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.

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.

Symptoms may vary according to the disorder's type and subtype present. SPD can affect one sense or multiple senses. While many people can present one or two symptoms, sensory processing disorder has to have a clear functional impact on the person's life.

Sensory-based motor disorder shows motor output that is disorganized as a result of incorrect processing of sensory information affecting postural control challenges, resulting in postural disorder, or developmental coordination disorder.

The SBMD subtypes are:

1. Dyspraxia

2. Postural disorder

Delirium develops rapidly over a short period of time and is characterized by a disturbance in cognition, manifested by confusion, excitement, disorientation, and a clouding of consciousness. Hallucinations and illusions are common, and some individuals may experience acute onset change of consciousness. It is a disorder that makes situational awareness and processing new information very difficult for those diagnosed. It usually has a high rate of onset ranging from minutes to hours and sometimes days, but it does not last for very long, only a few hours to weeks. Delirium can also be accompanied by a shift in attention, mood swings, violent or unordinary behaviors, and hallucinations. It can be caused by a preexisting medical condition. Delirium during a hospital stay can result in a longer stay and more risk of complications and long terms stays.

The syndrome rarely presents itself the same way in every patient. Some symptoms that occur may be:

- Constructional apraxia: difficulty in constructing: drawing, copying, designs, copying 3D models

- Topographical disorientation: difficulty finding one's way in the environment

- Optic ataxia: deficit in visually-guided reaching

- Ocular motor apraxia: inability to direct gaze, a breakdown (failure) in starting (initiating) fast eye movements

- Dressing apraxia: difficulty in dressing usually related to inability to orient clothing spatially, and to a disrupted awareness of body parts and the position of the body and its parts in relation to themselves and objects in the environment

- Right-left confusion: difficulty in distinguishing the difference between the directions left and right

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).

Topographical disorientation, also known as topographical agnosia and topographagnosia, is the inability to orient oneself in one's surroundings as a result of focal brain damage. This disability may result from the inability to make use of selective spatial information (e.g., environmental landmarks) or to orient by means of specific cognitive strategies such as the ability to form a mental representation of the environment, also known as a cognitive map. It may be part of a syndrome known as visuospatial dysgnosia.

Visuospatial dysgnosia is a loss of the sense of "whereness" in the relation of oneself to one's environment and in the relation of objects to each other. Visuospatial dysgnosia is often linked with topographical disorientation.

Visual agnosia is a broad category that refers to a deficiency in the ability to recognize visual objects. Visual agnosia can be further subdivided into two different subtypes: apperceptive visual agnosia and associative visual agnosia.

Individuals with apperceptive visual agnosia display the ability to see contours and outlines when shown an object, but they experience difficulty if asked to categorize objects. Apperceptive visual agnosia is associated with damage to one hemisphere, specifically damage to the posterior sections of the right hemisphere.

In contrast, individuals with associative visual agnosia experience difficulty when asked to name objects. Associative agnosia is associated with damage to both the right and left hemispheres at the occipitotemporal border. A specific form of associative visual agnosia is known as prosopagnosia. Prosopagnosia is the inability to recognize faces. For example, these individuals have difficulty recognizing friends, family and coworkers. However, individuals with prosopagnosia can recognize all other types of visual stimuli.

Auditory processing disorder (APD), also known as central auditory processing disorder (CAPD), is an umbrella term for a variety of disorders that affect the way the brain processes auditory information. Individuals with APD usually have normal structure and function of the outer, middle and inner ear (peripheral hearing). However, they cannot process the information they hear in the same way as others do, which leads to difficulties in recognizing and interpreting sounds, especially the sounds composing speech. It is thought that these difficulties arise from dysfunction in the central nervous system.

The American Academy of Audiology notes that APD is diagnosed by difficulties in one or more auditory processes known to reflect the function of the central auditory nervous system.

APD can affect both children and adults, although the actual prevalence is currently unknown. It has been suggested that males are twice as likely to be affected by the disorder as females, but there are no good epidemiological studies.

Developmental topographical disorientation (DTD) refers to the inability to orient from childhood despite the absence of any apparent brain damage, neurological condition or general cognitive defects. Individuals affected by DTD are unable to generate a mental representation of the environment (i.e. a cognitive map) and therefore unable to make use of it while orienting (a process that usually people go through while orienting). Not to be confused with healthy individuals who have a poor sense of direction, individuals affected by DTD get lost in very familiar surroundings, such as their house or neighborhood, daily.

Simultanagnosia (or simultagnosia) is a rare neurological disorder characterized by the inability of an individual to perceive more than a single object at a time. This type of visual attention problem is one of three major components (the others being optic ataxia and optic apraxia) of Bálint's syndrome, an uncommon and incompletely understood variety of severe neuropsychological impairments involving space representation (visuospatial processing). The term "simultanagnosia" was first coined in 1924 by Wolpert to describe a condition where the affected individual could see individual details of a complex scene but failed to grasp the overall meaning of the image.

Simultanagnosia can be divided into two different categories: dorsal and ventral. Ventral occipito-temporal lesions cause a mild form of the disorder, while dorsal occipito-parietal lesions cause a more severe form of the disorder.

Agnosias are sensory modality specific, usually classified as visual, auditory, or tactile. Associative visual agnosia refers to a subtype of visual agnosia, which was labeled by Lissauer (1890), as an inability to connect the visual percept (mental representation of something being perceived through the senses) with its related semantic information stored in memory, such as, its name, use, and description. This is distinguished from the visual apperceptive form of visual agnosia, "apperceptive visual agnosia", which is an inability to produce a complete percept, and is associated with a failure in higher order perceptual processing where feature integration is impaired, though individual features can be distinguished. In reality, patients often fall between both distinctions, with some degree of perceptual disturbances exhibited in most cases, and in some cases, patients may be labeled as integrative agnostics when they fit the criteria for both forms. Associative visual agnosias are often category-specific, where recognition of particular categories of items are differentially impaired, which can affect selective classes of stimuli, larger generalized groups or multiple intersecting categories. For example, deficits in recognizing stimuli can be as specific as familiar human faces or as diffuse as living things or non-living things.

An agnosia that affects hearing, "auditory sound agnosia", is broken into subdivisions based on level of processing impaired, and a "semantic-associative" form is investigated within the auditory agnosias.

Speech agnosia, or auditory verbal agnosia, refers to "an inability to comprehend spoken words despite intact hearing, speech production and reading ability". Patients report that they do indeed hear sounds being produced, but that the sounds are fundamentally unrecognizable/untranslatable.

1. EXAMINER: What did you eat for breakfast?

2. PATIENT: Breakfast, breakfast, it sounds familiar but it doesn't speak to me. (Obler & Gjerlow 1999:45)

Despite an inability to process what the speaker is saying, some patients have been reported to recognize certain characteristic information about the speaker's voice (such as being a man or woman).

Associative visual agnosia is a form of visual agnosia. It is an impairment in recognition or assigning meaning to a stimulus that is accurately perceived and not associated with a generalized deficit in intelligence, memory, language or attention. The disorder appears to be very uncommon in a "pure" or uncomplicated form and is usually accompanied by other complex neuropsychological problems due to the nature of the etiology. Afflicted individuals can accurately distinguish the object, as demonstrated by the ability to draw a picture of it or categorize accurately, yet they are unable to identify the object, its features or its functions.

Alzheimer's disease patients with constructional apraxia have unique symptoms. Their drawings contain fewer angles, spatial alterations, a lack of perspective and simplifications, which are uncharacteristic of left hemisphere or right hemisphere patients. Constructional disabilities are present early on in the disease and get progressively worse over time; however even patients with advanced Alzheimer's disease may be able to do some constructional tasks. Spontaneous drawing is affected early and is heavily dependent upon semantic memory; therefore simplifications in the drawing may be due to impaired access to semantic knowledge. As Alzheimer's disease progresses, the patient's ability to copy objects becomes increasingly impaired and they may lose the ability to correctly draw simple figures due to a motor loss in routine memories.

Symptoms generally include memory or learning impairments, with the inability to integrate parts coherently.There is a big range to the severity of this disease and often the symptoms that are shown in each patient vary as well. As ambiguous as the general symptoms may be, patients are often treated of their respective symptoms as they appear and how critical the conditions are.

Constructional apraxia is characterized by an inability or difficulty to build, assemble, or draw objects. Apraxia is a neurological disorder in which people are unable to perform tasks or movements even though they understand the task, are willing to complete it, and have the physical ability to perform the movements. Constructional apraxia may be caused by lesions in the parietal lobe following stroke or it may serve as an indicator for Alzheimer's disease.

Integrative agnosia is a sub-disease of agnosia, meaning the lack of integrating perceptual wholes within

knowledge. Integrative agnosia can be assessed by several experimental tests such as the Efron shape test, which

determines the specificity of the disease being Integrative.

This disease is often caused by brain trauma, producing medial ventral lesions to the extrastriate cortex. Affecting this region of the brain produces learning impairments: the inability to

integrate parts such as spatial distances or producing visual images from short or long-term memory.

There are a number of perceptual changes that can accompany HPPD. Typical symptoms of the disorder include: halos or auras surrounding objects, trails following objects in motion, difficulty distinguishing between colors, apparent shifts in the hue of a given item, the illusion of movement in a static setting, air assuming a grainy or textured quality (visual snow or static, by popular description, not to be confused with normal "blue field entoptic phenomenon"), distortions in the dimensions of a perceived object, and a heightened awareness of floaters. The visual alterations experienced by those with HPPD are not homogeneous and there appear to be individual differences in both the number and intensity of symptoms.

Visual aberrations can occur periodically in healthy individuals – e.g. afterimages after staring at a light, noticing floaters inside the eye, or seeing specks of light in a darkened room. However, in people with HPPD, symptoms are typically persistent enough that the individual cannot ignore them.

There is some uncertainty about to what degree visual snow constitutes a true HPPD symptom. There are many individuals who have never used a drug which could have caused the onset, but yet experience the same grainy vision reported by HPPD sufferers. There are a few potential reasons for this, the most obvious of which being the theory that the drug usage may exaggerate the intensity of visual snow. Another theory is that instead, there may be no change in the severity or magnitude of the visual snow, but perhaps the drug usage opens sensory pathways that result in the individual becoming more aware of any visual disturbances that may have simply not been noticed before the incidence of drug use. As for root cause of visual snow, some theories suggest that it is the result of thermal noise in the visual cortex or in the 'Optic Pathway' (encompassing photoreceptor cells on the retina, the optic nerve, and the optic chiasm), as eye tests for individuals who experience visual snow often reveal that physically, the eye is perfectly normal, and in many cases the individual still maintains 20/20 vision.

HPPD usually has a visual manifestation. Drugs affecting the auditory sense, like DiPT, may produce auditory disturbances, though there are few known cases. Some psychedelic drugs can produce temporary tinnitus-like symptoms as a side effect.

It also should be noted that the visuals do not constitute true hallucinations in the clinical sense of the word; people with HPPD recognize the visuals to be illusory, or pseudohallucinations, and thus maintain the ability to determine what is real (in contrast to some mental illnesses such as schizophrenia).

Optic ataxia is the inability to guide the hand toward an object using visual information where the inability cannot be explained by motor, somatosensory, visual field deficits or acuity deficits. Optic ataxia is seen in Bálint's syndrome where it is characterized by an impaired visual control of the direction of arm-reaching to a visual target, accompanied by defective hand orientation and grip formation. It is considered a specific visuomotor disorder, independent of visual space misperception.

Optic ataxia is also known as misreaching or dysmetria (), secondary to visual perceptual deficits. A patient with Bálint's syndrome likely has defective hand movements under visual guidance, despite normal limb strength. The patient is unable to grab an object while looking at the object, due to a discoordination of eye and hand movement. It is especially true with their contralesional hand.

Dysmetria refers to a lack of coordination of movement, typified by the undershoot or overshoot of intended position with the hand, arm, leg, or eye. It is sometimes described as an inability to judge distance or scale.

The reaching ability of the patient is also altered. It takes them longer to reach toward an object. Their ability to grasp an object is also impaired. The patient's performance is even more severely deteriorated when vision of either the hand or the target is prevented.

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

Patients with simultanagnosia, a component of Bálint's syndrome, have a restricted spatial window of visual attention and cannot see more than one object at a time in a scene that contains more than one object. For instance, if presented with an image of a table containing both food and various utensils, a patient will report seeing only one item, such as a spoon. If the patient's attention is redirected to another object in the scene, such as a glass, the patient will report that they see the glass but no longer see the spoon. As a result of this impairment, simultanagnosic patients often fail to comprehend the overall meaning of a scene.

In addition, patients note that one stationary object may spontaneously disappear from view as they become aware of another object in the scene.

Simultanagnosic patients often exhibit a phenomenon known as "local capture" where they only identify the local elements of stimuli containing local and global features. However, recent studies have demonstrated that implicit processing of the global structure can occur. With the appropriate stimulus conditions, explicit processing of the global form may occur. For example, a study performed with Navon hierarchical letters, which are large letters composed of smaller ones, revealed that the use of smaller and denser Navon letters biased the patient towards global processing.

Prosopagnosia, also called face blindness, is a cognitive disorder of face perception in which the ability to recognize familiar faces, including one's own face (self-recognition), is impaired, while other aspects of visual processing (e.g., object discrimination) and intellectual functioning (e.g., decision making) remain intact. The term originally referred to a condition following acute brain damage (acquired prosopagnosia), but a congenital or developmental form of the disorder also exists, which may affect up to 2.5% of the United States population. The specific brain area usually associated with prosopagnosia is the fusiform gyrus, which activates specifically in response to faces. The functionality of the fusiform gyrus allows most people to recognize faces in more detail than they do similarly complex inanimate objects. For those with prosopagnosia, the new method for recognizing faces depends on the less-sensitive object recognition system. The right hemisphere fusiform gyrus is more often involved in familiar face recognition than the left. It remains unclear whether the fusiform gyrus is only specific for the recognition of human faces or if it is also involved in highly trained visual stimuli.

There are two types of prosopagnosia: acquired and congenital (developmental). Acquired prosopagnosia results from occipito-temporal lobe damage and is most often found in adults. This is further subdivided into apperceptive and associative prosopagnosia. In congenital prosopagnosia, the individual never adequately develops the ability to recognize faces.

Though there have been several attempts at remediation, no therapies have demonstrated lasting real-world improvements across a group of prosopagnosics. Prosopagnosics often learn to use "piecemeal" or "feature-by-feature" recognition strategies. This may involve secondary clues such as clothing, gait, hair color, skin color, body shape, and voice. Because the face seems to function as an important identifying feature in memory, it can also be difficult for people with this condition to keep track of information about people, and socialize normally with others. Prosopagnosia has also been associated with other disorders that are associated with nearby brain areas: left hemianopsia (loss of vision from left side of space, associated with damage to the right occipital lobe), achromatopsia (a deficit in color perception often associated with unilateral or bilateral lesions in the temporo-occipital junction) and topographical disorientation (a loss of environmental familiarity and difficulties in using landmarks, associated with lesions in the posterior part of the parahippocampal gyrus and anterior part of the lingual gyrus of the right hemisphere). It is from the Greek: "prosopon" = "face" and "agnosia" = "not knowing".