Epileptic symptoms are frequently the product of the spread of overactivation occurring within one central foci that travels to lateral brain regions thereby causing an array of symptoms. Due to the massive amount of diversity in both the cognitive and motor functions that occur within the frontal lobes, there is an immense variety in the types of symptoms that can arise from epileptic seizures based on the side and topography of the focal origin. In general these symptoms can range anywhere from asymmetric and abnormal body positioning to repetitive vocal outbursts and repetitive jerking movements. The symptoms typically come in short bursts that last less than a minute and often occur while a patient is sleeping. In most cases, a patient will experience a physical or emotional Aura of tingling, numbness or tension prior to a seizure occurring. Fear is associated with temporal and frontal lobe epilepsies, but in FLE the fear is predominantly expressed on the person's face whereas in TLE the fear is subjective and internal, not perceptible to the observer.

Tonic posture and clonic movements are common symptoms among most of the areas of the frontal lobe, therefore the type of seizures associated with frontal lobe epilepsy are commonly called tonic-clonic seizures. Dystonic motor movements are common to both TLE and FLE, but are usually the first symptom in FLE episodes where they are quite brief and do not affect consciousness. The seizures are complex partial, simple partial, secondarily generalized or a combination of the three. These partial seizures are often misdiagnosed as psychogenic seizures. A wide range of more specific symptoms arise when different parts of the frontal cortex are affected.

- Supplementary motor area (SMA)

- The onset and relief of the seizure are quite abrupt.

- The tonic posturing in this area is unilateral or asymmetric between the left and right hemispheres. A somatosensory aura frequently precedes many large motor and vocal symptoms and most often the afflicted person is responsive.

- "Motor symptoms": Facial grimacing and complex automatisms like kicking and pelvic thrusting

- "Vocal symptoms": Laughing, yelling, or speech arrest.

- Primary motor cortex

- The primary motor cortex has jacksonian seizures that spread to adjacent areas of the lobe which often trigger a second round of seizures originating in another cortical area. The seizures are much simpler than those that originate in the SMA and are usually clonic or myoclonic movements with speech arrest. Some dystonic or contralateral adversive posturing may also be present.

- Medial frontal, cingulate gyrus, orbitofrontal, or frontopolar regions

- Motor symptoms of seizures in this area are accompanied by emotional feelings and viscerosensory symptoms. Motor and vocal agitation are similar to that of the SMA with short repetitive thrashing, pedaling, thrusting, laughing, screaming and/or crying.

- This is some of what can cause the misdiagnosis of a psychological disorder.

- Dorsolateral cortex

- This area does not seem to have many motor symptoms beyond tonic posturing or clonic movements. Contralateral or less commonly ipsilateral head turn and eye deviation are commonly associated with this area as well.

- Operculum

- Many of the symptoms associated with this area involve the head and digestive tract: swallowing, salivation, mastication and possibly gustatory hallucinations. Preceding the seizure the person is fearful and often has an epigastric aura. There is not much physical movement except clonic facial movements. Speech is often arrested.

Other medical conditions with similar symptoms include panic attacks, psychosis spectrum disorders, tardive dyskinesia, and occipital lobe epilepsy.

The signs of vertiginous epilepsy often occur without a change in the subject’s consciousness so that they are still aware while experiencing the symptoms. It is often described as a sudden onset of feeling like one is turning in one direction, typically lasting several seconds. Although subjects are aware during an episode, they often cannot remember specific details due to disorientation, discomfort, and/or partial cognitive impairment. This sensation of rotational movement in the visual and auditory planes is also known as a vertiginous aura (symptom), which can precede a seizure or may constitute a seizure itself. Auras are a “portion of the seizure that occur before consciousness is lost and for which memory is retained afterwards.” Auras can be focused in different regions of the brain and can thus affect different functions. Some such symptoms that may accompany vertiginous epilepsy include:

- Auditory hallucination

- Cognitive impairment

- Motor activity

- Ictal behavior

- Limbic auras

Many people tend to mistake dizziness as vertigo, and although they sound similar, dizziness is not considered a symptom of vertiginous epilepsy. Dizziness is the sensation of imbalance or floating, impending loss of consciousness, and/or confusion. This is different from vertigo which is characterized by the illusion of rotational movement caused by the “conflict between the signals sent to the brain by balance- and position-sensing systems of the body”.

Focal impaired awareness seizures are seizures which impair consciousness to some extent: they alter the person's ability to interact normally with their environment. They usually begin with a focal aware seizure, then spread to a larger portion of the temporal lobe, resulting in impaired consciousness. They may include autonomic and psychic features present in focal aware seizures.

Signs may include:

- Motionless staring

- Automatic movements of the hands or mouth

- Confusion and disorientation

- Altered ability to respond to others, unusual speech

- Transient aphasia (losing ability to speak, read, or comprehend spoken word)

These seizures tend to have a warning or aura before they occur, and when they occur they generally tend to last only 1–2 minutes. It is not uncommon for an individual to be tired or confused for up to 15 minutes after a seizure has occurred, although postictal confusion can last for hours or even days. Though they may not seem harmful, due to the fact that the individual does not normally seize, they can be extremely harmful if the individual is left alone around dangerous objects. For example, if a person with complex partial seizures is driving alone, this can cause them to run into the ditch, or worse, cause an accident involving multiple people. With this type, some people do not even realize they are having a seizure and most of the time their memory from right before or after the seizure is wiped. First-aid is only required if there has been an injury or if this is the first time a person has had a seizure.

Frontal lobe epilepsy, or FLE, is a neurological disorder that 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 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 simple partial seizures (that do not affect awareness or memory) or 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. Afflicted persons may or may not be aware that they are behaving in an abnormal manner, depending on the patient and type of seizure. A brief period of confusion known as a postictal state may sometimes follow a seizure occurring in the frontal lobes. However, these postictal states are often undetectable and generally do not last as long as the periods of confusion following seizures that occur in the temporal lobes.

There are many different causes of frontal lobe epilepsy ranging from genetics to head trauma that result in lesions in the frontal lobes. Although frontal lobe epilepsy is often misdiagnosed, tests such as prolonged EEG monitoring and/or a MRI scan of the frontal lobes can be administered in order to reveal the presence of a tumor or vascular malformation. Unlike most epileptic EEGs, the abnormalities in FLE EEGs precede the physical onset of the seizure and aid in localization of the seizure's origin. Medications such as anti-epileptic drugs can typically control the onset of seizures, however, if medications are ineffective the patient may undergo surgery to have focal areas of the frontal lobe removed.

Hypergraphia is the tendency for extensive and compulsive writing or drawing, and has been observed in persons with temporal lobe epilepsy who have experienced multiple seizures. Those with hypergraphia display extreme attention to detail in their writing. Some such patients keep diaries recording meticulous details about their everyday lives. In certain cases, these writings demonstrate extreme interest in religious topics. Also, these individuals tend to have poor penmanship. The novelist Fyodor Dostoyevsky showed symptoms of Geschwind syndrome, including hypergraphia. In some cases hypergraphia can manifest with compulsive drawing. Drawings by patients with hypergraphia exhibit repetition and a high level of detail, sometimes morphing writing with drawing

The list of symptoms differs somewhat by source. Generally included are the following:

1. Amnesia. Characterised by an inability to recall memories. Its nature is both anterograde and retrograde, meaning new memories cannot be formed and old memories cannot be recalled. The level of amnesia is considered to be profound.

2. Docility. Characterized by exhibiting diminished fear responses or reacting with unusually low aggression. This has also been termed "" or "tameness".

3. Dietary changes and hyperphagia. Characterized by eating inappropriate objects (pica), or overeating, or both.

4. Hyperorality. This was described by Ozawa et al. as "an oral tendency, or compulsion to examine objects by mouth".

5. Hypersexuality. Characterized by a heightened sex drive or a tendency to seek sexual stimulation from unusual or inappropriate objects.

6. Visual agnosia. Characterized by an inability to recognize familiar objects or people.

While this cluster of syndromes is common to such sources as 1997's "The Neuropsychiatry of Limbic and Subcortical Disorders", 2005's "Functional Neuroanatomy: Text and Atlas" and 1997's "Single-Photon Emission CT and MR Findings in Klüver-Bucy after Reye syndrome", an article in the "American Journal of Neuroradiology", the three vary thereafter.

Inconsistent criteria include:

- Hypermetamorphosis, characterized by Ozawa et al. as "an irresistible impulse to notice and react to everything within sight". This is included under the classification systems described by "The Neuropsychiatry of Limbic and Subcortical Disorders" and "Single-Photon Emission CT and MR Findings in Klüver-Bucy".

- Lack of emotional response, diminished emotional affect. This is a symptom under "The Neuropsychiatry of Limbic and Subcortical Disorders" and is included under "Single-Photon Emission CT and MR Findings in Klüver-Bucy" along with apathy under docility.

Focal aware seizures are seizures which affect only a small region of the brain, often the temporal lobes or structures found there such as the hippocampi. People who have focal aware seizures remain conscious. Focal aware seizures often precede larger focal impaired awareness seizures, where the abnormal electrical activity spreads to a larger area of the brain. This can result in a tonic-clonic seizure.

- Presentation

Focal onset aware seizures are a very subjective experience, and the symptoms vary greatly between people. This is due to the varying locations of the brain the seizures originate in e.g.: Rolandic. A focal aware seizure may go unnoticed by others or shrugged off by the sufferer as merely a "funny turn." Focal aware seizures usually start suddenly and are very brief, typically lasting 60 to 120 seconds.

Some common symptoms of a focal onset aware seizure, when the person is awake, are:

- preserved consciousness

- sudden and inexplicable feelings of fear, anger, sadness, happiness or nausea

- sensations of falling or movement

- experiencing of unusual feelings or sensations

- altered sense of hearing, smelling, tasting, seeing, and tactile perception (sensory illusions or hallucinations), or feeling as though the environment is not real (derealization) or dissociation from the environment or self (depersonalization)

- a sense of spatial distortion—things close by may appear to be at a distance

- déjà vu (familiarity) or jamais vu (unfamiliarity)

- laboured speech or inability to speak at all

- usually the event is remembered in detail

When the seizure occurs during sleep, the person will often become semi-conscious and act out a dream they were having while engaging with the real environment as normal. Objects and people usually appear normal or only slightly distorted to them, and will be able to communicate with them on an otherwise normal level.

However, since the person is still acting in the dream-like state from which they woke, they will assimilate any hallucinations or delusions into their communication, often speaking to a hallucinatory person or speaking of events or thoughts normally pertaining to the dream they were having or other hallucination.

While asleep symptoms include:

- onset usually in REM sleep

- dream like state

- appearance of full consciousness

- hallucinations or delusions

- behavior or visions typical in dreams

- ability to engage with the environment and other people as in full consciousness, though often behaving abnormally, erratically, or failing to be coherent

- complete amnesia or assimilating the memory as though it was a normal dream on regaining full consciousness

Although hallucinations may occur during focal aware seizures they are differentiated from psychotic symptoms by the fact that the person is usually aware that the hallucinations are not real.

- Jacksonian march

Jacksonian march or Jacksonian seizure is a phenomenon where a focal aware seizure spreads from the distal part of the limb toward the face (on same side of body). They involve a progression of the location of the seizure in the brain, which leads to a "march" of the motor presentation of symptoms.

Jacksonian seizures are initiated with abnormal electrical activity within the primary motor cortex. They are unique in that they travel through the primary motor cortex in succession, affecting the corresponding muscles, often beginning with the fingers. This is felt as a tingling sensation, or a feeling of waves through the fingers when touched together. It then affects the hand and moves on to more proximal areas on the same side of body. Symptoms often associated with a Jacksonian seizure are sudden head and eye movements, tingling, numbness, smacking of the lips, and sudden muscle contractions. Most of the time any one of these actions can be seen as normal movements, without being associated with the seizure occurring. They occur at no particular moment and last only briefly. They may result in secondary generalized seizure involving both hemispheres. They can also start at the feet, manifesting as tingling or pins and needles, and there are painful cramps in the foot muscles, due to the signals from the brain. Because it is a partial seizure, the postictal state is of normal consciousness .

A focal impaired awareness seizure is a seizure that is associated with unilateral cerebral hemisphere involvement and causes impairment of awareness or responsiveness, i.e. alteration of consciousness.

- Presentation

Focal impaired awareness seizures are often preceded by an aura. The seizure aura is a focal aware seizure. The aura may manifest itself as a feeling of déjà vu, jamais vu, fear, euphoria or depersonalization. The aura might also occur as a visual disturbance, such as tunnel vision or a change in the perceived size of objects. Once consciousness is impaired, the person may display automatisms such as lip smacking, chewing or swallowing. There may also be loss of memory (amnesia) surrounding the seizural event. The person may still be able to perform routine tasks such as walking, although such movements are not purposeful or planned. Witnesses may not recognize that anything is wrong.

Focal impaired awareness seizures might arise from any lobe of the brain. They most commonly arise from the temporal lobe, particularly the amygdala, hippocampus, and neocortical regions. A common associated brain abnormality is mesial temporal sclerosis. Mesial temporal sclerosis is a specific pattern of hippocampal neuronal loss accompanied by hippocampal gliosis and atrophy. Focal onset impaired awareness seizures occur when excessive and synchronous electrical brain activity causes the impaired awareness and responsiveness. The abnormal electrical activity might spread to the rest of the brain and cause a "focal to bilateral seizure" or a generalized tonic–clonic seizure. The newer classification of 2017 groups only focal and generalized seizures, and generalised seizures are those that involve both sides of the brain from the onset.

Patients with hypergraphia exhibit a wide variety of writing styles and content. While some write in a coherent, logical manner, others write in a more jumbled style (sometimes in a specific pattern). In some cases hypergraphia can manifest with compulsive drawing. Drawings by patients with hypergraphia exhibit repetition and a high level of detail, sometimes mixing both compulsive writing and drawing together.

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.

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.

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.

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.

Developmental topographical disorientation (DTD) refers to the inability to orient from childhood despite the absence of any apparent brain damage, neurological condition or general cognitive defects. Individuals affected by DTD are unable to generate a mental representation of the environment (i.e. a cognitive map) and therefore unable to make use of it while orienting (a process that usually people go through while orienting). Not to be confused with healthy individuals who have a poor sense of direction, individuals affected by DTD get lost in very familiar surroundings, such as their house or neighborhood, daily.

Gerstmann syndrome is characterized by four primary symptoms:

1. Dysgraphia/agraphia: deficiency in the ability to write

2. Dyscalculia/acalculia: difficulty in learning or comprehending mathematics

3. Finger agnosia/anomia: inability to distinguish the fingers on the hand

4. Left-right disorientation

Hypergraphia is a symptom of temporal lobe epilepsy, a condition of reoccurring seizures caused by excessive neuronal activity, but it is not a common symptom among patients. Less than 10 percent of patients with temporal lobe epilepsy exhibit characteristics of hypergraphia. Temporal lobe epilepsy patients may exhibit irritability, discomfort, or an increasing feeling of dread if their writing activity is disrupted. To elicit such responses when interrupting their writing suggests that hypergraphia is a compulsive condition, resulting in an obsessive motivation to write. A temporal lobe epilepsy may influence frontotemporal connections in such a way that the drive to write is increased in the frontal lobe, beginning with the prefrontal and premotor cortex planning out what to write, and then leading to the motor cortex (located next to the central fissure) executing the physical movement of writing.

Most temporal lobe epilepsy patients who suffer from hypergraphia can write words, but not all may have the capacity to write complete sentences that have meaning.

Benign occipital epilepsy of childhood (BOEC) is an idiopathic localization-related epilepsy and consists of an evolving group of syndromes. Most authorities include two subtypes, an early subtype with onset between three and five years, and a late onset between seven and 10 years. Seizures in BOEC usually feature visual symptoms such as scotoma or fortifications (brightly colored spots or lines) or amaurosis (blindness or impairment of vision). Convulsions involving one half the body, hemiconvulsions, or forced eye deviation or head turning are common. Younger patients typically experience symptoms similar to migraine with nausea and headache, and older patients typically complain of more visual symptoms. The EEG in BOEC shows spikes recorded from the occipital (back of head) regions. The EEG and genetic pattern suggest an autosomal dominant transmission as described by Ruben Kuzniecky, et al. Lately, a group of epilepsies termed Panayiotopoulos syndrome that share some clinical features of BOEC but have a wider variety of EEG findings are classified by some as BOEC.

Benign centrotemporal lobe epilepsy of childhood or benign Rolandic epilepsy is an idiopathic localization-related epilepsy that occurs in children between the ages of 3 and 13 years, with peak onset in prepubertal late childhood. Apart from their seizure disorder, these patients are otherwise normal. This syndrome features simple focal seizures that involve facial muscles and frequently cause drooling. Although most episodes are brief, seizures sometimes spread and generalize. Seizures are typically nocturnal and confined to sleep. The EEG may demonstrate spike discharges that occur over the centrotemporal scalp over the central sulcus of the brain (the Rolandic sulcus) that are predisposed to occur during drowsiness or light sleep. Seizures cease near puberty. Seizures may require anticonvulsant treatment, but sometimes are infrequent enough to allow physicians to defer treatment.

This disorder is often associated with brain lesions in the dominant (usually left) hemisphere including the angular and supramarginal gyri (Brodmann area 39 and 40 respectively) near the temporal and parietal lobe junction. There is significant debate in the scientific literature as to whether Gerstmann Syndrome truly represents a unified, theoretically motivated syndrome. Thus its diagnostic utility has been questioned by neurologists and neuropsychologists alike. The angular gyrus is generally involved in translating visual patterns of letter and words into meaningful information, such as is done while reading.

The bilateral form of FCMS ("also known as facio-labio-pharyngo-glosso-laryngo-brachial paralysis)" is consistent with the classic presentation of bilateral corticobulbar involvement. It is characterized by well-preserved automatic and reflex movements. It is caused by lesions in the cortical or subcortical region of the anterior opercular area surrounding the insula forming the gyri of the frontal, temporal, and parietal lobes.

The unilateral operculum syndrome is a very rare form of FCMS caused by the formation of unilateral lesions. In this form of FCMS, the unaffected hemisphere of the brain compensates for the unilateral lesion. Usually, this occurs when the unaffected region is the individual's dominant hemisphere.

Although largely used to describe unawareness of impairment after brain injury or stroke, the term 'anosognosia' is occasionally used to describe the lack of insight shown by some people with anorexia nervosa. They do not seem to recognize that they have a mental illness. There is evidence that 'anosognosia' related to schizophrenia may be the result of frontal lobe damage. E. Fuller Torrey, a psychiatrist and schizophrenia researcher, has stated that among those with schizophrenia and bipolar disorder, anosognosia is the most prevalent reason for not taking medications.

Relatively little has been discovered about the cause of the condition since its initial identification. Recent studies from the empirical data are prone to consider anosognosia a multi-componential syndrome or multi-faceted phenomenon. That is it can be manifested by failure to be aware of a number of specific deficits, including motor (hemiplegia), sensory (hemianaesthesia, hemianopia), spatial (unilateral neglect), memory (dementia), and language (receptive aphasia) due to impairment of anatomo-functionally discrete monitoring systems.

Anosognosia is relatively common following different causes of brain injury, such as stroke and traumatic brain injury; for example, anosognosia for hemiparesis, (weakness of one side of the body) with onset of acute stroke is estimated at between 10% and 18%. However, it can appear to occur in conjunction with virtually any neurological impairment. It is more frequent in the acute than in the chronic phase and more prominent for assessment in the cases with right hemispheric lesions than with the left. Anosognosia is not related to global mental confusion, cognitive flexibility, other major intellectual disturbances, or mere sensory/perceptual deficits.

The condition does not seem to be directly related to sensory loss but is thought to be caused by damage to higher level neurocognitive processes that are involved in integrating sensory information with processes that support spatial or bodily representations (including the somatosensory system). Anosognosia is thought to be related to unilateral neglect, a condition often found after damage to the non-dominant (usually the right) hemisphere of the cerebral cortex in which people seem unable to attend to, or sometimes comprehend, anything on a certain side of their body (usually the left).

Anosognosia can be selective in that an affected person with multiple impairments may seem unaware of only one handicap, while appearing to be fully aware of any others. This is consistent with the idea that the source of the problem relates to spatial representation of the body. For example, anosognosia for hemiplegia, or the paralysis of one side of the body, may occur with or without intact awareness of visuo-spatial unilateral neglect. This phenomenon of double dissociation can be an indicator of domain-specific disorders of awareness modules, meaning that in anosognosia, brain damage can selectively impact the self-monitoring process of one specific physical or cognitive function rather than a spatial location of the body.

There are also studies showing that the maneuver of vestibular stimulation could temporarily improve both the syndrome of spatial unilateral neglect and of anosognosia for left hemiplegia. Combining the findings of hemispheric asymmetry to the right, association with spatial unilateral neglect, and the temporal improvement on both syndromes, it is suggested there can be a spatial component underlying the mechanism of anosognosia for motor weakness and that neural processes could be modulated similarly. There were some cases of anosognosia for right hemiplegia after left hemisphere damage, but the frequency of this type of anosognosia has not been estimated.

Those diagnosed with Alzheimer's disease often display this lack of awareness and insist that nothing is wrong with them.

Anosognosia may occur as part of receptive aphasia, a language disorder that causes poor comprehension of speech and the production of fluent but incomprehensible sentences. A patient with receptive aphasia cannot correct his own phonetics errors and shows "anger and disappointment with the person with whom s/he is speaking because that person fails to understand her/him". This may be a result of brain damage to the posterior portion of the superior temporal gyrus, believed to contain representations of word sounds. With those representations significantly distorted, patients with receptive aphasia are unable to monitor their mistakes. Other patients with receptive aphasia are fully aware of their condition and speech inhibitions, but cannot monitor their condition, which is not the same as anosognosia and therefore cannot explain the occurrence of neologistic jargon.