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

Treatment for EDS usually involves treating the underlying causative factor(s). This may involve psychotherapy, substance abuse treatment, or medical treatment for diseases.

EDS has been successfully controlled in clinical trials using prescribed medications, including Carbamazepine, Ethosuximide, and Propranolol.

Hematological, biochemical and metabolic investigations on blood and urine between attacks are normal, as are karyotyping and EKG recordings. EKG recordings during attacks show sinus tachycardia. CT, MRI, EMG and nerve conduction studies produce normal results. EEG recordings are normal between attacks but show early-onset tachycardia during attacks. On the Neuropathic Pain Questionnaire patients indicated that pain during attacks is extremely unpleasant and typically felt deep, though also superficial on occasion. Aside from presentation of typical symptoms (see Signs and symptoms above) mutation of the gene "SCN9A" aids in appropriate diagnosis as this gene is mutated in 8 of 14 studied families.

There have not been sufficient studies conducted to make conclusive statements about prevalence nor who tends to suffer EHS. One study found that 13.5% of a sample of undergrads reported at least one episode over the course of their lives, with higher rates in those also suffering from sleep paralysis.

As of 2014, no clinical trials had been conducted to determine what treatments are safe and effective; a few case reports had been published describing treatment of small numbers of people (two to twelve per report) with clomipramine, flunarizine, nifedipine, topiramate, carbamazepine, methylphenidate. Studies suggest that education and reassurance can reduce the frequency of EHS episodes. There is some evidence that individuals with EHS rarely report episodes to medical professionals.

SPS is diagnosed by evaluating clinical findings and excluding other conditions. There is no specific laboratory test that confirms its presence. Underdiagnosis and misdiagnosis are common.

The presence of antibodies against GAD is the best indication of the condition that can be detected by blood and cerebrospinal fluid (CSF) testing. Anti-GAD65 is found in about 80 percent of SPS patients. Anti-thyroid, anti-intrinsic factor, anti-nuclear, anti-RNP, and anti-gliadin are also often present in blood tests. Electromyography (EMG) demonstrates involuntary motor unit firing in SPS patients. EMG can confirm the diagnosis by noting spasms in distant muscles as a result of subnoxious stimulation of cutaneous or mixed nerves. Responsiveness to diazepam helps confirm that the patient is suffering from SPS, as this decreases stiffness and motor unit potential firing.

The same general criteria are used to diagnose paraneoplastic SPS as the normal form of the condition. Once SPS is diagnosed, poor response to conventional therapies and the presence of cancer indicate that it may be paraneoplastic. CT scans are indicated for SPS patients who respond poorly to therapy to determine if this is the case.

A variety of conditions have similar symptoms to SPS, including myelopathies, dystonias, spinocerebellar degenerations, primary lateral sclerosis, neuromyotonia, and some psychogenic disorders. Tetanus, neuroleptic malignant syndrome, malignant hyperpyrexia, chronic spinal interneuronitis, serotonin syndrome, Multiple sclerosis, Parkinson's disease, and Isaacs syndrome should also be excluded.

Patients' fears and phobias often incorrectly lead doctors to think their symptoms are psychogenic, and they are sometimes suspected of malingering. It takes an average of six years after the onset of symptoms before the disease is diagnosed.

A consortium of academic clinicians and scientists was convened in 2013 to develop more defined diagnostic guidelines for this disorder in anticipation of furthering research, clinical trials, and clinical care for this patient subgroup. A second consortium meeting was convened at NIMH in 2014 to develop preliminary treatment guidelines. The following are the members of the PRC

At the time of first PANS presentation, note any family history of pharyngitis, impetigo, perianal dermatitis, and GAS infections. If possible, family members should have a throat swab cultured for GAS. Ongoing vigilance against GAS infections in any of the patient’s close contacts is important, as symptom exacerbations have been reported following exposure to a sibling with GAS (even when the PANDAS patient had no evidence of infection). Prompt medical attention to symptoms suggestive of streptococcal infection is important not only to protect the patient, but also siblings, who may be at an increased genetic risk for PANS.

Prenatal screening is not typically done for FHM, however it may be performed if requested. As penetrance is high, individuals found to carry mutations should be expected to develop signs of FHM at some point in life.

Most pharmacological treatments work poorly, but the best treatment is a low dosage of clonazepam, a muscle relaxant. Patients may also benefit from other benzodiazepines, phenobarbital, and other anticonvulsants such as valproic acid. Affected individuals have reported garlic to be effective for softening the attacks, but no studies have been done on this.

Carbamazepine is at least partly effective at reducing the number or severity of attacks in the majority of PEPD patients. High doses of this drug may be required, perhaps explaining the lack of effect in some individuals. While other anti-epileptic drugs, gabapentin and topiramate, have limited effect in some patients, they have not been shown to be generally effective. Opiate derived analgesics are also largely ineffective, with only sporadic cases of beneficial effect.

"See the equivalent section in the main migraine article."

People with FHM are encouraged to avoid activities that may trigger their attacks. Minor head trauma is a common attack precipitant, so FHM sufferers should avoid contact sports. Acetazolamide or standard drugs are often used to treat attacks, though those leading to vasoconstriction should be avoided due to the risk of stroke.

The progression of SPS depends on whether it is a typical or abnormal form of the condition and the presence of comorbidities. Early recognition and neurological treatment can limit its progression. SPS is generally responsive to treatment, but the condition usually progresses and stabilizes periodically. Even with treatment, quality of life generally declines as stiffness precludes many activities. Some patients require mobility aids due to the risk of falls. About 65 percent of SPS patients are unable to function independently. About ten percent of SPS patients require intensive care at some point; sudden death occurs in about the same number of patients. These deaths are usually caused by metabolic acidosis or an autonomic crisis.

The diagnosis of TRAPS may show an increased IgD level in a possibly affected individual, other methods to ascertain a definite finding is via the following:

- Blood test

- Genetic test

- Clinical evaluation

Paroxysmal Nonkinesigenic Dyskinesia (PNKD) is an episodic movement disorder first described by Mount and Reback in 1940 under the name "Familial paroxysmal choreoathetosis". It is a rare hereditary disease that affects various muscular and nervous systems in the body, passing to roughly fifty percent of the offspring.

The table below demonstrates the extensive and differential diagnosis of acquired epileptic aphasia along with Cognitive and Behavioral Regression:

Note: EEG = electroencephalographic; ESES = electrical status epilepticus of sleep; RL = receptive language; S = sociability

- Continuous spike and wave of slow-wave sleep (>85% of slow-wave sleep).

Parker and colleagues used a variety of standardised neuropsychological tests in their diagnosis of AJ's hyperthymesia. These included tests of memory, lateralisation, executive functions, language, calculations, IQ, and visual-spatial and visual-motor functions. They also devised novel tests to examine the extent of her memory abilities. These mostly consisted of questions pertaining to specific dates and events in history. Some of her personal recollections were verified with diary entries, as well as by her mother.

More recently, neuroscientist David Eagleman at Baylor College of Medicine developed a free on-line test for hyperthymesia. Participants first give their year of birth, and then are challenged to match dates to 60 famous events that happened between the time they were five years old and the present day. To qualify as potentially hyperthymestic, participants must achieve a score at least three standard deviations above the average. To prevent people from searching for answers on-line during the test, reaction time for each question is measured; answers must be chosen within 11 seconds to qualify for consideration. However, many of the questions are sourced in American culture and test results could have a strong cultural bias against non-Americans.

There are two lines of treatment for Pisa syndrome. The first line entails discontinuation or reduction in dose of the antipsychotic drug(s). The second line of treatment is an anticholinergic medication. A pharmacological therapy for Pisa syndrome caused by prolonged use of antipsychotic drugs has not been established yet.

Anticholinergic drugs have been reported to be extremely effective in 40% of the patients with the Pisa syndrome. Patients with Pisa syndrome that is resistant to anticholinergic drugs is mostly resolved by the reduction of the administration of the antipsychotic drugs as previously mentioned. While the specific pathology underlying idiopathic Pisa syndrome is unknown, the administration of anticholinergic drugs has provided resolution in known cases.

Because it is a rare and poorly understood condition, there is no definitive way to diagnose the Capgras delusion. Diagnosis is primarily made on psychological evaluation of the patient, who is most likely brought to a psychologist's attention by a family member or friend believed to be an imposter by the person under the delusion.

The syndrome can be difficult to diagnose and may be misdiagnosed as autism, pervasive developmental disorder, hearing impairment, learning disability, auditory/verbal processing disorder, attention deficit hyperactivity disorder, intellectual disability, childhood schizophrenia, or emotional/behavioral problems. An EEG (electroencephalogram) test is imperative to a diagnosis. Many cases of patients exhibiting LKS will show abnormal electrical brain activity in both the right and left hemispheres of the brain; this is exhibited frequently during sleep. Even though an abnormal EEG reading is common in LKS patients, a relationship has not been identified between EEG abnormalities and the presence and intensity of language problems. In many cases however, abnormalities in the EEG test has preceded language deterioration and improvement in the EEG tracing has preceded language improvement (this occurs in about half of all affected children). Many factors inhibit the reliability of the EEG data: neurologic deficits do not closely follow the maximal EEG changes in time.

The most effective way of confirming LKS is by obtaining overnight sleep EEGs, including EEGs in all stages of sleep. Many conditions like demyelination and brain tumors can be ruled out by using magnetic resonance imaging (MRI). In LKS, fluorodeoxyglucose (FDG) and positron emission tomography (PET) scanning can show decreased metabolism in one or both temporal lobes - hypermetabolism has been seen in patients with acquired epileptic aphasia.

Most cases of LKS do not have a known cause. Occasionally, the condition may be induced secondary to other diagnoses such as low-grade brain tumors, closed-head injury, neurocysticercosis, and demyelinating disease. Central Nervous System vasculitis may be associated with this condition as well.

Depending on subtype, many patients find that acetazolamide therapy is useful in preventing attacks. In some cases, persistent attacks result in tendon shortening, for which surgery is required.

Prenatal screening is not typically done for FHM, however it may be performed if requested. As penetrance is high, individuals found to carry mutations should be expected to develop signs of FHM at some point in life.

A ten-patient study conducted by Pareja et al. found that all patients diagnosed with CPH were responsive to indomethacin and were able to completely control their symptoms. Doses of the drug ranged from 25 mg per day to 150 mg per day with a median dose of 75 mg per 24-hour period.

Almost all cases of CPH respond positively and effectively to indometacin, but as much as 25 percent of patients discontinued use of the drug due to adverse side effects, namely complications in the gastrointestinal tract.

According to a case study by Milanlioglu et al., 100mg of lamotrigine, an antiepileptic drug, administered twice daily alleviated all painful symptoms. No side effects were noted after two months of treatment. Dosage of lamotrigine was decreased to 50mg a day after the first two months, and no symptoms or side-effects were recorded after a three-month followup.

Use of topiramate has also been found to be an effective treatment for CPH, but cluster headache medications have been found to have little effect.

Though outwardly similar to cluster headaches, chronic paroxysmal hemicrania is rather different, and the two headaches are not a subset of one or the other. Key differences include:

- Different gender distributions – CPH is more common in women than men, with opposite occurring with cluster headaches.

- CPH attacks occur more frequently, but are shorter.

- Individuals with CPH are far more responsive to indomethacin than individuals with cluster headaches.

- CPH attacks can be provoked by neck movement.

- In a study conducted by Sjaastad, heating a patient's body will cause the painful side of the forehead to sweat more in CPH patients, while there will be less sweating on that side for those suffering from cluster headaches.