Agnosia is the inability to recognize certain objects, persons or sounds. Agnosia is typically caused by damage to the brain (most commonly in the occipital or parietal lobes) or from a neurological disorder. Treatments vary depending on the location and cause of the damage. Recovery is possible depending on the severity of the disorder and the severity of the damage to the brain. Many more specific types of agnosia diagnoses exist, including: associative visual agnosia, astereognosis, auditory agnosia, auditory verbal agnosia, prosopagnosia, simultanagnosia, topographical disorientation, visual agnosia etc.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

Mild and major neurocognitive disorders are usually associated with but not restricted to the elderly. Unlike delirium, conditions under these disorders develop slowly and are characterized by memory loss. In addition to memory loss and cognitive impairment, other symptoms include aphasia, apraxia, agnosia, loss of abstract thought, behavioral/personality changes, and impaired judgment. There may also be behavioral disturbances including psychosis, mood, and agitation.

Mild and major neurocognitive disorders are differentiated based on the severity of their symptoms. Previously known as dementia, major neurocognitive disorder is characterized by significant cognitive decline and interference with independence, while mild neurocognitive disorder is characterized by moderate cognitive decline and does not interfere with independence. To be diagnosed, it must not be due to delirium or other mental disorder. They are also usually accompanied by another cognitive dysfunction. For non-reversible causes of dementia such as age, the slow decline of memory and cognition is lifelong. It can be diagnosed by screening tests such as the Mini Mental State Examination (MMSE).

The most prominent symptom of post-traumatic amnesia (PTA) is a loss of memory of the present time. As a result, patients are often unaware of their condition and may behave as if they are going about their regular lives. This can cause complications if patients are confined to a hospital and may lead to agitation, distress and/or anxiety. Many patients report feeling as though they were being "held prisoner" and being prevented from carrying on with their daily lives. Other symptoms include agitation, confusion, disorientation, and restlessness.

Patients also often display behavioral disturbances. Patients may shout, swear and behave in a disinhibited fashion. There have been cases in which patients who do not recognize anyone will ask for family members or acquaintances that they have not seen in years. Some patients exhibit childlike behavior. Other patients show uncharacteristically quiet, friendly and loving behavior. Although this behavior may seem less threatening because of its lack of aggressiveness, it may be equally worrisome.

PTA patients are often unaware of their surroundings and will ask questions repeatedly. Patients may also have a tendency to wander off, which can be a major concern in those who have suffered additional injuries at the time of trauma, such as injured limbs, as it may lead to the worsening of these secondary injuries.

Patients with psychoorganic syndrome often complain about headaches, dizziness, unsteadiness when walking, poor tolerance to the heat, stuffiness, atmospheric pressure changes, loud sounds, neurological symptoms.

The common reported psychological symptoms include:

- loss of memory and concentration

- emotional liability

- Clinical fatigue

- long term major depression

- severe anxiety

- reduced intellectual ability

The cognitive and behavioral symptoms are chronic and have little response to treatment.

Depending on lesion location, some patients may experience visual complications.

Delirium can be caused by the worsening of previous medical conditions, substance abuse or withdrawal, mental illness, severe pain, immobilization, sleep deprivation and hypnosis.

Other common causes that may increase the risk of delirium include infections of urinary tract, skin and stomach, pneumonia, old age, and poor nutrition.

Two types of confabulation are often distinguished:

- Provoked (momentary, or secondary) confabulations represent a normal response to a faulty memory, are common in both amnesia and dementia, and can become apparent during memory tests.

- Spontaneous (or primary) confabulations do not occur in response to a cue and seem to be involuntary. They are relatively rare, more common in cases of dementia, and may result from the interaction between frontal lobe pathology and organic amnesia.

Another distinction is that between:

- Verbal confabulations, spoken false memories are more common, and

- Behavioral confabulations, occur when an individual acts on their false memories.

WE is characterized by the presence of a triad of symptoms;

1. Ocular disturbances (ophthalmoplegia)

2. Changes in mental state (confusion)

3. Unsteady stance and gait (ataxia)

This triad of symptoms results from a deficiency in vitamin B which is an essential coenzyme. The aforementioned changes in mental state occur in approximately 82% of patients' symptoms of which range from confusion, apathy, inability to concentrate, and a decrease in awareness of the immediate situation they are in. If left untreated, WE can lead to coma or death. In about 29% of patients, ocular disturbances consist of nystagmus and paralysis of the lateral rectus muscles or other muscles in the eye. A smaller percentage of patients experience a decrease in reaction time of the pupils to light stimuli and swelling of the optic disc which may be accompanied by retinal hemorrhage. Finally, the symptoms involving stance and gait occur in about 23% of patients and result from dysfunction in the cerebellum and vestibular system. Other symptoms that have been present in cases of WE are stupor, low blood pressure (hypotension), elevated heart rate (tachycardia), as well as hypothermia, epileptic seizures and a progressive loss of hearing.

Interestingly, about 19% of patients have none of the symptoms in the classic triad at first diagnosis of WE; however, usually one or more of the symptoms develops later as the disease progresses.

People with WKS often show confabulation, spontaneous confabulation being seen more frequently than provoked confabulation. Spontaneous confabulations refer to incorrect memories that the patient holds to be true, and may act on, arising spontaneously without any provocation. Provoked confabulations can occur when a patient is cued to give a response, this may occur in test settings. The spontaneous confabulations viewed in WKS are thought to be produced by an impairment in source memory, where they are unable to remember the spatial and contextual information for an event, and thus may use irrelevant or old memory traces to fill in for the information that they cannot access. It has also been suggested that this behaviour may be due to executive dysfunction where they are unable to inhibit incorrect memories or because they are unable to shift their attention away from an incorrect response.

A person having an attack of TGA has almost no capacity to establish new memories, but generally appears otherwise mentally alert and lucid, possessing full knowledge of self-identity and identity of close family, and maintaining intact perceptual skills and a wide repertoire of complex learned behavior. The individual simply cannot recall anything that happened outside the last few minutes, while memory for more temporally distant events may or may not be largely intact. The degree of amnesia is profound, and, in the interval during which the individual is aware of his or her condition, is often accompanied by anxiety.

The diagnostic criteria for TGA, as defined for purposes of clinical research, include:

- The attack was witnessed by a capable observer and reported as being a definite loss of recent memory (anterograde amnesia).

- There was an absence of clouding of consciousness or other cognitive impairment other than amnesia.

- There were no focal neurological signs or deficits during or after the attack.

- There were no features of epilepsy, or active epilepsy in the past two years, and the patient did not have any recent head injury.

- The attack resolved within 24 hours.

Retrograde amnesia (RA) is a loss of memory-access to events that occurred, or information that was learned, before an injury or the onset of a disease. It tends to negatively affect episodic, autobiographical, and declarative memory while usually keeping procedural memory intact with no difficulty for learning new knowledge. RA can be temporally graded or more permanent based on the severity of its cause and is usually consistent with Ribot's Law: where subjects are more likely to lose memories closer to the traumatic incident than more remote memories. The type of information that is forgotten can be very specific, like a single event, or more general, resembling generic amnesia. It is not to be confused with anterograde amnesia, which deals with the inability to form new memories following the onset of an injury or disease.

Signs and symptoms of Fregoli's:

- delusions

- visual memory deficit

- deficit in self-monitoring

- deficit in self-awareness

- hallucinations

- deficit in executive functions

- deficit in cognitive flexibility

- history of seizure activity

- epileptogenic activity

The main symptom resulting from PCA is a decrease in visuospatial and visuoperceptual capabilities. Because the posterior region of the brain is home to the occipital lobe, which is responsible for visual processing, visual functions are impaired in PCA patients. The atrophy is progressive; early symptoms include difficulty reading, blurred vision, light sensitivity, issues with depth perception, and trouble navigating through space. Additional symptoms include apraxia, a disorder of movement planning, alexia, an impaired ability to read, and visual agnosia, an object recognition disorder. Damage to the ventral, or “what” stream, of the visual system, located in the temporal lobe, leads to the symptoms related to general vision and object recognition deficits; damage to the dorsal, or “where/how” stream, located in the parietal lobe, leads to PCA symptoms related to impaired movements in response to visual stimuli, such as navigation and apraxia.

As neurodegeneration spreads, more severe symptoms emerge, including the inability to recognize familiar people and objects, trouble navigating familiar places, and sometimes visual hallucinations. In addition, patients may experience difficulty making guiding movements towards objects, and may experience a decline in literacy skills including reading, writing, and spelling. Furthermore, if neural death spreads into other anterior cortical regions, symptoms similar to Alzheimer's disease, such as memory loss, may result. PCA patients with significant atrophy in one hemisphere of the brain may experience hemispatial neglect, the inability to see stimuli on one half of the visual field. Anxiety and depression are also common in PCA patients.

Fragmentation of memory is a memory disorder in when an individual is unable to associate the context of the memories to their autobiographical (episodic) memory. The explicit facts and details of the events may be known to the person (semantic memory). However, the facts of the events retrieve none of the effective and somatic elements of the experience. Therefore, the emotional and personal content of the memories can't be associated with the rest of the memory. Fragmentation of memory can occur for relatively recent events as well.

The impaired person usually suffers from physical damage to or underdevelopment of the hippocampus. This may be due to a genetic disorder or be the result of trauma, such as post-traumatic stress disorder. Brain dysfunction often has other related consequences, such as oversensitivity to some stimuli, impulsiveness, lack of direction in life, occasional aggressiveness, a distorted perception of oneself, and impaired ability to empathize with others, which is usually masked.

Confabulation is distinguished from lying as there is no intent to deceive and the person is unaware the information is false. Although individuals can present blatantly false information, confabulation can also seem to be coherent, internally consistent, and relatively normal.

Most known cases of confabulation are symptomatic of brain damage or dementias, such as aneurysm, Alzheimer's disease, or Wernicke–Korsakoff syndrome (a common manifestation of thiamine deficiency caused by alcoholism). Additionally confabulation often occurs in people who are suffering from anticholinergic toxidrome when interrogated about bizarre or irrational behaviour.

Confabulated memories of all types most often occur in autobiographical memory and are indicative of a complicated and intricate process that can be led astray at any point during encoding, storage, or recall of a memory. This type of confabulation is commonly seen in Korsakoff's syndrome.

This onset of TGA is generally fairly rapid, and its duration varies but generally lasts between 2 and 8 hours. A person experiencing TGA typically has memory only of the past few minutes or less, and cannot retain new information beyond that period of time. One of its bizarre features is perseveration, in which the victim of an attack faithfully and methodically repeats statements or questions, complete with profoundly identical intonation and gestures "as if a fragment of a sound track is being repeatedly rerun." This is found in almost all TGA attacks and is sometimes considered a defining characteristic of the condition. The individual experiencing TGA retains social skills and older significant memories, almost always including knowing his or her own identity and the identity of family members, and the ability to perform various complex learned tasks including driving and other learned behavior; one individual "was able to continue putting together the alternator of his car." Though outwardly appearing to be normal, a person with TGA is disoriented in time and space, perhaps knowing neither the year nor where they reside. Although confusion is sometimes reported, others consider this an imprecise observation, but an elevated emotional state (compared to patients experiencing Transient Ischemic Attack, or TIA) is common. In a large survey, 11% of individuals in a TGA state were described as exhibiting "emotionalism" and 14% "fear of dying". The attack lessens over a period of hours, with older memories returning first, and the repetitive fugue slowly lengthening so that the victim retains short-term memory for longer periods. While seemingly back to normal within 24 hours, there are subtle effects on memory that can persist longer. In the majority of cases there are no long-term effects other than a complete lack of recall for this period of the attack and an hour or two before its onset.

There is emerging evidence for observable impairments in a minority of cases weeks or even years following a TGA attack.

There is also evidence that the victim is aware that something is not quite right, even though they can't pinpoint it. Persons suffering from the attack may vocalize signs that 'they just lost their memory', or that they believed they had a stroke, although they aren't aware of the other signs that they are displaying. The main sign of this condition is the repetitive actions of something that is not usually repeated.

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

The severity of post-traumatic amnesia (PTA) is directly related to its duration, although a longer duration does not necessarily indicate more severe symptoms. The duration of PTA in brain-injured patients is a useful predictor of the expected long-term effects of the injury, along with the duration of loss of consciousness(LOC), and scores on the Glasgow Coma Scale (GCS), which measures degrees of consciousness, with higher scores indicating higher levels of functioning. A score of 3 indicates complete unconsciousness, and a score of 15 indicates normal functioning.

In patients experiencing PTA for the duration of:

Up to 1 hour – The injury is very mild in severity and full recovery is expected. The patient may experience a few minor post-concussive symptoms (e.g. headaches, dizziness).

1 – 24 hours – The injury is moderate in severity and full recovery is expected. The patient may experience some minor post-concussive symptoms (e.g. headaches, dizziness).

1 – 7 days – The injury is severe, and recovery may take weeks to months. The patient may be able to return to work, but may be less capable than before the injury.

1 – 2 weeks – The injury is very severe, and recovery is likely to take many months. The patient is likely to experience long-lasting cognitive effects such as decreased verbal and non-verbal intelligence as well as decreased performance on visual tests. Patients should, however, still be able to return to work.

2 – 12 weeks – The injury is very severe, and recovery is likely to take a year or more. The patient is likely to exhibit permanent deficits in memory and cognitive function, and the patient is unlikely to be able to return to work.

12+ weeks – injury is very severe and accompanied by significant disabilities that will require long-term rehabilitation and management. The patient is unlikely to be able to return to work.

Note: return to work is meant to indicate a return to a reasonable level of functionality, both in professional and personal arenas.

The long-term prognosis of PTA is generally positive. Many patients do recover a great deal of cognitive function, although they may not return to their pre-injury state.

Psychoorganic syndrome (POS) is a progressive disease comparable to presenile dementia. It consists of psychopathological complex of symptoms that are caused by organic brain disorders that involve a reduction in memory and intellect. Psychoorganic syndrome is often accompanied by asthenia.

Psychoorganic syndrome occurs during atrophy of the brain, most commonly during presenile and senile age (e.g. Alzheimer's disease, senile dementia). There are many causes, including cerebrovascular diseases, CNS damages to traumatic brain injury, intoxication, exposure to organic solvents such as toluene, chronic metabolic disorders, tumors and abscesses of the brain, encephalitis, and can also be found in cases of diseases accompanied by convulsive seizures. Psychoorganic syndrome may occur at any age but is most pronounced in elderly and senile age.

Depending on the nosological entity, the main symptoms of psychoorganic syndrome are expressed differently. For example, in atrophic cases such as Alzheimer's disease, the symptoms are more geared towards a memory disorder, while in Pick 's disease, mental disorders are more commonly expressed.

The Fregoli delusion, or the delusion of doubles, is a rare disorder in which a person holds a delusional belief that different people are in fact a single person who changes appearance or is in disguise. The syndrome may be related to a brain lesion and is often of a paranoid nature, with the delusional person believing themselves persecuted by the person they believe is in disguise.

A person with the Fregoli delusion can also inaccurately recall places, objects, and events. This disorder can be explained by "associative nodes". The associative nodes serve as a biological link of information about other people with a particular familiar face (to the patient). This means that for any face that is similar to a recognizable face to the patient, the patient will recall that face as the person they know.

The Fregoli delusion is classed both as a monothematic delusion, since it only encompasses one delusional topic, and as a delusional misidentification syndrome (DMS), a class of delusional beliefs that involves misidentifying people, places, or objects. Like Capgras delusion, psychiatrists believe it is related to a breakdown in normal face perception.

Witzelsucht (from the German "witzeln", meaning to joke or wisecrack, and "sucht", meaning addiction or yearning) is a set of rare neurological symptoms characterized by a tendency to make puns, or tell inappropriate jokes or pointless stories in socially inappropriate situations. A less common symptom is hypersexuality, the tendency to make sexual comments at inappropriate times or situations. Patients do not understand that their behavior is abnormal, therefore are nonresponsive to others' reactions. This disorder is most commonly seen in patients with frontal lobe damage, particularly right frontal lobe tumors or trauma. The disorder remains named in accordance with its reviewed definition by German neurologist Hermann Oppenheim; its first description as the less focused "Moria" ("stupidity"), by German neurologist Moritz Jastrowitz, was in 1888.

Due to similarity of symptoms of the disorder to the mannerisms of Batman's arch-rival Joker, it is sometimes known as 'The Joker Syndrome'

Hyperthymesia is the condition of possessing an extremely detailed autobiographical memory. People with hyperthymesia remember an abnormally vast number of their life experiences.

American neurobiologists Elizabeth Parker, Larry Cahill, and James McGaugh (2006) identified two defining characteristics of hyperthymesia: spending an excessive amount of time thinking about one's past, and displaying an extraordinary ability to recall specific events from one's past. The word "hyperthymesia" derives from Ancient Greek: "hyper-" ("excessive") and "thymesis" ("remembering").

There are seven major symptoms of Korsakoff's syndrome (amnestic-confabulatory syndrome):

1. anterograde amnesia, memory loss for events after the onset of the syndrome

2. retrograde amnesia, memory loss extends back for some time before the onset of the syndrome

3. amnesia of fixation, also known as fixation amnesia (loss of immediate memory, a person being unable to remember events of the past few minutes)

4. confabulation, that is, invented memories which are then taken by the patient as true due to gaps in memory, with such gaps sometimes associated with blackouts

5. minimal content in conversation

6. lack of insight

7. apathy – the patients lose interest in things quickly, and generally appear indifferent to change.

Benon R. and LeHuché R. (1920) described the characteristic signs of Korsakoff syndrome with some additional features: confabulation (false memories), fixation amnesia, paragnosia or false recognition of places, mental excitation, euphoria, etc.

Thiamine is essential for the decarboxylation of pyruvate, and deficiency during this metabolic process is thought to cause damage to the medial thalamus and mammillary bodies of the posterior hypothalamus, as well as generalized cerebral atrophy. These brain regions are all parts of the limbic system, which is heavily involved in emotion and memory.

Korsakoff's involves neuronal loss, that is, damage to neurons; gliosis, which is a result of damage to supporting cells of the central nervous system, and hemorrhage or bleeding also occurs in mammillary bodies. Damage to the dorsomedial nucleus or anterior group of the thalamus (limbic-specific nuclei) is also associated with this disorder. Cortical dysfunction may have arisen from thiamine deficiency, alcohol neurotoxicity, and/or structural damage in the diencephalon.

Originally, it was thought that a lack of initiative and a flat affect were important characteristics of emotional presentation in sufferers. Studies have questioned this, proposing that neither is necessarily a symptom of Korsakoff's. Research suggesting that Korsakoff's patients are emotionally unimpaired has made this a controversial topic. It can be argued that apathy, which usually characterizes Korsakoff's patients, reflects a deficit of emotional "expressions", without affecting the "experience" or perception of emotion.

Korsakoff's Syndrome causes deficits in declarative memory in most patients, but leaves implicit spatial, verbal, and procedural memory functioning intact. People who have Korsakoff's syndrome have deficits in the processing of contextual information. Context memories refers to the where and when of experiences, and is an essential part of recollection. The ability to store and retrieve this information, such as spatial location or temporal order information, is impaired.

Research has also suggested that Korsakoff patients have impaired executive functions, which can lead to behavioral problems and interfere with daily activities. It is unclear, however, which executive functions are affected most. Nonetheless, IQ is usually not affected by the brain damage associated with Korsakoff's syndrome.

At first it was thought that Korsakoff's patients used confabulation to fill in memory gaps. However, it has been found that confabulation and amnesia do not necessarily co-occur. Studies have shown that there is dissociation between provoked confabulation, spontaneous confabulation (which is unprovoked), and false memories. That is, patients could be led to believe certain things had happened which actually had not, but so could people without Korsakoff’s syndrome.

Amnesia is a deficit in memory caused by brain damage, disease, or psychological trauma. Amnesia can also be caused temporarily by the use of various sedatives and hypnotic drugs. The memory can be either wholly or partially lost due to the extent of damage that was caused. There are two main types of amnesia: retrograde amnesia and anterograde amnesia. Retrograde amnesia is the inability to retrieve information that was acquired before a particular date, usually the date of an accident or operation. In some cases the memory loss can extend back decades, while in others the person may lose only a few months of memory. Anterograde amnesia is the inability to transfer new information from the short-term store into the long-term store. People with this type of amnesia cannot remember things for long periods of time. These two types are not mutually exclusive; both can occur simultaneously.

Case studies also show that amnesia is typically associated with damage to the medial temporal lobe. In addition, specific areas of the hippocampus (the CA1 region) are involved with memory. Research has also shown that when areas of the diencephalon are damaged, amnesia can occur. Recent studies have shown a correlation between deficiency of RbAp48 protein and memory loss. Scientists were able to find that mice with damaged memory have a lower level of RbAp48 protein compared to normal, healthy mice. In people suffering with amnesia, the ability to recall "immediate information" is still retained, and they may still be able to form new memories. However, a severe reduction in the ability to learn new material and retrieve old information can be observed. Patients can learn new procedural knowledge. In addition, priming (both perceptual and conceptual) can assist amnesiacs in the learning of fresh non-declarative knowledge. Amnesic patients also retain substantial intellectual, linguistic, and social skill despite profound impairments in the ability to recall specific information encountered in prior learning episodes. The term is ; .

The signs and symptoms of frontal lobe disorder can be indicated by Dysexecutive syndrome which consists of a number of symptoms which tend to occur together. Broadly speaking, these symptoms fall into three main categories; cognitive (movement and speech), emotional or behavioural. Although many of these symptoms regularly co-occur, it is common to encounter patients who have several, but not all of these symptoms. This is one reason why some researchers are beginning to argue that dysexecutive syndrome is not the best term to describe these various symptoms. The fact that many of the dysexecutive syndrome symptoms can occur alone has led some researchers to suggest that the symptoms should not be labelled as a "syndrome" as such. Some of the latest imaging research on frontal cortex areas suggests that executive functions may be more discrete than was previously thought.

Signs/symptoms can be divided as follows: