate, and is in turn imitated by, a number of other diseases that affect the blood vessels of the brain diffusely such as fibromuscular dysplasia and thrombotic thrombocytopenic purpura.

Treatment is first with many different high-dose steroids, namely glucocorticoids. Then, if symptoms do not improve additional immunosuppression such as cyclophosphamide are added to decrease the immune system's attack on the body's own tissues. Cerebral vasculitis is a very rare condition that is difficult to diagnose, and as a result there are significant variations in the way it is diagnosed and treated.

Having cancer (current or previous) is currently one of the most prevalent out of all conditions among patients. High blood pressure, Chronic lung conditions, Alcohol abuse, Kidney failure, Malnutrition are another major risk factors.

While recent case series (n=9-80) studies have found a mortality rate of 20-40%, a large (n=1641) 2009 study reported a mortality rate of 7.5%.

Most cases of Fournier gangrene are infected by both aerobic and anaerobic bacteria. Resulting mortality increases in individuals lacking access not only to pragmatic resources such as sanitation and medical care, but to psychosocial resources as well.

A 2006 Turkish study reported 46% of those diagnosed with Fourniers had elevated blood sugars. There have been additional findings that seemingly link Fourniers with immunosuppression and alcoholism. One study reported approximately one third of those diagnosed with Fournier had alcoholism with resulting diabetes and malnutrition, while another 10% had been medical immunosuppressed either via chemotherapy, steroids, or malignancy.

Granulomatous meningoencephalitis (GME) is an inflammatory disease of the central nervous system (CNS) of dogs and, rarely, cats. It is a form of meningoencephalitis. GME is likely second only to encephalitis caused by "canine distemper virus" as the most common cause of inflammatory disease of the canine CNS. The disease is more common in female toy dogs of young and middle age. It has a rapid onset. The lesions of GME exist mainly in the white matter of the cerebrum, brainstem, cerebellum, and spinal cord. The cause is only known to be noninfectious and is considered at this time to be idiopathic. Because lesions resemble those seen in allergic meningoencephalitis, GME is thought to have an immune-mediated cause, but it is also thought that the disease may be based on an abnormal response to an infectious agent. One study searched for viral DNA from "canine herpesvirus", "canine adenovirus", and "canine parvovirus" in brain tissue from dogs with GME, necrotizing meningoencephalitis, and necrotizing leukoencephalitis (see below for the latter two conditions), but failed to find any.

The condition is rare.

The typical age range of those affected by the condition is about 23–66 years of age. It usually occurs in smokers. The male to female ratio has been reported as 1.95:1, and 2.31:1.

Anterior spinal artery syndrome is necrosis of tissue in the anterior spinal artery or its branches. It is characterised by pain which radiates at onset and sudden quadraplegia (paralysis of all four limbs) or paraplegia (paralysis of the lower body). Within days, flaccid limbs become spastic and hyporeflexia (underactive nerve responses) turns into hyperreflexia (overactive nerve responses) and extensor plantar nerve responses. Sensory loss to pain and temperature also occurs up to the level of damage on the spinal cord, as damage to different areas will affect different parts of the body.

In diagnosis, other causes of abrupt paralysis should be excluded such as cord compression, transverse myelitis (inflammation of the spinal cord) and Guillain–Barré syndrome. A specific cause of the infarction should be looked for, such as diabetes, polyarteritis nodosa (inflammatory damage of vessels) or systemic lupus erythematosus. Neurosyphilis is also a known cause. Other causes include:

Treatment is supportive and aims to relieve symptoms. The prognosis is dependent upon individual circumstances and factors.

Posterior spinal artery syndrome is much rarer than its anterior counterpart as the white matter structures that are present are much less vulnerable to ischemia since they have a better blood supply. When posterior spinal artery syndrome does occur, dorsal columns are damaged and ischemia may spread into the posterior horns. Clinically the syndrome presents as a loss of tendon reflexes and loss of joint position sense

For several decades, the term "tropical spastic paraparesis" was used to describe a chronic and progressive clinical syndrome that affected adults living in equatorial areas of the world. This condition was initially thought to be associated with infectious agents (such as Treponema pertenue and Treponema pallidum, which cause inflammation of the central nervous system) and with chronic nutritional deficiencies (such as avitaminosis) or exposure to potentially toxic foods (such as bitter cassava).

Tropical myeloneuropathies are classified as two separate syndromes: tropical ataxic neuropathy (TAN) and tropical spastic paraparesis (TSP). They are placed together because they are found in tropical countries, although tropical spastic paraparesis

has occurred in temperate countries (e.g., Japan).

The prognosis for Tropical spastic paraparesis indicates some improvement in a percentage of cases due to immunosuppressive treatment. A higher percentage will eventually lose the ability to walk within a ten-year interval.

Necrotizing funisitis is a very severe form of funisitis in which the tissue that makes-up the umbilical cord starts to die. It is associated with congenital syphilis. It is now rare, and seen almost exclusively in the preterm infant. The majority of affected infants are stillborn, or die within a few weeks of birth.

Acute esophageal necrosis made an appearance on an American medical drama show, . Jan Garavaglia, the show's host, receives a female body, that at time of the autopsy had a severe case of acute esophageal necrosis due to chronic alcoholism.

Myelopathy describes any neurologic deficit related to the spinal cord. When due to trauma, it is known as (acute) spinal cord injury. When inflammatory, it is known as myelitis. Disease that is vascular in nature is known as vascular myelopathy. The most common form of myelopathy in human, "cervical spondylotic myelopathy (CSM)", is caused by arthritic changes (spondylosis) of the cervical spine, which result in narrowing of the spinal canal (spinal stenosis) ultimately causing compression of the spinal cord. In Asian populations, spinal cord compression often occurs due to a different, inflammatory process affecting the posterior longitudinal ligament.