Older people with cognitive impairment appear to improve somewhat with light therapy.

Cognitive deficit or cognitive impairment is an inclusive term to describe any characteristic that acts as a barrier to the cognition process.

The term may describe

- deficits in overall intelligence (as with intellectual disabilities),

- specific and restricted deficits in cognitive abilities (such as in learning disorders like dyslexia),

- neuropsychological deficits (such as in attention, working memory or executive function),

- or it may describe drug-induced impairment in cognition and memory (such as that seen with alcohol, glucocorticoids, and the benzodiazepines.)

It usually refers to a durable characteristic, as opposed to altered level of consciousness, which may be acute and reversible. Cognitive deficits may be inborn or caused by environmental factors such as brain injuries, neurological disorders, or mental illness.

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

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

Symptoms of DES fall into three broad categories: cognitive, emotional and behavioural. Many of the symptoms can be seen as a direct result of impairment to the central executive component of working memory, which is responsible for attentional control and inhibition. Although many of the symptoms regularly co-occur, it is common to encounter patients who have several, but not all symptoms. The accumulated effects of the symptoms have a large impact on daily life.

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

Cognitive symptoms refer to a person's ability to process thoughts. Cognition primarily refers to memory, the ability to learn new information, speech, and reading comprehension. Deficits within this area cause many problems with every day life decisions.

One of the main difficulties for an individual with DES is planning and reasoning. Impaired planning and reasoning affect the individual's ability to realistically assess and manage the problems of every day living. New problems and situations may be especially poorly handled because of the inability to transfer previous knowledge to the new event. An individual that has DES may have a short attention span due to impairment in attentional control. This may alter the individual's ability to focus, and as such have difficulty with reading and following a storyline or conversation. For instance, they can easily lose track of conversations which can make it difficult to hold a meaningful conversation and may result in avoiding social interactions.

Individuals with DES will have very poor working memory and short term memory due to executive dysfunction. The dysfunction can range from mild and subtle to severe and obvious. There is a tremendous variability in the manifestations of executive dysfunction with strong influences often apparent from the afflicted person's personality, life experiences and intellect. Individuals with DES may suffer from confabulation, which is the spontaneous reporting of events that never happened. This can affect their autobiographical memory. It is thought that patients may not be able to assess the accuracy of memory retrieval and therefore elaborate on implausible memories.

Individuals with dementia, delirium or other severe psychiatric illnesses combined with DES often have disturbed sleep patterns. Some will not recognize that it is night-time and may become upset when someone tries to correct them.

In psychology and neuroscience, executive dysfunction, or executive function deficit, is a disruption to the efficacy of the executive functions, which is a group of cognitive processes that regulate, control, and manage other cognitive processes. Executive dysfunction can refer to both neurocognitive deficits and behavioural symptoms. It is implicated in numerous psychopathologies and mental disorders, as well as short-term and long-term changes in non-clinical executive control.

Executive dysfunction is not the same as dysexecutive syndrome, a term coined by Alan Baddeley to describe a common pattern of dysfunction in executive functions, such as deficiencies in planning, abstract thinking, flexibility and behavioural control. This group of symptoms, usually resulting from brain damage, tend to occur together. However, the existence of dysexecutive syndrome is controversial.

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

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

Cognitive symptoms from steroids appear within the first few weeks of treatment, appear to be dose dependent, and may or may not be accompanied by steroid psychosis or other Cushing's-type symptoms.

The symptoms include deficits in

- verbal and non-verbal memory

- working memory

- attention

- sustained concentration

- executive function

- psychomotor speed

- academic or occupational performance.

These symptoms have been shown to improve within months to a year after discontinuing glucocorticoid medication, but residual impairments following prolonged steroid use can remain.

Perseveration according to psychology, psychiatry, and speech-language pathology, is the repetition of a particular response (such as a word, phrase, or gesture) regardless of the absence or cessation of a stimulus. It is usually caused by a brain injury or other organic disorder. Symptoms include "lacking ability to transition or switch ideas appropriately with the social context, as evidenced by the repetition of words or gestures after they have ceased to be socially relevant or appropriate", or the "act or task of doing so", and are not better described as stereotypy (a highly repetitive idiosyncratic behaviour).

In a broader sense, it is used for a wide range of functionless behaviours that arise from a failure of the brain to either inhibit prepotent responses or to allow its usual progress to a different behavior, and includes impairment in set shifting and task switching in social and other contexts.

The primary definition of perseveration in biology and clinical psychiatry involves some form of response repetition or the inability to undertake set shifting (changing of goals, tasks or activities) as required, and is usually evidenced by behaviours such as words and gestures continuing to be repeated despite absence or cessation of a stimulus.

More broadly in clinical psychology, it describes mental or physical behaviours which are not excessive in terms of quantity but are apparently both functionless and involve a narrow range of behaviours, and are not better described as stereotypy (a highly repetitive idiosyncratic behaviour).

In general English, perseveration (vb: "to perseverate") refers to insistent or redundant repetition, not necessarily in a clinical context.

Although largely used to describe unawareness of impairment after brain injury or stroke, the term 'anosognosia' is occasionally used to describe the lack of insight shown by some people with anorexia nervosa. They do not seem to recognize that they have a mental illness. There is evidence that 'anosognosia' related to schizophrenia may be the result of frontal lobe damage. E. Fuller Torrey, a psychiatrist and schizophrenia researcher, has stated that among those with schizophrenia and bipolar disorder, anosognosia is the most prevalent reason for not taking medications.

A few possible explanations for anosodiaphoria exist:

1. The patient is aware of the deficit but does not fully comprehend it or its significance for functioning

2. May be related to an affective communication disorder and defective arousal. These emotional disorders cannot account for the verbal explicit denial of illness of anosognosia.

Other explanations include reduced emotional experience, impaired emotional communication, alexithymia, behavioral abnormalities, dysexecutive syndrome, and the frontal lobes.

Anosognosia (, ; from Ancient Greek ἀ- "a-", "without", νόσος "nosos", "disease" and γνῶσις "gnōsis", "knowledge") is a deficit of self-awareness, a condition in which a person with some disability seems unaware of its existence. It was first named by the neurologist Joseph Babinski in 1914. Anosognosia results from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere, and is thus a neurological disorder. While this distinguishes the condition from denial, which is a psychological defense mechanism, attempts have been made at a unified explanation. Anosognosia is sometimes accompanied by asomatognosia, a form of neglect in which patients deny ownership of their limbs.

Aboulia has been known to clinicians since 1838. However, in the time since its inception, the definition of aboulia has been subjected to many different forms, some contradictory. Aboulia has been described as a loss of drive, expression, loss of behavior and speech output, slowing and prolonged speech latency, and reduction of spontaneous thought content and initiative. The clinical features most commonly associated with aboulia are:

- Difficulty in initiating and sustaining purposeful movements

- Lack of spontaneous movement

- Reduced spontaneous speech

- Increased response-time to queries

- Passivity

- Reduced emotional responsiveness and spontaneity

- Reduced social interactions

- Reduced interest in usual pastimes

Especially in patients with progressive dementia, it may affect feeding. Patients may continue to chew or hold food in their mouths for hours without swallowing it. The behavior may be most evident after these patients have eaten part of their meals and no longer have strong appetites.

Aboulia or abulia (from , meaning "will", with the prefix -a), in neurology, refers to a lack of will or initiative and can be seen as a disorder of diminished motivation (DDM). Aboulia falls in the middle of the spectrum of diminished motivation, with apathy being less extreme and akinetic mutism being more extreme than aboulia. A patient with aboulia is unable to act or make decisions independently. It may range in severity from subtle to overwhelming. It is also known as Blocq's disease (which also refers to abasia and astasia-abasia). Aboulia was originally considered to be a disorder of the will.

Perseveration of thought indicates an inability to switch ideas or responses. An example of perseveration is, during a conversation, if an issue has been fully explored and discussed to a point of resolution, it is not uncommon for something to trigger the reinvestigation of the matter. This can happen at any time during a conversation.

Physical brain injury, trauma or damage

- Perseveration is particularly common with those who have had traumatic brain injury.

- Perseveration is sometimes a feature of frontal lobe lesions, and of other conditions involving dysfunction or dysregulation within the frontal lobe. This is especially true when the lateral orbitofrontal cortex or inferior prefrontal convexity (Brodmann areas 47/12) are affected.

- Perseveration is also sometimes seen as a symptom of aphasia.

Other neurological conditions

- Perseveration may also refer to the obsessive and highly selective interests of individuals on the autism spectrum. This term is most connected to Asperger syndrome.

- In attention deficit hyperactivity disorder (ADHD), perseveration or "hyperfocus" commonly occurs as an impairment of set shifting and task switching. The resistance to transition may be a coping mechanism or the brain's method to compensate for the lack of ability to regulate the application of attention.

- In people who are both intellectually gifted and suffer a learning disability, the state of hyperfocus and flow can be confounded with perseverance.

- Apart from their direct symptoms, people with obsessive–compulsive disorder can have specific problems with set shifting and inhibition of prepotent responses.

Confounds (conditions with similar appearing symptoms)

- Perseveration may be confused with habitual behaviours in a number of other conditions and disorders, such as obsessive–compulsive disorder, including post-traumatic stress disorder (PTSD), body dysmorphic disorder, trichotillomania, and habit problems. However, in animal experiments it can be shown when repetitive behaviour is a cognitive perseveration rather than a motor disorder. For example, under low doses of amphetamine an animal will perseverate in maintaining an arbitrary object preference even when different motor responses are required to maintain that preference.

Unproven:

- Several researchers have tried to connect perseveration with a lack of memory inhibition (the person repeats the answer because they have not been able to forget a past question and move on to the current subject); however, this connection could not be found, or was small.

Symptoms of OBS vary with the disease that is responsible. However, the more common symptoms of OBS are confusion; impairment of memory, judgment, and intellectual function; and agitation. Often these symptoms are attributed to psychiatric illness, which causes a difficulty in diagnosis.

Neurological disorders can be categorized according to the primary location affected, the primary type of dysfunction involved, or the primary type of cause. The broadest division is between central nervous system disorders and peripheral nervous system disorders. The Merck Manual lists brain, spinal cord and nerve disorders in the following overlapping categories:

- Brain:

- Brain damage according to cerebral lobe "(see also 'lower' brain areas such as basal ganglia, cerebellum, brainstem)":

- Frontal lobe damage

- Parietal lobe damage

- Temporal lobe damage

- Occipital lobe damage

- Brain dysfunction according to type:

- Aphasia (language)

- Dysgraphia (writing)

- Dysarthria (speech)

- Apraxia (patterns or sequences of movements)

- Agnosia (identifying things or people)

- Amnesia (memory)

- Spinal cord disorders (see spinal pathology, injury, inflammation)

- Peripheral neuropathy and other Peripheral nervous system disorders

- Cranial nerve disorder such as Trigeminal neuralgia

- Autonomic nervous system disorders such as dysautonomia, Multiple System Atrophy

- Seizure disorders such as epilepsy

- Movement disorders of the central and peripheral nervous system such as Parkinson's disease, Essential tremor, Amyotrophic lateral sclerosis, Tourette's Syndrome, Multiple Sclerosis and various types of Peripheral Neuropathy

- Sleep disorders such as Narcolepsy

- Migraines and other types of Headache such as Cluster Headache and Tension Headache

- Lower back and neck pain (see Back pain)

- Central neuropathy (see Neuropathic pain)

- Neuropsychiatric illnesses (diseases and/or disorders with psychiatric features associated with known nervous system injury, underdevelopment, biochemical, anatomical, or electrical malfunction, and/or disease pathology e.g. Attention deficit hyperactivity disorder, Autism, Tourette's syndrome and some cases of obsessive compulsive disorder as well as the neurobehavioral associated symptoms of degeneratives of the nervous system such as Parkinson's disease, essential tremor, Huntington's disease, Alzheimer's disease, multiple sclerosis and organic psychosis.)

Many of the diseases and disorders listed above have neurosurgical treatments available (e.g. Tourette's Syndrome, Parkinson's disease, Essential tremor and Obsessive compulsive disorder).

- Delirium and dementia such as Alzheimer's disease

- Dizziness and vertigo

- Stupor and coma

- Head injury

- Stroke (CVA, cerebrovascular attack)

- Tumors of the nervous system (e.g. cancer)

- Multiple sclerosis and other demyelinating diseases

- Infections of the brain or spinal cord (including meningitis)

- Prion diseases (a type of infectious agent)

- Complex regional pain syndrome (a chronic pain condition)

Neurological disorders in non-human animals are treated by veterinarians.

Nonverbal learning disorder (also known as nonverbal learning disability, NLD, or NVLD) is a learning disorder characterized by verbal strengths as well as visual-spatial, motor, and social skills difficulties. It is sometimes confused with Asperger Syndrome or high IQ. Nonverbal learning disorder has never been included in the American Psychiatric Association's "Diagnostic and Statistical Manual of Mental Disorders" or the World Health Organization's "International Classification of Diseases".

Neuroscientists have learned a lot about the role of the brain in numerous cognitive mechanisms by understanding corresponding disorders. Similarly, neuroscientists have come to learn a lot about music cognition by studying music-specific disorders. Even though music is most often viewed from a "historical perspective rather than a biological one" music has significantly gained the attention of neuroscientists all around the world. For many centuries music has been strongly associated with art and culture. The reason for this increased interest in music is because it "provides a tool to study numerous aspects of neuroscience, from motor skill learning to emotion".

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

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.

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.

A reading disability is a condition in which a sufferer displays difficulty reading resulting primarily from neurological factors. Developmental Dyslexia, Alexia (acquired dyslexia), and Hyperlexia (word-reading ability well above normal for age and IQ).

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.