The international classification of sleep disorder (ICSD-3) [4] defines DSWPD as: (1) a significant delay in the phase of the major sleep episode in relation to the desired or required sleep time and wake-up time for at least 3 months. When patients are allowed to choose their ad libitum schedule, they will exhibit improved sleep quality and duration for age and maintain a delayed phase of the 24-h sleep-wake pattern. Additionally, the delay in the timing of the habitual sleep period is demonstrated on sleep log and, when possible, on actigraphy, which should include both work/school and free days. Moreover, these symptoms should not be better explained by any other disorder, medication, or substance use.

Seven to sixteen percent of adolescents are reported to have DSWPD. About 10 % of patients presenting with insomnia have DSWPD. The disorder is characterized by a habitual delay in the sleep-wake cycle by 2 h or more as compared to normally acceptable social standards. This leads to difficulty in falling asleep at socially acceptable time. Once sleep onset occurs, the sleep is typically of normal duration, which leads to difficulty waking up on time for school, work, or other activities. The onset typically occurs in adolescence but sometime onset is seen at an even earlier age. The onset may follow environmental, psychological, or medical stresses. Untreated, it can persist in adulthood; however, biological advance in sleep phase with increasing age may resolve the condition. Untreated, the patient can turn to stimulants, which may cause substance abuse issues. The patients tend to have evening-type chronotype and are prone to mood disorders.

There are multiple factors that predispose or precipitate this disorder. Family history is present in 40 % of the patients. Additionally, polymorphisms in Per3, arylalkylamine N-acetyltransferase, human leukocyte antigen, and Clock genes such as BMAL have been suggested to be associated with DSWPD. Environmental factors such as decreased exposure to light during morning and midday may also influence it. Social, behavioral, and occupational factors requiring activities in evening hours may also contribute to DSWPD. Diagnosis is based on the history and sleep logs. Actigraphy spanning over 14 days, including weekend or off days, will help to identify delay on free nights. Dim light melatonin onset (DLMO) and core body temperature rhythm are in synch with the delayed sleep onset. Behaviorally induced delay has to be differentiated from DSWPD. Detail history can help differentiate DSWPD from behavioral symptoms. In DSWPD, sleep quality and quantity is normal once the patient is sleeping at the desired time. Additionally, core body temperature and DLMO are not in synch with the late sleep onset in behavioral symptoms.

Treatment involves phototherapy in the morning, reduced bright light exposure in evenings, and melatonin to advance the sleep phase.

JME is a relatively common and easily recognizable epilepsy syndrome , which has been described for over 200 years. In 1989, The International League Against Epilepsy (ILAE) reported that JME appears around puberty and is characterized by seizures with bilateral, single or repetitive, arrhythmic, irregular myoclonic jerks, predominantly in the arms. Jerks may cause some patients to fall suddenly. No disturbance of consciousness is noticeable. The disorder may be inherited, and sex distribution is equal. Often, there are generalized tonic–clonic seizures and, less often, infrequent absences. The seizures usually occur shortly after awakening and are often precipitated by sleep deprivation. Interictal and ictal EEGs have rapid, generalized, often irregular spike–waves and polyspike–waves; there is no close phase correlation between EEG spikes and jerks. Frequently, the patients are photosensitive. Response to appropriate drugs is good [10]. The prevalence of JME has been estimated to be 0.1 to 0.2 per 100,000 with a peak age of onset of 12–18 years. Three seizure types occur in patients with JME: (1) early morning myoclonic jerks, (2) generalized tonic–clonic seizures, and (3) absence seizures with the myoclonic jerks being the most common and absence being the least. All three seizure types are seen in a third of patients. These patients are typically brought to medical attention after a generalized seizure, which follows the onset of myoclonic jerks by 1.3–3.3 years. Circadian distribution of the seizures is a major feature of the syndrome with most myoclonic jerks and generalized seizures occurring in the early morning hours and during awakenings from sleep [11]. In a study, the occurrence of generalized seizures was noted between 6 am–12 pm [12]. In about 15 % of patients, the seizures are provoked by flickering light. This phenomenon is called a photoparoxysmal response, which can also be seen on EEG when flashing light induces an electrographic seizure on the EEG [13]. Some of the most common precipitating factors are sleep deprivation and alcohol consumption [11]. The diagnosis is assisted by the presence of polyspike and wave discharges on EEG. Broad spectrum antiepileptic drugs like valproic acid, lamotrigine, and levetiracetam are effective in controlling the seizures [14].