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.

Relatively little has been discovered about the cause of the condition since its initial identification. Recent studies from the empirical data are prone to consider anosognosia a multi-componential syndrome or multi-faceted phenomenon. That is it can be manifested by failure to be aware of a number of specific deficits, including motor (hemiplegia), sensory (hemianaesthesia, hemianopia), spatial (unilateral neglect), memory (dementia), and language (receptive aphasia) due to impairment of anatomo-functionally discrete monitoring systems.

Anosognosia is relatively common following different causes of brain injury, such as stroke and traumatic brain injury; for example, anosognosia for hemiparesis, (weakness of one side of the body) with onset of acute stroke is estimated at between 10% and 18%. However, it can appear to occur in conjunction with virtually any neurological impairment. It is more frequent in the acute than in the chronic phase and more prominent for assessment in the cases with right hemispheric lesions than with the left. Anosognosia is not related to global mental confusion, cognitive flexibility, other major intellectual disturbances, or mere sensory/perceptual deficits.

The condition does not seem to be directly related to sensory loss but is thought to be caused by damage to higher level neurocognitive processes that are involved in integrating sensory information with processes that support spatial or bodily representations (including the somatosensory system). Anosognosia is thought to be related to unilateral neglect, a condition often found after damage to the non-dominant (usually the right) hemisphere of the cerebral cortex in which people seem unable to attend to, or sometimes comprehend, anything on a certain side of their body (usually the left).

Anosognosia can be selective in that an affected person with multiple impairments may seem unaware of only one handicap, while appearing to be fully aware of any others. This is consistent with the idea that the source of the problem relates to spatial representation of the body. For example, anosognosia for hemiplegia, or the paralysis of one side of the body, may occur with or without intact awareness of visuo-spatial unilateral neglect. This phenomenon of double dissociation can be an indicator of domain-specific disorders of awareness modules, meaning that in anosognosia, brain damage can selectively impact the self-monitoring process of one specific physical or cognitive function rather than a spatial location of the body.

There are also studies showing that the maneuver of vestibular stimulation could temporarily improve both the syndrome of spatial unilateral neglect and of anosognosia for left hemiplegia. Combining the findings of hemispheric asymmetry to the right, association with spatial unilateral neglect, and the temporal improvement on both syndromes, it is suggested there can be a spatial component underlying the mechanism of anosognosia for motor weakness and that neural processes could be modulated similarly. There were some cases of anosognosia for right hemiplegia after left hemisphere damage, but the frequency of this type of anosognosia has not been estimated.

Those diagnosed with Alzheimer's disease often display this lack of awareness and insist that nothing is wrong with them.

Anosognosia may occur as part of receptive aphasia, a language disorder that causes poor comprehension of speech and the production of fluent but incomprehensible sentences. A patient with receptive aphasia cannot correct his own phonetics errors and shows "anger and disappointment with the person with whom s/he is speaking because that person fails to understand her/him". This may be a result of brain damage to the posterior portion of the superior temporal gyrus, believed to contain representations of word sounds. With those representations significantly distorted, patients with receptive aphasia are unable to monitor their mistakes. Other patients with receptive aphasia are fully aware of their condition and speech inhibitions, but cannot monitor their condition, which is not the same as anosognosia and therefore cannot explain the occurrence of neologistic jargon.

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.

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.

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.

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).

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.

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.

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.

Jargon aphasia is a type of fluent aphasia in which an individual's speech is incomprehensible, but appears to make sense to the individual. Persons experiencing this condition will either replace a desired word with another that sounds or looks like the original one, or has some other connection to it, or they will replace it with random sounds. Accordingly, persons with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they can't find with sounds.

People affected by jargon aphasia usually are elderly and/or people who have damage to the neural pathways of certain parts of the brain. This is usually the result of the following conditions[2]:

- Stroke

- Traumatic Brain Injury

- Epilepsy

- Migraine

- Brain Tumor

- Alzheimer's Disease

- Parkinson's Disease

Since jargon is associated with fluent (Wernicke’s) aphasia, it is usually caused by damage of the temporal lobe, and more specifically, Wernicke’s area. After the condition is diagnosed, a Computerized Tomography (CT) or Magnetic Resonance Imaging (MRI) scan is typically used to determine the location and severity of the brain damage that has caused the aphasia[2].

There have been cases in which aphasia has developed after damage to only the right hemisphere of the brain. These cases are few and far between, and usually involve unique circumstances for the individual. Most commonly, these results can stem from brain organization that is different than the general population, or a heavier than normal reliance on the right hemisphere of the brain[7].

Reduplicative paramnesia has been reported in the context of a number of neurological disorders, including stroke, intracerebral hemorrhage, tumor, dementia, encephalopathy and various psychiatric disorders.

Taken from the Benson and colleagues study, the following excerpt illustrates some of the core features of the delusion. The patient had suffered a head injury after a fall in his home. The impact had caused a fractured skull and frontal lobe damage to both sides (although more pronounced on the right) owing to the formation of intracerebral hematomas:

The illusory relocation to a familiar place, such as a home or town the patient knows well, is a common theme, although occasionally the patient believes they are resident in more fantastical or exotic locations (such as, in one case, Timbuktu).

Anton–Babinski syndrome is mostly seen following a stroke, but may also be seen after head injury. Neurologist Macdonald Critchley describes it thus:

The sudden development of bilateral occipital dysfunction is likely to produce transient physical and psychical effects in which mental confusion may be prominent. It may be some days before the relatives, or the nursing staff, stumble onto the fact that the patient has actually become sightless. This is not only because the patient ordinarily does not volunteer the information that they have become blind, but he furthermore misleads his entourage by behaving and talking as though they were sighted. Attention is aroused however when the patient is found to collide with pieces of furniture, to fall over objects, and to experience difficulty in finding his way around. They may try to walk through a wall or through a closed door on his way from one room to another. Suspicion is still further alerted when they begin to describe people and objects around them which, as a matter of fact, are not there at all.

Thus we have the twin symptoms of anosognosia (or lack of awareness of defect) and confabulation, the latter affecting both speech and behaviour.

Anton–Babinski syndrome may be thought of ideally as the opposite of blindsight, blindsight occurring when part of the visual field is not consciously experienced, but some reliable perception does in fact occur.

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.

Somatoparaphrenia is a type of monothematic delusion where one denies ownership of a limb or an entire side of one's body. Even if provided with undeniable proof that the limb belongs to and is attached to their own body, the patient produces elaborate confabulations about whose limb it really is, or how the limb ended up on their body. In some cases, delusions become so elaborate that a limb may be treated and cared for as if it were a separate being.

Somatoparaphrenia differs from a similar disorder, asomatognosia, which is characterized as loss of recognition of half of the body or a limb, possibly due to paralysis or unilateral neglect. For example, asomatognosic patients may mistake their arm for the doctor's. However, they can be shown their limb and this error is temporarily corrected.

Somatoparaphrenia has been reported to occur predominately in the left arm of one's body, and it is often accompanied by left-sided paralysis and anosognosia (denial or lack of awareness) of the paralysis. The link between somatoparaphrenia and paralysis has been documented in many clinical cases and while the question arises as to whether paralysis is necessary for somatoparaphrenia to occur, anosognosia is not, as documented by cases with somatoparaphrenia and paralysis with no anosognosia.

Dejerine–Roussy syndrome is most commonly preceded by numbness in the affected side. In these cases, numbness is replaced by burning and tingling sensations, widely varying in degree of severity across all cases. The majority of those reported are cases in which the symptoms are severe and debilitating. Burning and tingling can also be accompanied by hypersensitivity, usually in the form of dysaesthesia or allodynia. Less commonly, some patients develop severe ongoing pain with little or no stimuli.

Allodynia is pain from a stimulus that would normally not cause pain. For example, there is a patient who experiences unrelenting pain when a breeze touches his skin. Most patients experiencing allodynia, experience pain with touch and pressure, however some can be hypersensitive to temperature.

Dysaesthesia is defined as pain due to thalamic lesioning. This form of neuropathic pain can be any combination of itching, tingling, burning, or searing experienced spontaneously or from stimuli.

Allodynia and dysaesthesia replace numbness between one week and a few months after a thalamic stroke. In general, once the development of pain has stopped, the type and severity of pain will be unchanging and if untreated, persist throughout life. Consequentially, many will undergo some form of pain treatment and adjust to their new lives as best they can.

Pain associated with Dejerine–Roussy syndrome is sometimes coupled with anosognosia or somatoparaphrenia which causes a patient having undergone a right-parietal, or right-sided stroke to deny any paralysis of the left side when indeed there is, or deny the paralyzed limb(s) belong to them. Although debatable, these symptoms are rare and considered part of a "thalamic phenomenon", and are not normally considered a characteristic of Dejerine–Roussy syndrome.

It has been suggested that damage to the posterior cerebral regions (temporoparietal junction) of the cortex may play a significant role in the development of somatoparaphrenia. However, more recent studies have shown that damage to deep cortical regions such as the posterior insula and subcortical structures such as the basal ganglia, the thalamus and the white matter connecting the thalamus to the cortex may also play a significant role in the development of somatoparaphrenia. It has also been suggested that involvement of deep cortical and subcortical grey structures of the temporal lobe may contribute to reduce the sense of familiarity experienced by somatoparaphrenic patients for their paralyzed limb.

Post-stroke depression (PSD) is considered the most frequent and important neuropsychiatric consequence of stroke. Approximately one-third of stroke survivors experience major depression. Moreover, this condition can have an adverse effect on cognitive function, functional recovery and survival.

The Diagnostic and Statistical Manual (DSM) IV categorizes post-stroke depression as “mood disorder due to a general medical condition” (i.e. stroke) with the specifiers of depressive features, major depressive-like episodes, manic features, or mixed features. Utilizing patient data from acute hospital admission, community surveys, or out patient clinics previous studies have identified two types of depressive disorders associated with cerebral ischemia: major depression, which occurs in up to 25% of patients; and minor depression, which has been defined for research purposes by DSM-IV criteria as a depressed mood or loss of interest and at least two but fewer than four symptoms of major depression. Minor depression occurs in up to 30% of patients following stroke.

Prevalence clearly varies over time with an apparent peak 3–6 months after stroke and subsequent decline in prevalence at one-year reaches about to 50% of initial rates. Robinson and colleagues characterized the natural course of major depression after stroke with spontaneous remission typically 1 to 2 years after stroke However, it was also noted that in few cases depression becomes chronic and may persist more than 3 years following stroke . On the other hand, minor depression appeared to be more variable, with both short term and long term depression occurring in these patients .

Post-stroke depression is highly prevalent among both men and women post-stroke, however, it appears that post-stoke depression is more common in women when prevalence is compared between the sexes.

Women were twice as likely to experience post-stroke depression than men. It is hypothesized, based on CT scanning, that of the two sexes experiencing post-stroke depression, women who had post-stroke depression had a higher rate of left hemisphere lesions than men. However, risk of post-stroke depression can not be determined effectively based on the location of the lesion in the brain and more research in this area is needed.

It has also been postulated that the risk of developing post-stroke depression in male patients is partly linked to having a high level of limitations and disability in functioning, especially in performing activities of daily living (ADL's), as a result of their stroke; the greater the limitation, the greater the severity. Risk of developing depression post-stroke in women is partly linked to a history of psychological disorders as well as limitations involving cognition as a result of their stroke.

The scientific community is divided into two “camps” supporting opposing views: some propose a primary biological mechanism with stroke affecting neural circuits involved in mood regulation which in turn causes post-stroke depression, while other researchers claim that post stroke depression is caused by social and psychological stressors that emerge as a result of stroke.

While an integrated bio-psycho-social model including both biological and psychosocial aspects of post stroke depression seems warranted, a number of studies clearly suggest that biological mechanisms play a major role in the development of post stroke depression.

1. stroke patients show a higher rate of depression compared to orthopedic patients with disabilities of comparable severity.

2. Several studies proposed an association with specific lesions (left anterior and basal ganglia lesions and lesions close to frontal pole) and occurrence of post stroke depression.

3. Some studies reported an association between post-stroke mania and right orbital frontal, basotemporal, basal ganglia lesions.

4. It has been shown that patients with anosognosia who are unaware of their disability still develop post stroke depression.

Despite this evidence, the association of post-stroke depression to specific brain lesions is still vague and needs replication from various independent groups. Furthermore, the cause of post stroke depression at a functional level is not clear.

The only biological model was proposed by Robinson and co-workers: They hypothesized that the depletion of monoaminergic amines occurring after stroke play a role in post stroke-depression. They point out that norepinephrinergic and serotonergic nuclei send projections to the frontal cortex and arc posteriorly, running through the deep layers of the cortex, where they arborize and send terminal projections into the superficial cortical layers. These norepinephrinergic and serotoninergic pathways are disrupted in basal ganglia and frontal lobe lesions – sites that are shown to be associated with post stroke depression.

However, this model is far from being universally accepted and there are serious objections both to their model and findings showing the association between post-stroke depression and lesion sites.

Interestingly, depression-like behaviors are demonstrated in a mouse model of cortical intracerebral hemorrhage.

Dejerine-Roussy is a rare pain syndrome. Individuals with emerging Dejerine–Roussy syndrome usually report they are experiencing unusual pain or sensitivity that can be allodynic in nature or triggered by seemingly unrelated stimuli (sounds, tastes). Symptoms are typically lateralized and may include vision loss or loss of balance (position sense). Workup should be performed by a neurologist and brain imaging to look for evidence of infarction or tumor should be obtained.

During the final stages, the patient is completely dependent upon caregivers. Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech. Despite the loss of verbal language abilities, people can often understand and return emotional signals. Although aggressiveness can still be present, extreme apathy and exhaustion are much more common symptoms. People with Alzheimer's disease will ultimately not be able to perform even the simplest tasks independently; muscle mass and mobility deteriorates to the point where they are bedridden and unable to feed themselves. The cause of death is usually an external factor, such as infection of pressure ulcers or pneumonia, not the disease itself.

Progressive deterioration eventually hinders independence, with subjects being unable to perform most common activities of daily living. Speech difficulties become evident due to an inability to recall vocabulary, which leads to frequent incorrect word substitutions (paraphasias). Reading and writing skills are also progressively lost. Complex motor sequences become less coordinated as time passes and AD progresses, so the risk of falling increases. During this phase, memory problems worsen, and the person may fail to recognise close relatives. Long-term memory, which was previously intact, becomes impaired.

Behavioural and neuropsychiatric changes become more prevalent. Common manifestations are wandering, irritability and labile affect, leading to crying, outbursts of unpremeditated aggression, or resistance to caregiving. Sundowning can also appear. Approximately 30% of people with AD develop illusionary misidentifications and other delusional symptoms. Subjects also lose insight of their disease process and limitations (anosognosia). Urinary incontinence can develop. These symptoms create stress for relatives and carers, which can be reduced by moving the person from home care to other long-term care facilities.

If the area of the brain affected contains one of the three prominent central nervous system pathways—the spinothalamic tract, corticospinal tract, and the posterior column–medial lemniscus pathway, symptoms may include:

- hemiplegia and muscle weakness of the face

- numbness

- reduction in sensory or vibratory sensation

- initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), excessive reflexes, and obligatory synergies.

In most cases, the symptoms affect only one side of the body (unilateral). Depending on the part of the brain affected, the defect in the brain is "usually" on the opposite side of the body. However, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate a stroke.In addition to the above CNS pathways, the "brainstem" gives rise to most of the twelve cranial nerves. A brainstem stroke affecting the brainstem and brain, therefore, can produce symptoms relating to deficits in these cranial nerves:

- altered smell, taste, hearing, or vision (total or partial)

- drooping of eyelid (ptosis) and weakness of ocular muscles

- decreased reflexes: gag, swallow, pupil reactivity to light

- decreased sensation and muscle weakness of the face

- balance problems and nystagmus

- altered breathing and heart rate

- weakness in sternocleidomastoid muscle with inability to turn head to one side

- weakness in tongue (inability to stick out the tongue or move it from side to side)

If the "cerebral cortex" is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

- aphasia (difficulty with verbal expression, auditory comprehension, reading and writing; Broca's or Wernicke's area typically involved)

- dysarthria (motor speech disorder resulting from neurological injury)

- apraxia (altered voluntary movements)

- visual field defect

- memory deficits (involvement of temporal lobe)

- hemineglect (involvement of parietal lobe)

- disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)

- lack of insight of his or her, usually stroke-related, disability

If the "cerebellum" is involved, ataxia might be present and this includes:

- altered walking gait

- altered movement coordination

- vertigo and or disequilibrium

Loss of consciousness, headache, and vomiting usually occur more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing the brain.

If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.