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.

Conduction aphasics will show relatively well-preserved auditory comprehension, which may even be completely functional. Spontaneous speech production will be fluent and generally grammatically and syntactically correct. Intonation and articulation will also be preserved. Speech will often contain paraphasic errors: phonemes and syllables will be dropped or transposed (e.g., "snowball" → "snowall", "television" → "vellitision", "ninety-five percent" → "ninety-twenty percent"). The hallmark deficit of this disorder, however, is in repetition. Patients will show a marked inability to repeat words or sentences when prompted by an examiner. After saying a sentence to a person with conduction aphasia, he or she will be able to paraphrase the sentence accurately but will not be able to repeat it, possibly because their "motor speech error processing is disrupted by inaccurate forward predictions, or because detected errors are not translated into corrective commands due to damage to the auditory-motor interface". When prompted to repeat words, patients will be unable to do so, and produce many paraphasic errors. For example, when prompted with "bagger", a patient may respond with, "gabber". Oral reading can also be poor.

However, patients recognize their paraphasias and errors and will try to correct them, with multiple attempts often necessary for success. This recognition is due to preserved auditory error detection mechanisms. Error sequences frequently fit a pattern of incorrect approximations featuring known morphemes that "a") share one or more similarly located phonemes but "b") differ in at least one aspect that makes the substituted morpheme(s) semantically distinct. This repetitive effort to approximate the appropriate word or phrase is known as "conduite d’approche". For example, when prompted to repeat "Rosenkranz", a German-speaking patient may respond with, "rosenbrau... rosenbrauch... rosengrau... bro... grosenbrau... grossenlau, rosenkranz... kranz... rosenkranz".

Conduction aphasia is a relatively mild language impairment, and most patients return to day-to-day life. Symptoms of conduction aphasia, as with other aphasias, can be transient, lasting only several hours or a few days. As aphasias and other language disorders are frequently due to stroke, their symptoms can change and evolve over time, or simply disappear. This is due to healing in the brain after inflammation or hemorrhage, which leads to decreased local impairment. Furthermore, plastic changes in the brain may lead to the recruitment of new pathways to restore lost function. For example, the right hemisphere speech systems may learn to correct for left-hemisphere damage. However, chronic conduction aphasia is possible, without transformation to other aphasias. These patients show prolonged, profound deficits in repetition, frequent phonemic paraphasias, and "conduite d'approche" during spontaneous speech.

There are three main types of anomia:

- Word selection anomia occurs when the patient knows how to use an object and can correctly select the target object from a group of objects, and yet cannot name the object. Some patients with word selection anomia may exhibit selective impairment in naming particular types of objects, such as animals or colors. In the subtype known as color anomia, the patient can distinguish between colors but cannot identify them by name or name the color of an object. The patients can separate colors into categories, but they cannot name them.

- Semantic anomia is a disorder in which the meaning of words becomes lost. In patients with semantic anomia, a naming deficit is accompanied by a recognition deficit. Thus, unlike patients with word selection anomia, patients with semantic anomia are unable to select the correct object from a group of objects, even when provided with the name of the target object.

- Disconnection anomia results from the severing of connections between sensory and language cortices. Patients with disconnection anomia may exhibit modality-specific anomia, where the anomia is limited to a specific sensory modality, such as hearing. For example, a patient who is perfectly capable of naming a target object when it is presented via certain sensory modalities like audition or touch, may be unable to name the same object when the object is presented visually. Thus, in such a case, the patient's anomia arises as a consequence of a disconnect between his/her visual cortex and language cortices.

Conduction aphasia, also called associative aphasia, is a relatively rare form of aphasia. An acquired language disorder, it is characterized by intact auditory comprehension, fluent (yet paraphasic) speech production, but poor speech repetition. They are fully capable of understanding what they are hearing, but fail to encode phonological information for production. This deficit is load-sensitive as patients show significant difficulty repeating phrases, particularly as the phrases increase in length and complexity and as they stumble over words they are attempting to pronounce. Patients will display frequent errors during spontaneous speech, such as substituting or transposing sounds. They will also be aware of their errors, and will show significant difficulty correcting them. For example: "Clinician: Now, I want you to say some words after me. Say ‘boy’. Patient: Boy. Clinician: Home. Patient: Home. Clinician: Seventy-nine. Patient: Ninety-seven. No … sevinty-sine … siventy-nice…. Clinician: Let’s try another one. Say ‘refrigerator’. Patient: Frigilator … no? how about … frerigilator … no frigaliterlater … aahh! It’s all mixed up!"

Shallice and Warrington (1970) were able to differentiate two variants of

this constellation: the reproduction and the repetition type. These authors suggested an exclusive deficit of auditory-verbal short-term memory in repetition conduction aphasia whereas the other variant was assumed to reflect disrupted phonological encoding mechanism, afflicting confrontation tasks such as repetition, reading and naming in a similar manner.

Left-hemisphere damage involving auditory regions often result in speech deficits. Lesions in this area that damage the sensorimotor dorsal stream suggest that the sensory system aid in motor speech. Studies have suggested that conduction aphasia is a result of damage specifically to the left superior temporal gyrus and/or the left supra marginal gyrus. The classical explanation for conduction aphasia is that of a disconnection between the brain areas responsible for speech comprehension (Wernicke's area) and speech production (Broca's area), due specifically to damage to the arcuate fasciculus, a deep white matter tract. Patients are still able to comprehend speech because the lesion does not disrupt the ventral stream pathway.

Pure alexia, also known as agnosic alexia or alexia without agraphia or pure word blindness, is one form of alexia which makes up "the peripheral dyslexia" group. Individuals who have pure alexia suffer from severe reading problems while other language-related skills such as naming, oral repetition, auditory comprehension or writing are typically intact.

Pure alexia is also known as: "alexia without agraphia", "letter-by-letter dyslexia", "spelling dyslexia", or "word-form dyslexia". Another name for it is "Dejerine syndrome", after Joseph Jules Dejerine, who described it in 1892; however, when using this name, it should not be confused with medial medullary syndrome which shares the same eponym.

Auditory verbal agnosia can be referred to as a pure aphasia because it has a high degree of specificity. Despite an inability to comprehend speech, patients with auditory verbal agnosia typically retain the ability to hear and process non-speech auditory information, speak, read and write. This specificity suggests that there is a separation between speech perception, non-speech auditory processing, and central language processing. In support of this theory, there are cases in which speech and non-speech processing impairments have responded differentially to treatment. For example, some therapies have improved writing comprehension in patients over time, while speech remained critically impaired in those same patients.

The term "pure word deafness" is something of a misnomer. By definition, individuals with pure word deafness are not deaf – in the absence of other impairments, these individuals have normal hearing for all sounds, including speech. The term "deafness" originates from the fact that individuals with AVA are unable to "comprehend" speech that they hear. The term "pure word" refers to the fact that comprehension of verbal information is selectively impaired in AVA. For this reason, AVA is distinct from other auditory agnosias in which the recognition of nonspeech sounds is impaired. Classical (or pure) auditory agnosia is an inability to process environmental sounds. Interpretive or receptive agnosia (amusia) is an inability to understand music.

Patients with pure word deafness complain that speech sounds simply do not register, or that they tend not to come up. Other claims include speech sounding as if it were in a foreign language, the words having a tendency to run together, or the feeling that speech was simply not connected to the patient's voice.

Anomic aphasia (anomia) is a type of aphasia characterized by problems recalling words, names, and numbers. Speech is fluent and receptive language is not impaired in someone with anomic aphasia. Subjects often use circumlocutions (speaking in a roundabout way) in order to avoid a name they cannot recall or to express a certain word they cannot remember. Sometimes the subject can recall the name when given clues. Additionally, patients are able to speak with correct grammar; the main problem is finding the appropriate word to identify an object or person.

Sometimes subjects may know what to do with an object, but still not be able to give a name to the object. For example, if a subject is shown an orange and asked what it is called, the subject may be well aware that the object can be peeled and eaten, and may even be able to demonstrate this by actions or even verbal responses – however, they cannot recall that the object is called an "orange". Sometimes, when a person with this condition is multilingual, they might confuse the language they are speaking in trying to find the right word (inadvertent code-switching).

Pure alexia results from cerebral lesions in circumscribed brain regions and therefore belongs to the group of acquired reading disorders, alexia, as opposed to developmental dyslexia found in children who have difficulties in learning to read.

There is no uniform performance among patients with auditory verbal agnosia; therefore it is not possible to attribute specific phonetic or phonological deficits to the syndrome. In order to diagnose AVA, two intact abilities need to be established:

- Words that are heard must have undergone adequate acoustic analysis as evidenced by correct repetition;

- The semantic representation of the word must be intact as evidenced by immediate comprehension of the word when presented in written form.

If both of these criteria are met "and" lack of auditory verbal comprehension is apparent, a diagnosis of AVA may follow.

In at least one instance, the Boston Diagnostic Aphasia Examination has been used to profile AVA. This method was able to show that the patient experienced marked difficulty in speech perception with minor to no minor deficits in production, reading, and writing, fitting the profile of AVA. While this provides a well-known example, other verbal-audio test batteries can and have also been used to diagnose pure speech deafness.

Social-emotional agnosia is generally diagnosed through the use of two tests, the Faux Pas Test and the Strange Stories Test. Both of these tests are used to show deficits in theory of mind, the recognition of mental states of others. For people with social-emotional agnosia, it is mainly the emotional states that are difficult for them to recognize. Studies have shown that subjects with amygdala damage perform poorly on both the Faux Pas test and the Strange Stories test.

Social-emotional agnosia, also known as emotional agnosia or expressive agnosia, is the inability to perceive facial expressions, body language, and voice intonation. A person with this disorder is unable to non-verbally perceive others' emotions in social situations, limiting normal social interactions. The condition causes a functional blindness to subtle non-verbal social-emotional cues in voice, gesture, and facial expression. People with this form of agnosia have difficulty in determining and identifying the motivational and emotional significance of external social events, and may appear emotionless or agnostic (uncertainty or general indecisiveness about a particular thing). Symptoms of this agnosia can vary depending on the area of the brain affected. Social-emotional agnosia often occurs in individuals with schizophrenia and autism. It is difficult to distinguish from, and has been found to co-occur with, alexithymia.

Unilateral injury to the medial aspect of the brain's frontal lobe can trigger reaching, grasping and other purposeful movements in the contralateral hand. With anteromedial frontal lobe injuries, these movements are often exploratory reaching movements in which external objects are frequently grasped and utilized functionally, without the simultaneous perception on the part of the patient that they are "in control" of these movements. Once an object has been acquired and is maintained in the grasp of this "frontal variant" form of alien hand, the patient often has difficulty with voluntarily releasing the object from grasp and can sometimes be seen to be peeling the fingers of the hand back off the grasped object using the opposite controlled hand to enable the release of the grasped object (also referred to as tonic grasping or the "instinctive grasp reaction"). Some (for example, the neurologist Derek Denny-Brown) have referred to this behavior as "magnetic apraxia"

Goldberg and Bloom described a woman who suffered a large cerebral infarction of the medial surface of the left frontal lobe in the territory of the left anterior cerebral artery which left her with the frontal variant of the alien hand involving the right hand. There were no signs of callosal disconnection nor was there evidence of any callosal damage. The patient displayed frequent grasp reflexes; her right hand would reach out and grab objects without releasing them. In regards to tonic grasping, the more the patient tried to let go of the object, the more the grip of the object tightened. With focused effort the patient was able to let go of the object, but if distracted, the behaviour would re-commence. The patient could also forcibly release the grasped object by peeling her fingers away from contact with the object using the intact left hand. Additionally, the hand would scratch at the patient's leg to the extent that an orthotic device was required to prevent injury. Another patient reported not only tonic grasping towards objects nearby, but the alien hand would take hold of the patient's penis and engage in public masturbation.

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.

Cortical deafness is a rare form of sensorineural hearing loss caused by damage to the primary auditory cortex. Cortical deafness is an auditory disorder where the patient is unable to hear sounds but has no apparent damage to the anatomy of the ear (see auditory system), which can be thought of as the combination of auditory verbal agnosia and auditory agnosia. Patients with cortical deafness cannot hear any sounds, that is, they are not aware of sounds including non-speech, voices, and speech sounds. Although patients appear and feel completely deaf, they can still exhibit some reflex responses such as turning their head towards a loud sound.

Cortical deafness is caused by bilateral cortical lesions in the primary auditory cortex located in the temporal lobes of the brain. The ascending auditory pathways are damaged, causing a loss of perception of sound. Inner ear functions, however, remains intact. Cortical deafness is most often cause by stroke, but can also result from brain injury or birth defects. More specifically, a common cause is bilateral embolic stroke to the area of Heschl's gyri. Cortical deafness is extremely rare, with only twelve reported cases. Each case has a distinct context and different rates of recovery.

It is thought that cortical deafness could be a part of a spectrum of an overall cortical hearing disorder. In some cases, patients with cortical deafness have had recovery of some hearing function, resulting in partial auditory deficits such as auditory verbal agnosia. This syndrome might be difficult to distinguish from a bilateral temporal lesion such as described above.

Many studies have shown that disconnection syndromes such as aphasia, agnosia, apraxia, pure alexia and many others are not caused by direct damage to functional neocortical regions. They can also be present on only one side of the body which is why these are categorized as hemispheric disconnections. The cause for hemispheric disconnection is if the interhemispheric fibers, as mentioned earlier, are cut or reduced.

An example is commissural disconnect in adults which usually results from surgical intervention, tumor, or interruption of the blood supply to the corpus callosum or the immediately adjacent structures. Callosal disconnection syndrome is characterized by left ideomotor apraxia and left-hand agraphia and/or tactile anomia, and is relatively rare.

Other examples include commissurotomy, the surgical cutting of cerebral commissures to treat epilepsy and callosal agenesis which is when individuals are born without a corpus callosum. Those with callosal agenesis can still perform interhemispheric comparisons of visual and tactile information but with deficits in processing complex information when performing the respective tasks.

Since cortical deafness and auditory agnosia have many similarities, diagnosing the disorder proves to be difficult. Bilateral lesions near the primary auditory cortex in the temporal lobe are important criteria. Cortical deafness requires demonstration that brainstem auditory responses are

normal, but cortical evoked potentials are impaired. Brainstem auditory evoked potentials (BAEP), also referred to as brainstem auditory evoked responses (BAER) show the neuronal activity in the auditory nerve, cochlear nucleus, superior olive, and inferior colliculus of the brainstem. They typically have a response latency of no more than six milliseconds with an amplitude of approximately one microvolt. The latency of the responses gives critical information: if cortical deafness is applicable, LLR (long-latency responses) are completely abolished and MLR (middle latency responses) are either abolished or significantly impaired. In auditory agnosia, LLRs and MLRs are preserved.

Another important aspect of cortical deafness that is often overlooked is that patients "feel" deaf. They are aware of their inability to hear environmental sounds, non-speech and speech sounds. Patients with auditory agnosia can be unaware of their deficit, and insist that they are not deaf. Verbal deafness and auditory agnosia are disorders of a selective, perceptive and associative nature whereas cortical deafness relies on the anatomic and functional disconnection of the auditory cortex from acoustic impulses.

Source amnesia is the inability to remember where, when or how previously learned information has been acquired, while retaining the factual knowledge. This branch of amnesia is associated with the malfunctioning of one's explicit memory. It is likely that the disconnect between having the knowledge and remembering the context in which the knowledge was acquired is due to a dissociation between semantic and episodic memory – an individual retains the semantic knowledge (the fact), but lacks the episodic knowledge to indicate the context in which the knowledge was gained.

Memory representations reflect the encoding processes during acquisition. Different types of acquisition processes (e.g.: reading, thinking, listening) and different types of events (e.g.: newspaper, thoughts, conversation) will produce mental depictions that perceptually differ from one another in the brain, making it harder to retrieve where information was learned when placed in a different context of retrieval. Source monitoring involves a systematic process of slow and deliberate thought of where information was originally learned. Source monitoring can be improved by using more retrieval cues, discovering and noting relations and extended reasoning.

Individuals with frontal lobe damage have deficits in temporal context memory; source memory can also exhibit deficits in those with frontal lobe damage. It appears that those with frontal lobe damage have difficulties with recency and other temporal judgements (e.g., placing events in the order they occurred), and as such they are unable to properly attribute their knowledge to appropriate sources (i.e., suffer source amnesia). Those individuals with frontal lobe damage have normal recall of facts, but they make significantly more errors in source memory than control subjects, with these effects becoming apparent as shortly as 5 minutes after the learning experience. Individuals with frontal lobe damage often mistakenly attribute the knowledge they have to some other source (e.g., they read it somewhere, saw it on TV, etc.) but rarely attribute it to having learned it over the course of the experiment. It appears that frontal lobe damage causes a disconnection between semantic and episodic memory – in that the individuals cannot associate the context in which they acquired the knowledge to the knowledge itself.

Anterograde amnesia is a loss of the ability to create new memories after the event that caused the amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.

People with anterograde amnesic syndromes may present with widely varying degrees of forgetfulness. Some with severe cases have a combined form of anterograde and retrograde amnesia, sometimes called global amnesia.

In the case of drug-induced amnesia, it may be short-lived and patients can recover from it. In the other case, which has been studied extensively since the early 1970s, patients often have permanent damage, although some recovery is possible, depending on the nature of the pathophysiology. Usually, some capacity for learning remains, although it may be very elementary. In cases of pure anterograde amnesia, patients have recollections of events prior to the injury, but cannot recall day-to-day information or new facts presented to them after the injury occurred.

In most cases of anterograde amnesia, patients lose declarative memory, or the recollection of facts, but they retain nondeclarative memory, often called procedural memory. For instance, they are able to remember and in some cases learn how to do things such as talking on the phone or riding a bicycle, but they may not remember what they had eaten earlier that day for lunch. One extensively studied anterograde amnesiac patient, codenamed H.M., demonstrated that despite his amnesia preventing him from learning new declarative information, procedural memory consolidation was still possible, albeit severely reduced in power. He, along with other patients with anterograde amnesia, were given the same maze to complete day after day. Despite having no memory of having completed the maze the day before, unconscious practice of completing the same maze over and over reduced the amount of time needed to complete it in subsequent trials. From these results, Corkin et al. concluded despite having no declarative memory (i.e. no conscious memory of completing the maze exists), the patients still had a working procedural memory (learning done unconsciously through practice). This supports the notion that declarative and procedural memory are consolidated in different areas of the brain. In addition, patients have a diminished ability to remember the temporal context in which objects were presented. Certain authors claim the deficit in temporal context memory is more significant than the deficit in semantic learning ability (described below).

The following two case reports are examples of the Capgras delusion in a psychiatric setting:

The following case is an instance of the Capgras delusion resulting from a neurodegenerative disease:

The age of onset of seizures is typically between three and five, though onset can occur at an earlier or later age. The syndrome shows clear parallels to West syndrome, enough to suggest a connection.

Daily multiple seizures are typical in LGS. Also typical is the broad range of seizures that can occur, larger than that of any other epileptic syndrome. The most frequently occurring seizure type is tonic seizures, which are often nocturnal (90%); the second most frequent are myoclonic seizures, which often occur when the person is over-tired.

Atonic, atypical absence, tonic, complex partial, focalized and tonic–clonic seizures are also common. Additionally, about half of patients will have status epilepticus, usually the nonconvulsive type, which is characterized by dizziness, apathy, and unresponsiveness. The seizures can cause sudden falling (or spasms in tonic, atonic and myoclonic episodes) and/or loss of balance, which is why patients often wear a helmet to prevent head injury.

In addition to daily multiple seizures of various types, children with LGS frequently have arrested/slowed psycho-motor development and behavior disorders.

The syndrome is also characterized by an (between-seizures) EEG featuring slow spike-wave complexes.

Capgras delusion is a psychiatric disorder in which a person holds a delusion that a friend, spouse, parent, or other close family member (or pet) has been replaced by an identical impostor. The Capgras delusion is classified as a delusional misidentification syndrome, a class of delusional beliefs that involves the misidentification of people, places, or objects. It can occur in acute, transient, or chronic forms. Cases in which patients hold the belief that time has been "warped" or "substituted" have also been reported.

The delusion most commonly occurs in patients diagnosed with paranoid schizophrenia, but has also been seen in patients suffering from brain injury and dementia. It presents often in individuals with a neurodegenerative disease, particularly at an older age. It has also been reported as occurring in association with diabetes, hypothyroidism, and migraine attacks. In one isolated case, the Capgras delusion was temporarily induced in a healthy subject by the drug ketamine. It occurs more frequently in females, with a female:male ratio of approximately 3:2. It is worth noting that there is historical and quite probably modern use of the Political decoy as well as Celebrity lookalike, and impersonation is used by criminals, as well. Although 'delusion' is defined as when a patient holds a false belief "in spite of incontrovertible evidence", such evidence is difficult to produce (in the case of Capgras symptoms), whether lookalikes exist or not. This does not deter psychiatrists from prescribing pharmaceutical chemicals for persons describing these situations with little, if any, investigation into the claims, though it seems even one actual encounter with a genuine impersonator (whether sinister or not) has a notably unnerving effect on future interactions with that actual person, and possibly leading to paranoia of others being impersonated. Carefully targeted identity thefts in this sense can cause quite a few real problems, ranging from confusion to petty theft, business and domestic situations going awry, sexual relationship sabotage or confusion (possibility of unplanned pregnancy and risk of STD exposure), and financial fraud.

Diaschisis (from Greek διάσχισις meaning "shocked throughout") is a sudden loss (or change) of function in a portion of the brain connected to a distant, but damaged, brain area. The site of the originally damaged area and of the diaschisis are connected to each other by neurons. The loss of the damaged structure disrupts the function of the remaining intact systems and causes a physiological imbalance. The injury is produced by an acute focal disturbance in an area of the brain, from traumatic brain injury or stroke, for example. Some function may be restored with gradual readjustment of the intact but suppressed areas through intervention and the brain's natural neuroplasticity.

The term "diaschisis" was coined by Constantin von Monakow in 1914. Currently the term "diaschisis" is used to describe a depression of regional neuronal metabolism and cerebral blood flow caused by in an anatomically separate but functionally related neuronal region.

Von Monakow's concept of neurophysical changes in distant brain tissue to the focal lesion led to a widespread clinical interest. Doctors were interested in how diaschisis could describe the signs and symptoms of brain lesions that could not be explained.

The areas of the brain are connected by vast organized neuronal pathways that allow one area of the brain to influence other areas more distal to it. Understanding these dense pathways helps to link a lesion causing brain damage in one area of the brain to degeneration in a more distal brain area. A focal lesion causes damage that also disturbs the structural and functional connectivity to the brain areas distal to the lesion.

The primary mechanism of diaschisis is functional deafferentation, which is the loss of the input of information from the part of the brain that is now damaged. The decrease in information and neural firing to the distal brain area causes those synaptic connections to weaken and initiates a change in the structural and functional connectivity around that area. This leads to diaschisis. Diaschisis is also influenced by many other factors, including stoke, brain swelling, and neuroanatomical disconnection. The severity of these factors is manifested in altered neuronal excitability, hypo-metabolism, and hypo perfusion.

There are two types of diaschisis. The first is focal diaschisis, which refers to the remote neurophysiological changes that are caused by a focal lesion based on von Monakow's definition. The second type of diaschisis is non-focal diaschisis and it focuses on the changes in the strength and direction of neural pathways and connectivity between brain areas. This type of diaschisis has only been a topic in recent study as a result of the advancement of brain imaging tools and technology. These new tools allow for better understanding of the organization of the brain connectivity and further investigation into new types of diaschisis, like non-focal or connectional diascisis. This new type of diaschisis relates much more closely to clinical findings.

Lennox–Gastaut syndrome (LGS) is a childhood-onset epilepsy that most often appears between the second and sixth year of life. LGS is characterized by a triad of signs including frequent seizures of multiple types, an abnormal EEG pattern of less than 2.5 Hz slow spike wave activity, and moderate to severe intellectual impairment.