The 'core' neuroacanthocytosis syndromes are chorea acanthocytosis and McLeod syndrome. Acanthocytes are nearly always present in these conditions and they share common clinical features. Some of these features are also seen in the other neurological syndromes associated with neuroacanthocytosis.

A common feature of the core syndromes is chorea: involuntary dance-like movements. In neuroacanthocytosis, this is particularly prominent in the face and mouth which can cause difficulties with speech and eating. These movements are usually abrupt and irregular and present during both rest and sleep.

Individuals with neuroacanthocytosis also often suffer from parkinsonism, the uncontrolled slowness of movements, and dystonia, abnormal body postures. Many affected individuals also have cognitive (intellectual) impairment and psychiatric symptoms such as anxiety, paranoia, depression, obsessive behavior, and pronounced emotional instability. Seizures may also be a symptom of neuroacanthocytosis.

Onset differs between individual neuroacanthocytosis syndromes but is usually between ages 20 and 40. Affected individuals usually live for 10–20 years after onset.

Tics are movements or sounds "that occur intermittently and unpredictably out of a background of normal motor activity", having the appearance of "normal behaviors gone wrong". The tics associated with Tourette's change in number, frequency, severity and anatomical location. Waxing and waning—the ongoing increase and decrease in severity and frequency of tics—occurs differently in each individual. Tics may also occur in "bouts of bouts", which vary for each person.

Coprolalia (the spontaneous utterance of socially objectionable or taboo words or phrases) is the most publicized symptom of Tourette's, but it is not required for a diagnosis of Tourette's and only about 10% of Tourette's patients exhibit it. Echolalia (repeating the words of others) and palilalia (repeating one's own words) occur in a minority of cases, while the most common initial motor and vocal tics are, respectively, eye blinking and throat clearing.

In contrast to the abnormal movements of other movement disorders (for example, choreas, dystonias, myoclonus, and dyskinesias), the tics of Tourette's are temporarily suppressible, nonrhythmic, and often preceded by an unwanted premonitory urge. Immediately preceding tic onset, most individuals with Tourette's are aware of an urge, similar to the need to sneeze or scratch an itch. Individuals describe the need to tic as a buildup of tension, pressure, or energy which they consciously choose to release, as if they "had to do it" to relieve the sensation or until it feels "just right". Examples of the premonitory urge are the feeling of having something in one's throat, or a localized discomfort in the shoulders, leading to the need to clear one's throat or shrug the shoulders. The actual tic may be felt as relieving this tension or sensation, similar to scratching an itch. Another example is blinking to relieve an uncomfortable sensation in the eye. These urges and sensations, preceding the expression of the movement or vocalization as a tic, are referred to as "premonitory sensory phenomena" or premonitory urges. Because of the urges that precede them, tics are described as semi-voluntary or ""unvoluntary"", rather than specifically "involuntary"; they may be experienced as a "voluntary", suppressible response to the unwanted premonitory urge. Published descriptions of the tics of Tourette's identify sensory phenomena as the core symptom of the syndrome, even though they are not included in the diagnostic criteria.

While individuals with tics are sometimes able to suppress their tics for limited periods of time, doing so often results in tension or mental exhaustion. People with Tourette's may seek a secluded spot to release their symptoms, or there may be a marked increase in tics after a period of suppression at school or at work. Some people with Tourette's may not be aware of the premonitory urge. Children may be less aware of the premonitory urge associated with tics than are adults, but their awareness tends to increase with maturity. They may have tics for several years before becoming aware of premonitory urges. Children may suppress tics while in the doctor's office, so they may need to be observed while they are not aware they are being watched. The ability to suppress tics varies among individuals, and may be more developed in adults than children.

Although there is no such thing as a "typical" case of Tourette syndrome, the condition follows a fairly reliable course in terms of the age of onset and the history of the severity of symptoms. Tics may appear up to the age of eighteen, but the most typical age of onset is from five to seven. A 1998 study published by Leckman and colleagues from the Yale Child Study Center showed that the ages of highest tic severity are eight to twelve (average ten), with tics steadily declining for most patients as they pass through adolescence. The most common, first-presenting tics are eye blinking, facial movements, sniffing and throat clearing. Initial tics present most frequently in midline body regions where there are many muscles, usually the head, neck and facial region. This can be contrasted with the stereotyped movements of other disorders (such as stims and stereotypies of the autism spectrum disorders), which typically have an earlier age of onset, are more symmetrical, rhythmical and bilateral, and involve the extremities (e.g., flapping the hands). Tics that appear early in the course of the condition are frequently confused with other conditions, such as allergies, asthma, and vision problems: pediatricians, allergists and ophthalmologists are typically the first to see a child with tics.

Most cases of Tourette's in older individuals are mild and almost unrecognizable. When symptoms are severe enough to warrant referral to clinics, obsessive–compulsive disorder (OCD) and attention-deficit hyperactivity disorder (ADHD) are often associated with Tourette's. In children with tics, the additional presence of ADHD is associated with functional impairment, disruptive behavior, and tic severity. Compulsions resembling tics are present in some individuals with OCD; "tic-related OCD" is hypothesized to be a subgroup of OCD, distinguished from non-tic related OCD by the type and nature of obsessions and compulsions. Not all persons with Tourette's have ADHD or OCD or other comorbid conditions, although in clinical populations, a high percentage of patients presenting for care do have ADHD. One author reports that a ten-year overview of patient records revealed about 40% of patients with Tourette's have "TS-only" or "pure TS", referring to Tourette syndrome in the absence of ADHD, OCD and other disorders. Another author reports that 57% of 656 patients presenting with tic disorders had uncomplicated tics, while 43% had tics plus comorbid conditions. People with "full-blown Tourette's" have significant comorbid conditions in addition to tics.

The characteristic symptom of Costeff syndrome is the onset of progressively worsening eyesight caused by degeneration of the optic nerve (optic atrophy) within the first few years of childhood, with the majority of affected individuals also developing motor disabilities later in childhood. Occasionally, people with Costeff syndrome may also experience mild cognitive disability.

It is type of 3-methylglutaconic aciduria, the hallmark of which is an increased level in the urinary concentrations of 3-methylglutaconic acid and 3-methylglutaric acid; this can allow diagnosis as early as at one year of age.

Those with Costeff syndrome typically experience the first symptoms of visual deterioration within the first few years of childhood, which manifests as the onset of progressively decreasing visual acuity. This decrease tends to continue with age, even after childhood.

The majority of people with Costeff syndrome develop movement problems and motor disabilities later in childhood, the two most significant of which are choreoathetosis and spasticity. The former causes involuntary erratic, jerky, and twisting movements (see chorea and athetosis), whereas the latter causes twitches and spastic tendencies.

These two symptoms are often severe enough to seriously disable an individual; among 36 people with Costeff syndrome, 17 experienced major motor disability as a result of choreoathetosis, and 12 experienced spasticity-related symptoms severe enough to do the same.

Ataxia (loss of muscle coordination) and speech impairment caused by dysarthria also occur in roughly 50% of cases, but are rarely seriously disabling.

Some individuals with Costeff disease also display mild cognitive impairment, though such cases are relatively infrequent.

In the long term, many paroxysmal symptoms occur along with AHC, and while these symptoms vary in strength depending on the person, they are consistent features of AHC. It is thought that some of these symptoms are brought on or worsened by hemiplegic attacks, though it is not known for certain. Patients suffer persistent motor, movement (ataxia), and cognitive deficits. These deficits become more apparent over time and include developmental delays, social problems, and retardation. It is rare for someone with AHC not to have cognitive deficits, but a study in Japan did find two patients who met all of the diagnostic criteria for AHC but who were not mentally impaired. It is not known whether AHC is a progressive disease, but severe attacks are suspected to cause damage which result in permanent loss of function. 100% of children studied in the USA have had some form of mental impairment, which is usually described as mild to moderate, but varies greatly among individuals.

Tics are sudden, repetitive, nonrhythmic movements (motor tics) and utterances (phonic tics) that involve discrete muscle groups. Motor tics are movement-based tics, while phonic tics are involuntary sounds produced by moving air through the nose, mouth, or throat.

Tourette's was classified by the fourth version of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM-IV-TR) as one of several tic disorders "usually first diagnosed in infancy, childhood, or adolescence" according to type (motor or phonic tics) and duration (transient or chronic). Transient tic disorders consisted of multiple motor tics, phonic tics or both, with a duration between four weeks and twelve months. Chronic tic disorder was either single or multiple, motor or phonic tics (but not both), which were present for more than a year. Tourette's is diagnosed when multiple motor tics, and at least one phonic tic, are present for more than a year. The fifth version of the DSM (DSM-5), published in May 2013, reclassified Tourette's and tic disorders as motor disorders listed in the neurodevelopmental disorder category, and replaced transient tic disorder with provisional tic disorder, but made few other significant changes.

Tic disorders are defined only slightly differently by the World Health Organization International Statistical Classification of Diseases and Related Health Problems, ICD-10; code F95.2 is for combined vocal and multiple motor tic disorder [de la Tourette].

Although Tourette's is the more severe expression of the spectrum of tic disorders, most cases are mild. The severity of symptoms varies widely among people with Tourette's, and mild cases may be undetected.

At least 50% of AHC sufferers also suffer from epilepsy, and AHC is often misdiagnosed as epilepsy because of this. These epileptic events are distinguished from other episodes by an alteration of consciousness, as well as frequent tonic or tonic-clonic activity. Epileptic episodes are generally rare, though they do increase with age. Due to the rarity of epileptic episodes, there are few EEG confirmations of them.

The hallmark of the neuroacanthocytosis syndromes is the presence of acanthocytes in peripheral blood. "Acanthocytosis" originated from the Greek word "acantha", meaning thorn. Acanthocytes are spiculated red blood cells and can be caused by altered distribution of membrane lipids or membrane protein/skeleton abnormalities. In neuroacanthocytosis, acanthocytes are caused by protein but not lipid membrane abnormalities

Movement disorders are clinical syndromes with either an excess of movement or a paucity of voluntary and involuntary movements, unrelated to weakness or spasticity. Movement disorders are synonymous with basal ganglia or extrapyramidal diseases. Movement disorders are conventionally divided into two major categories- "hyperkinetic" and "hypokinetic".

Hyperkinetic movement disorders refer to dyskinesia, or excessive, often repetitive, involuntary movements that intrude upon the normal flow of motor activity.

Hypokinetic movement disorders refer to akinesia (lack of movement), hypokinesia (reduced amplitude of movements), bradykinesia (slow movement) and rigidity. In primary movement disorders, the abnormal movement is the primary manifestation of the disorder. In secondary movement disorders, the abnormal movement is a manifestation of another systemic or neurological disorder.

Symptoms typically present in the 3rd or 4th decade of life, but have been seen as early as the age of 14. It presents with torsion dystonia, particularly when presenting at a younger age, which then progresses to parkinsonism with or without ongoing dystonia. Often the two symptoms coexist.The parkinsonian features of x-linked dystonia parkinsonism include festinating gait, bradykinesia, blepharospasm, and postural instability. It often lacks a resting tremor, helping to differentiate it from Parkinson's disease.

This is characterized by attacks of involuntary movements (dystonia, chorea, or ballism), which are typically triggered by sudden voluntary movements, but can also be triggered by involuntary movements as well (for example, hyperventilating). These voluntary movements usually involve whole body activity such as standing, walking, and running. The age of onset is typically in childhood or early adolescence with most cases reporting improvement or complete remission with aging. Attacks last from seconds to minutes and are known to be at higher risk of occurring during stress, fear, cold, heat, or menstruation.

The paroxysmal dyskinesias are mainly classified by their triggers and on the basis of the duration and frequency of the attacks. The three main types are paroxysmal kinesigenic dyskinesia (PKD), paroxysmal non-kinesigenic dyskinesia (PNKD) and paroxysmal exercise-induced (exertion-induced) dyskinesia (PED).

Most children with Allan–Herndon–Dudley syndrome have weak muscle tone (hypotonia) and underdevelopment of many muscles (muscle hypoplasia). As they get older, they usually develop joint deformities called contractures, which restrict the movement of certain joints. Abnormal muscle stiffness (spasticity), muscle weakness, and involuntary movements of the arms and legs also limit mobility. As a result, many people with Allan–Herndon–Dudley syndrome are unable to walk independently and become wheelchair-bound by adulthood.

Tics should be distinguished from other causes of tourettism, stereotypies, chorea, dyskinesias, myoclonus, and obsessive-compulsive disorder.

Motor disorders are malfunctions of the nervous system that cause involuntary or uncontrollable movements or actions of the body (Stone). These disorders can cause lack of intended movement or an excess of involuntary movement (Mandal). Symptoms of motor disorders include tremors, jerks, twitches, spasms, contractions, or gait problems.

The disease typically starts in one limb, typically one leg. Progressive dystonia results in clubfoot and tiptoe walking. The symptoms can spread to all four limbs around age 18, after which progression slows and eventually symptoms reach a plateau. There can be regression in developmental milestones (both motor and mental skills) and failure to thrive in the absence of treatment.

In addition, SS is typically characterized by signs of parkinsonism that may be relatively subtle. Such signs may include slowness of movement (bradykinesia), tremors, stiffness and resistance to movement (rigidity), balance difficulties, and postural instability. Approximately 25 percent also have abnormally exaggerated reflex responses (hyperreflexia), particularly in the legs. These symptoms can result in a presentation that is similar in appearance to that of Parkinson's Disease.

Many patients experience improvement with sleep, are relatively free of symptoms in the morning, and develop increasingly severe symptoms as the day progresses (i.e., diurnal fluctuation). Accordingly, this disorder has sometimes been referred to as "progressive hereditary dystonia with diurnal fluctuations." Yet some SS patients do not experience such diurnal fluctuations, causing many researchers to prefer other disease terms.

- Other symptoms - footwear

- excessive wear at toes, but little wear on heels, thus replacement of shoes every college term/semester.

- Other symptoms - handwriting

- near normal handwriting at infants/kindergarten (ages 3–5 school) years.

- poor handwriting at pre-teens (ages 8–11 school) years.

- very poor (worse) handwriting during teen (qv GCSE/A level-public exams) years.

- bad handwriting (worsening) during post-teen (qv university exams) years.

- very bad handwriting (still worsening) during adult (qv post-graduate exams) years.

- worsening pattern of sloppy handwriting best observed by school teachers via termly reports.

- child sufferer displays unhappy childhood facial expressions (depression.?)

ICD10 diagnosis codes are:

- F95.0 Transient tic disorder

- F95.1 Chronic motor or vocal tic disorder

- F95.2 Combined vocal and multiple motor tic disorder [Gilles de la Tourette]

- F95.8 Other tic disorders

- F95.9 Tic disorder, unspecified

Chorea-acanthocytosis (ChAc, also called Choreoacanthocytosis), is a rare hereditary disease caused by a mutation of the gene that directs structural proteins in red blood cells. It belongs to a group of four diseases characterized under the name Neuroacanthocytosis. When a patient's blood is viewed under a microscope, some of the red blood cells appear thorny. These thorny cells are called acanthocytes.

Other effects of the disease may include epilepsy, behaviour changes, muscle degeneration, and neuronal degradation similar to Huntington's Disease. The average age of onset of symptoms is 35 years. The disease is incurable and inevitably leads to premature death.

Some more information about Chorea-acanthocytosis is that it is a very complex autosomal recessive adult-onset neurodegenerative disorder. It often shows itself as a mixed movement disorder, in which chorea, tics, dystonia and even parkinsonism may appear as a symptom.

This disease is also characterized by the presence of a few different movement disorders including chorea, dystonia etc.

Chorea-acanthocytosis is considered an autosomal recessive disorder, although a few cases with autosomal dominant inheritance have been noted.

ARSACS is usually diagnosed in early childhood, approximately 12–24 months of age when a child begins to take their first steps. At this time it manifests as a lack of coordination and balance resulting in frequent falls. Some of the signs and symptoms include:

- Stiffness of the legs

- Appendicular and trunk ataxia

- Hollow foot and hand deformities

- Ataxic dysarthria

- Distal muscle wasting

- Horizontal gaze nystagmus

- Spasticity

Giant axonal neuropathy usually appears in infancy or early childhood, and is progressive. Early signs of the disorder often present in the peripheral nervous system, causing individuals with this disorder to have problems walking. Later, normal sensation, coordination, strength, and reflexes become affected. Hearing or vision problems may also occur. Abnormally kinky hair is characteristic of giant axonal neuropathy, appearing in almost all cases. As the disorder progresses, central nervous system becomes involved, which may cause a gradual decline in mental function, loss of control of body movement, and seizures.

The oculogyric crises usually occur in the later half of the day and during these episodes patients undergo extreme agitation and irritability along with uncontrolled head and neck movements. Apart from the aforementioned symptoms, patients can also display Parkinsonism, sleep disturbances, small head size (microcephaly), behavioral abnormalities, weakness, drooling, and gastrointestinal symptoms.

Congenital mirror movement disorder (CMM disorder) is a rare genetic neurological disorder which is characterized by mirrored movement, sometimes referred to as associated or synkinetic movement, most often in the upper extremity of the body. These movements are voluntary intentional movements on one, ipsilateral, side of the body that are mirrored simultaneously by involuntary movements on the contralateral side.

The reproduction of involuntary movement usually happens along the head-tail axis, having a left-right symmetry. For example, if someone were to voluntarily make a fist with their left hand, their right hand would do the same. In most cases, the accompanying contralateral involuntary movements are much weaker than the ipsilateral voluntary ones, although the extent and magnitude of the mirrored movement vary across patients. This disorder has not yet been found to be associated with any other neurologic disease or cognitive disability, and currently, no cures nor means to improve signs or symptoms have been found.

The congenital mirror movements begin in infancy and persist throughout the patient’s life, often with very little improvement, or deterioration. Consequently, patients who do suffer from this movement disorder have serious difficulty carrying out tasks that require manual dexterity or precision, such as playing a two handed musical instrument or typing on a keyboard, for their whole lives. Patients also often experience discomfort or pain in the upper limbs due to prolonged use of the same muscles. Therefore, quality of life can be severely hampered.

CMM disorder’s prevalence in the world is thought to be less than 1 in 1 million people. Because of its rarity, researchers suggest that some mildly affected individuals may never be diagnosed. It is important not to confuse congenital mirror movement disorders, a rare genetically based neurologic disease, with acquired mirror movement disorders that present themselves during one’s lifetime due to other reasons (stroke for example).

Costeff syndrome, or 3-methylglutaconic aciduria type III, is a genetic disorder caused by mutations in the "OPA3" gene. It is typically associated with the onset of visual deterioration (optic atrophy) in early childhood followed by the development of movement problems and motor disability in later childhood, occasionally along with mild cases of cognitive deficiency. The disorder is named after Hanan Costeff, the doctor who first described the syndrome in 1989.

Sepiapterin reductase deficiency is an inherited pediatric disorder characterized by movement problems, and most commonly displayed as a pattern of involuntary sustained muscle contractions known as dystonia. Symptoms are usually present within the first year of age, but diagnosis is delayed due to physicians lack of awareness and the specialized diagnostic procedures. Individuals with this disorder also have delayed motor skills development including sitting, crawling, and need assistance when walking. Additional symptoms of this disorder include intellectual disability, excessive sleeping, mood swings, and an abnormally small head size. SR deficiency is a very rare condition. The first case was diagnosed in 2001, and since then there have been approximately 30 reported cases. At this time, the condition seems to be treatable, but due to a lack of overall awareness and a series of atypical procedures used to diagnose this condition pose a dilemma.

Geniospasm is movement disorder of the mentalis muscle.

It is a benign genetic disorder linked to chromosome 9q13-q21 where there are episodic involuntary up and down movements of the chin and lower lip. The movements consist of rapid fluttering or trembling at about 8 Hz superimposed onto a once per three seconds movement of higher amplitude and occur symmetrically in the V shaped muscle. The tongue and buccal floor muscles may also be affected but to a much lesser degree.

The movements are always present but extreme episodes may be precipitated by stress, concentration or emotion and commence in early childhood.

The condition is extremely rare and in a study in 1999 only 23 families in the world were known to be affected, although it may be under-reported. Inheritance is aggressively autosomal dominant. In at least two studies the condition appeared spontaneously in the families.

The condition responds very well to regular botulinus toxin injections into the mentalis muscle which paralyse the muscle but cause no impairment of facial expression or speech.

X-linked dystonia parkinsonism (XDP), also known as Lubag Syndrome or X-linked Dystonia of Panay, is a rare x-linked progressive movement disorder with high penetrance found almost exclusively in males from the Panay, Philippines. It is characterized by dystonic movements first typically occurring in the 3rd and 4th decade of life. The dystonic movements often either coexist or develop into parkinsonism within 10 years of disease onset.