A July, 2012, study suggested that mesenchymal stem cell therapy could delay the progression of neurological deficits in patients with MSA-cerebellar type, suggesting the potential of mesenchymal stem cell therapy as a treatment candidate of MSA.

The rate of MSA is estimated at 4.6 cases per 100,000 people. This disease is more common in men than in women, with studies showing ratios ranging from between 1.4:1 to ratios as high as 1.9:1. Chef Kerry Simon died from complications of MSA.

Parkinson-plus syndromes are usually more rapidly progressive and less likely to respond to antiparkinsonian medication than PD. However, the additional features of the diseases may respond to medications not used in PD.

Current therapy for Parkinson-plus syndromes is centered around a multidisciplinary treatment of symptoms.

These disorders have been linked to pesticide exposure.

Parkinson-plus syndromes, also known as disorders of multiple system degeneration, is a group of neurodegenerative diseases featuring the classical features of Parkinson's disease (tremor, rigidity, akinesia/bradykinesia, and postural instability) with additional features that distinguish them from simple idiopathic Parkinson's disease (PD). Some consider Alzheimer's disease to be in this group. Parkinson-plus syndromes are either inherited genetically or occur sporadically.

The atypical parkinsonian or Parkinson-plus syndromes are often difficult to differentiate from PD and each other. They include multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). Dementia with Lewy bodies (DLB), may or may not be part of the PD spectrum, but it is increasingly recognized as the second-most common type of neurodegenerative dementia after Alzheimer's disease. These disorders are currently lumped into two groups, the synucleinopathies and the tauopathies. They may coexist with other pathologies.

Additional Parkinson-plus syndromes include Pick's disease and olivopontocerebellar atrophy. The latter is characterized by ataxia and dysarthria, and may occur either as an inherited disorder or as a variant of multiple system atrophy. MSA is also characterized by autonomic failure, formerly known as Shy–Drager syndrome.

Clinical features that distinguish Parkinson-plus syndromes from idiopathic PD include symmetrical onset, a lack of or irregular resting tremor, and a reduced response to dopaminergic drugs (including levodopa). Additional features include bradykinesia, early-onset postural instability, increased rigidity in axial muscles, dysautonomia, alien limb syndrome, supranuclear gaze palsy, apraxia, involvement of the cerebellum including the pyramidal cells, and in some instances significant cognitive impairment.

Olivopontocerebellar atrophy (OPCA) is the degeneration of neurons in specific areas of the brain – the cerebellum, pons, and inferior olives. OPCA is present in several neurodegenerative syndromes, including inherited and non-inherited forms of ataxia (such as the hereditary spinocerebellar ataxia known as Machado–Joseph disease) and multiple system atrophy (MSA), with which it is primarily associated.

OPCA may also be found in the brains of individuals with prion disorders and inherited metabolic diseases. The characteristic areas of brain damage that indicate OPCA can be seen by imaging the brain using CT scans or MRI studies.

The term was originally coined by Joseph Jules Dejerine and André Thomas.

Olivopontocerebellar atrophy is hereditary, but has an unknown genetic basis. There are two forms:

A few non-hereditary diseases formerly categorized as olivopontocerebellar atrophy have been reclassified as forms of multiple system atrophy as well as to four hereditary types, that have been currently reclassified as four different forms of spinocerebellar ataxia:

Hereditary motor and sensory neuropathy with proximal dominance (HMSN-P) is an autosomal dominant neurodegenerative disorder that is defined by extensive involuntary and spontaneous muscle contractions, asthenia, and atrophy with distal sensory involvement following. The disease starts presenting typically in the 40s and is succeeded by a slow and continuous onslaught. Muscle spasms and muscle contractions large in number are noted, especially in the earliest stages. The presentation of HMSN-P is quite similar to amyotrophic lateral sclerosis and has common neuropathological findings. Sensory loss happens as the disease progresses, but the amount of sensation lost varies from case to case. There have been other symptoms of HMSN-P reported such as urinary disturbances and a dry cough.

Two large families in Japan have been identified with the disease locus to chromosome 3q. From descendants of Japan, HMSN-P was brought to Brazil, from there it is a pretty isolated disease. Through clinical studies, researchers identified that TFG mutations on chromosome 3q13.2 causes HMSN-P. "The presence of TFG/ubiquitin- and/or TDP-43-immunopositive cytoplasmic inclusions in motor neurons and cytosolic aggregation composed of TDP-43 in cultured cells expressing mutant TFG indicate a novel pathway of motor neuron death"

One family of 68 individuals over 5 generations was studied and the prevalence of disease among the family members suggests that it is indicative of dominant inheritance that is not sexually linked. This is supported by the fact that the disease failed to skip generations even in the absence of intermarriages and that disease incidence was independent of sex. The current findings suggest that the cause of the disease could be narrowed down to one enzymatic defect that is involved in the development of neuroectodermal tissue, however the exact molecular mechanisms are currently unknown. The other symptoms that arise such as bone defects and diabetes may be secondary to this enzymatic defect.

DAMP—deficits in attention, motor control and perception—is a controversial psychiatric concept conceived by Christopher Gillberg.

DAMP is similar to minimal brain dysfunction (MBD), a concept that was formulated in the 1960s. Both concepts are related to certain psychiatric conditions, such as hyperactivity. The concept of MBD was strongly criticized by Sir Michael Rutter [Gillberg, 2003, p. 904] and several other researchers, and this led to its abandonment in the 1980s. At the same time, research showed that something similar was needed. One alternative concept was ADHD (Attention-Deficit Hyperactivity Disorder). Gillberg proposed another alternative: DAMP. Gillberg's concept was formulated in the early 1980s, and the term itself was introduced in a paper that Gillberg published in 1986 (see Gillberg [1986]). (DAMP is essentially MBD without the etiological assumptions.)

The concept of DAMP met with considerable criticism. For example, Sir Michael Rutter stated that the concept of DAMP (unlike ADHD) was "muddled" and "lacks both internal coherence and external discriminative validity ... it has no demonstrated treatment or prognostic implications"; he concluded that the concept should be abandoned. Another example is the criticism of Per-Anders Rydelius, Professor of Child Psychiatry at the Karolinska Institute, who argued that the definition of DAMP was too vague: "the borderline between DAMP and conduct disorders [is] unclear ... the borderline between DAMP and ADHD [is] unclear"; he concluded that "the concept is in need of revision". And in 2000, Eva Kärfve, a sociologist at the University of Lund, published a book which argued that Gillberg's work on DAMP should be rejected.

Perhaps the strongest criticism of DAMP is that Gillberg and his co-workers in Gothenburg are almost the only people doing research on DAMP. Indeed, in a review of DAMP published by Gillberg in 2003, it was noted that there were only "about 50" research papers that had been published on DAMP and that the "vast majority of these have either originated in the author's own clinical and research setting or have been supervised and/or co-authored by him" [Gillberg, 2003, p. 904]. This is in contrast to ADHD, on which "several thousand papers" had been published [Gillberg, 2003, p. 905]. As far as clinical practice goes, DAMP has been primarily accepted only in Gillberg's native Sweden and in Denmark [Gillberg, 2003, p. 904], and even in those countries acceptance is mixed.

In 2003, Gillberg revised his definition of DAMP. The new definition is as follows:

1. ADHD as defined in DSM-IV;

2. Developmental Coordination Disorder (DCD) as defined in DSM-IV;

3. condition not better accounted for by cerebral palsy; and

4. IQ should be higher than about 50 [Gillberg, 2003: box 1]. (In the WHO system, this would be a hyperkinetic disorder combined with a developmental disorder of motor function.) About half of children with ADHD are believed to also have DCD [Gillberg, 2003; Martin et al., 2006].

Strong criticism of DAMP, however, has continued. In particular, it has been observed that "the validity and utility of DAMP will remain unclear until stronger evidence of the special status of the overlap between its constituent disorders is provided".

In 2005, there was an hour-long television program broadcast on Swedish TV, questioning why Sweden, almost alone in the world, would accept the DAMP construct. The program featured critical commentary from Sir Michael Rutter. It also considered some of the controversies over Gillberg's Gothenburg study.

The concept of DAMP (deficits in attention, motor control, and perception) has been in clinical use in Scandinavia for about 20 years. DAMP is diagnosed on the basis of concomitant attention deficit/hyperactivity disorder and developmental coordination disorder in children who do not have severe learning disability or cerebral palsy. In clinically severe form it affects about 1.5% of the general population of school age children; another few per cent are affected by more moderate variants. Boys are overrepresented; girls are currently probably underdiagnosed. There are many comorbid problems/overlapping conditions, including conduct disorder, depression/anxiety, and academic failure. There is a strong link with autism spectrum disorders in severe DAMP. Familial factors and pre- and perinatal risk factors account for much of the variance. Psychosocial risk factors appear to increase the risk of marked psychiatric abnormality in DAMP. Outcome in early adult age was psychosocially poor in one study in almost 60% of unmedicated cases. There are effective interventions available for many of the problems encountered in DAMP.

The exact pathophysiological mechanism of Flynn–Aird syndrome is unknown. However, several theories are in place with regards to the nature of this disease including the presence of a genetically defective enzyme involving a neuroectodermal tissue constituent. This explanation provides evidence for the late onset of the condition, the intricate findings, the varied nature of the disorder, as well as the genetic incidence. In addition, some aspects of the condition may be linked to a suppressing (S) gene due to the fact that only a small amount of stigmata appeared while the defects were still transmitted in the family studied. A suppressing gene down regulates the phenotypic expression of another gene, especially of a mutant gene. Other abnormalities may be due to endocrine system diseases.

Nonverbal learning disorder (also known as nonverbal learning disability, NLD, or NVLD) is a learning disorder characterized by verbal strengths as well as visual-spatial, motor, and social skills difficulties. It is sometimes confused with Asperger Syndrome or high IQ. Nonverbal learning disorder has never been included in the American Psychiatric Association's "Diagnostic and Statistical Manual of Mental Disorders" or the World Health Organization's "International Classification of Diseases".

REM sleep behavior disorder or RBD is the most common REM sleep parasomnia in which muscle atonia is absent. This allows the individual to act out their dreams and may result in repeated injury—bruises, lacerations, and fractures—to themselves or others. Patients may take self-protection measures by tethering themselves to bed, using pillow barricades, or sleeping in an empty room on a mattress.

Demographically, 90% of RBD patients are males, and most are older than 50 years of age.

Typical clinical features of REM sleep behavior disorder are:

- Male gender predilection

- Mean age of onset 50–65 years (range 20–80 years)

- Vocalisation, screaming, swearing that may be associated with dreams

- Motor activity, simple or complex, that may result in injury to patient or bed-partner

- Occurrence usually in latter half of sleep period (REM sleep)

- May be associated with neurodegenerative disease

Acute RBD, occurs mostly as a result of a side-effect in prescribed medication—usually antidepressants. But if not then 55% of the time the cause is unknown the other 45% the cause is associated with alcohol.

Chronic RBD is idiopathic, meaning of unknown origin, or associated with neurological disorders. There is a growing association of chronic RBD with neurodegenerative disorders—Parkinson's disease, multiple system atrophy (MSA), or dementia—as an early indicator of these conditions by as much as 10 years.

Patients with narcolepsy also are more likely to develop RBD.

Considered to be neurologically based, nonverbal learning disorder is characterized by verbal strengths as well as visual-spatial, motor, and social skills difficulties. People with this disorder may not at times comprehend nonverbal cues such as facial expression or tone of voice. Challenges with mathematics and handwriting are common.

While various nonverbal impairments were recognized since early studies in child neurology, there is ongoing debate as to whether/or the extent to which existing conceptions of NLD provide a valid diagnostic framework. As originally presented "nonverbal disabilities" (p. 44) or "disorders of nonverbal learning" (p. 272) was a category encompassing non-linguistic learning problems (Johnson and Myklebust, 1967). "Nonverbal learning disabilities" were further discussed by Myklebust in 1975 as representing a subtype of learning disability with a range of presentations involving "mainly visual cognitive processing," social imperception, a gap between higher verbal ability and lower performance IQ, as well as difficulty with handwriting. Later neuropsychologist Byron Rourke sought to develop consistent criteria with a theory and model of brain functioning that would establish NLD as a distinct syndrome (1989).

Questions remain about how best to frame the perceptual, cognitive and motor issues associated with NLD.

The DSM-5 (Diagnostic and Statistical Manual) and ICD-10 (International Classification of Diseases) do not include NLD as a diagnosis.

Assorted diagnoses have been discussed as sharing symptoms with NLD—these conditions include Right hemisphere brain damage and Developmental Right Hemisphere Syndrome, Developmental Coordination Disorder, Social-Emotional Processing Disorder, Asperger syndrome, Gerstmann syndrome and others.

Labels for specific associated issues include visual-spatial deficit, dyscalculia, dysgraphia, as well as dyspraxia.

In their 1967 book "Learning Disabilities; Educational Principles and Practices", Doris J. Johnson and Helmer R. Myklebust characterize how someone with these kinds of disabilities appears in a classroom: "An example is the child who fails to learn the meaning of the actions of others...We categorize this child as having a deficiency in social perception, meaning that he has an inability which precludes acquiring the significance of basic nonverbal aspects of daily living, though his verbal level of intelligence falls within or above the average." (p. 272). In their chapter "Nonverbal Disorders Of Learning" (p. 272-306) are sections titled "Learning Though Pictures," (274) "Gesture," (281) "Nonverbal Motor Learning," (282) "Body Image," (285) "Spatial Orientation," (290) "Right-Left Orientation," (292) "Social Imperception," (295) "Distractibility, Perseveration, and Disinhibition." (298)

Distal trisomy 10 is a rare chromosomal disorder that causes several physical defects and intellectual disability.

Humans, like all sexually reproducing species, have somatic cells that are in diploid [2N] state, meaning that N represent the number of chromosomes, and 2 the number of their copies. In humans, there are 23 chromosomes, but there are two sets of them, one from mother and one from father, totaling in 46, that are arranged according to their size, function and genes they carry. Each cell is supposed to have two of each, but sometimes due to mutations or malfunctions during cell division, mistakes are made that cause serious health problems. One such error is the cause of Distal trisomy 10q disorder.

Each chromosome has two arms, labeled p (for petite, or short) and q (for long). If both arms are equal in length, the chromosome is said to be metacentric. If arms' lengths are unequal, chromosome is said to be submetacentric, and if p arm is so short that is hard to observe, but still present, then the chromosome is acrocentric. In Distal Trisomy 10q disorder, end or distal portion of the q (long) arm of the chromosome number 10 appears to be present three times, rather than two times as it is supposed to be. This extra arm results in chromosome 10 trisomy, meaning that three arms are present. Depending on the length of the aberrant arm, the severity can vary from case to case. Often the source of this chromosomal error is a translocation in one of the parents. Sometimes it occurs spontaneously, in which case it is termed "de novo".

This syndrome has a large range of outcomes depending on how much chromosomal material is involved. Outcomes include: very slow postnatal growth, hypotonia, lack of coordination skills and mild to severe cases of intellectual disability, digestive issues, and heart and kidney problems. Individuals with this disorder can also be distinguished by their facial features. Number of support groups do exist in the United States, where affected families can meet and discuss problems they encounter, possible treatments and can find emotional support.

Recurrent Isolated Sleep Paralysis is an inability to perform voluntary movements at sleep onset, or upon waking from sleep.

EEM syndrome (or Ectodermal dysplasia, Ectrodactyly and Macular dystrophy syndrome) is an autosomal recessive congenital malformation disorder affecting tissues associated with the ectoderm (skin, hair, nails, teeth), and also the hands, feet and eyes.

The risk of chemotherapy-induced nausea and vomiting varies based on the type of treatment received, as well as several outside factors. Some types of chemotherapy are more prone to causing nausea and vomiting than others. Some chemotheraputic agents may not cause nausea and vomiting on their own, but may when used in combination with other agents. Regimens that are linked to a high incidence (90% or higher) of nausea and vomiting are referred to as "highly emetogenic chemotherapy", and those causing a moderate incidence (30–90%) of nausea and vomiting are referred to as "moderately emetogenic chemotherapy".

Some highly emetogenic agents and chemotherapy regimens include:

- Cisplatin

- Dacarbazine

- Cyclophosphamide (>1500 mg/m)

- Carmustine (>250 mg/m)

- Mechlorethamine

- Streptozocin

- ABVD

- MOPP/COPP/BEACOPP

- CBV

- VIP

- BEP

- AC

Some moderately emetogenic agents and regimens include:

- Carboplatin

- Methotrexate

- Doxorubicin/Adriamycin

- Docetaxel

- Paclitaxel

- Etoposide

- Ifosfamide

- Cyclophosphamide (≤1500 mg/m)

- CHOP/CHOP-R

Besides the type of treatment, personal factors may put a patient at greater risk for CINV. Other risk factors include:

- Female sex

- Patient age (under 55 years old)

- History of light alcohol use

- History of previous CINV

- History of nausea and vomiting during pregnancy

- History of motion sickness

- Anxiety or depression

- Anticipation of CINV

Magnesium deficiency causes neurogenic inflammation in a rat model. Researchers have theorized that since substance P which appears at day five of induced magnesium deficiency, is known to stimulate in turn the production of other inflammatory cytokines including IL-1, Interleukin 6 (IL-6), and TNF-alpha (TNFα), which begin a sharp rise at day 12, substance P is a key in the path from magnesium deficiency to the subsequent cascade of neuro-inflammation. In a later study, researchers provided rats dietary levels of magnesium that were reduced but still within the range of dietary intake found in the human population, and observed an increase in substance P, TNF alpha (TNFα) and Interleukin-1 beta (IL-1β), followed by exacerbated bone loss. These and other data suggest that deficient dietary magnesium intake, even at levels not uncommon in humans, may trigger neurogenic inflammation and lead to an increased risk of osteoporosis.

Inhalation of an agonist for the beta-2 adrenergic receptor, such as Salbutamol, Albuterol (US), is the most common treatment for asthma. Polymorphisms of the beta-2 receptor play a role in tachyphylaxis. Expression of the Gly-16 allele (glycine at position 16) results in greater receptor downregulation by endogenous catecholamines at baseline compared to Arg-16. This results in a greater single-use bronchodilator response in individuals homozygous for Arg-16 compared to Gly-16 homozygotes. However, with regular beta-2 agonist use, asthmatic Arg-16 individuals experience a significant decline in bronchodilator response. This decline does not occur in Gly-16 individuals. It has been proposed that the tachyphylactic effect of regular exposure to exogenous beta-2 agonists is more apparent in Arg-16 individuals because their receptors have not been downregulated prior to agonist administration.

EEM syndrome is caused by mutations in the "P-cadherin" gene ("CDH3"). Distinct mutations in "CDH3" (located on human chromosome 16) are responsible for the macular dystrophy and spectrum of malformations found in EEM syndrome, due in part to developmental errors caused by the resulting inability of "CDH3" to respond correctly to the "P-cadherin" transcription factor p63.

The gene for p63 ("TP73L", found on human chromosome 3) may also play a role in EEM syndrome. Mutations in this gene are associated with the symptoms of EEM and similar disorders, particularly ectrodactyly.

EEM syndrome is an autosomal recessive disorder, which means the defective gene is located on an autosome, and two copies of the defective gene - one from each parent - are required to inherit the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder.

Neurogenic inflammation is inflammation arising from the local release by afferent neurons of inflammatory mediators such as Substance P, Calcitonin Gene-Related Peptide (CGRP), neurokinin A (NKA), and endothelin-3 (ET-3). TRPA1 channels stimulated by lipopolysaccharide (LPS) may also cause acute neurogenic inflammation.

Once released, these neuropeptides induce the release of histamine from adjacent mast cells. In turn, histamine evokes the release of substance P and calcitonin gene-related peptide; thus, a bidirectional link between histamine and neuropeptides in neurogenic inflammation is established.

Neurogenic inflammation appears to play an important role in the pathogenesis of numerous diseases including migraine, psoriasis, asthma, vasomotor rhinitis, fibromyalgia, eczema, rosacea, dystonia, and multiple chemical sensitivity.

In migraine, stimulation of the trigeminal nerve causes neurogenic inflammation via release of neuropeptides including Substance P, nitric oxide, vasoactive intestinal polypeptide, 5-HT, Neurokinin A and CGRP. leading to a "sterile neurogenic inflammation."

In a patient fully withdrawn from opioids, going back to an intermittent schedule or maintenance dosing protocol, a fraction of the old tolerance level will rapidly develop, usually starting two days after therapy is resumed and, in general, leveling off after day 7. Whether this is caused directly by opioid receptors modified in the past or affecting a change in some metabolic set-point is unclear. Increasing the dose will usually restore efficacy; relatively rapid opioid rotation may also be of use if the increase in tolerance continues.

P′′ is a primitive computer programming language created by Corrado Böhm in 1964 to describe a family of Turing machines.

DPB is idiopathic, which means an exact physiological, environmental, or pathogenic cause of the disease is unknown. However, several factors are suspected to be involved with its pathogenesis (the way in which the disease works).

The major histocompatibility complex (MHC) is a large genomic region found in most vertebrates that is associated with the immune system. It is located on chromosome 6 in humans. A subset of MHC in humans is human leukocyte antigen (HLA), which controls the antigen-presenting system, as part of adaptive immunity against pathogens such as bacteria and viruses. When human cells are infected by a pathogen, some of them can present parts of the pathogen's proteins on their surfaces; this is called "antigen presentation". The infected cells then become targets for types of cytotoxic T-cells, which kill the infected cells so they can be removed from the body.

Genetic predisposition for DPB susceptibility has been localized to two HLA haplotypes (a nucleotide or gene sequence difference between paired chromosomes, that is more likely to occur among a common ethnicity or trait) common to people of East Asian descent. HLA-B54 is associated with DPB in the Japanese, while HLA-A11 is associated with the disease in Koreans. Several genes within this region of class I HLA are believed to be responsible for DPB, by allowing increased susceptibility to the disease. The common genetic background and similarities in the HLA profile of affected Japanese and Korean individuals were considered in the search for a DPB gene. It was suggested that a mutation of a suspected disease-susceptibility gene located somewhere between HLA-B and HLA-A had occurred on an ancestral chromosome carrying both HLA-B54 and HLA-A11. Further, it is possible that a number of genetic recombination events around the disease locus (location on a chromosome) could have resulted in the disease being associated with HLA-B54 in the Japanese and HLA-A11 in Koreans. After further study, it was concluded that a DPB susceptibility gene is located near the HLA-B locus at chromosome 6p21.3. Within this area, the search for a genetic cause of the disease has continued.

Because many genes belonging to HLA remain unidentified, positional cloning (a method used to identify a specific gene, when only its location on a chromosome is known) has been used to determine that a mucin-like gene is associated with DPB. In addition, diseases caused by identified HLA genes in the DPB-susceptibility region have been investigated. One of these, bare lymphocyte syndrome I (BLS I), exhibits a number of similarities with DPB in those affected, including chronic sinusitis, bronchiolar inflammation and nodules, and the presence of "H. influenzae". Also like DPB, BLS I responds favorably to erythromycin therapy by showing a resolution of symptoms. The similarities between these two diseases, the corresponding success with the same mode of treatment, and the fact that the gene responsible for BLS I is located within the DPB-causing area of HLA narrows the establishment of a gene responsible for DPB. Environmental factors such as inhaling toxic fumes and cigarette smoking are not believed to play a role in DPB, and unknown environmental and other non-genetic causes—such as unidentified bacteria or viruses—have not been ruled out.

Cystic fibrosis (CF), a progressive multi-system lung disease, has been considered in the search for a genetic cause of DPB. This is for a number of reasons. CF, like DPB, causes severe lung inflammation, abundant mucus production, infection, and shows a genetic predominance among Caucasians of one geographic group to the rarity of others; whereas DPB dominates among East Asians, CF mainly affects individuals of European descent. While no gene has been implicated as the cause of DPB, mutation in a specific gene—much more likely to occur in Europeans—causes CF. This mutation in the CF-causing gene is not a factor in DPB, but a unique polymorphism (variation) in this gene is known to occur in many Asians not necessarily affected by either disease. It is being investigated whether this gene in any state of mutation could contribute to DPB.

A study done in 1995 of 811 university students in the United States found 5.2% of that population had results indicating they were talkaholics. A similar study from the same year with students from New Zealand found similar results, with 4.7% scoring above 40.