Frontal lobe epilepsy (FLE) is a neurological disorder which is a subtype of the larger group of epilepsy and then focal epilepsy is characterized by brief, recurring seizures that arise in the frontal lobes of the brain, often while the patient is sleeping. It is the second most common type of focal  epilepsy after temporal lobe epilepsy (TLE), and is related to the temporal form by the fact that both forms are characterized by the occurrence of partial (focal) seizures. Partial seizures occurring in the frontal lobes can occur in one of two different forms: either “focal aware”, the old term was simple partial seizures (that do not affect awareness or memory) “focal unaware” the old term was complex partial seizures (that affect awareness or memory either before, during or after a seizure). The symptoms and clinical manifestations of frontal lobe epilepsy can differ depending on which specific area of the frontal lobe is affected.The onset of a seizure may be hard to detect since the frontal lobes contain and regulate many structures and functions about which relatively little is known. Due to the lack of knowledge surrounding the functions associated with the frontal lobes, seizures occurring in these regions of the brain may produce unusual symptoms which can often be misdiagnosed as a psychiatric disorder, non-epileptic seizure or a sleep disorder.During the onset of a seizure, the patient may exhibit abnormal body posturing, sensorimotor tics, or other abnormalities in motor skills. In some cases, uncontrollable laughing or crying may occur during a seizure.
A common deletion found in one-third of CPEO patients is a 4,977 base pair segment found between a 13 base pair repeat.The mtDNA that is affected maybe a single or multiple point deletion, with associated nuclear DNA deletions. One study showed that mtDNA deletion seen in CPEO patients also had an associated nuclear DNA deletion of the Twinkle gene which encodes specific mitochondrial protein; Twinkle.Whether a tissue is affected is correlated with the amount of oxidative demands in relation to the amount of mtDNA deletion.In most cases, PEO occurs due to a sporadic deletion or duplication within the mitochondrial DNA. However, transmission from the mother to the progeny appears only in few cases. Both autosomal dominant and autosomal recessive inheritance can occur, autosomal recessive inheritance being more severe. Dominant and recessive forms of PEO can be caused by genetic mutations in the ANT1, POLG, POLG2 and PEO1 genes. Diagnosis
It is important to differentiate CPEO from other pathologies that may cause an ophthalmoplegia. There are specific therapies used for these pathologies.CPEO is diagnosed via muscle biopsy. On examination of muscle fibers stained with Gömöri trichrome stain, one can see an accumulation of enlarged mitochondria. This produces a dark red staining of the muscle fibers given the name "ragged red fibers". While ragged red fibers are seen in normal aging, amounts in excess of normal aging give a diagnosis of a mitochondrial myopathy.