The non-stimulant wake-promoting medications approved for use in narcolepsy include modafinil and armodafinil. Their pharmacology is not completely understood, but these medications "appear to influence brain chemistry that increases wakefulness." They elevate hypothalamic histamine levels, and they are known to bind to the dopamine transporter, thereby inhibiting dopamine reuptake. Modafinil can cause uncomfortable side effects, including nausea, headache, and a dry mouth for some patients, while other patients report no noticeable improvement even on relatively high dosages. They may also "interact with low-dose contraceptives, potentially reducing efficacy, although the scientific data supporting this claim is weak and rests on poorly documented anecdotes." New histamine-directed wake-promoting medications are currently under development (see Histamine-directed medications).

Atomoxetine (or reboxetine in Europe) is an adrenergic reuptake inhibitor which increases wakefulness (generally less strongly than the medications which act on dopamine) and which has been argued to have a "clear use in the therapeutic arsenal against narcolepsy and hypersomnia although undocumented by clinical trials."

Ritanserin is a serotonin antagonist that has "been shown to improve daytime alertness and subjective sleep quality in patients on their usual narcolepsy medications." It is intended as an adjunct (supplement to another main therapeutic agent), and although it is not available in the US, it is available in Europe.

Although anti-depressants, in general, have not been found to be helpful for treatment of idiopathic hypersomnia, bupropion specifically is known to have wake-promoting effects. "It is a low potency nonspecific monoamine reuptake inhibitor that also has DAT [dopamine-reuptake] inhibitory effects."

Sleep promoting medications can help by ensuring effective sleep as well as sleep at an appropriate time.

Sodium oxybate is an orphan drug which was designed specifically for the treatment of narcolepsy. It has been shown to promote deep sleep and improve daytime sleepiness (as well as cataplexy) in patients with narcolepsy; however, "its effects in those with idiopathic hypersomnia are not well characterized." Common side effects include nausea, dizziness, and hallucinations. A 2016 study by Leu-Semenescu et al. found sodium oxybate improved daytime sleepiness in idiopathic hypersomnia to the same degree as in patients with narcolepsy type 1, and the drug improved severe sleep inertia in 71% of the hypersomnia patients.

In a test tube model, clarithromycin (an antibiotic approved by the FDA for the treatment of infections) was found to return the function of the GABA system to normal in patients with primary hypersomnias. Investigators therefore treated a few patients with off-label clarithromycin, and most felt their symptoms improved with this treatment. In order to help further determine whether clarithromycin is truly beneficial for the treatment of narcolepsy and idiopathic hypersomnia, a small, double-blind, randomized, controlled clinical trial was completed in 2012. "In this pilot study, clarithromycin improved subjective sleepiness in GABA-related hypersomnia. Larger trials of longer duration are warranted." In 2013, a retrospective review evaluating longer-term clarithromycin use showed efficacy in a large percentage of patients with GABA-related hypersomnia. “It is important to note that the positive effect of clarithromycin is secondary to a benzodiazepine antagonist-like effect, not its antibiotic effects, and treatment must be maintained.”

People with narcolepsy can be substantially helped, but not cured. Treatment is tailored to the individual, based on symptoms and therapeutic response. The time required to achieve optimal control of symptoms is highly variable and may take several months or longer. Medication adjustments are frequently necessary, and complete control of symptoms is seldom possible. While oral medications are the mainstay of formal narcolepsy treatment, lifestyle changes are also important.

The main treatment of excessive daytime sleepiness in narcolepsy is central nervous system stimulants such as methylphenidate, amphetamine, dextroamphetamine, modafinil, and armodafinil. In late 2007 an alert for severe adverse skin reactions to modafinil was issued by the FDA.

Another drug that is used is atomoxetine, a non-stimulant and a norepinephrine reuptake inhibitor (NRI), which has no addiction liability or recreational effects. In many cases, planned regular short naps can reduce the need for pharmacological treatment of the EDS, but only improve symptoms for a short duration. A 120-minute nap provided benefit for 3 hours in patient alertness whereas a 15-minute nap provided no benefit. Daytime naps are not a replacement for nighttime sleep. Ongoing communication between the health care provider, patient, and the patient's family members is important for optimal management of narcolepsy.

Another FDA-approved treatment option for narcolepsy is sodium oxybate, also known as sodium gamma-hydroxybutyrate (GHB). It can be used for cataplexy associated with narcolepsy and excessive daytime sleepiness associated with narcolepsy.

Narcolepsy has sometimes been treated with selective serotonin reuptake inhibitors and tricyclic antidepressants, such as clomipramine, imipramine, or protriptyline, as well as other drugs that suppress REM sleep. Venlafaxine, an antidepressant which blocks the reuptake of serotonin and norepinephrine, has shown usefulness in managing symptoms of cataplexy, however, it has notable side-effects including sleep disruption.

Sodium oxybate and gamma-hydroxybutyrate has been found to be effective at reducing the number of cataplexy episodes. Sodium oxybate is generally safe. Sodium oxybate is typically the recommended treatment.

If the above treatment is not possible venlafaxine is recommended. Evidence for benefit is not as good.

Previous treatments include tricyclic antidepressants such as imipramine, clomipramine or protriptyline. Monoamine oxidase inhibitors may be used to manage both cataplexy and the REM sleep-onset symptoms of sleep paralysis and hypnagogic hallucinations.

Though no large trials have taken place which focus on the treatment of sleep paralysis, several drugs have promise in case studies. Two trials of GHB for people with narcolepsy demonstrated reductions in sleep paralysis episodes.

Medical treatment starts with education about sleep stages and the inability to move muscles during REM sleep. People should be evaluated for narcolepsy if symptoms persist. The safest treatment for sleep paralysis is for people to adopt healthier sleeping habits. However, in more serious cases tricyclic antidepressants or selective serotonin reuptake inhibitors (SSRIs) may be used. Despite the fact that these treatments are prescribed there is currently no drug that has been found to completely interrupt episodes of sleep paralysis a majority of the time.

PLMD is often treated with anti-Parkinson medication; it may also respond to anticonvulsants, benzodiazepines, and narcotics. Patients must stay on these medications in order to experience relief, because there is no known cure for this disorder.

PLMs tend to be exacerbated by tricyclic antidepressants, SSRIs, stress, and sleep deprivation. It is also advised not to consume caffeine, alcohol, or antidepressants as these substances could worsen the PLMD symptoms.

Other medications aimed at reducing or eliminating the leg jerks or the arousals can be prescribed. Non-ergot derived dopaminergic drugs (pramipexole and ropinirole) are preferred. Other dopaminergic agents such as co-careldopa, co-beneldopa, pergolide, or lisuride may also be used. These drugs decrease or eliminate both the leg jerks and the arousals. These medications are also successful for the treatment of restless legs syndrome.

In one study, co-careldopa was superior to dextropropoxyphene in decreasing the number of leg kicks and the number of arousals per hour of sleep. However, co-careldopa and, to a lesser extent, pergolide may shift the leg movements from the nighttime to the daytime.

Clonazepam (Klonopin), in doses of 1 mg has been shown to improve objective and subjective measures of sleep.

Research suggests that hypnosis may be helpful in alleviating some types and manifestations of sleep disorders in some patients. "Acute and chronic insomnia often respond to relaxation and hypnotherapy approaches, along with sleep hygiene instructions." Hypnotherapy has also helped with nightmares and sleep terrors. There are several reports of successful use of hypnotherapy for parasomnias specifically for head and body rocking, bedwetting and sleepwalking.

Hypnotherapy has been studied in the treatment of sleep disorders in both adults and children.

A review of the evidence in 2012 concluded that current research is not rigorous enough to make recommendations around the use of acupuncture for insomnia. The pooled results of two trials on acupuncture showed a moderate likelihood that there may be some improvement to sleep quality for individuals with a diagnosis insomnia. This form of treatment for sleep disorders is generally studied in adults, rather than children. Further research would be needed to study the effects of acupuncture on sleep disorders in children.

Although "there has been no cure of chronic hypersomnia", there are several treatments that may improve patients' quality of life, depending on the specific cause or causes of hypersomnia that are diagnosed.

Secondary hypersomnias are extremely numerous.

Hypersomnia can be secondary to disorders such as clinical depression, multiple sclerosis, encephalitis, epilepsy, or obesity. Hypersomnia can also be a symptom of other sleep disorders, like sleep apnea. It may occur as an adverse effect of taking certain medications, of withdrawal from some medications, or of drug or alcohol abuse. A genetic predisposition may also be a factor. In some cases it results from a physical problem, such as a tumor, head trauma, or dysfunction of the autonomic or central nervous system.

Sleep apnea is the most frequent cause of secondary hypersomnia, affecting up to 4% of middle-aged adults, mostly men. Upper airway resistance syndrome (UARS) is a clinical variant of sleep apnea that can also cause hypersomnia. Just as other sleep disorders (like narcolepsy) can coexist with sleep apnea, the same is true for UARS. There are many cases of UARS in which EDS persists after CPAP treatment, indicating an additional cause, or causes, of the hypersomnia and requiring further evaluation.

Sleep movement disorders, such as restless legs syndrome (RLS) and periodic limb movement disorder (PLMD or PLMS) can also cause secondary hypersomnia. Although RLS does commonly cause EDS, PLMS does not. There is no evidence that PLMS plays "a role in the etiology of daytime sleepiness. In fact, two studies showed no correlation between PLMS and objective measures of EDS. In addition, EDS in these patients is best treated with psychostimulants and not with dopaminergic agents known to suppress PLMS."

Neuromuscular diseases and spinal cord diseases often lead to sleep disturbances due to respiratory dysfunction causing sleep apnea, and they may also cause insomnia related to pain. "Other sleep alterations, such as periodic limb movement disorders in patients with spinal cord disease, have also been uncovered with the widespread use of polysomnography."

Primary hypersomnia in diabetes, hepatic encephalopathy, and acromegaly is rarely reported, but these medical conditions may also be associated with the secondary hypersomnias sleep apnea and periodic limb movement disorder (PLMD).

Chronic fatigue syndrome and fibromyalgia can also be associated with hypersomnia. Regarding chronic fatigue syndrome, it is "characterized by persistent or relapsing fatigue that does not resolve with sleep or rest. Polysomnography shows reduced sleep efficiency and may include alpha intrusion into sleep EEG. It is likely that a number of cases labeled as chronic fatigue syndrome are unrecognized cases of upper airway resistance syndrome" or other sleep disorders, such as narcolepsy, sleep apnea, PLMD, etc.

Similarly to chronic fatigue syndrome, fibromyalgia also may be associated with anomalous alpha wave activity (typically associated with arousal states) during NREM sleep. Also, researchers have shown that disrupting stage IV sleep consistently in young, healthy subjects causes a significant increase in muscle tenderness similar to that experienced in "neurasthenic musculoskeletal pain syndrome". This pain resolved when the subjects were able to resume their normal sleep patterns.

Chronic kidney disease is commonly associated with sleep symptoms and excessive daytime sleepiness. For those on dialysis, approximately 80% have sleep disturbances. Sleep apnea can occur 10 times as often in uremic patients than in the general population and can affect up to 30-80% of patients on dialysis, though nighttime dialysis can improve this. About 50% of dialysis patients have hypersomnia, as severe kidney disease can cause uremic encephalopathy, increased sleep-inducing cytokines, and impaired sleep efficiency. About 70% of dialysis patients are affected by insomnia, and RLS and PLMD affect 30%, though these may improve after dialysis or kidney transplant.

Most forms of cancer and their therapies can cause fatigue and disturbed sleep, affecting 25-99% of patients and often lasting for years after treatment completion. "Insomnia is common and a predictor of fatigue in cancer patients, and polysomnography demonstrates reduced sleep efficiency, prolonged initial sleep latency, and increased wake time during the night." Paraneoplastic syndromes can also cause insomnia, hypersomnia, and parasomnias.

Autoimmune diseases, especially lupus and rheumatoid arthritis are often associated with hypersomnia, as well. Morvan's syndrome is an example of a more rare autoimmune illness that can also lead to hypersomnia. Celiac disease is another autoimmune disease associated with poor sleep quality (which may lead to hypersomnia), "not only at diagnosis but also during treatment with a gluten-free diet." There are also some case reports of central hypersomnia in celiac disease. And RLS "has been shown to be frequent in celiac disease," presumably due to its associated iron deficiency.

Hypothyroidism and iron deficiency with or without (iron-deficiency anemia) can also cause secondary hypersomnia. Various tests for these disorders are done so they can be treated. Hypersomnia can also develop within months after viral infections such as Whipple's disease, mononucleosis, HIV, and Guillain–Barré syndrome.

Behaviorally induced insufficient sleep syndrome must also be considered in the differential diagnosis of secondary hypersomnia. This disorder occurs in individuals who fail to get sufficient sleep for at least three months. In this case, the patient has chronic sleep deprivation although he or she is not necessarily aware of it. This situation is becoming more prevalent in western society due to the modern demands and expectations placed upon the individual.

Many medications can also lead to secondary hypersomnia. Therefore, a patient's complete medication list should be carefully reviewed for sleepiness or fatigue as side effects. In these cases, careful withdrawal from the possibly offending medication(s) is needed; then, medication substitution can be undertaken.

Mood disorders, like depression, anxiety disorder and bipolar disorder, can also be associated with hypersomnia. The complaint of EDS in these conditions is often associated with poor sleep at night. "In that sense, insomnia and EDS are frequently associated, especially in cases of depression." Hypersomnia in mood disorders seems to be primarily related to "lack of interest and decreased energy inherent in the depressed condition rather than an increase in sleep or REM sleep propensity". In all cases with these mood disorders, the MSLT is normal (not too short and no SOREMPs).

Current research at the University of Utah is investigating whether sodium oxybate, also known as Gamma-Hydroxybutyric acid is an effective treatment for AHC. Thus far, only a small number of patients have been sampled, and no conclusive results are yet available. While some success has been had thus far with the drug, AHC patients have been known to respond well initially to other drugs, but then the effectiveness will decline over time. Currently, sodium oxybate is used as a narcolepsy-cataplexy treatment, though in the past it has been used controversially in nutritional supplements. This drug was chosen to test because of a possible link between the causes of narcolepsy-cataplexy and AHC.

The most common drug used to treat AHC is flunarizine. Flunarizine functions by acting as a calcium channel blocker. Other drugs, in order of frequency of use are benzodiazepines, carbamazapine, barbiturates, and valproic acid. Flunarizine is prescribed for the purpose of reducing the severity of AHC attacks and the number of episodes, though it rarely stops attacks altogether. Minimizing the attacks may help reduce damage to the body from hemiplegic attacks and improve long-term outcomes as far as mental and physical disabilities are concerned.

Experts differ in their confidence in flunarizine's effectiveness. Some studies have found it to be very effective in reducing the duration, severity, and frequency of hemiplegic attacks. It is generally considered the best treatment available, but this drug is thought by some to be of little benefit to AHC patients. Many patients suffer adverse effects without seeing any improvement. Flunarizine also causes problems because it is difficult for patients to obtain, as it is not readily available in the United States.

People with PLMD often do not know the cause of their excessive daytime sleepiness and their limb movements are reported by a spouse or sleep partner.

PLMD is diagnosed with the aid of a polysomnogram or PSG. PLMD is diagnosed by first finding PLMS (periodic limb movements of sleep) on a PSG, then integrating that information with a detailed history from the patient and/or bed partner. PLMS can range from a small amount of movement in the ankles and toes, to wild flailing of all four limbs. These movements, which are more common in the legs than arms, occur for between 0.5 and 5 seconds, recurring at intervals of 5 to 90 seconds. A formal diagnosis of PLMS requires three periods during the night, lasting from a few minutes to an hour or more, each containing at least 30 movements followed by partial arousal or awakening.

Treatment of any kind of complex visual hallucination requires an understanding of the different pathologies in order to correctly diagnose and treat. If a person is taking a pro-hallucinogenic medication, the first step is to stop taking it. Sometimes improvement will occur spontaneously and pharmacotherapy is not necessary. While there is not a lot of evidence of effective pharmacological treatment, antipsychotics and anticonvulsants have been used in some cases to control hallucinations. Since peduncular hallucinosis occurs due to an excess of serotonin, modern antipsychotics are used to block both dopamine and serotonin receptors, preventing the overstimulation of the lateral geniculate nucleus. The drug generically called carbamazepine increases GABA, which prevents the LGN from firing, thereby increasing the inhibition of the LGN. Regular antipsychotics as well as antidepressants can also be helpful in reducing or eliminating peduncular hallucinosis.

More invasive treatments include corrective surgery such as cataract surgery, laser photocoagulation of the retina, and use of optical correcting devices. Tumor removal can also help to relieve compression in the brain, which can decrease or eliminate peduncular hallucinosis. Some hallucinations may be due to underlying cardiovascular disease, so in these cases the appropriate treatment includes control of hypertension and diabetes. As described, the type of treatment varies widely depending on the causation behind the complex visual hallucinations.

Favorable response to treatment with the ADHD drug methylphenidate (Ritalin) has been reported, but this treatment option is not acceptable to all patient families.

Dr. Lane Robson, of The Children’s Clinic in Calgary, Alberta, says "If a child is having a wetting episode once a month, medicating them daily is probably not a good treatment. If it’s a daily issue, you may have to make that decision."

Episodes of giggle incontinence are embarrassing and socially incapacitating, diminishing the quality of life. Those having the condition learn to adapt by avoiding activities that may bring on laughter. Other approaches include limiting fluid intake, trying to remain seated, and concealing leakage by wearing absorbent pads and dark clothing.

Non-epileptic seizures are paroxysmal events that mimic an epileptic seizure but do not involve abnormal, rhythmic discharges of cortical neurons. They are caused by either physiological or psychological conditions. The latter is discussed more fully in psychogenic non-epileptic seizures.

[Please could somebody add an actual description of what happens when somebody has a seizure or 'paroxysmal event'?!]

Possible causes include:

- Syncope (fainting)

- Reflex anoxic seizures

- Breath-holding spells of childhood

- Hypoglycaemia

- Cataplexy

- Hyperekplexia, also called startle syndrome

- Migraine

- Narcolepsy

- Non-epileptic myoclonus

- Opsoclonus

- Parasomnias, including night terrors

- Paroxysmal kinesigenic dyskinesia

- Repetitive or ritualistic behaviours

- Tics

- AADC Deficiency

Other visual hallucinations tend to stem from psychological disorders. Whereas a person with a psychological disorder thinks their hallucinations are real, people with peduncular hallucinosis normally know that the visual hallucinations they see are not real. Peduncular hallucinations are independent of seizures, unlike some other visual hallucinations.

One drug that has been tried is Miglustat. Miglustat is a glucosylceramide synthase inhibitor, which inhibits the synthesis of glycosphingolipids in cells. It has been shown to delay the onset of disease in the NPC mouse, and published data from a multi-center clinical trial of Miglustat in the United States and England and from case reports suggests that it may ameliorate the course of human NPC.

Several other treatment strategies are under investigation in cell culture and animal models of NPC. These include, cholesterol mobilization, neurosteroid (a special type of hormone that affects brain and other nerve cells) replacement using allopregnanolone, rab overexpression to bypass the trafficking block (Pagano lab) and Curcumin as an anti-inflammatory and calcium modulatory agent. The pregnane X receptor has been identified as a potential target.

Neural stem cells have also been investigated in an animal model, and clear evidence of life extension in the mouse model has been shown.

Low cholesterol diets are often used, but there is no evidence of efficacy.

In April 2009, hydroxypropyl-beta-cyclodextrin (HPbCD) was approved under compassionate use by the U.S. Food and Drug Administration (FDA) to treat Addison and Cassidy Hempel, identical twin girls suffering from Niemann–Pick type C disease. Medi-ports, similar to ports used to administer chemotherapy drugs, were surgically placed into the twins' chest walls and allow doctors to directly infuse HPbCD into their bloodstreams. Treatment with cyclodextrin has been shown to delay clinical disease onset, reduced intraneuronal storage and secondary markers of neurodegeneration, and significantly increased lifespan in both the Niemann–Pick type C mice and feline models. This is the second time in the United States that cyclodextrin alone has been administered in an attempt treat a fatal pediatric disease. In 1987, HPbCD was used in a medical case involving a boy suffering from severe hypervitaminosis A.

On May 17, 2010, the FDA granted Hydroxypropyl-beta-cyclodextrin orphan drug status and designated HPbCD cyclodextrin as a potential treatment for Niemann–Pick type C disease. On July 14, 2010, Dr. Caroline Hastings of UCSF Benioff Children's Hospital Oakland filed additional applications with the FDA requesting approval to deliver HPbCD directly into the central nervous systems of the twins in an attempt to help HPbCD cross the blood–brain barrier. The request was approved by the FDA on September 23, 2010, and bi-monthly intrathecal injections of HPbCD into the spine were administered starting in October 2010.

On December 25, 2010, the FDA granted approval for HPbCD to be delivered via IV to an additional patient, Peyton Hadley, aged 13, under an IND through Rogue Regional Medical Center in Medford, Oregon. Soon after in March 2011, approval was sought for similar treatment of his sibling, Kayla, age 11, and infusions of HPbCD began shortly after. Both have since begun intrathecal treatments beginning in January 2012.

In April 2011, the National Institutes of Health (NIH), in collaboration with the Therapeutics for Rare and Neglected Diseases Program (TRND), announced they were developing a clinical trial utilizing cyclodextrin for Niemann–Pick type C patients.

On September 20, 2011, the European Medicines Agency (EMA) granted HPbCD orphan drug status and designated the compound as a potential treatment for Niemann–Pick type C disease.

On December 31, 2011, the FDA granted approval for IV HPbCD infusions for a fifth child in the United States, Chase DiGiovanni, under a compassionate use protocol. The child was 29 months old at the time of his first intravenous infusion, which was started in January 2012.

Due to unprecedented collaboration between individual physicians and parents of children afflicted with NPC, approximately 15 patients worldwide have received HPbCD cyclodextrin therapy under compassionate use treatment protocols. Treatment involves a combination of intravenous therapy (IV), intrathecal therapy (IT) and intracerebroventricular (ICV) cyclodextrin therapy.

On January 23, 2013, a formal clinical trial to evaluate HPβCD cyclodextrin therapy as a treatment for Niemann–Pick disease, type C was announced by scientists from the NIH's National Center for Advancing Translational Sciences (NCATS) and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). A Phase I clinical trial is currently being conducted at the NIH Clinical Center.

The affective spectrum is a spectrum of affective disorders (mood disorders). It is a grouping of related psychiatric and medical disorders which may accompany bipolar, unipolar, and schizoaffective disorders at statistically higher rates than would normally be expected. These disorders are identified by a common positive response to the same types of pharmacologic treatments. They also aggregate strongly in families and may therefore share common heritable underlying physiologic anomalies.

Affective spectrum disorders include:

- Attention deficit hyperactivity disorder

- Bipolar disorder

- Body dysmorphic disorder

- Bulimia nervosa and other eating disorders

- Cataplexy

- Dysthymia

- Generalized anxiety disorder

- Hypersexuality

- Irritable bowel syndrome

- Impulse-control disorders

- Kleptomania

- Migraine

- Major depressive disorder

- Obsessive-compulsive disorder

- Oppositional defiant disorder

- Panic disorder

- Posttraumatic stress disorder

- Premenstrual dysphoric disorder

- Social anxiety disorder

- Fibromyalgia

The following may also be part of the spectrum accompanying affective disorders.

- Chronic pain

- Intermittent explosive disorder

- Pathological gambling

- Personality disorder

- Pyromania

- Substance abuse and addiction (includes alcoholism)

- Trichotillomania

Also, there are now studies linking heart disease.

Many of the terms above overlap. The American Psychiatric Association's definitions of these terms can be found in the "Diagnostic and Statistical Manual of Mental Disorders" (DSM).