Socioeconomic correlates of health have been well established in the study of heart disease, lung cancer, and diabetes. Many of the explanations for the increased incidence of these conditions in people with lower socioeconomic status (SES) suggest they are the result of poor diet, low levels of exercise, dangerous jobs (exposure to toxins etc.) and increased levels of smoking and alcohol intake in socially deprived populations. Hesdorffer et al. found that low SES, indexed by poor education and lack of home ownership, was a risk factor for epilepsy in adults, but not in children in a population study. Low socioeconomic status may have a cumulative effect for the risk of developing epilepsy over a lifetime.

There were also observations that hippocampal sclerosis was associated with vascular risk factors. Hippocampal sclerosis cases were more likely than Alzheimer's disease to have had a history of stroke (56% vs. 25%) or hypertension (56% vs. 40%), evidence of small vessel disease (25% vs. 6%), but less likely to have had diabetes mellitus (0% vs. 22%).

Although the theory is controversial, there is a link between febrile seizures (seizures coinciding with episodes of fever in young children) and subsequent temporal lobe epilepsy, at least epidemiologically.

The causes of TLE include mesial temporal sclerosis, traumatic brain injury, brain infections, such as encephalitis and meningitis, hypoxic brain injury, stroke, cerebral tumours, and genetic syndromes. Temporal lobe epilepsy is not the result of psychiatric illness or fragility of the personality.

The cause of MS is unknown; however, it is believed to occur as a result of some combination of genetic and environmental factors such as infectious agents. Theories try to combine the data into likely explanations, but none has proved definitive. While there are a number of environmental risk factors and although some are partly modifiable, further research is needed to determine whether their elimination can prevent MS.

MS is more common in people who live farther from the equator, although exceptions exist. These exceptions include ethnic groups that are at low risk far from the equator such as the Samis, Amerindians, Canadian Hutterites, New Zealand Māori, and Canada's Inuit, as well as groups that have a relatively high risk close to the equator such as Sardinians, inland Sicilians, Palestinians and Parsis. The cause of this geographical pattern is not clear. While the north-south gradient of incidence is decreasing, as of 2010 it is still present.

MS is more common in regions with northern European populations and the geographic variation may simply reflect the global distribution of these high-risk populations. Decreased sunlight exposure resulting in decreased vitamin D production has also been put forward as an explanation. A relationship between season of birth and MS lends support to this idea, with fewer people born in the northern hemisphere in November as compared to May being affected later in life. Environmental factors may play a role during childhood, with several studies finding that people who move to a different region of the world before the age of 15 acquire the new region's risk to MS. If migration takes place after age 15, however, the person retains the risk of their home country. There is some evidence that the effect of moving may still apply to people older than 15.

Approximately 2 million people in the world suffer from multiple sclerosis Tumefactive multiple sclerosis cases make up 1 to 2 of every 1000 multiple sclerosis cases. This means that only around 2000 people in the world suffer of tumefactive MS. Of those cases, there is a higher percentage of females affected than males. The median age of onset is 37 years.

As in general MS, there are differences for gender, ethnicity and geographic location. Based on epidemiological studies, there are about 3 times more female MS patients than male patients, indicating a possibility of an increased risk due to hormones. Among different ethnic groups, MS is the most common among Caucasians and seems to have a greater incidence at latitudes above 40° as compared to at the equator. While these associations have been made, it is still unclear how they result in an increased risk of MS onset.

Prognosis is poor, however, current analysis suggests that those associated with thymoma, benign or malignant, show a less favorable prognosis (CASPR2 Ab positive).

Most common cause of autoimmune encephalitis after acute demyelinating encephalitis in England. More than 500 cases have been reported in literature till 2013. In California Encephalitis Project it was found >4 times as frequently as herpes simplex virus type 1 (HSV-1), varicella-zoster virus (VZV), and West Nile virus (WNV). Among patients with first-onset schizophrenia incidence varies between 6–10%.

- Age – frequently 5–76 years, Median age of patients was 23 years

- Sex – 80% Female

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

Glucocorticoid medications have been known to be associated with significant side effects involving behavior and mood, regardless of previous psychiatric or cognitive condition, since the early 1950s. But cognitive side effects of steroid medications involving memory and attention are not as widely publicized and may be misdiagnosed as separate conditions, such as attention deficit disorder (ADHD or ADD) in children or early Alzheimer's disease in elderly patients.

The pathology of the tumefactive demyelinating lesion (TDL) is heterogeneous. In acute phase, the plaques of lesions were characterized by massive demyelination with relatively axonal preservation associated with reactive astrocytosis and infiltration of macrophages. In plaques of chronic lesions, demyelinated lesions with relative axonal preservation and sharply defined margins were major findings. And myelin-laden macrophages accumulate at the edges of plaques and stay inactive

There are several conditions can produce tumefactive lesions. This is known because in some special cases the etiology can be identified. For example, there are some cases of NMO, misidentified as MS and treated with interferon-beta by mistake. Some of these patients developed tumefactive lesions. Anyway, it is important to have into account that NMO itself can also produce them

Some other cases have been found related to viral infection, some others related to NMOSD, others could be paraneoplastic. Also some cases could be related to hormonal treatments

Other possible cause are immunomodulatory combinations. In particular, it has been found that switching from standard MS therapies to fingolimod can trigger tumefactive lesions in some MS patients

While standard multiple sclerosis process has an autoimmune response after the breach of the blood-brain barrier, in tumefactive MS things do not process in the same way, and demyelinating lesions do not always show antibody damage. Subjects with tumefactive multiple sclerosis display elevated levels of choline (Cho)/creatine ratio and increased lactate which is associated with demylinating diseases. Cases also display oligoclonal bands in the cerebrospinal fluid.

The disease is heterogeneous and the lesions do not always comply with the requirements for multiple sclerosis diagnosis (dissemination in time and space). In these cases it is only possible to speak about tumefactive demyelination (TD).

In general, it is accepted that the two main causes of pseudo-tumoral lesions are Marburg multiple sclerosis and acute disseminated encephalomyelitis (ADEM). Tumefactive demyelination of the spinal cord is rare but it has been reported

Damage is not confined to the demyelinating area. Wallerian degeneration outside the lesions has been reported.

Focal seizures (also called partial seizures and localized seizures) are seizures which affect initially only one hemisphere of the brain. The brain is divided into two hemispheres, each consisting of four lobes – the frontal, temporal, parietal and occipital lobes. A focal seizure is generated in and affects just one part of the brain – a whole hemisphere or part of a lobe. Symptoms will vary according to where the seizure occurs. In the frontal lobe symptoms may include a wave-like sensation in the head; in the temporal lobe, a feeling of déjà vu; in the parietal lobe, a numbness or tingling; and in the occipital lobe, visual disturbance or hallucination.

Normal aging, although not responsible for causing memory disorders, is associated with a decline in cognitive and neural systems including memory (long-term and working memory). Many factors such as genetics and neural degeneration have a part in causing memory disorders. In order to diagnose Alzheimer's disease and dementia early, researchers are trying to find biological markers that can predict these diseases in younger adults. One such marker is a beta-amyloid deposit which is a protein that deposits on the brain as we age. Although 20-33% of healthy elderly adults have these deposits, they are increased in elderly with diagnosed Alzheimer's disease and dementia.

Additionally, traumatic brain injury, TBI, is increasingly being linked as a factor in early-onset Alzheimer's disease.

One study examined dementia severity in elderly schizophrenic patients diagnosed with Alzheimer's disease and dementia versus elderly schizophrenic patients without any neurodegenerative disorders. In most cases, if schizophrenia is diagnosed, Alzheimer's disease or some form of dementia in varying levels of severity is also diagnosed. It was found that increased hippocampal neurofibrillary tangles and higher neuritic plaque density (in the superior temporal gyrus, orbitofrontal gyrus, and the inferior parietal cortex) were associated with increased severity of dementia. Along with these biological factors, when the patient also had the apolipoprotein E (ApoE4) allele (a known genetic risk factor for Alzheimer's disease), the neuritic plaques increased although the hippocampal neurofibrillary tangles did not. It showed an increased genetic susceptibility to more severe dementia with Alzheimer's disease than without the genetic marker.

As seen in the examples above, although memory does degenerate with age, it is not always classified as a memory disorder. The difference in memory between normal aging and a memory disorder is the amount of beta-amyloid deposits, hippocampal neurofibrillary tangles, or neuritic plaques in the cortex. If there is an increased amount, memory connections become blocked, memory functions decrease much more than what is normal for that age and a memory disorder is diagnosed.

The cholinergic hypothesis of geriatric memory dysfunction is an older hypothesis that was considered before beta-amyloid deposits, neurofibrillary tangles, or neuritic plaques. It states that by blocking the cholinergic mechanisms in control subjects you can examine the relationship between cholinergic dysfunction and normal aging and memory disorders because this system when dysfunctional creates memory deficits.

The prognosis of this disease is very variable and can take three different courses: a monophasic, not remitting;

remitting;

and finally, progressive, with increase in deficits.

Regions of the brain with a high density of glucocorticoid receptors (GRs) including the hippocampus, hypothalamus, and prefrontal cortex are particularly sensitive to elevated circulating levels of glucocorticoids even in the absence of stress. Scientific studies have mainly focused on the impact of glucocorticoids on the hippocampus because of its role in memory processes and on the prefrontal cortex for its role in attention and executive function.

Elevated glucocorticoid activity is associated with down-regulation of GRs (known as "glucocorticoid cascade hypothesis"), which diminishes neuroreparative activity and attenuates neurogenesis that can result in decreased hippocampal volume with prolonged glucocorticoid exposure.

Variations in individual sensitivity to glucocorticoid medications may be due to either GR hypofunction or hyperfunction. Similarly, variations in individual hypothalamic-pituitary-adrenal (HPA) axis responsiveness can modulate the type and number of side effects.

Ocular dysmetria is a form of dysmetria that involves the constant under- or over-shooting of the eyes when attempting to focus gaze on something.

Ocular dysmetria indicates lesions in the cerebellum, which is the brain region responsible for coordinating movement. It is a symptom of several neurological conditions including multiple sclerosis.

It is a condition that can cause symptoms similar to sea sickness.

Source of information: Mult-sclerosis.org

The list of these diseases depends of the author, but usually are included:

- multiple sclerosis, normally defined by the dissemination in time and space of demyelinating lesions, with two (or sometimes three) clinical presentations:

- Relapsing-Onset multiple sclerosis, the most known and extended variant, normally consisting of two distinct clinical phases (Remitent-Recidivant, RRMS, and Secondary Progressive, SPMS)

- Progressive-Onset MS, most known as Primary progressive MS including a special genetic variant named rapidly progressive multiple sclerosis.

- Optic-spinal MS, or opticospinal, clinical and pathological variant of multiple sclerosis which often include visual symptoms and have a more severe course than typical MS. Though multiple scars (scleroses) are present in CNS, and they comply with the dissemination criteria, and sometimes is classified as clinically definite multiple sclerosis, currently is considered outside the scope of Multiple Sclerosis and inside the scope of Devic's disease, though it is uncertain if this applies to all cases. Also a variant affecting mainly the spinal cord and the cortex has been proposed

- Neuromyelitis optica (NMO), and its associated "spectrum of disorders" (NMOSD), currently considered a common syndrome for at least three separated diseases:, mainly produced by AQP4 autoimmune channelopathy, though other variants exists, some with anti-MOG and some others idiopathic. Some researchers think that there could exist an overlapping between Anti-NMDA receptor encephalitis cases and neuromyelitis optica or acute disseminated encephalomyelitis.

- Anti-MOG associated spectrum, often clinically presented as an anti-MOG autoimmune encephalomyelitis, but can also appear as negative NMO or atypical multiple sclerosis

- CRION (Chronic relapsing inflammatory optic neuritis): A distinct clinical entity from other inflammatory demyelinating diseases including multiple sclerosis (MS), neuromyelitis optica-immunoglobulin G (NMO-IgG) spectrum disease, and idiopathic relapsing optic neuritis.

- Acute disseminated encephalomyelitis or ADEM, a closely related disorder in which a known virus or vaccine triggers autoimmunity against myelin.

- Acute hemorrhagic leukoencephalitis, possibly a variant of Acute disseminated encephalomyelitis

- Balo concentric sclerosis, an unusual presentation of plaques forming concentrenic circles, which can sometimes get better spontaneously.

- Schilder disease or diffuse myelinoclastic sclerosis: is a rare disease that presents clinically as a pseudotumoural demyelinating lesion; and is more common in children.

- Marburg multiple sclerosis, an aggressive form, also known as malignant, fulminant or acute MS.

- Tumefactive multiple sclerosis: lesions whose size is more than 2 cm, with mass effect, oedema and/or ring enhancement

- Solitary sclerosis: This variant has been recently proposed (2012) by Mayo Clinic researches. though it was also reported by other groups more or less at the same time. It is defined as isolated demyelinating lesions which produce a progressive myelopathy similar to primary progressive MS, and is currently considered a synonym for tumefactive multiple sclerosis.

Some inflammatory conditions are associated with the presence of scleroses in the CNS. Optic neuritis (monophasic and recurrent) and Transverse myelitis (monophasic and recurrent)

As MS is an active field for research, the list is not closed or definitive. For example, some diseases like Susac's syndrome (MS has an important vascular component), leukoaraiosis, myalgic encephalomyelitis (aka chronic fatigue syndrome) or autoimmune variants of peripheral neuropathies like Guillain–Barré syndrome or progressive inflammatory neuropathy could be included assuming the autoimmune model. Also Leukodystrophy (which see) and its sub-conditions: Adrenoleukodystrophy and Adrenomyeloneuropathy could be in the list. Venous induced demyelination has also been proposed as a hypothetical MS variant produced by CCSVI.

Recent research has identified some possible new variants, like the possibility to separate primary progressive MS, PPMS, after recent findings seem to point that it is pathologically a very different disease.

Also an OPA1 variant and aKIR4.1 multiple sclerosis variant was reported in 2012 and later reported again, which could be considered a different disease (as Devic disease did before), and can represent up to a 47% of the MS cases. Finally, there exist some reports of an aquaporine-related multiple sclerosis, related to vegetal aquaporine proteins.

Originally found in neuromyelitis optica, this autoantibody has been associated with other conditions. Its current spectrum is as following:

- Seropositive Devic's disease, according to the diagnostic criteria described above

- Limited forms of Devic's disease, such as single or recurrent events of longitudinally extensive myelitis, and bilateral simultaneous or recurrent optic neuritis

- Asian optic-spinal MS - this variant can present brain lesions like MS.

- Longitudinally extensive myelitis or optic neuritis associated with systemic autoimmune disease

- Optic neuritis or myelitis associated with lesions in specific brain areas such as the hypothalamus, periventricular nucleus, and brainstem

- Some cases of tumefactive multiple sclerosis

Diffuse myelinoclastic sclerosis, sometimes referred to as Schilder's disease, is a very infrequent neurodegenerative disease that presents clinically as pseudotumoural demyelinating lesions, that make its diagnosis difficult. It usually begins in childhood, affecting children between 5 and 14 years old, but cases in adults are possible.

This disease is considered one of the borderline forms of multiple sclerosis because some authors consider them different diseases and others MS variants. Other diseases in this group are neuromyelitis optica (NMO), Balo concentric sclerosis and Marburg multiple sclerosis.

Natalizumab (Tysabri) was approved in 2004 by the FDA for multiple sclerosis (MS). It was subsequently withdrawn from the market by its manufacturer after it was linked with three cases of PML. All 3 initial cases were taking natalizumab in combination with interferon beta-1a. After a safety review the drug was returned to the market in 2006 as a monotherapy for MS under a special prescription program. As of May 2011, over 130 cases of PML had been reported in MS patients, all in patients who had taken natalizumab for more than a year. While none of them had taken the drug in combination with other disease-modifying treatments, previous use of MS treatments increases the risk of PML between 3 and 4-fold. The estimated prevalence of PML in MS is 1.5 cases per thousand natalizumab users. Around 20% of MS patients with PML die, and most of the rest are very disabled.

A person with MS developed PML and died during a 4-year course of dimethyl-fumarate.

Balo lesions have been reported alone, but also associated to standard multiple sclerosis, neuromyelitis optica, CADASIL and progressive multifocal leukoencephalopathy

Incidence of demyelinating diseases vary from disorder to disorder. Some conditions, such as Tabes dorsalis appear predominantly in males and begins in mid-life. Optic neuritis on the other hand, occurs preferentially in females typically between the ages of 30 and 35. Other conditions such as multiple sclerosis vary in prevalence depending on the country and population. This condition can appear in children as well as adults.

Balo concentric sclerosis in children has been reported to behave different from adults

PML is most common in people with HIV1 infection; prior to the advent of effective antiretroviral therapy, as many as 5% of people with AIDS eventually developed PML. It is unclear why PML occurs more frequently in AIDS than in other immunosuppressive conditions; some research suggests the effects of HIV on brain tissue, or on JCV itself, make JCV more likely to become active in the brain and increase its damaging inflammatory effects.

PML can occur in people on chronic immunosuppressive therapy like corticosteroids, for organ transplant, in people with cancer (such as Hodgkin’s disease, leukemia, or lymphoma) and individuals with autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, psoriasis, sarcoidosis, and systemic lupus erythematosus with or without biological therapies that depress the immune response and allow JC virus reactivation. These therapies include efalizumab, belatacept, rituximab, natalizumab, infliximab, cytotoxic chemotherapy, corticosteroids, and various transplant drugs such as tacrolimus.