Socioeconomic correlates of health have been well established in the study of heart disease, lung cancer, and diabetes. Many of the explanations for the increased incidence of these conditions in people with lower socioeconomic status (SES) suggest they are the result of poor diet, low levels of exercise, dangerous jobs (exposure to toxins etc.) and increased levels of smoking and alcohol intake in socially deprived populations. Hesdorffer et al. found that low SES, indexed by poor education and lack of home ownership, was a risk factor for epilepsy in adults, but not in children in a population study. Low socioeconomic status may have a cumulative effect for the risk of developing epilepsy over a lifetime.

Epilepsy is a relatively common disorder, affecting between 0.5-1% of the population, and frontal lobe epilepsy accounts for about 1-2% of all epilepsies. The most common subdivision of epilepsy is symptomatic partial epilepsy, which causes simple partial seizures, and can be further divided into temporal and frontal lobe epilepsy. Although the exact number of cases of frontal lobe epilepsy is not currently known, it is known that FLE is the less common type of partial epilepsy, accounting for 20-30% of operative procedures involving intractable epilepsy. The disorder also has no gender or age bias, affecting males and females of all ages. In a recent study, the mean subject age with frontal lobe epilepsy was 28.5 years old, and the average age of epilepsy onset for left frontal epilepsy was 9.3 years old whereas for right frontal epilepsy it was 11.1 years old.

Although the theory is controversial, there is a link between febrile seizures (seizures coinciding with episodes of fever in young children) and subsequent temporal lobe epilepsy, at least epidemiologically.

The causes of TLE include mesial temporal sclerosis, traumatic brain injury, brain infections, such as encephalitis and meningitis, hypoxic brain injury, stroke, cerebral tumours, and genetic syndromes. Temporal lobe epilepsy is not the result of psychiatric illness or fragility of the personality.

There were also observations that hippocampal sclerosis was associated with vascular risk factors. Hippocampal sclerosis cases were more likely than Alzheimer's disease to have had a history of stroke (56% vs. 25%) or hypertension (56% vs. 40%), evidence of small vessel disease (25% vs. 6%), but less likely to have had diabetes mellitus (0% vs. 22%).

The origins of frontal lobe seizures range from tumors to head trauma to genetics. 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. Head trauma frequently causes damage to the frontal lobe and can cause seizures directly or indirectly through gliosis. Seizures originating directly from head trauma usually occur within a few months, but occasionally they can take years to manifest. On occasion encephalitis can cause frontal lobe seizures but it is most often associated with temporal lobe affliction. The main genetic cause of frontal lobe epilepsy is an autosomal dominant disease called Autosomal Dominant Nocturnal Frontal Lobe Epilepsy, which involves mutations in 2 nicotinic acetylcholine receptor genes. A genetic mutation on chromosome 22 has also been associated with another genetic form of the disorder.

In adults, many of the symptoms diminish over time. Although it has been suggested that a similar diminishing of symptoms occurs in children as well, it appears more likely that most do not overcome their deficits, but instead simply learn to adjust.

Although a specific cause has not been identified to always induce vertiginous epilepsy there have been a number of supported hypotheses to how these seizures come about, the most common being traumatic injury to the head. Other causes include tumor or cancers in the brain, stroke with loss of blood flow to the brain, and infection. A less tested hypothesis that some believe may play a larger role in determining who is affected by this disease is a genetic mutation that predisposes the subject for vertiginous epilepsy. This hypothesis is supported by occurrences of vertiginous epilepsy in those with a family history of epilepsy.

Vertiginous epilepsies are included in the category of the partial epilepsy in which abnormal electrical activity in the brain is localized. With current research, it is presumed that the most likely cause to produce vertigo are epilepsies occurring in the lateral temporal lobe. These abnormal electrical activities can either originate from within the temporal lobe or may propagate from an epilepsy in a neighboring region of the brain. Epilepsies in the parietal and occipital lobes commonly propagate into the temporal lobe inducing a vertiginous state. This electrical propagation across the brain explains why so many different symptoms may be associated with the vertiginous seizure. The strength of the electrical signal and its direction of propagation in the brain will also determine which associated symptoms are noticeable.

Reduplicative paramnesia is the delusional belief that a place or location has been duplicated, existing in two or more places simultaneously, or that it has been 'relocated' to another site. It is one of the delusional misidentification syndromes and, although rare, is most commonly associated with acquired brain injury, particularly simultaneous damage to the right cerebral hemisphere and to both frontal lobes.

Klüver–Bucy syndrome is a syndrome resulting from bilateral lesions of the medial temporal lobe (including amygdaloid nucleus). Klüver–Bucy syndrome may present with compulsive eating, hypersexuality, insertion of inappropriate objects in the mouth (hyperorality), visual agnosia, and .

Vertiginous epilepsy is infrequently the first symptom of a seizure, characterized by a feeling of vertigo. When it occurs there is a sensation of rotation or movement that lasts for a few seconds before full seizure activity. While the specific causes of this disease are speculative there are several methods for diagnosis, the most important being the patient's recall of episodes. Most times, those diagnosed with vertiginous seizures are left to self-manage their symptoms or are able to use anti-epileptic medication to dampen the severity of their symptoms. Vertiginous epilepsy has also been referred to as Epileptic vertigo, Vestibular epilepsy, Vestibular seizures, and Vestibulogenic seizures in different cases, but vertiginous epilepsy is the preferred term.

Topographical disorientation, also known as topographical agnosia and topographagnosia, is the inability to orient oneself in one's surroundings as a result of focal brain damage. This disability may result from the inability to make use of selective spatial information (e.g., environmental landmarks) or to orient by means of specific cognitive strategies such as the ability to form a mental representation of the environment, also known as a cognitive map. It may be part of a syndrome known as visuospatial dysgnosia.

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.

Focal seizures (also called partial seizures and localized seizures) are seizures which affect initially only one hemisphere of the brain. The brain is divided into two hemispheres, each consisting of four lobes – the frontal, temporal, parietal and occipital lobes. A focal seizure is generated in and affects just one part of the brain – a whole hemisphere or part of a lobe. Symptoms will vary according to where the seizure occurs. In the frontal lobe symptoms may include a wave-like sensation in the head; in the temporal lobe, a feeling of déjà vu; in the parietal lobe, a numbness or tingling; and in the occipital lobe, visual disturbance or hallucination.

Geschwind syndrome, also known as Gastaut-Geschwind, is a group of behavioral phenomena evident in some people with temporal lobe epilepsy. It is named for one of the first individuals to categorize the symptoms, Norman Geschwind, who published prolifically on the topic from 1973 to 1984. There is controversy surrounding whether it is a true neuropsychiatric disorder. Temporal lobe epilepsy causes chronic, mild, interictal (i.e. between seizures) changes in personality, which slowly intensify over time. Geschwind syndrome includes five primary changes; hypergraphia, hyperreligiosity, atypical (usually reduced) sexuality, circumstantiality, and intensified mental life. Not all symptoms must be present for a diagnosis. Only some people with epilepsy or temporal lobe epilepsy show features of Geschwind syndrome.

Strokes are one of the most common causes of Foix-Chavany-Marie Syndrome. The type of strokes associated with this syndrome include embolic and thrombotic strokes. Strokes affecting the middle cerebral artery and the branches that pass through or near the operculum are characteristic of FCMS.

People with Geschwind syndrome reported higher rates of atypical or altered sexuality. In approximately half of affected individuals hyposexuality is reported. Less commonly, cases of hypersexuality have been reported.

Symptoms of infections specifically HIV and Herpes simplex encephalitis can cause FCMS. Numerous lesions can develop with HIV infections, which likely result in the development of FCMS.

Musicogenic epilepsy is a form of reflex epilepsy with seizures elicited by special stimuli.

It has probably been described for the first time in 1605 by the French philosopher and scholar Joseph Justus Scaliger (1540-1609). Later publications were, in the eighteenth century, among others, by the German physician Samuel Schaarschmidt, in the nineteenth century 1823 by the British physician John C. Cooke, 1881 by the British neurologist and epileptologist William Richard Gowers, as well as in 1913 by the Russian neurologist, clinical neurophysiologist and psychiatrist Vladimir Mikhailovich Bekhterev. In 1937 the British neurologist Macdonald Critchley coined the term for the first time and classified it as a form of reflex epilepsy.

Most patients have temporal lobe epilepsy. Listening, probably also thinking or playing, of usually very specific music with an emotional content triggers focal seizures with or without loss of awareness, occasionally also evolving to bilateral tonic-clonic seizures.

Although musicality is at least in non-musicians predominantly located in the right temporal lobe, the seizure onset may also be left-hemispherical. Of the approximately 100 patients reported in the literature so far, about 75% had temporal lobe epilepsy, women were slightly more affected, and the mean age of onset was about 28 years. Ictal EEG and SPECT findings as well as functional MRI studies localized the epileptogenic area predominantly in the right temporal lobe. Treatment with epilepsy surgery leading to complete seizure freedom has been reported.

Topographical disorientation is the inability to orient in the surrounding as a result of focal brain damage.

Topographical Disorientation has been studied for decades using case studies of patients who have selectively lost their ability to find their way within large-scale, locomotor environments. Several dozen case reports of topographical disorientation have been presented over the last century. Studying these people will aid in the understanding of the complex, multi-component behavior of navigation. Topographical disorientation may result from a stroke or part of a progressive illness, hemispatial neglect, dementia, Alzheimer's disease.

Certain drugs have been known to induce hypergraphia including donepezil. In one case study, a patient taking donepezil reported an elevation in mood and energy levels which led to hypergraphia and other excessive forms of speech (such as singing). Six other cases of patients taking donepezil and experiencing mania have been previously reported. These patients also had cases of dementia, cognitive impairment from a cerebral aneurysm, bipolar I disorder, and/or depression. Researchers are unsure why donepezil can induce mania and hypergraphia. It could potentially result from an increase in acetylcholine levels, which would have an effect on the other neurotransmitters in the brain.

Another potential cause of hypergraphia is from one of the body's neurotransmitters, dopamine (DA). Dopamine has been known to decrease latent inhibition, which causes a decrease in the ability to habituate to different stimuli. Low latent inhibition leads to an excessive level of stimulation and could contribute to the onset of hypergraphia and general creativity. This research implies that there is a direct correlation between the levels of DA between neuronal synapses and the level of creativity exhibited by the patient. DA agonists increase the levels of DA between synapses which results in higher levels of creativity, and the opposite is true for DA antagonists.

Hypoacusis is defined as impairment in hearing or deafness. Hypoacusis is one of five etiologies of musical hallucinations, and is the most common in the case studies reviewed by Evers and Ellgers. According to Sanchez et al. 2011, there have been suggestions that pontine lesions could alter the central auditory system's function causing hypoacusis and musical hallucinations.

Hypergraphia is a behavioral condition characterized by the intense desire to write or draw. Forms of hypergraphia can vary in writing style and content. It is a symptom associated with temporal lobe changes in epilepsy, which is the cause of the Geschwind syndrome, a mental disorder. Structures that may have an effect on hypergraphia when damaged due to temporal lobe epilepsy are the hippocampus and Wernicke's area. Aside from temporal lobe epilepsy, chemical causes may be responsible for inducing hypergraphia.

Gerstmann syndrome is a neuropsychiatric disorder that is characterized by a constellation of symptoms that suggests the presence of a lesion in a particular area of the brain. (It should not be confused with Gerstmann-Sträussler-Scheinker syndrome, which is a transmissible spongiform encephalopathy.) Damage to the inferior parietal lobule of the dominant hemisphere results in Gerstmann's syndrome.

It is named for Josef Gerstmann.

Intoxication accounts for a small percentage of musical hallucination cases. Intoxication leads to either withdrawal or inflammatory encephalopathy, which are major contributors to musical hallucinations. Some of the drugs that have been found to relate to musical hallucinations include salicylates, benzodiazepines, pentoxifylline, propranolol, clomipramine, amphetamine, quinine, imipramine, a phenothiazine, carbamazepine, marijuana, paracetamol, phenytoin, procaine, and alcohol. General anesthesia has also been association with musical hallucinations.

In a case study by Gondim et al. 2010, a seventy–seven-year-old woman with Parkinson's disease (PD) was administered amantadine after a year of various other antiparkinsonian treatments. Two days into her treatment, she started to experience musical hallucinations, which consisted of four musical pieces. The music persisted until three days after cessation of the drug. Although the patient was taking other medications at the same time, the timing of onset and offset suggested that amantadine either had a synergistic effect with the other drugs or simply caused the hallucinations. Although the case wasn't specific to intoxication, it leads to the idea that persons with PD who are treated with certain drugs can experience musical hallucinations.