Certain types of seizures are associated with the somatosensory system. Cortical injury may lead to loss of thermal sensation or the ability to discriminate pain. An aura involving thermal and painful sensations is a phenomenon known to precede the onset of an epileptic seizure or focal seizure. Another type of seizure, called a sensory Jacksonian seizure involves an abnormal, localizable, cutaneous sensation but does not have apparent stimulus. This sensation may progress along a limb or to adjacent cutaneous body areas, reflecting abnormal neuronal firing in the postcentral gyrus where an epileptic discharge is propagated. These episodes in which patients are consciously aware during a seizure have been useful for identifying problems associated with the somatosensory cortex. Patients can describe the nature of the seizure and how they feel during it.

Patients may experience numbness, prickling or tingling sensations (paresthesias), or the feeling a limb has "fallen asleep" (an indicator of nerve compression), burning, cutting or other sensations.

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.

Episodes that include complex hyperactivity of the proximal portions of the limbs that lead to increased overall motor activity are called hypermotor seizures. When associated with bizarre movements and vocalizations these seizures are often misdiagnosed as pseudoseizures or other episodic movement disorders such as psychogenic movement disorders, familial paroxysmal dystonic choreoathetosis, paroxysmal kinesogenic choreoathetosis, or episodic ataxia type 1. Hypermotor seizure in children are often confused with pavor nocturnus (night terrors). 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.

Damage to the corpus callosum can give rise to "purposeful" actions in the sufferer's non-dominant hand (an individual who is left-hemisphere-dominant will experience the left hand becoming alien, and the right hand will turn alien in the person with right-hemisphere dominance).

In "the callosal variant", the patient's hand counteracts voluntary actions performed by the other, "good" hand. Two phenomena that are often found in patients with callosal alien hand are "agonistic dyspraxia" and "diagonistic dyspraxia".

Agonistic dyspraxia involves compulsive automatic execution of motor commands by one hand when the patient is asked to perform movements with the other hand. For example, when a patient with callosal damage was instructed to pull a chair forward, the affected hand would decisively and impulsively push the chair backwards.

Agonistic dyspraxia can thus be viewed as an involuntary competitive interaction between the two hands directed toward completion of a desired act in which the affected hand competes with the unaffected hand to complete a purposive act originally intended to be performed by the unaffected hand.

Diagonistic dyspraxia, on the other hand, involves a conflict between the desired act in which the unaffected hand has been engaged and the interfering action of the affected hand which works to oppose the purpose of the desired act intended to be performed by the unaffected hand. For instance, when Akelaitis's patients underwent surgery to the corpus callosum to reduce epileptic seizures, one patient's left alien hand would frequently interfere with the right hand. For instance, while trying to turn over to the next page with the right hand, his left hand would try to close the book.

In another case of callosal alien hand, the patient did not suffer from intermanual conflict between the hands but rather from a symptom characterized by involuntary mirror movements of the affected hand. When the patient was asked to perform movements with one hand, the other hand would involuntarily perform a mirror image movement which continued even when the involuntary movement was brought to the attention of the patient, and the patient was asked to restrain the mirrored movement. The patient suffered from a ruptured aneurysm near the anterior cerebral artery, which resulted in the right hand being mirrored by the left hand. The patient described the left hand as frequently interfering and taking over anything the patient tried to do with the right hand. For instance, when trying to grasp a glass of water with the right hand with a right side approach, the left hand would involuntary reach out and grasp hold of the glass through a left side approach.

More recently, Geschwind et al. described the case of a woman who suffered severe coronary heart disease. One week after undergoing coronary artery bypass grafting, she noticed that her left hand started to "live a life of its own". It would unbutton her gown, try to choke her while asleep and would automatically fight with the right hand to answer the phone. She had to physically restrain the affected hand with the right hand to prevent injury, a behavior which has been termed "self-restriction". The left hand also showed signs of severe ideomotor apraxia. It was able to mimic actions but only with the help of mirror movements executed by the right hand (enabling synkinesis). Using magnetic resonance imaging (MRI), Geschwind et al. found damage to the posterior half of the callosal body, sparing the anterior half and the splenium extending slightly into the white matter underlying the right cingulate cortex.

Alien hand syndrome (AHS) is a condition in which a person experiences their limbs acting seemingly on their own, without control over the actions. The term is used for a variety of clinical conditions and most commonly affects the left hand. There are many similar names used to describe the various forms of the condition but they are often used inappropriately. The afflicted person may sometimes reach for objects and manipulate them without wanting to do so, even to the point of having to use the controllable hand to restrain the alien hand. While under normal circumstances, thought, as intent, and action can be assumed to be deeply mutually entangled, the occurrence of alien hand syndrome can be usefully conceptualized as a phenomenon reflecting a functional "disentanglement" between thought and action.

Alien hand syndrome is best documented in cases where a person has had the two hemispheres of their brain surgically separated, a procedure sometimes used to relieve the symptoms of extreme cases of epilepsy and epileptic psychosis, e.g., temporal lobe epilepsy. It also occurs in some cases after brain surgery, stroke, infection, tumor, aneurysm, migraine and specific degenerative brain conditions such as Alzheimer's disease and Creutzfeldt–Jakob disease. Other areas of the brain that are associated with alien hand syndrome are the frontal, occipital, and parietal lobes.

Allochiria (from the Greek meaning "other hand") is a neurological disorder in which the patient responds to stimuli presented to one side of their body as if the stimuli had been presented at the opposite side. It is associated with spatial s, usually symmetrical, of stimuli from one side of the body (or of the space) to the opposite one. Thus a touch to the left side of the body will be reported as a touch to the right side, which is also known as somatosensory allochiria. If the auditory or visual senses are affected, sounds (a person's voice for instance) will be reported as being heard on the opposite side to that on which they occur and objects presented visually will be reported as having been presented on the opposite side. Often patients may express allochiria in their drawing while copying an image. Allochiria often co-occurs with unilateral neglect and, like hemispatial neglect, the disorder arises commonly from damage to the right parietal lobe.

Allochiria is often confused with alloesthesia, also known as false allochiria. True allochiria is a symptom of dyschiria and unilateral neglect. Dyschiria is a disorder in the localization of sensation due to various degrees of dissociation and cause impairment in one side causing the inability to tell which side of the body was touched.

Optic ataxia is the inability to guide the hand toward an object using visual information where the inability cannot be explained by motor, somatosensory, visual field deficits or acuity deficits. Optic ataxia is seen in Bálint's syndrome where it is characterized by an impaired visual control of the direction of arm-reaching to a visual target, accompanied by defective hand orientation and grip formation. It is considered a specific visuomotor disorder, independent of visual space misperception.

Optic ataxia is also known as misreaching or dysmetria (), secondary to visual perceptual deficits. A patient with Bálint's syndrome likely has defective hand movements under visual guidance, despite normal limb strength. The patient is unable to grab an object while looking at the object, due to a discoordination of eye and hand movement. It is especially true with their contralesional hand.

Dysmetria refers to a lack of coordination of movement, typified by the undershoot or overshoot of intended position with the hand, arm, leg, or eye. It is sometimes described as an inability to judge distance or scale.

The reaching ability of the patient is also altered. It takes them longer to reach toward an object. Their ability to grasp an object is also impaired. The patient's performance is even more severely deteriorated when vision of either the hand or the target is prevented.

Some telltale signs suggesting Bálint's syndrome following bilateral brain insults may include:

- limitation to perceive only stimuli that is presented at 35 to 40 degrees to the right. They are able to move their eyes but cannot fixate on specific visual stimuli. (ataxia)

- patient's field of attention is limited to one object at a time. making activities like reading difficult because each letter is perceived separately.(ataxia)

- figure/ground defects in which a patient can see either the background but not the object residing somewhere in the whole scene, or conversely can see the object but sees no background around it (simultanagnosia)

- a patient, while attempting to put one foot into a slipper by trying to insert the foot into a nonexistent slipper several inches from the real slipper, even as the patient focuses on the actual slipper (oculomotor apraxia)

- a patient raising a fork or spoon containing food to a point on the patient's face above or below the mouth, and possibly finding the mouth by trial and error by manually moving the utensil on the face (optic ataxia)

Dejerine–Roussy syndrome is most commonly preceded by numbness in the affected side. In these cases, numbness is replaced by burning and tingling sensations, widely varying in degree of severity across all cases. The majority of those reported are cases in which the symptoms are severe and debilitating. Burning and tingling can also be accompanied by hypersensitivity, usually in the form of dysaesthesia or allodynia. Less commonly, some patients develop severe ongoing pain with little or no stimuli.

Allodynia is pain from a stimulus that would normally not cause pain. For example, there is a patient who experiences unrelenting pain when a breeze touches his skin. Most patients experiencing allodynia, experience pain with touch and pressure, however some can be hypersensitive to temperature.

Dysaesthesia is defined as pain due to thalamic lesioning. This form of neuropathic pain can be any combination of itching, tingling, burning, or searing experienced spontaneously or from stimuli.

Allodynia and dysaesthesia replace numbness between one week and a few months after a thalamic stroke. In general, once the development of pain has stopped, the type and severity of pain will be unchanging and if untreated, persist throughout life. Consequentially, many will undergo some form of pain treatment and adjust to their new lives as best they can.

Pain associated with Dejerine–Roussy syndrome is sometimes coupled with anosognosia or somatoparaphrenia which causes a patient having undergone a right-parietal, or right-sided stroke to deny any paralysis of the left side when indeed there is, or deny the paralyzed limb(s) belong to them. Although debatable, these symptoms are rare and considered part of a "thalamic phenomenon", and are not normally considered a characteristic of Dejerine–Roussy syndrome.

Disconnection syndrome is a general term for a number of neurological symptoms caused by damage to the white matter axons of communication pathways—via lesions to association fibers or commissural fibers—in the cerebrum, independent of any lesions to the cortex. The behavioral effects of such disconnections are relatively predictable in adults. Disconnection syndromes usually reflect circumstances where regions A and B still have their functional specializations except in domains that depend on the interconnections between the two regions.

Callosal syndrome, or split-brain, is an example of a disconnection syndrome from damage to the corpus callosum between the two hemispheres of the brain. Disconnection syndrome can also lead to aphasia, left-sided apraxia, and tactile aphasia, among other symptoms. Other types of disconnection syndrome include conduction aphasia (lesion of the association tract connecting Broca’s area and Wernicke’s), agnosia, apraxia, pure alexia, etc.

Allochiria has been observed mainly in the context of neglect which is usually due to a lesion that affects the right parietal lobe. In patients with allochiria, their sensibility is retained completely but the patient is not clear as to which side of the body has been touched. Their power of localization is retained but error exists to the side touched and they often refer the irritation to the corresponding part of the limb. In the patients' mind there is doubt or error as to which side of the body is touched.

There are multiple definitions of allochiria. According to Musser, allochiria is the reference of a sensory stimulus to the corresponding location on the opposite location on the opposite side of the body. Judson Bury says that a patient may refer to an impression on one side to a corresponding place on the opposite side of the body. Thus, if a patient is pricked on one limb, he may say that he feels it on the other. Overall, even though different author's definition differs on points such as the type of stimulus, and the symmetry between the site of the stimulus and the seat of its localization, they all agree that an essential feature of allochiria is the deflection of a sensation to the wrong side of the body, which is true allochiria. In none of these definitions is any stress laid on the state of the patient's knowledge of a right or left side and the symptoms are seen as an error in localization.

Obsersteiner laid stress that there is in allochiria no defect in vertical localization but merely confusion in the patient's mind between the opposite sides of the body and come to look upon the symptom as simply any form of bad mistake in localization.

There is in the patient's mind doubt or error as to the side touched while sensibility including the power of localization is otherwise retained. Allochiria has been described as occurring in nerve lesions, Hemiplegia, disseminated sclerosis Multiple sclerosis, tabes dorsalis, unilateral injury to the spinal cord, Ménière's disease, hysteria, symmetrical gangrene, and in connection with touch, pain, the "muscle sense," the temperature sense, sight, smell, taste, hearing, and the electrical reactions.

Allochiria can occur in relation to any or every segment of the body. In some cases allochiria may be , and in others it may be restricted to certain regions of the body, or even only to one part of the body. Allochiria is marked to have connections with a variety of senses and sometimes only certain kinds of stimuli can arouse the appropriate feeling of one sidedness.

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.

Anosodiaphoria is a condition in which a person who suffers disability due to brain injury seems indifferent to the existence of their handicap. Anosodiaphoria is specifically used in association with indifference to paralysis. It is a somatosensory agnosia, or a sign of neglect syndrome. It might be specifically associated with defective functioning of the frontal lobe of the right hemisphere.

Joseph Babinski first used the term anosodiaphoria in 1914 to describe a disorder of the body schema in which patients verbally acknowledge a clinical problem (such as hemiparesis) but fail to be concerned about it. Anosodiaphoria follows a stage of anosognosia, in which there may be verbal, explicit denial of the illness, and after several days to weeks, develop the lack of emotional response. Indifference is different from denial because it implies a lack of caring on the part of the patient whom otherwise acknowledges his or her deficit.

An epileptic aura is the consequence of the activation of functional cortex by abnormal, unilateral, and brief neuronal discharge. In addition to being a warning sign to an upcoming seizure, the nature of an aura can give insight into the localization and lateralization of the seizure or migraine.

Not everyone experiences an aura with a seizure, but the most common auras include motor, somatosensory, visual, and auditory symptoms. The activation in the brain during an aura can spread through multiple regions continuously or discontinuously, on the same side or to both sides.

Auras are particularly common in focal seizures. If the motor cortex is involved in the over excitation of neurons, motor auras can result. Likewise, somatosensory auras (such as tingling, numbness, and pain) can result if in the somatosensory cortex. When the primary somatosensory cortex is activated, more discrete parts on the opposite side of the body and the secondary somatosensory areas result in symptoms ipsilateral to the seizure focus.

Visual auras can be simple or complex. Simple visual symptoms can include static, flashing, or moving lights/shapes/colors caused mostly by abnormal activity in the primary visual cortex. Complex visual auras can include people, scenes, and objects which results from stimulation of the temporo-occipital junction and is lateralized to one hemifield. Auditory auras can also be simple (ringing, buzzing) or complex (voices, music). Simple symptoms can occur from activation in the primary auditory cortex and complex symptoms from the temporo-occipital cortex at the location of the auditory association areas.

Dejerine-Roussy is a rare pain syndrome. Individuals with emerging Dejerine–Roussy syndrome usually report they are experiencing unusual pain or sensitivity that can be allodynic in nature or triggered by seemingly unrelated stimuli (sounds, tastes). Symptoms are typically lateralized and may include vision loss or loss of balance (position sense). Workup should be performed by a neurologist and brain imaging to look for evidence of infarction or tumor should be obtained.

Similarly to vision loss, hearing loss can vary from full or partial inability to detect some or all frequencies of sound which can typically be heard by members of their species. For humans, this range is approximately 20 Hz to 20 kHz at ~6.5 dB, although a 10 dB correction is often allowed for the elderly. Primary causes of hearing loss due to an impaired sensory system include long-term exposure to environmental noise, which can damage the mechanoreceptors responsible for receiving sound vibrations, as well as multiple diseases, such as HIV or meningitis, which damage the cochlea and auditory nerve, respectively.

Hearing loss may be gradual or sudden. Hearing loss may be very mild, resulting in minor difficulties with conversation, or as severe as complete deafness. The speed with which hearing loss occurs may give clues as to the cause. If hearing loss is sudden, it may be from trauma or a problem with blood circulation. A gradual onset is suggestive of other causes such as aging or a tumor. If you also have other associated neurological problems, such as tinnitus or vertigo, it may indicate a problem with the nerves in the ear or brain. Hearing loss may be unilateral or bilateral. Unilateral hearing loss is most often associated with conductive causes, trauma, and acoustic neuromas. Pain in the ear is associated with ear infections, trauma, and obstruction in the canal.

The causes of CCAS lead to variations in symptoms, but a common core of symptoms can be seen regardless of etiology. Causes of CCAS include cerebellar agenesis, dysplasia and hypoplasia, cerebellar stroke, tumor, cerebellitis, trauma, and neurodegenerative diseases. CCAS can also be seen in children with prenatal, early postnatal, or developmental lesions. In these cases there are lesions of the cerebellum resulting in cognitive and affect deficits. The severity of CCAS varies depending on the site and extent of the lesion. In the original report that described this syndrome, patients with bihemispheric infarction, pancerebellar disease, or large unilateral posterior inferior cerebellar artery (PICA) infarcts had more cognitive deficits than patients with small right PICA infarcts, small right anterior interior cerebellar artery infarcts or superior cerebellar artery (SCA) territory. Overall, patients with damage to either the posterior lobe of the cerebellum or with bilateral lesions had the greatest severity of symptoms, whereas patients with lesions in the anterior lobe had less severe symptoms. In children, it was found that those with astrocytoma performed better than those with medulloblastoma on neuropsychological tests. When diagnosing a patient with CCAS, medical professionals must remember that CCAS has many different causes.

The CCAS has been described in both adults and children. The precise manifestations may vary on an individual basis, likely reflecting the precise location of the injury in the cerebellum. These investigators subsequently elaborated on the affective component of the CCAS, i.e., the neuropsychiatric phenomena. They reported that patients with injury isolated to the cerebellum may demonstrate distractibility, hyperactivity, impulsiveness, disinhibition, anxiety, ritualistic and stereotypical behaviors, illogical thought and lack of empathy, aggression, irritability, ruminative and obsessive behaviors, dysphoria and depression, tactile defensiveness and sensory overload, apathy, childlike behavior, and inability to comprehend social boundaries and assign ulterior motives.

The CCAS can be recognized by the pattern of deficits involving executive function, visual-spatial cognition, linguistic performance and changes in emotion and personality. Underdiagnosis may reflect lack of familiarity of this syndrome in the scientific and medical community. The nature and variety of the symptoms may also prove challenging. Levels of depression, anxiety, lack of emotion, and affect deregulation can vary between patients. The symptoms of CCAS are often moderately severe following acute injury in adults and children, but tend to lessen with time. This supports the view that the cerebellum is involved with the regulation of cognitive processes.

An aura is a perceptual disturbance experienced by some with migraines or seizures before either the headache or seizure begins. It often manifests as the perception of a strange light, an unpleasant smell, or confusing thoughts or experiences. Some people experience aura without a subsequent migraine or seizure (see silent migraine). Auras vary by individual experience; some people experience smells, lights, or hallucinations. Less known symptoms of the eye include disturbances, where the eyes roll in the back of the head caused by photosensitivity. A sufferer of this type of aura may experience tearfulness of the eyes and uncontrollable sensations of light followed by reduced symptoms after approximately 20 minutes; it is the rarest type of aura.

When occurring, auras allow people who have epilepsy time to prevent injury to themselves and/or others. The time between the appearance of the aura and the migraine lasts from a few seconds up to an hour. The aura can stay with a migraine sufferer for the duration of the migraine; depending on the type of aura, it can leave the person disoriented and confused. It is not uncommon for migraine sufferers to experience more than one type of aura during the migraine. Most people who have auras have the same type of aura every time.

Auras can also be confused with sudden onset of panic, panic attacks or anxiety attacks creating difficulties in diagnosis. The differential diagnosis of patients who experience symptoms of paresthesias, derealization, dizziness, chest pain, tremors, and palpitations can be quite challenging.

Patients with autotopagnosia exhibit an inability to locate parts of their own body, the body of an examiner’s, or the parts of a representation of a human body. Deficiencies can be in localizing parts of a certain area of the body, or the entire body.

Some patients demonstrating the symptoms of autotopagnosia have a decreased ability to locate parts of other multipart object. Patients are considered to suffer from “pure” autotopagnosia, however, if their deficiency is specific to body part localization. Patients suffering from “pure” autotopagnosia often have no problems carrying out tasks involved in everyday life that require body part awareness. Patients have difficulty locating body parts when directly asked, but can carry out activities such as putting on pants without difficulty. Patients can describe the function and appearance of body parts, yet they are still unable to locate them.

Damage to the left parietal lobe can result in what is called Gerstmann syndrome. It can include right-left confusion, a difficulty with writing Agraphia and a difficulty with mathematics Acalculia. In addition, it can also produce language deficiencies Aphasia and an inability to recognize objects normally Agnosia.

Other related disorders include:

- Apraxia: an inability to perform skilled movements despite understanding of the movements and intact sensory and motor systems.

- Finger agnosia: An inability to name the fingers, move a specific finger upon being asked, and/or recognize which finger has been touched when an examiner touches one.

Hemispatial neglect results most commonly from strokes and brain unilateral injury to the right cerebral hemisphere, with rates in the critical stage of up to 80% causing visual neglect of the left-hand side of space. Neglect is often produced by massive strokes in the middle cerebral artery region and is variegated, so that most sufferers do not exhibit all of the syndrome's traits. Right-sided spatial neglect is rare because there is redundant processing of the right space by both the left and right cerebral hemispheres, whereas in most left-dominant brains the left space is only processed by the right cerebral hemisphere. Although it most strikingly affects visual perception ('visual neglect'), neglect in other forms of perception can also be found, either alone or in combination with visual neglect.

For example, a stroke affecting the right parietal lobe of the brain can lead to neglect for the left side of the visual field, causing a patient with neglect to behave as if the left side of sensory space is nonexistent (although they can still turn left). In an extreme case, a patient with neglect might fail to eat the food on the left half of their plate, even though they complain of being hungry. If someone with neglect is asked to draw a clock, their drawing might show only the numbers 12 to 6, or all 12 numbers might be on one half of the clock face with the other half distorted or blank. Neglect patients may also ignore the contralesional side of their body; for instance, they might only shave, or apply make-up to, the non-neglected side. These patients may frequently collide with objects or structures such as door frames on the side being neglected.

Neglect may also present as a delusional form, where the patient denies ownership of a limb or an entire side of the body. Since this delusion often occurs alone, without the accompaniment of other delusions, it is often labeled as a monothematic delusion.

Neglect not only affects present sensation but memory and recall perception as well. A patient suffering from neglect may also, when asked to recall a memory of a certain object and then draw said object, draw only half of the object. It is unclear, however, if this is due to a perceptive deficit of the memory (to the patient having lost pieces of spatial information of the memory) or whether the information within the memory is whole and intact but simply being ignored, the same way portions of a physical object in the patient's presence would be ignored.

Some forms of neglect may also be very mild—for example, in a condition called extinction where competition from the ipsilesional stimulus impedes perception of the contralesional stimulus. These patients, when asked to fixate on the examiner's nose, can detect fingers being wiggled on the affected side. If the examiner were to wiggle his or her fingers on both the affected and unaffected sides of the patient, the patient will report seeing movement only on the ipsilesional side.

Many types of sense loss occur due to a dysfunctional sensation process, whether it be ineffective receptors, nerve damage, or cerebral impairment. Unlike agnosia, these impairments are due to damages prior to the perception process.

Since astasis itself is more a symptom than a disease, it is more often seen associated with other signs and symptoms. People who have astasis often experience

- Odd gyrations

- Tightrope balancing deficits (in which a person attempts to balance on a tightrope in order to test balance and motor coordination)

- Near falling deficits (which is a test in which the patient is slightly pushed in order to check their ability to regain posture)

- Exaggerated effort deficits (which is an overcompensation test used to determine motor coordination ability)

- Atypical postures and weakness

- Paralysis

- Jumping fits (in which motor control is partially or totally lost)

- Tremors

One study described a patient with astasis as lying in bed with a normal body posture. When the patient was sitting, he tilted his body to the left. When he was asked to stand up, the patient rotated his trunk axis to the left (left shoulder going backwards), and tilted his body to that same side, showing resistance to passive correction of posture in both of these planes. He was unable to stand and fell backwards and towards the left.