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.

Episodic dyscontrol syndrome (EDS, or sometimes just dyscontrol), is a pattern of abnormal, episodic, and frequently violent and uncontrollable social behavior in the absence of significant provocation; it can result from limbic system diseases, disorders of the temporal lobe, or abuse of alcohol or other psychoactive substances.

EDS may affect children or adults.

The condition manifests itself as attacks lasting from a few minutes to several hours. Episodes only happen when the individual is awake, and they remain conscious throughout the attack. Symptoms are most severe in youth and lessen with age. Sufferers can have multiple attacks on a daily basis or may have periods of weeks or months between attacks. Symptoms experienced during attacks can vary and include dystonia, chorea, athetosis, ballismus, or a combination.

While not the same in all people, there are several common triggers that can precipitate an attack:

- Moderate to high consumption of stimulants, such as alcohol, caffeine, or nicotine.

- Low amounts of energy due to hunger, lack of sleep, illness, or physical fatigue.

- Moderate to high presence of stress.

- Menstruation and ovulation.

The most distinctive feature of PEPD is episodic burning pain of the rectum, ocular, and mandibular regions. It should be stressed that while pain often originates or is centered in these areas it can also spread or be diffuse in nature. Pain experienced by patients with this disorder should not be underestimated as women with the disorder who have also given birth describe PEPD pain as worse than labor pain. Concomitant with this pain is typically flushing, often in an area associated with the pain.

During attacks in infants, the child often looks startled or terrified and can scream inconsolably. These attacks can be precipitated by injections, defecation, wiping of the perineum, eating, or the consumption of oral medication. When attacks occur due to such precipitation, pain and flushing are often present in the area of attack precipitation, though symptoms may also be diffuse in nature.

Other symptoms may include hypersalivation when attacks are localized in the mandibular region, or leg weakness after foot trauma. A prominent non-physical symptom are tonic non-epileptic seizures. Such seizures are more common in infancy and childhood than during adulthood. In older children, inconsolable screaming usually precedes such attack, followed by apnea, paleness, and stiffness. Such stiffness can last from seconds to a few minutes.

Attack precipitants are usually physical in nature, such as defecation, eating, or taking medicine. Some less common precipitants are micturition, coitus, and painful stimuli. There are also non-physical precipitants, such as the thought or sight of food. In general attacks tend to occur in the precipitated area, though this is not always the case. While some individuals have described a build-up to attacks, in general they tend to be abrupt. The duration of these attacks can be from a few seconds to two hours.

Patients are largely normal between attacks. The only notable interictal problem is constipation, likely due to apprehension of precipitating an attack. This symptom often decreases with age, likely due to coping mechanisms such as the use of stool softeners.

Patients with stiff person syndrome (SPS) suffer progressive stiffness in their truncal muscles, which become rigid and stiff because the lumbar and abdominal muscles engage in constant contractions. Initially, stiffness occurs in the thoracolumbar paraspinal and

abdominal muscles. It later affects the proximal leg and abdominal wall muscles. The stiffness leads to a change in posture, and patients develop a rigid gait. Persistent lumbar hyperlordosis often occurs as it progresses. The muscle stiffness initially fluctuates, sometimes for days or weeks, but eventually begins to consistently impair mobility. As the disease progresses, patients sometimes become unable to walk or bend. Chronic pain is common and worsens over time but sometimes acute pain occurs as well. Stress, cold weather, and infections lead to an increase in symptoms, and sleep decreases them.

SPS patients suffer superimposed spasms and extreme sensitivity to touch and sound. These spasms primarily occur in the proximal limb and axial muscles. There are co-contractions of agonist and antagonist muscles. Spasms usually last for minutes and can recur over hours. Attacks of spasms are unpredictable and are often caused by fast movements, emotional distress, or sudden sounds or touches. In rare cases, facial muscles, hands, feet, and the chest can be affected and unusual eye movements and vertigo occur. There are brisk stretch reflexes and clonus occurs in patients. Late in the disease's progression, hypnagogic myoclonus can occur. Tachycardia and hypertension are sometimes also present.

Because of the spasms, patients may become increasingly fearful, require assistance, and lose the ability to work, leading to depression, anxiety, and phobias, including agoraphobia and dromophobia. Most patients are psychologically normal and respond reasonably to their situations.

Paraneoplastic SPS tends to affect the neck and arms more than other variations. It progresses very quickly, is more painful, and is more likely to include distal pain than classic SPS. Patients with paraneoplastic SPS generally lack other autoimmune issues but may have other paraneoplastic conditions.

Stiff-limb syndrome is a variant of SPS. This syndrome develops into full SPS about 25 percent of the time. Stiffness and spasms are usually limited to the legs and hyperlordoisis generally does not occur. The stiffness begins in one limb and remains most prominent there. Sphincter and brainstem issues often occur with stiff-limb syndrome. Progressive encephalomyelitis with rigidity, another variant of the condition, includes symptoms of SPS with brainstem issues and autonomic disturbances. It involves polio-encephalomyelitis in the spine and brainstem. There is cerebellar and brainstem involvement. In some cases, the limbic system is affected, as well. Most patients have upper motoneuron issues and autonomic disturbances. Jerking man syndrome or jerking SPS is another subtype of the condition. It begins like classical SPS and progresses for several years, up to 14 in some cases. It is then distinguished by the development of myoclonus as well as seizures and ataxia in some cases.

Typically, episodic ataxia presents as bouts of ataxia induced by startle, stress, or exertion. Some patients also have continuous tremors of various motor groups, known as myokymia. Other patients have nystagmus, vertigo, tinnitus, diplopia or seizures.

The predominant symptom of Pisa syndrome is dystonia. Dystonia is a neurological movement disorder characterized by sustained muscle contraction leading to abnormal posture, twisting, and repetitive movement. In Pisa Syndrome specifically there is commonly a tonic flexion of the trunk of the body to one side, leading to a slight lean (reminiscent of the Leaning Tower of Pisa, hence the name "Pisa syndrome"). This is usually associated with a backward axial rotation of the spine and indifferent to markedly abnormal posture. Patients diagnosed with Pisa Syndrome usually experience either acute dystonia or tardive dystonia, also known as tardive dyskinesia. Differential diagnosis between the two may be hard to accomplish without a complete patient history, since both types of dystonia may occur simultaneously in a patient. These symptoms generally disappear after discontinuation of the antipsychotic drug. The time of onset of symptoms may vary depending on drug being administered and the neurological characteristics of the patient in question.

Pleurothotonus, commonly known as Pisa syndrome, is a rare neurological disorder which occurs due to prolonged exposure to antipsychotic drugs (which may also be referred to as neuroleptics). It is characterized by dystonia, and abnormal and sustained involuntary muscle contraction. This may cause twisting or jerking movements of the body or a body part. Although Pisa syndrome develops most commonly in those undergoing long-term treatment with antipsychotics, it has been reported less frequently in patients receiving other medications, such as an acetylcholinesterase inhibitor. However, it has also been seen in those with other diseases causing neurodegeneration and in those who are not receiving any medication (idiopathic Pisa syndrome). The characteristic development of Pisa syndrome consists of two types of dystonia: acute dystonia and tardive dystonia (also known as tardive dyskinesia). The underlying pathology of drug-induced Pisa syndrome is very complex, and development may be due to an underlying dopaminergic-cholinergic imbalance, or serotonergic/noradrenergic dysfunction.

Exploding head syndrome is classified as a parasomnia and a sleep-related dissociative disorder by the 2005 International Classification of Sleep Disorders and is an unusual type of auditory hallucination in that it occurs in people who are not fully awake.

Exploding head syndrome (EHS), alternately termed episodic cranial sensory shock, is a benign condition in which a person hears loud "imagined" noises (such as a bomb exploding, a gunshot, or a cymbal crash) or experiences an explosive feeling when falling asleep or waking up. These noises have a sudden onset, are typically brief in duration, and are often jarring for the person. Neither the cause nor the mechanism is known. Though harmless in and of themselves, episodes have been known to create distress or impairment in the lives of individuals.

Paroxysmal extreme pain disorder (PEPD), originally named familial rectal pain syndrome, is a rare disorder whose most notable features are pain in the mandibular, ocular and rectal areas as well as flushing. PEPD often first manifests at the beginning of life, perhaps even "in utero", with symptoms persisting throughout life. PEPD symptoms are reminiscent of primary erythromelalgia, as both result in flushing and episodic pain, though pain is typically present in the extremities for primary erythromelalgia. Both of these disorders have recently been shown to be allelic, both caused by mutations in the voltage-gated sodium channel Na1.7 encoded by the gene "SCN9A". A different mutation in "SCN9A" causes congenital insensitivity to pain.

A diagnosis of EDS has been used as a defense in court for persons accused of committing violent crimes including murder.

The various symptoms of EA are caused by dysfunction of differing areas. Ataxia, the most common symptom, is due to misfiring of Purkinje cells in the cerebellum. This is either due to direct malfunction of these cells, such as in EA2, or improper regulation of these cells, such as in EA1. Seizures are likely due to altered firing of hippocampal neurons (KCNA1 null mice have seizures for this reason).

Stiff person syndrome (SPS), also known as stiff man syndrome (SMS), is a rare neurologic disorder of unclear cause characterized by progressive rigidity and stiffness. The stiffness primarily affects the truncal muscles and is superimposed by spasms, resulting in postural deformities. Chronic pain, impaired mobility, and lumbar hyperlordosis are common symptoms.

SPS occurs in about one in a million people and is most commonly found in middle-aged people. A small minority of patients have the paraneoplastic variety of the condition. Variants of the condition, such as stiff-limb syndrome which primarily affects a specific limb, are often seen.

SPS was first described in 1956. Diagnostic criteria were proposed in the 1960s and refined two decades later. In the 1990s and 2000s the roles of antibodies in the condition became more clear. SPS patients generally have GAD antibodies, which seldom occur in the general population. In addition to blood to tests for GAD, electromyography tests can help confirm the condition's presence.

Benzodiazepine-class drugs are the most common treatment; they are used for symptom relief from stiffness. Other common treatments include Baclofen, intravenous immunoglobin and rituximab. There has been limited but encouraging success with stem-cell treatment.

Paroxysmal hypertension is episodic and volatile high blood pressure, which may be due to stress of any sort, or from a pheochromocytoma, a type of tumor involving the adrenal medulla. Patients with paroxysmal hypertension who test negative for pheochromocytoma are said to be suffering from a clinical entity called "pseudopheochromocytoma." This disorder is due to episodic dopamine discharge and has been observed predominantly in hypertensive women, that had episodes that shared similar characteristics of pheochromocytoma but testing proved negative and had ruled out the tumor. In patients with pseudopheochromocytoma dopamine was found to be significantly increased post-paroxysm. The paroxysm is said to be similar to the hypertensive episodes described by Page. These episodes commonly occur after diencephalic stimulation. Therefore, pseudopheochromocytoma, shares many characteristics of "Page's syndrome."

Pseudopheochromocytoma, colloquially known as page's syndrome, is caused predominantly by episodic dopamine discharge, stressors including pain or anxiety, or possibly repressed emotions caused by prior emotional trauma and commonly, a repressive way of coping emotionally. Therefore, treatment of pseudopheochromocytoma is aimed at psychological support and intervention with antidepressants, but also treatment with alpha and then beta blockers in resistant cases.

FHM signs overlap significantly with those of migraine with aura. In short, FHM is typified by migraine with aura associated with hemiparesis and, in FHM1, cerebellar degeneration. This cerebellar degeneration can result in episodic or progressive ataxia. FHM can also present with the same signs as benign familial infantile convulsions (BFIC) and alternating hemiplegia of childhood. Other symptoms are altered consciousness (in fact, some cases seem related to head trauma), gaze-evoked nystagmus and coma. Aura symptoms, such as numbness and blurring of vision, typically persist for 30–60 minutes, but can last for weeks and months. An attack resembles a stroke, but unlike a stroke, it resolves in time. These signs typically first manifest themselves in the first or second decade of life.

Hyperekplexia ("exaggerated surprise") is a neurologic disorder classically characterised by pronounced startle responses to tactile or acoustic stimuli and hypertonia. The hypertonia may be predominantly truncal, attenuated during sleep and less prominent after a year of age. Classic hyperekplexia is caused by genetic mutations in a number of different genes, all of which play an important role in glycine neurotransmission. Glycine is used by the central nervous system as an inhibitory neurotransmitter. Hyperekplexia is generally classified as a genetic disease, but some disorders can mimic the exaggerated startle of hyperekplexia.

Individuals with CPH suffer multiple short, severe headaches a day, often more than five, with most lasting between 5 and 30 minutes each. When compared to cluster headaches, CPH attacks are typically shorter. Each headache is centered around the eye, temple and forehead and is localized to one side of the head. While redness and watering of the eye are associated with CPH, patients typically do not experience nausea or vomiting.

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.

The three main signs of hyperekplexia are generalized stiffness, excessive startle beginning at birth and nocturnal myoclonus. Affected individuals are fully conscious during episodes of stiffness, which consist of forced closure of the eyes and an extension of the extremities followed by a period of generalised stiffness and uncontrolled falling at times. Initially, the disease was classified into a "major" and a "minor" form, with the minor form being characterized by an excessive startle reflex, but lacking stiffness. There is only genetic evidence for the existence of the major form.

Other signs and symptoms of hyperekplexia may include episodic neonatal apnea, excessive movement during sleep and the head-retraction reflex. The link to some cases of Sudden Infant Death remains controversial.

Witzelsucht (from the German "witzeln", meaning to joke or wisecrack, and "sucht", meaning addiction or yearning) is a set of rare neurological symptoms characterized by a tendency to make puns, or tell inappropriate jokes or pointless stories in socially inappropriate situations. A less common symptom is hypersexuality, the tendency to make sexual comments at inappropriate times or situations. Patients do not understand that their behavior is abnormal, therefore are nonresponsive to others' reactions. This disorder is most commonly seen in patients with frontal lobe damage, particularly right frontal lobe tumors or trauma. The disorder remains named in accordance with its reviewed definition by German neurologist Hermann Oppenheim; its first description as the less focused "Moria" ("stupidity"), by German neurologist Moritz Jastrowitz, was in 1888.

Due to similarity of symptoms of the disorder to the mannerisms of Batman's arch-rival Joker, it is sometimes known as 'The Joker Syndrome'

Many secondary conditions have been reported to be possible causes of CPH, according to Mehta et al., most of which are arterial abrasions or tumors. These include aneurysms in the circle of Willis, middle cerebral artery infarction, parietal arteriovenous malformation, cavernous sinus and petrous ridge meningiomas, pituitary adenoma, Pancoast tumor, gangliocytoma of the sella turcica, and malignant frontal tumors. This accentuates the urgency for those diagnosed with CPH to receive an MRI head scan.

Hyperreligiosity is a psychiatric disturbance in which a person experiences intense religious beliefs or experiences that interfere with normal functioning. Hyperreligiosity generally includes abnormal beliefs and a focus on religious content, which interferes with work and social functioning. Hyperreligiosity may occur in a variety of disorders including epilepsy, psychotic disorders and frontotemporal lobar degeneration. Hyperreligiosity is a symptom of Geschwind syndrome, which is associated with temporal lobe epilepsy.