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.

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.

Patients who experience full awareness with explicit recall may have suffered an enormous trauma. Some patients experience post traumatic stress disorder (PTSD), leading to long-lasting after-effects such as nightmares, night terrors, flashbacks, insomnia, and in some cases even suicide. Some cases of awareness alert the patient to intra-operative errors.

A study from Sweden in 2002 attempted to follow up 18 patients for approximately 2 years after having been previously diagnosed with awareness under anesthesia. Four of the nine interviewed patients were still severely disabled due to psychiatric/psychological after-effects. All of these patients had experienced anxiety during the period of awareness, but only one had stated feeling pain. Another three patients had less severe, transient mental symptoms, although they could cope with these in daily life. Two patients denied any lasting effects from their awareness episode.

There are two states of consciousness that may be present:

- Awareness: That is, patients seem to be cognizant responding to commands but with no postoperative recall or memory of the events.

- Awareness and recall: That is, patients can recall events postoperatively, but were not necessarily conscious enough to respond to commands.

The incidence of a state with both responses in diverse degrees is also possible. The drugs that induce paralysis would also prevent responding to commands.

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.

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.

In the UK, the formal rules for the diagnosis of brainstem death have undergone only minor modifications since they were first published in 1976. The most recent revision of the UK's Department of Health Code of Practice governing use of that procedure for the diagnosis of death reaffirms the preconditions for its consideration. These are:

1. There should be no doubt that the patient’s condition – deeply comatose, unresponsive and requiring artificial ventilation—is due to irreversible brain damage of known cause.

2. There should be no evidence that this state is due to depressant drugs.

3. Primary hypothermia as the cause of unconsciousness must have been excluded, and

4. Potentially reversible circulatory, metabolic and endocrine disturbances likewise.

5. Potentially reversible causes of apnoea (dependence on the ventilator), such as muscle relaxants and cervical cord injury, must be excluded.

With these pre-conditions satisfied, the definitive criteria are:

1. Fixed pupils which do not respond to sharp changes in the intensity of incident light.

2. No corneal reflex.

3. Absent oculovestibular reflexes – no eye movements following the slow injection of at least 50ml of ice-cold water into each ear in turn (the caloric reflex test).

4. No response to supraorbital pressure.

5. No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation.

6. No observed respiratory effort in response to disconnection of the ventilator for long enough (typically 5 minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least 6.0 kPa (6.5 kPa in patients with chronic carbon dioxide retention). Adequate oxygenation is ensured by pre-oxygenation and diffusion oxygenation during the disconnection (so the brainstem respiratory centre is not challenged by the ultimate, anoxic, drive stimulus). This test—the apnoea test—is dangerous – and may prove lethal.

Two doctors, of specified status and experience, are required to act together to diagnose death on these criteria and the tests must be repeated after “a short period of time ... to allow return of the patient’s arterial blood gases and baseline parameters to the pre-test state”. These criteria for the diagnosis of death are not applicable to infants below the age of two months.

Characteristics of paroxysmal sympathetic hyperactivity include:

- fever

- tachycardia

- hypertension

- tachypnea

- hyperhidrosis or diaphoresis

- dystonic posturing

- pupillary dilation

- flushing

In cases where PSH episodes develop post-injury, specifically traumatic brain injury, symptoms typically develop quickly, usually within a week. Symptom onset has been seen to average 5.9 days post-injury. Episodes vary in duration and occurrence. Episodes can last as little as a few minutes or as long as ten hours, and they can occur multiple times a day. Episode duration has been seen to average 30.8 minutes and occur five to six times a day. Episodes can occur naturally or arise from external triggers. Common triggers include pain or stimulation, body turning or movements, and bladder distention. Bladder distention has been observed in patients being treated in intensive care units with the concurrent use of catheters. Symptoms of PSH can last from weeks to years following initial onset. As episodes persist over time, they have been found to become less frequent in occurrence but last for prolonged periods.

Brainstem death is a clinical syndrome defined by the absence of reflexes with pathways through the brainstem—the “stalk” of the brain, which connects the spinal cord to the mid-brain, cerebellum and cerebral hemispheres—in a deeply comatose, ventilator-dependent patient.

Identification of this state carries a very grave prognosis for survival; cessation of heartbeat often occurs within a few days although it may continue for weeks or even months if intensive support is maintained.

In the United Kingdom, the formal diagnosis of brainstem death by the procedure laid down in the official Code of Practice permits the diagnosis and certification of death on the premise that a person is dead when consciousness and the ability to breathe are permanently lost, regardless of continuing life in the body and parts of the brain, and that death of the brainstem alone is sufficient to produce this state.

This concept of brainstem death is also accepted as grounds for pronouncing death for legal purposes in India and Trinidad & Tobago. Elsewhere in the world the concept upon which the certification of death on neurological grounds is based is that of permanent cessation of all function in all parts of the brain—whole brain death—with which the reductionist United Kingdom concept should not be confused. The United States' President's Council on Bioethics made it clear, in its White Paper of December 2008, that the United Kingdom concept and clinical criteria are not considered sufficient for the diagnosis of death in the United States of America.

Paroxysmal sympathetic hyperactivity (PSH) is a syndrome that causes episodes of increased activity of the sympathetic nervous system. Hyperactivity of the sympathetic nervous system can manifest as increased heart rate, increased respiration, increased blood pressure, diaphoresis, and hyperthermia.

Previously, this syndrome has been identified as general dysautonomia but now is considered a specific form of it. It has also been referred to as paroxysmal sympathetic instability with dystonia, or PAID, and sympathetic storm. Recently, however, studies have adopted the name paroxysmal sympathetic hyperactivity to ensure specificity. PSH is observed more in younger patients than older ones. It is also seen more commonly in men than women. There is no known reason why this is the case, although it is suspected pathophysiological links may exist. In patients surviving traumatic brain injury, the occurrence of these episodes is one in every three. PSH can also be associated with severe anoxia, subarachnoid and intracerebral hemorrhage, and hydrocephalus.

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.

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.

Transneuronal degeneration can be grouped into two general categories: anterograde and retrograde.

Diffuse axonal injury (DAI) is a brain injury in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area. DAI is one of the most common and devastating types of traumatic brain injury, and is a major cause of unconsciousness and persistent vegetative state after severe head trauma. It occurs in about half of all cases of severe head trauma and may be the primary damage that occurs in concussion. The outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness. Those who do wake up often remain significantly impaired.

DAI can occur in every degree of severity from very mild or moderate to very severe. Concussion may be a milder type of diffuse axonal injury.

Anterograde transneuronal degeneration is degeneration caused by loss of inputs; it occurs when a neuron in the central nervous system is damaged and causes the degeneration of a postsynaptic neuron associated with a similar function as the presynaptic neuron. It is often termed "dying forward," and is also referred to as trans-synaptic degeneration. Anterograde degeneration can occur at a late stage of brain injury and result in diaschisis.

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.

Alcohol-related dementia presents as a global deterioration in intellectual function with memory not being specifically affected, but it may occur with other forms of dementia, resulting in a wide range of symptoms. Certain individuals with alcohol-related dementia present with damage to the frontal lobes of their brain causing disinhibition, loss of planning and executive functions, and a disregard for the consequences of their behavior. Other types of alcohol-related dementia such as Korsakoff's Syndrome cause the destruction of certain areas of the brain, where changes in memory, primarily a loss of short term memory, are the main symptom. Most presentations of alcohol dementia are somewhere along the spectrum between a global dementia and Korsakoff's psychosis, and may include symptoms of both.

Individuals affected by alcohol-related dementia may develop memory problems, language impairment, and an inability to perform complex motor tasks such as getting dressed. Heavy alcohol abuse also damages the nerves in arms and legs, i.e. peripheral neuropathy, as well as the cerebellum that controls coordination thereby leading to the development of cerebellar ataxia. These patients frequently have problems with sensation in their extremities and may demonstrate unsteadiness on their feet.

Alcohol-related dementia can produce a variety of psychiatric problems including psychosis (disconnection from reality), depression, anxiety, and personality changes. Patients with alcoholic dementia often develop apathy, related to frontal lobe damage, that may mimic depression. People with alcoholism are more likely to become depressed than people without alcoholism, and it may be difficult to differentiate between depression and alcohol dementia.

The syndrome of subjective doubles is a rare delusional misidentification syndrome in which a person experiences the delusion that he or she has a double or Doppelgänger with the same appearance, but usually with different character traits, that is leading a life of its own. The syndrome is also called the syndrome of doubles of the self, delusion of subjective doubles, or simply subjective doubles. Sometimes, the patient is under the impression that there is more than one double. A double may be projected onto any person, from a stranger to a family member.

This syndrome is often diagnosed during or after the onset of another mental disorder, such as schizophrenia or other disorders involving psychotic hallucinations. There is no widely accepted method of treatment, as most patients require an individualized therapy. The prevalence of this disease is relatively low, as few cases have been reported since the disease was defined in 1978 by George Christodoulou. However, subjective doubles is not clearly defined in literature, and therefore, may be under-reported.

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.

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.

The symptoms of the syndrome of subjective doubles are not clearly defined in medical literature, however, there are some defining features of the delusion:

- The existence of the delusion, by definition, is not a widely accepted cultural belief.

- The patient insists that the double he/she sees is real even when presented with contradictory evidence.

- Paranoia and/or spatial visualization ability impairments are present.

Similarities to other disorders are often noted in literature. Prosopagnosia, or the inability to recognize faces, may be related to this disorder due to the similarity of symptoms. Subjective doubles syndrome is also similar to delusional autoscopy, also known as an out-of-body experience, and therefore is occasionally referred to as an "autoscopic type" delusion. However, subjective doubles delusion differs from an autoscopic delusion: autoscopy often occurs during times of extreme stress, and can usually be treated by relieving the said stressor.

The syndrome of subjective doubles is usually accompanied by another mental disorder or organic brain syndrome, and may appear during or after the onset of the other disorder. Often, co-occurrence of subjective doubles with other types of delusional misidentification syndromes, especially Capgras syndrome, also occurs.

Several variations of the syndrome have been reported in literature:

- The doubles may appear at different ages of oneself.

- Some patients describe their double as both a physically and psychologically identical copy, rather than a purely physical copy. This is also known as clonal pluralization of the self, another type of delusional misidentification syndrome that may or may not be the same type of disorder (see #Controversy, below). In this case, depersonalization may be a symptom.

- Reverse subjective doubles occurs when the patient believes his/her own self (either physical or mental) is being transformed into another person. (see the case of Mr. A in #Presentation)

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:

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.

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.

Alcohol-related dementia is a broad term currently preferred among medical professionals. Many experts use the terms alcohol (or alcoholic) dementia to describe a specific form of ARD, characterized by impaired executive function (planning, thinking, and judgment). Another form of ARD is known as wet brain (Wernicke-Korsakoff syndrome), characterized by short term memory loss and thiamine (vitamin B1) deficiency. ARD patients often have symptoms of both forms, i.e. impaired ability to plan, apathy, and memory loss. ARD may occur with other forms of dementia (mixed dementia). The diagnosis of ARD is widely recognized but rarely applied, due to a lack of specific diagnostic criteria.

On many non-medical websites, the terms wet brain and alcohol-related dementia are often used interchangeably, creating significant confusion. Additionally, the term alcohol-induced persistent dementia is another non-specific name that is sometimes used.