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.

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.

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.

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].

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.

For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause.

Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies.

Agnosia is the inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. Agnosia only affects a single modality, such as vision or hearing. More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information.

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.

The affected individual may not realize that they have a visual problem and may complain of becoming "clumsy" or "muddled" when performing familiar tasks such as setting the table or simple DIY.

Anosognosia, a lack of awareness of the deficit, is common and can cause therapeutic resistance. In some agnosias, such as prosopagnosia, awareness of the deficit is often present; however shame and embarrassment regarding the symptoms can be a barrier in admission of a deficiency. Because agnosias result from brain lesions, no direct treatment for them currently exists, and intervention is aimed at utilization of coping strategies by patients and those around them. Sensory compensation can also develop after one modality is impaired in agnostics

General principles of treatment:

- restitution

- repetitive training of impaired ability

- development of compensatory strategies utilizing retained cognitive functions

Partial remediation is more likely in cases with traumatic/vascular lesions, where more focal damage occurs, than in cases where the deficit arises out of anoxic brain damage, which typically results in more diffuse damage and multiple cognitive impairments. However, even with forms of compensation, some afflicted individuals may no longer be able to fulfill the requirements of their occupation or perform common tasks, such as, eating or navigating. Agnostics are likely to become more dependent on others and to experience significant changes to their lifestyle, which can lead to depression or adjustment disorders.

The term "reduplicative paramnesia" was first used in 1903 by psychiatrist Arnold Pick to describe a condition in a patient with suspected Alzheimer's disease who insisted that she had been moved from Pick's city clinic to one she claimed looked identical but was in a familiar suburb. To explain the discrepancy she further claimed that Pick and the medical staff worked at both locations.

In retrospect, however, the phenomenon has been found to have been first reported by the Swiss naturalist Charles Bonnet in 1788, who described a woman who also had what would now be called Cotard delusion. Henry Head and Paterson and Zangwill later reported on soldiers who had the delusional belief that their hospital was located in their home town, although in these cases traumatic brain injury seemed to be the most likely cause.

It wasn't until 1976 that serious consideration was given to the disorder, when three cases were reported by Benson and colleagues. Benson not only described striking reduplication syndromes in his patients, but also attempted to explain the phenomena in terms of the neurocognitive deficits also present in the patients. This was one of the first attempts to give a neuropsychological explanation for the disorder.

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.

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.

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.

One form of treatment that has produced a more integrated body awareness is mirror therapy, in which the individual who denies that the affected limb belongs to their body looks into a mirror at the limb. Patients looking into the mirror state that the limb does belong to them; however body ownership of the limb does not remain after the mirror is taken away.

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.

Of the millions experiencing strokes worldwide, over 30,000 in the United States alone have developed some form of Dejerine–Roussy syndrome. 8% of all stroke patients will experience central pain syndrome, with 5% experiencing moderate to severe pain. The risk of developing Dejerine–Roussy syndrome is higher in older stroke patients, about 11% of stroke patients over the age of 80.

The imbalance in sensation characterized by Dejerine–Roussy syndrome can be argued through a model addressing a system of inputs and outputs that the brain must constantly process throughout life, suggesting latent plasticity. The right and left hemispheres of the brain both play important roles in the sensory input and output. When a stroke damages one hemisphere, it is proposed that the other hemisphere will cope with the discrepancies in a specific manner. The left hemisphere tends to "gloss over" discrepancies from inputs, eliciting either denial or rationalization defense mechanisms in order to stabilize said discrepancy. In contrast, the right hemisphere does the opposite, and will focus on the discrepancy, and motivate action to be taken to restore equilibrium. Therefore, damage to the left hemisphere can cause both an indifference to pain and hypersensitivity to pain (dysaesthesia or allodynia), while damage to the right hemisphere can cause denial as a defense mechanism (anosognosia and somatoparaphrenia).

The insular cortex, part of the cerebral cortex, is responsible for self-sensation, including the degree of pain perceived by the body, and for self-awareness and defense mechanisms. The insular cortex is often lesioned by a stroke. Particularly, the posterior insula has been mapped to correlate to pain experienced by an individual. In addition, it has been proven that the posterior insula receives a substantial amount of the inputs of the brain, and can be treated with visual, kinesthetic, and auditory inputs.

Diabetes mellitus increases the risk of stroke by 2 to 3 times. While intensive blood sugar control has been shown to reduce small blood vessel complications such as kidney damage and damage to the retina of the eye it has not been shown to reduce large blood vessel complications such as stroke.

At present, there is no definitive evidence to support that any particular measure is effective in preventing AD. Global studies of measures to prevent or delay the onset of AD have often produced inconsistent results.

Epidemiological studies have proposed relationships between certain modifiable factors, such as diet, cardiovascular risk, pharmaceutical products, or intellectual activities among others, and a population's likelihood of developing AD. Only further research, including clinical trials, will reveal whether these factors can help to prevent AD.

The early stages of Alzheimer's disease are difficult to diagnose. A definitive diagnosis is usually made once cognitive impairment compromises daily living activities, although the person may still be living independently. The symptoms will progress from mild cognitive problems, such as memory loss through increasing stages of cognitive and non-cognitive disturbances, eliminating any possibility of independent living, especially in the late stages of the disease.

Life expectancy of people with AD is less. Following diagnosis it typically ranges from three to ten years.

Fewer than 3% of people live more than fourteen years. Disease features significantly associated with reduced survival are an increased severity of cognitive impairment, decreased functional level, history of falls, and disturbances in the neurological examination. Other coincident diseases such as heart problems, diabetes or history of alcohol abuse are also related with shortened survival. While the earlier the age at onset the higher the total survival years, life expectancy is particularly reduced when compared to the healthy population among those who are younger. Men have a less favourable survival prognosis than women.

Pneumonia and dehydration are the most frequent immediate causes of death brought by AD, while cancer is a less frequent cause of death than in the general population.

The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation although the size of the effect is small with 833 people have to be treated for 1 year to prevent one stroke. Other modifiable risk factors include high blood cholesterol levels, diabetes mellitus, cigarette smoking (active and passive), drinking lots of alcohol and drug use, lack of physical activity, obesity, processed red meat consumption, and unhealthy diet. Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances). Drugs, most commonly amphetamines and cocaine, can induce stroke through damage to the blood vessels in the brain and acute hypertension. Migraine with aura doubles a person's risk for ischemic stroke.

High levels of physical activity reduce the risk of stroke by about 26%. There is a lack of high quality studies looking at promotional efforts to improve lifestyle factors. Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advice on diet, exercise, smoking and alcohol use. Medication is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.