Mind-blindness is a cognitive disorder where an individual is unable to attribute mental states to others. As a result of this kind of social and empathetic cognitive deficit, the individual is incapable in putting himself "into someone else's shoes" and cannot conceptualize, understand or predict knowledge, thoughts and beliefs, emotions, feelings and desires, behaviour, actions and intentions of another person. Such an ability to develop a mental awareness of what is in the other minds is known as the theory of mind (ToM), and the "Mind-blindness" Theory asserts that children who delay in this development often are or will be autistic and Asperger's syndrome (AS) patients. In addition to autism and AS, ToM and mind-blindness research has recently been extended to other disorders such as schizophrenia, dementia, bipolar disorders, antisocial personality disorders as well as normal aging.

Mind-blindness is a state where the ToM has not been developed or lost in an individual. The ToM is implicit in neurotypical individuals. This enables one to make automatic interpretations of events taking into consideration the mental states of people, their desires and beliefs. Simon Baron-Cohen described an individual lacking a ToM would perceive the world in a confusing and frightening manner; leading to a withdrawal from society.

An alternative approach to the social impairment observed in mind-blindness focuses on emotion of subjects. Based on empirical evidence, Uta Frith concluded that the processing of complex cognitive emotions is impaired compared to simpler emotions. In addition, attachment does not seem to fail in the early childhood of autistics. This suggests that emotion is a component of social cognition that is separable from mentalizing.

Lombardo and Cohen updated the theory and pinpointed some additional factors that play an important part in ToM of autistic patients. They highlighted that the middle cingulated cortex which is outside the traditional mentalizing region was underactive in autistic patients, while the rest of ToM activation was normal. This region was important in deciding how much to invest in a person and hence required mentalization.

Treatment of OBS varies with the causative disorder or disease. It is important to note that it is not a primary diagnosis and a cause needs to be sought out and treated.

Reduced affect display, sometimes referred to as emotional blunting, is a condition of reduced emotional reactivity in an individual. It manifests as a failure to express feelings (affect display) either verbally or non-verbally, especially when talking about issues that would normally be expected to engage the emotions. Expressive gestures are rare and there is little animation in facial expression or vocal inflection. Reduced affect can be symptomatic of autism, schizophrenia, depression, posttraumatic stress disorder, depersonalization disorder, schizoid personality disorder or brain damage. It may also be a side effect of certain medications (e.g., antipsychotics and antidepressants). Individuals with blunted or flat affect show different regional brain activity when compared with typical individuals.

Reduced affect should be distinguished from apathy, which explicitly refers to a lack of emotion, whereas reduced affect is a lack of emotional expression regardless of whether emotion is actually reduced or not.

A restricted or constricted affect is a reduction in an individual's expressive range and the intensity of emotional responses.

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.

The Faux Pas test measures how socially adept one is in certain situations. For this test, a faux pas is considered a statement or action that accidentally offends another person. During the test, the subject or patient is told of various social situations and later asked if one of the people in the story would be offended in the situation. A person with impaired social skills would have difficulty in detecting the faux pas made by characters in the stories.

An organic brain syndrome (OBS), also known as an organic brain disease/disorder (OBD), an organic mental syndrome (OMS), or an organic mental disorder (OMD), is a syndrome or disorder of mental function whose cause is alleged to be known as organic (physiologic) rather than purely of the mind. These names are older and nearly obsolete general terms from psychiatry, referring to many physical disorders that cause impaired mental function. They are meant to exclude psychiatric disorders (mental disorders). Originally, the term was created to distinguish physical (termed "organic") causes of mental impairment from psychiatric (termed "functional") disorders, but during the era when this distinction was drawn, not enough was known about brain science (including neuroscience, cognitive science, neuropsychology, and mind-brain correlation) for this cause-based classification to be more than educated guesswork labeled with misplaced certainty, which is why it has been deemphasized in current medicine.

"Acute" organic brain syndrome is (by definition) a recently appearing state of mental impairment, as a result of intoxication, drug overdose, infection, pain, and many other physical problems affecting mental status. In medical contexts, "acute" means "of recent onset". As is the case with most acute disease problems, acute organic brain syndrome is often temporary, although this does not guarantee that it will not recur (happen again) or progress to become chronic, that is, long-term. A more specific medical term for the "acute" subset of organic brain syndromes is delirium.

"Chronic" organic brain syndrome is long-term. For example, some forms of chronic drug or alcohol dependence can cause organic brain syndrome due to their long-lasting or permanent toxic effects on brain function. Other common causes of chronic organic brain syndrome sometimes listed are the various types of dementia, which result from permanent brain damage due to strokes, Alzheimer's disease, or other damaging causes which are not reversible.

Though OBS was once a common diagnosis in the elderly, until the understanding of the various types of dementias it is related to a disease process and is not an inevitable part of aging. In some of the older literature, there was an attempt to separate organic brain syndrome from dementia, but this was related to an older world view in which dementia was thought to be a part of normal aging, and thus did not represent a special disease process. The later identification of various dementias as clear pathologies is an example of the types of pathological problems discovered to be associated with mental states, and is one of the areas which led to abandonment of all further attempts to clearly define and use OBS as a term.

Developmental regression is when a child loses an acquired function or fails to progress beyond a prolonged plateau after a period of relatively normal development. Developmental regression could be due to metabolic disorders, progressive hydrocephalus, worsening of seizures, increased spasticity, worsening of movement disorders or parental misconception of acquired milestones. The timing of onset of developmental regression can be established by repeated medical evaluations, prior photographs and home movies. Whether the neurologic decline is predominantly affecting the gray matter or the white matter of the brain needs to be ascertained. Seizures or EEG changes, movement disorders, blindness with retinal changes, personality changes and dementia are features suggestive of grey matter involvement.

An idée fixe is a preoccupation of mind believed to be firmly resistant to any attempt to modify it, a fixation. The name originates from the French "idée", "idea" and "fixe", "fixed."

Thought blocking (also known as ), a phenomenon that occurs in people with psychiatric illnesses (usually schizophrenia), occurs when a person's speech is suddenly interrupted by silences that may last a few seconds to a minute or longer. When the person begins speaking again, after the block, they will often speak about a subject unrelated to what was being discussed when blocking occurred. It is described as being experienced as an unanticipated, quick and total emptying of the mind. People with schizophrenia commonly experience thought blocking and may comprehend the experience in peculiar ways. For example a person with schizophrenia might remark that another person has removed their thoughts from their brain.

When doctors diagnose thought blocking, it is important that they consider other causes of pauses in speech and expression, such as petit mal seizures, aphasia, hesitation brought on by anxiety, or slow thought processes. When looking for schizophrenia they may look for thought blocking. It is a common issue with schizophrenia patients.

Most of the treatments for thought insertion are not specific to the symptom, but rather the symptom is treated through treatment of the psychopathology that causes it. However, one case report considers a way to manage thought insertion through performing thoughts as motor actions of speech. In other words, the patient would speak his thoughts out loud in order to re-give himself the feeling of agency as he could hear himself speaking and then contributing the thought to himself.

Anton–Babinski syndrome, also known as visual anosognosia, is a rare symptom of brain damage occurring in the occipital lobe. Those who suffer from it are "cortically blind", but affirm, often quite adamantly and in the face of clear evidence of their blindness, that they are capable of seeing. Failing to accept being blind, the sufferer dismisses evidence of their condition and employs confabulation to fill in the missing sensory input. It is named after Gabriel Anton and Joseph Babinski.

Why patients with Anton–Babinski syndrome deny their blindness is unknown, although there are many theories. One hypothesis is that damage to the visual cortex results in the inability to communicate with the speech-language areas of the brain. Visual imagery is received but cannot be interpreted; the speech centers of the brain confabulate a response.

This is often seen in immunosuppressed patients with JC virus. Specifically, patients being treated with natalizumab—a monoclonal antibody currently used as a staple in treatment for multiple sclerosis—are quickly becoming classical examples of Anton–Babinski syndrome.

Patients have also reported visual anosognosia after suffering from ischemic vascular cerebral disease. A 96-year-old man, who was admitted to an emergency room complaining of a severe headache and sudden loss of vision, was discovered to have suffered from a posterior cerebral artery thrombosis and consequently lost his vision. He adamantly claimed he was able to see despite an ophthalmologic exam proving otherwise. An MRI of his brain proved that his right occipital lobe was ischemic. Similarly, a 56-year-old woman was admitted to the emergency room in a confused state and with severely handicapped psychomotor skills. Ocular movements and pupil reflexes were still intact, but the patient could not name objects and was not aware of light changes in the room, and seemed unaware of her visual deficit.

Thought insertion is defined by the ICD-10 as feeling as if one's thoughts are not one's own, but rather belong to someone else and have been inserted into one's mind. The person experiencing thought insertion will not necessarily know where the thought is coming from, but is able to distinguish between their own thoughts and those inserted into their minds. However, patients do not experience all thoughts as inserted, only certain ones, normally following a similar content or pattern. This phenomenon is classified as a delusion. A person with this delusional belief is convinced of the veracity of their beliefs and is unwilling to accept such diagnosis.

Thought insertion is a common symptom of psychosis and occurs in many mental disorders and other medical conditions. However, thought insertion is most commonly associated with schizophrenia. Thought insertion, along with thought broadcasting, thought withdrawal, thought blocking and other first rank symptoms, is a primary symptom and should not be confused with the delusional explanation given by the respondent. Although normally associated with some form of psychopathology, thought insertion can also be experienced in those considered nonpathological, usually in spiritual contexts, but also in culturally influenced practices such as mediumship and automatic writing.

Examples of thought insertion:

"She said that sometimes it seemed to be her own thought 'but I don't get the feeling that it is'. She said her 'own thoughts might say the same thing', 'but the feeling isn't the same', 'the feeling is that it is somebody else's'"

"I look out the window and I think that the garden looks nice and the grass looks cool, but the thoughts of Eamonn Andrews come into my mind. There are no other thoughts there, only his. He treats my mind like a screen and flashes thoughts onto it like you flash a picture"

"The subject has thoughts that she thinks are the thoughts of other people, somehow occurring in her own mind. It is not that the subject thinks that other people are making her think certain thoughts as if by hypnosis or psychokinesis, but that other people think the thoughts using the subject's mind as a psychological medium."

Solipsism syndrome refers to a psychological state in which a person feels that the world is not external to his or her mind. Periods of extended isolation may predispose people to this condition. In particular, the syndrome has been identified as a potential concern for individuals living in outer space for extended periods of time.

Aphantasia is the suggested name for a condition where one does not possess a functioning mind's eye and cannot visualize imagery. The phenomenon was first described by Francis Galton in 1880, but has remained largely unstudied since. Interest in the phenomenon renewed after the publication of a study conducted by a team led by Prof. Adam Zeman of the University of Exeter, which also coined the term "aphantasia". Research on the subject is still scarce, but further studies are planned.

Diagnosis is not very advanced and is based on the telltale nodding seizures of the victims. When stunted growth and mental disability are also present, probability of nodding syndrome is high. In the future, neurological scans may also be used in diagnosis. As there is no known cure for the disease, treatment has been directed at symptoms, and has included the use of anticonvulsants such as sodium valproate and phenobarbitol. Anti-malaria drugs have also been administered, to unknown effect.

Apotemnophia / Body Integrity Disorder (BIID) is a is a rare, infrequently studied and highly secretive condition in which there is a mismatch between the mental body image and the physical body. Apotemnomphilia is characterized by an intense desire for amputation of a limb. Currently BIID is not included in the International Statistical Classification of Diseases 11 or the Diagnostic and Statistical Manual of Mental Disorders IV. It is often not known to surgeons, neurologists and psychiatrists. BIID individuals typically avoid healthcare and often act out their desires by pretending they are disabled or perform actual self-amputation.

A 2012 study concluded, based on interviews with 54 individuals, that the main rationale for their desire for body modification (amputation) was to feel complete or to feel satisfied inside. Based on the results of the survey, researchers concluded that psychotherapy was often supportive, but did not help diminishing BIID symptoms. Individuals reported that antidepressants were helpful in reducing depressive symptoms related to BIID, but that antipsychotics were not. Actual amputation of the limb was effective in all 7 cases who had surgical treatment.

Individuals experiencing solipsism syndrome feel that the world is not 'real' in the sense of being external to their own minds. The syndrome is characterized by feelings of loneliness, detachment and indifference to the outside world. Solipsism syndrome is not currently recognized as a psychiatric disorder by the American Psychiatric Association, though it shares similarities with depersonalization disorder, which is recognized. Solipsism syndrome is distinct from solipsism, which is not a psychological state but rather a philosophical position, namely that nothing exists or can be known to exist outside of one's own mind; advocates of this philosophy do not necessarily suffer from solipsism syndrome, and sufferers do not necessarily subscribe to solipsism as a school of intellectual thought.

Periods of extended isolation may predispose people to solipsism syndrome. In particular, the syndrome has been identified as a potential challenge for astronauts and cosmonauts on long-term missions,

and these concerns influence the design of artificial habitats.

In psychiatry, thought withdrawal is the delusional belief that thoughts have been 'taken out' of the patient's mind, and the patient has no power over this. It often accompanies thought blocking. The patient may experience a break in the flow of their thoughts, believing that the missing thoughts have been withdrawn from their mind by some outside agency. This delusion is one of Schneider's first rank symptoms for schizophrenia. Because thought withdrawal is characterized as a delusion, according to the DSM-IV TR it represents a positive symptom of schizophrenia.

Aphantasia is similar to invisible disabilities such as face blindness, word blindness, and tone deafness, though aphantasia itself has not been associated with any functional deficits.

The prognosis of ICOE-G is unclear, although available data indicate that remission occurs in 50–60% of patients within 2–4 years of onset. Seizures show a dramatically good response to carbamazepine in more than 90% of patients. However, 40–50% of patients may continue to have visual seizures and infrequent secondarily generalized convulsions, particularly if they have not been appropriately treated with antiepileptic drugs.

The differential diagnosis of ICOE-G is mainly from symptomatic occipital epilepsy and migraine where misdiagnosis is high. The differential diagnosis from migraine should be easy because elementary visual hallucinations of occipital seizures develop rapidly within seconds, are brief in duration (2–3 minutes) are usually colored and circular. These are fundamentally different from the visual aura of migraine which develops slowly in minutes, is longer lasting ≥5 minutes and mainly achromatic with linear patterns.

Symptomatic occipital epilepsy often imitates ICOE-G; neuroophthalmological examination and brain imaging may be normal. Thus, high resolution MRI is required to detect subtle lesions.

The differentiation of ICOE-G from Panayiotopoulos syndrome is straightforward. The seizures of ICOE-G are purely occipital, brief, frequent and diurnal. Conversely seizures in Panayiotopoulos syndrome manifest with autonomic manifestations, they are lengthy and infrequent; visual symptoms are rare and not the sole manifestation of a seizure.

The prognosis of a patient with acquired cortical blindness depends largely on the original cause of the blindness. For instance, patients with bilateral occipital lesions have a much lower chance of recovering vision than patients who suffered a transient ischemic attack or women who experienced complications associated with eclampsia. In patients with acquired cortical blindness, a permanent complete loss of vision is rare. The development of cortical blindness into the milder cortical visual impairment is a more likely outcome. Furthermore, some patients regain vision completely, as is the case with transient cortical blindness associated with eclampsia and the side effects of certain anti-epilepsy drugs.

Recent research by Krystel R. Huxlin and others on the relearning of complex visual motion following V1 damage has offered potentially promising treatments for individuals with acquired cortical blindness. These treatments focus on retraining and retuning certain intact pathways of the visual cortex which are more or less preserved in individuals who sustained damage to V1. Huxlin and others found that specific training focused on utilizing the "blind field" of individuals who had sustained V1 damage improved the patients' ability to perceive simple and complex visual motion. This sort of 'relearning' therapy may provide a good workaround for patients with acquired cortical blindness in order to better make sense of the visual environment.