Paroxysmal nocturnal dystonia or hypnogenic paroxysmal dystonia are other names given to describe FLE symptoms but are simply just FLE.Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is the best understood form of frontal lobe epilepsy but is often misdiagnosed as sleep apnea. Both disorders are characterized by awakening during the night which leads to daytime sleepiness. Some symptoms of sleep apnea overlap with those of ADNFLE, such as sudden awakening accompanied by a feeling of choking and on occasion motor activity which makes diagnosis difficult based on symptoms alone. Video surveillance as well as EEG is occasionally needed to differentiate between the two disorders. It has been reported that sleep apnea might be associated with epilepsy which would account for some of the misdiagnoses. Causes
The origins of frontal lobe seizures can be different deviations. One of the major reasons for FLE is abnormal cognitive development or sometimes congenital abnormal brain development. Other reasons are:

Tumors
Head Trauma
GeneticApart from the above-mentioned reason, there are a few unknown factors that can trigger the seizures:
Sleep deprivation
Waking up
Stress
Hormonal changes, such as during menstruation
Alcohol
Certain medications
Illegal substances

Tumors
Tumors account for about one-third of all frontal lobe epilepsy cases. Low-grade tumors such as gangliogliomas, low-grade gliomas, and epidermoid tumors are most common, but many high-grade tumors were most likely once involved with seizures. Other lesions on the frontal lobe such as hamartomas and nodular heterotopias can cause frontal lobe symptoms as well. Birth defects such as vascular malformation are known to cause seizures, especially arteriovenous malformations, and cavernous angiomas.
Essential fructosuria, caused by a deficiency of the enzyme hepatic fructokinase, is a clinically benign condition characterized by the incomplete metabolism of fructose in the liver, leading to its excretion in urine. Fructokinase (sometimes called ketohexokinase) is the first enzyme involved in the degradation of fructose to fructose-1-phosphate in the liver.This defective degradation does not cause any clinical symptoms, fructose is either excreted unchanged in the urine or metabolized to fructose-6-phosphate by alternate pathways in the body, most commonly by hexokinase in adipose tissue and muscle. Cause
Essential fructosuria is a genetic condition that is inherited in an autosomal recessive manner. Mutations in the KHK gene, located on chromosome 2p23.3-23.2 are responsible. The incidence of essential fructosuria has been estimated at 1:130,000. The actual incidence is likely higher, because those affected are asymptomatic. Diagnosis
A diagnosis of essential fructosuria is typically made after a positive routine test for reducing sugars in the urine. An additional test with glucose oxidase must also be carried out (with a negative result indicating essential fructosuria) as a positive test for reducing sugars is most often a result of glucosuria secondary to diabetes mellitus. The excretion of fructose in the urine is not constant, it depends largely on dietary intake. Treatment
No treatment is indicated for essential fructosuria, while the degree of fructosuria depends on the dietary fructose intake, it does not have any clinical manifestations. The amount of fructose routinely lost in urine is quite small. Other errors in fructose metabolism have greater clinical significance.