According to the 2017 "Survey of Pediatric Acute-Onset Neuropsychiatric Syndrome Characteristics and Course" these symptoms may occur in PANS patients:

Some patients meet criteria for PANS, but have a severe presentation and/or follow a chronic static or chronic deteriorating course. These patients warrant more aggressive evaluations, as they may also meet criteria for Autoimmune Encephalitis, Steroid Responsive Encephalitis with Thyroiditis, CNS vasculitis, antiphospholipid antibody syndrome, or lupus cerebritis, and thus may qualify for aggressive immunomodulatory therapy.

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.

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.?)

There are multiple symptoms that can help this disease to be diagnosed, this disease is marked by the presence of acanthocytes in blood (these acanthocytes can sometimes be absent or even make a late appearance in the course of the disease.) and neurodegeneration causing a choreiform movement disorder.

Another one of them would be that this disease should be considered in patients who have elevated levels of acanthocytes in a peripheral blood film.

The serum creatine kinase is often elevated in the body of the people who are affected by this disease.

People afflicted by this disease also experience a loss of neurons. Loss of neurons is a hallmark of neurodegenerative diseases. Due to the generally non-regenerative nature of neuronal cells in the adult central nervous system, this results in an irreversible and fatal process of neurodegeneration. There is also the presence of several movement related disorders including chorea, dystonia and bradykinesia, one of the more incapacitating ones includes Truncal spasms.

In those with SS, symptoms typically dramatically improve with low-dose administration of levodopa (L-dopa). L-DOPA exists as a biochemically significant metabolite of the amino acid phenylalanine, as well as a biological precursor of the catecholamine dopamine, a neurotransmitter. (Neurotransmitters are naturally produced molecules that may be sequestered following the propagation of an action potential down a nerve towards the axon terminal, which in turn may cross the synaptic junction between neurons, enabling neurons to communicate in a variety of ways.) Low-dose L-dopa usually results in near-complete or total reversal of all associated symptoms for these patients. In addition, the effectiveness of such therapy is typically long term, without the complications that often occur for those with Parkinson's disease who undergo L-dopa treatment. Thus, most experts indicate that this disorder is most appropriately known as dopa-responsive dystonia (SS).

No data are available on mortality associated with SS, but patients surviving beyond the fifth decade with treatment have been reported. However, in severe, early autosomal recessive forms of the disease, patients have been known to pass away during childhood. Girls seem to be somewhat more commonly affected. The disease less commonly begins during puberty or after age 20, and very rarely, cases in older adults have been reported.

Due to commonly being misdiagnosed, it is common for the disease to remain untreated. When left untreated, patients often need achilles tendon surgery by the age of 21. They will also struggle with walking, an ability that will degrade throughout the day. Power napping can provide temporary relief in untreated patients. It also impairs development into adulthood, reduces balance, and reduces calf muscle development. Socially, it can result in depression, lack of social skills, and inability to find employment.

Males

In males the symptoms of Danon Disease are more severe. Features of Danon Disease in males are:

- An early age of onset of muscle weakness and heart disease (onset in childhood or adolescence)

- Some learning problems or intellectual disability can be present

- Muscle weakness can be severe and can affect endurance and the ability to walk

- Heart disease (cardiomyopathy) can be severe and can lead to a need for medications. It usually progress to heart failure, commonly complicated by atrial fibrillation and embolic strokes with severe neurological disability, leading to death unless heart transplant is performed.

- Cardiac conduction abnormalities can occur. Wolff-Parkinson-White syndrome is a common conduction pattern in Danon disease.

- Symptoms are usually gradually progressive

- Some individuals may have visual disturbances, and/or retinal pigment abnormalities

- Danon Disease is rare and unfamiliar to most physicians. It can be mistaken for other forms of heart disease and/or muscular dystrophies, including Pompe disease.

Females

In females the symptoms of Danon Disease are less severe. Common symptoms of Danon Disease in females are:

- A later age of onset of symptoms. Many females will not have obvious symptoms until late adolescence or even adulthood.

- Learning problems and intellectual disability are usually ABSENT

- Muscle weakness is often absent or subtle. Some females will tire easily with exercise

- Cardiomyopathy) is often absent in childhood. Some women will develop this in adulthood. Cardiomyopathy can be associated with atrial fibrillation and embolic strokes.

- Cardiac conduction abnormalities can occur. Wolff-Parkinson-White syndrome is a common conduction pattern in Danon disease.

- Symptoms in females progress more slowly than in males.

- Some females may have visual disturbances, and/or retinal pigment abnormalities

- Danon Disease is rare and unfamiliar to most physicians. The milder and more subtle symptoms in females can make it more difficult to diagnose females with Danon Disease

Symptoms categorized as physically visible symptoms include chorea, dystonia, spasticity, and rigidity, all physical symptoms of the body associated with movement disorders. The symptoms accompanying neuroferritinopathy affecting movement are also progressive, becoming more generalized with time. Usually during the first ten years of onset of the disease only one or two limbs are directly affected.

Distinctive symptoms of neuroferritinopathy are chorea, found in 50% of diagnosed patients, dystonia, found in 43% of patients, and parkinsonism, found in 7.5% of patients. Full control of upper limbs on the body generally remains until late onset of the disease. Over time, symptoms seen in a patient can change from one side of the body to the opposite side of the body, jumping from left to right or vice versa. Another route that the physically visible symptoms have been observed to take is the appearance, disappearance, and then reappearance once more of specific symptoms.

While these symptoms are the classic indicators of neuroferritinopathy, symptoms will vary from patient to patient.

Danon disease (or glycogen storage disease Type IIb) is a metabolic disorder.Danon disease is an X-linked lysosomal and glycogen storage disorder associated with hypertrophic cardiomyopathy, skeletal muscle weakness, and intellectual disability.

SCA6 is typified by progressive and permanent cerebellar dysfunction. These cerebellar signs include ataxia and dysarthria, likely caused by cerebellar atrophy. Prior to diagnosis and the onset of major symptoms, patients often report a feeling of "wooziness" and momentary imbalance when turning corners or making rapid movements. The age at which symptoms first occur varies widely, from age 19 to 71, but is typically between 43 and 52. Other major signs of SCA6 are the loss of vibratory and proprioceptive sensation and nystagmus.

While most patients present with these severe progressive symptoms, others, sometimes within the same family, display episodic non-progressive symptoms more similar to episodic ataxia. Still others present with symptoms common to both SCA6 and familial hemiplegic migraine.

Symptoms categorized as medically tested and diagnosed include iron accumulation in the brain, basal ganglia cavitation, and neurodegeneration. Patients who are diagnosed with neuroferritinopathy have abnormal iron accumulation in the brain within the neurons and glia of the striatum and cerebellar cortices. Along with the accumulation of iron in the brain, neuroferritinopathy typically causes severe neuronal loss as well.

Secondary symptoms may also arise. It is possible that the initial iron accumulation will cause additional neuronal damage and neuronal death. The damaged neurons may be replaced by other cells in an effort to reverse the neurodegeneration. These cells often have a higher iron content. The breakdown of the blood brain barrier may also occur due to the loss of neurons and will subsequently allow more iron to access the brain and accumulate over time.

Neuroferritinopathy is mainly seen in those who have reached late adulthood and is generally seen to slowly progress throughout many decades in a lifetime with the mean age of onset being 39 years old. A loss of cognition is generally only seen with late stages of the disease. Diagnosed patients are seen to retain most of their cognitive functioning until the most progressive stages of the illness sets in.

Jansky–Bielschowsky disease is an extremely rare autosomal recessive genetic disorder that is part of the neuronal ceroid lipofuscinosis (NCL) family of neurodegenerative disorders. It is caused by the accumulation of lipopigments in the body due to a deficiency in tripeptidyl peptidase I as a result of a mutation in the TPP1 gene. Symptoms appear between ages 2 and 4 and consist of typical neurodegenerative complications: loss of muscle function (ataxia), drug resistant seizures (epilepsy), apraxia, development of muscle twitches (myoclonus), and vision impairment. This late-infantile form of the disease progresses rapidly once symptoms are onset and ends in death between age 8 and teens. The prevalence of Jansky–Bielschowsky disease is unknown, however NCL collectively affects an estimated 1 in 100,000 individuals worldwide. Jansky–Bielschowsky disease is also known as: late-infantile Batten disease, LINCL, or neuronal ceroid lipofuscinosis.

There are three main types of the disease each with its own distinctive symptoms.

Type I infantile form, infants will develop normally until about a year old. At this time, the affected infant will begin to lose previously acquired skills involving the coordination of physical and mental behaviors. Additional neurological and neuromuscular symptoms such as diminished muscle tone, weakness, involuntary rapid eye movements, vision loss, and seizures may become present. With time, the symptoms worsen and children affected with this disorder will experience a decreased ability to move certain muscles due to muscle rigidity. The ability to respond to external stimuli will also decrease. Other symptoms include neuroaxonal dystrophy from birth, discoloration of skin, Telangiectasia or widening of blood vessels.

Type II adult form, symptoms are milder and may not appear until the individual is in his or her 30s. Angiokeratomas, an increased coarsening of facial features, and mild intellectual impairment are likely symptoms.

Type III is considered an intermediate disorder. Symptoms vary and can include to be more severe with seizures and mental retardation, or less severe with delayed speech, a mild autistic like presentation, and/or behavioral problems.

Some of the possible symptoms that can occur with metabolic disorders are: lethargy, weight loss, jaundice, seizures, to name a few. The symptoms expressed would vary with the type of metabolic disorder. There are four categories of symptoms: acute symptoms, late-onset acute symptoms, progressive general symptoms and permanent symptoms.

Tourette’s syndrome is a neurological disorder characterized by recurrent involuntary movements (motor tics) and involuntary noises (vocal tics). The reason Tourette’s syndrome and other tic disorders are being considered for placement in the obsessive compulsive spectrum is because of the phenomenology and co-morbidity of the disorders with obsessive compulsive disorder. Within the population of patients with OCD up to 40% have a history of a tic disorder and 60% of people with Tourette’s syndrome have obsessions and/or compulsions. Plus 30% of people with Tourette’s syndrome have full-scale OCD. Course of illness is another factor that suggests correlation because it has been found that tics displayed in childhood are a predictor of obsessive and compulsive symptoms in late adolescence and early adulthood. However, the association of Tourette’s and tic disorders with OCD is challenged by neuropsychology and pharmaceutical treatment. Whereas OCD is treated with SSRI’s, tics are treated with dopamine blockers and alpha-2 agonists.

Hypochondriasis is excessive preoccupancy or worry about having a serious illness. These thoughts cause a person a great deal of anxiety and stress. The prevalence of this disorder is the same for men and women. Hypochondriasis is normally recognized in early adult age. Those that suffer with hypochondriasis are constantly thinking of their body functions, minor bumps and bruises as well as body images. Hypochondriacs go to numerous outpatient facilities for confirmation of their own diagnosis. Hypochondriasis is the belief that something is wrong but it is not known to be a delusion.

This form differs from the infantile principally in the relative lack of cardiac involvement. The onset is more insidious and has a slower progression. Cardiac involvement may occur but is milder than in the infantile form. Skeletal involvement is more prominent with a predilection for the lower limbs.

Late onset features include impaired cough, recurrent chest infections, hypotonia, progressive muscle weakness, delayed motor milestones, difficulty swallowing or chewing and reduced vital capacity.

Prognosis depends on the age of onset on symptoms with a better prognosis being associated with later onset disease.

The infantile form usually comes to medical attention within the first few months of life. The usual presenting features are cardiomegaly (92%), hypotonia (88%), cardiomyopathy (88%), respiratory distress (78%), muscle weakness (63%), feeding difficulties (57%) and failure to thrive (50%).

The main clinical findings include floppy baby appearance, delayed motor milestones and feeding difficulties. Moderate hepatomegaly may be present. Facial features include macroglossia, wide open mouth, wide open eyes, nasal flaring (due to respiratory distress), and poor facial muscle tone. Cardiopulmonary involvement is manifested by increased respiratory rate, use of accessory muscles for respiration, recurrent chest infections, decreased air entry in the left lower zone (due to cardiomegaly), arrhythmias and evidence of heart failure.

Median age at death in untreated cases is 8.7 months and is usually due to cardiorespiratory failure.

Paraphrenia (from – beside, near + φρήν – intellect, mind) is a mental disorder characterized by an organized system of paranoid delusions with or without hallucinations (the positive symptoms of schizophrenia) without deterioration of intellect or personality (its negative symptom).

This disorder is also distinguished from schizophrenia by a lower hereditary occurrence, less premorbid maladjustment, and a slower rate of progression. Onset of symptoms generally occurs later in life, near the age of 60. The prevalence of the disorder among the elderly is between 0.1 and 4%

Paraphrenia is not included in the DSM-5; psychiatrists often diagnose patients presenting with paraphrenia as having atypical psychoses, delusional disorder, psychoses not otherwise specified, schizoaffective disorders, and persistent persecutory states of older adults. Recently, mental health professionals have also been classifying paraphrenia as very late-onset schizophrenia-like psychosis.

In the Russian psychiatric manuals paraphrenia (or paraphrenic syndrome) is the last stage of development of paranoid schizophrenia. "Systematized paraphrenia" (with systematized delusions i. e. delusions with complex logical structure) and "expansive-paranoid paraphrenia" (with expansive/grandiose delusions and persecutory delusions) are the variants of paranoid schizophrenia (). You see sometimes "systematized paraphrenia" with delusional disorder ().

Some early signs of HIBMs includes:

- Difficulty walking on heels, and difficulty running;

- Weak index finger;

- Frequent loss of balance.

- On muscle biopsy, the typical finding includes inclusion bodies, rimmed vacuoles and accumulation of aberrant proteins similar to those found in senile plaques of Alzheimer's disease (amyloid beta, hyperphosphorylated tau, amongst others)

Neurodegeneration with brain iron accumulation (NBIA) is a group of inherited neurological disorders in which iron accumulates in the basal ganglia, resulting in progressive dystonia, Parkinsonism, spasticity, optic atrophy or retinal degeneration and neuropsychiatric abnormalities. NBIA disorders have been associated with genes in synapse and lipid metabolism related pathways. Describes a group of disorders characterized by an accumulation of brain iron and the presence of axonal spheroids in the central nervous system. Iron accumulation can occur any where in the brain, with accumulation typically occurring in globus pallidus, substantia nigra, pars reticula, striatum and cerebellar dentate nuclei. Symptoms can include various movement disorders, seizures, visual disturbances, and cognitive decline, usually in combination. The known causes of NBIA disorders are mutations in genes directly involved in iron metabolism, impaired phospholipid and ceramide metabolism, lysosomal disorders, as well as mutations in genes with unknown functions. Onset can occur at different ages, from early childhood to late adulthood. Magnetic resonance imaging (MRI) is used to distinguish between the different forms of NBIA due to the accumulation of iron in different areas of the brain. Patients typically fall into two different categories: (1) early onset, rapid progression or (2) late onset, slow progression. The first type is considered to be the classic presentation, while the second type is the atypical presentation. Phenotypes of the different disorders appear to be dependent on age, i.e. amount of iron accumulation and cognitive ability.

Sandhoff disease symptoms are clinically indeterminable from Tay–Sachs disease. The classic infantile form of the disease has the most severe symptoms and is incredibly hard to diagnose at this early age. The first signs of symptoms begin before 6 months of age and the parents’ notice when the child begins regressing in their development. If the children had the ability to sit up by themselves or crawl they will lose this ability. This is caused by a slow deterioration of the muscles in the child’s body from the buildup of GM2 gangliosides. Since the body is unable to create the enzymes it needs within the central nervous system it is unable to attach to these gangliosides to break them apart and make them non-toxic. With this buildup there are several symptoms that begin to appear such as muscle/motor weakness, sharp reaction to loud noises, blindness, deafness, inability to react to stimulants, respiratory problems and infections, mental retardation, seizures, cherry red spots in the retina, enlarged liver and spleen (hepatosplenomegaly), pneumonia, or bronchopneumonia.

The other two forms of Sandhoff disease have similar symptoms but to a lesser extent. Adult and juvenile forms of Sandhoff disease are more rare than the infantile form. In these cases victims suffer cognitive impairment (retardation) and a loss of muscle coordination that impairs and eventually destroys their ability to walk; the characteristic red spots in the retina also develop. The adult form of the disease, however, is sometimes milder, and may only lead to muscle weakness that impairs walking or the ability to get out of bed.

The main symptoms of paraphrenia are paranoid delusions and hallucinations. The delusions often involve the individual being the subject of persecution, although they can also be erotic, hypochondriacal, or grandiose in nature. The majority of hallucinations associated with paraphrenia are auditory, with 75% of patients reporting such an experience; however, visual, tactile, and olfactory hallucinations have also been reported. The paranoia and hallucinations can combine in the form of “threatening or accusatory voices coming from neighbouring houses [and] are frequently reported by the patients as disturbing and undeserved". Patients also present with a lack of symptoms commonly found in other mental disorders similar to paraphrenia. There is no significant deterioration of intellect, personality, or habits and patients often remain clean and mostly self-sufficient. Patients also remain oriented well in time and space.

Paraphrenia is different from schizophrenia because, while both disorders result in delusions and hallucinations, individuals with schizophrenia exhibit changes and deterioration of personality whereas individuals with paraphrenia maintain a well-preserved personality and affective response.

Hereditary inclusion body myopathies (HIBM) are a heterogeneous group of very rare genetic disorders which have different symptoms. Generally, they are neuromuscular disorders characterized by muscle weakness developing in young adults. Hereditary inclusion body myopathies comprise both autosomal recessive and autosomal dominant muscle disorders that have a variable expression (phenotype) in individuals, but all share similar structural features in the muscles.

HIBMs are a group of muscle wasting disorders, which are uncommon in the general world population. One autosomal recessive form of HIBM is known as IBM2 or GNE myopathy, which is a common genetic disorder amongst people of Iranian Jewish descent. IBM2 has also been identified in other minorities throughout the world, including people of Asian (Japanese and others), European, and South American origin, as well as Muslim people in the Middle Eastern, Palestinian, and Iranian origin. In Japan and many East Asian countries, this disorder is known as Distal Myopathy with Rimmed Vacuoles (DMRV).

IBM2 causes progressive muscle weakness and wasting. Muscle wasting usually starts around the age of 20 – 30 years, although young onset at 17 and old onset at 52 has been recorded. As such, it affects the most productive times of our lives. It can progress to marked disability within 10 – 15 years, confining many people with IBM2 to a wheelchair. The weakness and severity can vary from person to person. In some, weakness in the legs is noticed first. In few others, the hands are weakened more rapidly than the legs. Weakness is progressive, which means the muscle becomes weaker over time. IBM2 does not seem to affect the brain, internal organs or sensation. The quadriceps are relatively spared, and remain strong until the late stages of disease, which is the reason IBM2 is often referred to as Quadriceps Sparing Myopathy (QSM).

Most cases of autosomal recessive cerebellar ataxia are early onset, usually around the age of 20. People with this type of ataxia share many characteristic symptoms including:

- frequent falls due to poor balance

- imprecise hand coordination

- postural or kinetic tremor of extremities or trunk

- dysarthria

- dysphasia

- vertigo

- diplopia

- lower extremity tendon reflexes

- dysmetria

- minor abnormalities in ocular saccades

- attention defects

- impaired verbal working memory and visuospatial skills

- Normal life expectancy

Autosomal recessive ataxias are generally associated with a loss of proprioception and vibration sense. Arreflexia is more common in autosomal recessive ataxia than autosomal dominant ataxias. Also, they tend to have more involvement outside of the nervous system. Mutations in subunit of the mitochondrial DNA polymerase (POLG) have been found to be a potential cause of autosomal recessive cerebellar ataxia.