Clinically, anosognosia is often assessed by giving patients an anosognosia questionnaire in order to assess their metacognitive knowledge of deficits. However, neither of the existing questionnaires applied in the clinics are designed thoroughly for evaluating the multidimensional nature of this clinical phenomenon; nor are the responses obtained via offline questionnaire capable of revealing the discrepancy of awareness observed from their online task performance. The discrepancy is noticed when patients showed no awareness of their deficits from the offline responses to the questionnaire but demonstrated reluctance or verbal circumlocution when asked to perform an online task. For example, patients with anosognosia for hemiplegia may find excuses not to perform a bimanual task even though they do not admit it is because of their paralyzed arms.

A similar situation can happen on patients with anosognosia for cognitive deficits after traumatic brain injury when monitoring their errors during the tasks regarding their memory and attention (online emergent awareness) and when predicting their performance right before the same tasks (online anticipatory awareness). It can also occur among patients with dementia and anosognosia for memory deficit when prompted with dementia-related words, showing possible pre-attentive processing and implicit knowledge of their memory problems. More interestingly, patients with anosognosia may overestimate their performance when asked in first-person formed questions but not from a third-person perspective when the questions referring to others.

When assessing the causes of anosognosia within stroke patients, CT scans have been used to assess where the greatest amount of damage is found within the various areas of the brain. Stroke patients with mild and severe levels of anosognosia (determined by response to an anosognosia questionnaire) have been linked to lesions within the temporoparietal and thalamic regions, when compared to those who experience moderate anosognosia, or none at all. In contrast, after a stroke, people with moderate anosognosia have a higher frequency of lesions involving the basal ganglia, compared to those with mild or severe anosognosia.

In order to assess an individual for agnosia, it must be verified that the individual is not suffering from a loss of sensation, and that both their language abilities and intelligence are intact. In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality. To make a diagnosis, the distinction between apperceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual is suffering from a form of apperceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual is suffering from a form of associative agnosia, they will not be able to match different examples of a stimulus. For example, an individual who has been diagnosed with associative agnosia in the visual modality would not be able to match pictures of a laptop that is open with a laptop that is closed.

Using verbal descriptions may be helpful for individuals with certain types of agnosia. Individuals such as prosopagnosics may find it useful to listen to a description of their friend or family member and recognize them based on this description more easily than through visual cues.

In regard to anosognosia for neurological patients, no long-term treatments exist. As with unilateral neglect, caloric reflex testing (squirting ice cold water into the left ear) is known to temporarily ameliorate unawareness of impairment. It is not entirely clear how this works, although it is thought that the unconscious shift of attention or focus caused by the intense stimulation of the vestibular system temporarily influences awareness. Most cases of anosognosia appear to simply disappear over time, while other cases can last indefinitely. Normally, long-term cases are treated with cognitive therapy to train patients to adjust for their inoperable limbs (though it is believed that these patients still are not "aware" of their disability). Another commonly used method is the use of feedback – comparing clients' self-predicted performance with their actual performance on a task in an attempt to improve insight.

Neurorehabilitation is difficult because, as anosognosia impairs the patient's desire to seek medical aid, it may also impair their ability to seek rehabilitation. A lack of awareness of the deficit makes cooperative, mindful work with a therapist difficult. In the acute phase, very little can be done to improve their awareness, but during this time, it is important for the therapist to build a therapeutic alliance with patients by entering their phenomenological field and reducing their frustration and confusion. Since severity changes over time, no single method of treatment or rehabilitation has emerged or will likely emerge.

In regard to psychiatric patients, empirical studies verify that, for individuals with severe mental illnesses, lack of awareness of illness is significantly associated with both medication non-compliance and re-hospitalization. Fifteen percent of individuals with severe mental illnesses who refuse to take medication voluntarily under any circumstances may require some form of coercion to remain compliant because of anosognosia. Coercive psychiatric treatment is a delicate and complex legal and ethical issue.

One study of voluntary and involuntary inpatients confirmed that committed patients require coercive treatment because they fail to recognize their need for care. The patients committed to the hospital had significantly lower measures of insight than the voluntary patients.

Anosognosia is also closely related to other cognitive dysfunctions that may impair the capacity of an individual to continuously participate in treatment. Other research has suggested that attitudes toward treatment can improve after involuntary treatment and that previously committed patients tend later to seek voluntary treatment.

Sensory modality testing allows practitioners to assess for generalized versus specific deficits, distinguishing visual agnosias from optic aphasia, which is a more generalized deficit in semantic knowledge for objects that spans multiple sensory modalities, indicating an impairment in the semantic representations themselves.

Specialists, like ophthalmologists or audiologists, can test for perceptual abilities. Detailed testing is conducted, using specially formulated assessment materials, and referrals to neurological specialists is recommended to support a diagnosis via brain imaging or recording techniques. The separate stages of information processing in the object recognition model are often used to localize the processing level of the deficit.

Testing usually consists of object identification and perception tasks including:

- object-naming tasks

- object categorization or figure matching

- drawing or copying real objects or images or illustrations

- unusual views tests

- overlapping line drawings

- partially degraded or fragmented image identification

- face or feature analysis

- fine line judgment

- figure contour tracking

- visual object description

- object-function miming

- tactile ability tests (naming by touch)

- auditory presentation identification

Someone with jargon aphasia may exhibit the following behaviors[4]:

- Intermixing real words and nonsensical words while speaking or writing

- Failing to recognize mistakes being made while speaking or writing

- Using real words in incorrect situations

- Frequent, repetitive uttering of low frequency words

- The inability to say or write a specific word or phrase

Some of the specific types of language errors that occur are[5]:

Lexical (real word):

Semantic - Real word that was semantically related to target. ("dog" instead of "cat")

Formal - Real word that shared either the initial phoneme or at least 50% of phonemes with target. ("dog" instead of "desk" or "dog" instead of "frog")

Mixed - Real word that was both semantically and phonologically related to target. ("bicycle" instead of "motorcycle")

Visual - Real word of an item similar in visual form to the target. ("ball" instead of "orange")

Unrelated - Real word that was not related to the target in any obvious way. ("dog" instead of "apple")

Non-lexical (nonword):

Phonological - Nonword that shared either the initial phoneme or at least 50% of phonemes with target. ("deg" instead of "dog")

Neologistic - Nonword not reaching the criterion for phonological relatedness (i.e., sharing less than 50% of phonemes with the target and with a different initial phoneme). Nonwords that are pseudo compound words. ("kib" instead of "dog")

Other Errors:

Don’t know - Indication that response was unknown or if item was not responded to at all. ("I don’t know" or silence)

Description - Attempts to describe as opposed to name item. (Multiple word responses)

Jargon aphasia must be diagnosed through a series of tests. Since the number of individuals that have aphasia after suffering a stroke is high, a test is usually carried out soon after the stroke occurs. There is a list of basic exercises to help assess a person’s language skills, such as:

- Naming objects that begin with a certain letter

- Reading or writing

- Holding a conversation

- Understanding directions and commands

There is also a common test used, called the Boston Diagnostic Aphasia Examination test, which incorporates exercises that extensively review the person’s language skills[2].

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.

Indifference to illness may have an adverse impact on a patient's engagement in neurological rehabilitation, cognitive rehabilitation and physical rehabilitation. Patients are not likely to implement rehabilitation for a condition about which they are indifferent. Although anosognosia often resolves in days to weeks after stroke, anosodiaphoria often persists. Therefore, the therapist has to be creative in their rehabilitation approach in order to maintain the interest of the patient.

The only way to treat aphasia is with speech and language therapy (SLT). It will not completely restore the person’s prior level of communication, but SLT can lead to a massive improvement of jargon aphasia. Recipients of this treatment typically achieve better use of residual language abilities, improved language skills, and the ability to communicate in a different way by making up for missing words in their speech[2].

One specific method that has shown to lead to improvements with certain symptoms is “phonological component analysis”, or PCA for short. Participants in PCA therapy tend to improve in the ability to name specific items that they are test on, as well as the decrease in use of nonwords to describe said items. Seeing promising results from this type of therapy has led to much optimism in hopes of developing more treatment methods for jargon aphasia[6].

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.

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.

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.

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.

Of the many medical imaging techniques available, single photon emission computed tomography (SPECT) appears to be superior in differentiating Alzheimer's disease from other types of dementia, and this has been shown to give a greater level of accuracy compared with mental testing and medical history analysis. Advances have led to the proposal of new diagnostic criteria.

PiB PET remains investigational, but a similar PET scanning radiopharmaceutical called florbetapir, containing the longer-lasting radionuclide fluorine-18, has recently been tested as a diagnostic tool in Alzheimer's disease, and given FDA approval for this use.

Amyloid imaging is likely to be used in conjunction with other markers rather than as an alternative. Volumetric MRI can detect changes in the size of brain regions. Measuring those regions that atrophy during the progress of Alzheimer's disease is showing promise as a diagnostic indicator. It may prove less expensive than other imaging methods currently under study.

In 2011 An FDA panel voted unanimously to recommend approval of florbetapir, which is currently used in an investigational study. The imaging agent can help to detect Alzheimer's brain plaques, but will require additional clinical research before it can be made available commercially.

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.

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.

Expensive and invasive, the above treatments are not guaranteed to work, and are not meeting the needs of patients. There is a need for a new, less expensive, less invasive form of treatment, two of which are postulated below.

- Spinal cord stimulation has been studied in the last couple of years. In a long case study, 8 patients were given spinal cord stimulation via insertion of a percutaneous lead at the appropriate level of the cervical or thoracic spine. Between 36 and 149 months after the stimulations, the patients were interviewed. 6 of the 8 had received initial pain relief, and three experienced long-term pain relief. Spinal cord stimulation is cheaper than brain stimulation and less invasive, and is thus a more promising option for pain treatment.

- In 2007, Dr. V. S. Ramachandran and his lab proposed that caloric stimulation might be effective in treating Dejerine–Roussy syndrome. They hypothesized that if cold water was streamed into the ear down the auditory canal, the symptoms associated with Dejerine–Roussy syndrome would be alleviated. Ramachandran stated that he had carried out provisional experiments on two patients and believed that their reactions supported his theory.

When a stroke has been diagnosed, various other studies may be performed to determine the underlying cause. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary since the cause of stroke varies with age, comorbidity and the clinical presentation. The following are commonly used techniques:

- an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral arteries;

- an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream);

- a Holter monitor study to identify intermittent abnormal heart rhythms;

- an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation);

- blood tests to determine if blood cholesterol is high, if there is an abnormal tendency to bleed, and if some rarer processes such as homocystinuria might be involved.

For hemorrhagic strokes, a CT or MRI scan with intravascular contrast may be able to identify abnormalities in the brain arteries (such as aneurysms) or other sources of bleeding, and structural MRI if this shows no cause. If this too does not identify an underlying reason for the bleeding, invasive cerebral angiography could be performed but this requires access to the bloodstream with an intravascular catheter and can cause further strokes as well as complications at the insertion site and this investigation is therefore reserved for specific situations. If there are symptoms suggesting that the hemorrhage might have occurred as a result of venous thrombosis, CT or MRI venography can be used to examine the cerebral veins.

For diagnosing ischemic stroke in the emergency setting:

- CT scans ("without" contrast enhancements)

- MRI scan

For diagnosing hemorrhagic stroke in the emergency setting:

- CT scans ("without" contrast enhancements)

- MRI scan

For detecting chronic hemorrhages, MRI scan is more sensitive.

For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT documents cerebral blood flow and PET with FDG isotope the metabolic activity of the neurons.