The best way to see if anomic aphasia has developed is by using verbal as well as imaging tests. The combination of the two tests seem to be most effective, since either test done alone may give false positives or false negatives. For example, the verbal test is used to see if there is a speech disorder, and whether it is a problem in speech production or in comprehension. Patients with Alzheimer's disease have speech problems that are linked to dementia or progressive aphasias which can include anomia. The imaging test, mostly done using MRI scans, is ideal for lesion mapping or viewing deterioration in the brain. However, imaging cannot diagnose anomia on its own because the lesions may not be located deep enough to damage the white matter or damage the arcuate fasciculus. However, anomic aphasia is very difficult to associate with a specific lesion location in the brain. Therefore, the combination of speech tests and imaging tests has the highest sensitivity and specificity.

It is important to first do a hearing test, in case the patient cannot clearly hear the words or sentences needed in the speech repetition test. In the speech tests, the person is asked to repeat a sentence with common words; if the person cannot identify the word but he or she can describe it, then the person is highly likely to have anomic aphasia. However, to be completely sure, the test is given while a test subject is in an fMRI scanner, and the exact location of the lesions and areas activated by speech are pinpointed. Few simpler or cheaper options are available, so lesion mapping and speech repetition tests are the main ways of diagnosing anomic aphasia.

"Aphasia is usually first recognized by the physician who treats the person for his or her brain injury. Most individuals will undergo a magnetic resonance imaging (MRI) or computed tomography (CT) scan to confirm the presence of a brain injury and to identify its precise location." In circumstances where a person is showing possible signs of aphasia, the physician will refer him or her to a speech-language pathologist (SLP) for a comprehensive speech and language evaluation. SLPs will examine the individual's ability to express him or herself through speech, understand language in written and spoken forms, write independently, and perform socially.

The American Speech, Language, Hearing Association (ASHA) states a comprehensive assessment should be conducted in order to analyze the patient's communication functioning on multiple levels; as well as the effect of possible communication deficits on activities of daily living. Typical components of an aphasia assessment include: case history, self report, oral-motor examination, language skills, identification of environmental and personal factors, and the assessment results. A comprehensive aphasia assessment includes both formal and informal measures.

Formal assessments:

- Boston Diagnostic Aphasia Examination (BDAE): diagnoses the presence and type of aphasia, focusing on location of lesion and the underlying linguistic processes.

- Western Aphasia Battery - Revised (WAB): determines the presence, severity, and type of aphasia; and can also determine baseline abilities of patient.

- Communication Activities of Daily Living - Second Edition (CADL-2): measures functional communication abilities; focuses on reading, writing, social interactions, and varying levels of communication.

- Revised Token Test (RTT): assess receptive language and auditory comprehension; focuses on patient's ability to follow directions.

Informal Assessments:

Informal assessments aide in the diagnosis of patients with suspected aphasia.

- Conversational Speech and Language Sample

- Family Interview

- Case History or Medical Chart Review

- Behavioral Observations

Diagnostic information should be scored and analyzed appropriately. Treatment plans and individual goals should be developed based on diagnostic information, as well as patient and caregiver needs, desires, and priorities.

Following are some precautions that should be taken to avoid aphasia, by decreasing the risk of stroke, the main cause of aphasia:

- Exercising regularly

- Eating a healthy diet

- Keeping alcohol consumption low and avoiding tobacco use

- Controlling blood pressure

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

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.

The nature of the alleged mental representations that underlie the act of pointing to target body parts have been a controversial issue. Originally, it was diagnosed as the effects of general mental deterioration or of aphasia on the task of pointing to body parts on verbal command. However, contemporary neuropsychological therapy seeks to establish the independence of autotopagnosia from other disorders. With such a general definition, a patient that presents with a dysfunction of or failure in accessing one of four mental representation systems suffers from autotopagnosia. Through observational testing, the type of mental misrepresentation of the body can be deduced: whether "semantic", "visuospatial", "somatosensory", or "motor misrepresentations". Neuropsychological tests can provide a proper diagnosis in regards to the specificity of patient’s agnosic condition.

1) Test 1: Body Part Localization: Free vision and no vision conditions

2) Test 2: On-line positioning of body vis-à-vis objects

3) Test 3: Localization of objects on the body surface

4) Test 4: Body part semantic knowledge

5) Test 5: Matching body parts: Effect of viewing angle

When addressing Wernicke’s aphasia, according to Bakheit et al. (2007), the lack of awareness of the language impairments, a common characteristic of Wernicke’s aphasia, may impact the rate and extent of therapy outcomes. Klebic et al. (2011) suggests that people benefit from continuing therapy upon discharge from the hospital to ensure generalization. Robey (1998) determined that at least 2 hours of treatment per week is recommended for making significant language gains. Spontaneous recovery may cause some language gains, but without speech-language therapy, the outcomes can be half as strong as those with therapy.

When addressing Broca’s aphasia, better outcomes occur when the person participates in therapy, and treatment is more effective than no treatment for people in the acute period. Two or more hours of therapy per week in acute and post-acute stages produced the greatest results. High intensity therapy was most effective, and low intensity therapy was almost equivalent to no therapy.

People with global aphasia are sometimes referred to as having irreversible aphasic syndrome, often making limited gains in auditory comprehension, and recovering no functional language modality with therapy. With this said, people with global aphasia may retain gestural communication skills that may enable success when communicating with conversational partners within familiar conditions. Process-oriented treatment options are limited, and people may not become competent language users as readers, listeners, writers, or speakers no matter how extensive therapy is. However, people’s daily routines and quality of life can be enhanced with reasonable and modest goals. After the first month, there is limited to no healing to language abilities of most people. There is a grim prognosis leaving 83% who were globally aphasic after the first month they will remain globally aphasic at the first year. Some people are so severely impaired that their existing process-oriented treatment approaches offer signs of progress, and therefore cannot justify the cost of therapy.

Perhaps due to the relative rareness of conduction aphasia, few studies have specifically studied the effectiveness of therapy for people with this type of aphasia. From the studies performed, results showed that therapy can help to improve specific language outcomes. One intervention that has had positive results is auditory repetition training. Kohn et al. (1990) reported that drilled auditory repetition training related to improvements in spontaneous speech, Francis et al. (2003) reported improvements in sentence comprehension, and Kalinyak-Fliszar et al. (2011) reported improvements in auditory-visual short-term memory.

Most acute cases of aphasia recover some or most skills by working with a speech-language pathologist. Recovery and improvement can continue for years after the stroke. After the onset of Aphasia, there is approximately a six-month period of spontaneous recovery; during this time, the brain is attempting to recover and repair the damaged neurons. Improvement varies widely, depending on the aphasia's cause, type, and severity. Recovery also depends on the person's age, health, motivation, handedness, and educational level.

There is no one treatment proven to be effective for all types of aphasias. The reason that there is no universal treatment for aphasia is because of the nature of the disorder and the various ways it is presented, as explained in the above sections. Aphasia is rarely exhibited identically, implying that treatment needs to be catered specifically to the individual. Studies have shown that, although there is no consistency on treatment methodology in literature, there is a strong indication that treatment in general has positive outcomes. Therapy for aphasia ranges from increasing functional communication to improving speech accuracy, depending on the person's severity, needs and support of family and friends. Group therapy allows individuals to work on their pragmatic and communication skills with other individuals with aphasia, which are skills that may not often be addressed in individual one-on-one therapy sessions. It can also help increase confidence and social skills in a comfortable setting.

Evidence dose not support the use of transcranial direct current stimulation (tDCS) for improving aphasia after stroke.

Specific treatment techniques include the following:

- Copy and Recall Therapy (CART) - repetition and recall of targeted words within therapy may strengthen orthographic representations and improve single word reading, writing, and naming

- Visual Communication Therapy (VIC) - the use of index cards with symbols to represent various components of speech

- Visual Action Therapy (VAT) - typically treats individuals with global aphasia to train the use of hand gestures for specific items

- Functional Communication Treatment (FCT) - focuses on improving activities specific to functional tasks, social interaction, and self-expression

- Promoting Aphasic's Communicative Effectiveness (PACE) - a means of encouraging normal interaction between people with aphasia and clinicians. In this kind of therapy the focus is on pragmatic communication rather than treatment itself. People are asked to communicate a given message to their therapists by means of drawing, making hand gestures or even pointing to an object

- Melodic Intonation Therapy (MIT) - aims to use the intact melodic/prosodic processing skills of the right hemisphere to help cue retrieval of words and expressive language

- Other - i.e. drawing as a way of communicating, trained conversation partners

Semantic feature analysis (SFA) -a type of aphasia treatment that targets word-finding deficits. It is based on the theory that neural connections can strengthened by using using related words and phrases that are similar to the target word, to eventually activate the target word in the brain. SFA can be implemented in multiple forms such as verbally, written, using picture cards, etc. The SLP provides prompting questions to the individual with aphasia in order for the person to name the picture provided. Studies show that SFA is an effective intervention for improving confrontational naming.

Melodic intonation therapy is used to treat non-fluent aphasia and has proved to be effective in some cases. However, there is still no evidence from randomized controlled trials confirming the efficacy of MIT in chronic aphasia. MIT is used to help people with aphasia vocalize themselves through speech song, which is then transferred as a spoken word. Good candidates for this therapy include people who have had left hemisphere strokes, non-fluent aphasias such as Broca's, good auditory comprehension, poor repetition and articulation, and good emotional stability and memory. An alternative explanation is that the efficacy of MIT depends on neural circuits involved in the processing of rhythmicity and formulaic expressions (examples taken from the MIT manual: “I am fine,” “how are you?” or “thank you”); while rhythmic features associated with melodic intonation may engage primarily left-hemisphere subcortical areas of the brain, the use of formulaic expressions is known to be supported by right-hemisphere cortical and bilateral subcortical neural networks.

According to the National Institute on Deafness and Other Communication Disorders (NIDCD), involving family with the treatment of an Aphasic loved one is ideal for all involved, because while it will no doubt assist in their recovery, it will also make it easier for members of the family to learn how best to communicate with them.

According to Bates et al. (2005), "the primary goal of rehabilitation is to prevent complications, minimize impairments, and maximize function". The topics of intensity and timing of intervention are widely debated across various fields. Results are contradictory: some studies indicate better outcomes with early intervention, while other studies indicate starting therapy too early may be detrimental to the patient's recovery. Recent research suggests, that therapy be functional and focus on communication goals that are appropriate for the patient's individual lifestyle.

Specific treatment considerations for working with individuals with Wernicke's aphasia (or those who exhibit deficits in auditory comprehension) include using familiar materials,using shorter and slower utterances when speaking, giving direct instructions, and using repetition as needed.

Neuroplasticity: Role in Recovery

Neuroplasticity is defined as the brain's ability to reorganize itself, lay new pathways, and rearrange existing ones, as a result of experience. Neuronal changes after damage to the brain such as collateral sprouting, increased activation of the homologous areas, and map extension demonstrate the brain's neuroplastic abilities. According to Thomson, "Portions of the right hemisphere, extended left brain sites, or both have been shown to be recruited to perform language functions after brain damage. All of the neuronal changes recruit areas not originally or directly responsible for large portions of linguistic processing. Principles of neuroplasticity have been proven effective in neurorehabilitation after damage to the brain. These principles include: incorporating multiple modalities into treatment to create stronger neural connections, using stimuli that evoke positive emotion, linking concepts with simultaneous and related presentations, and finding the appropriate intensity and duration of treatment for each individual patient.

There is no method available to completely cure anomic aphasia. However, there are treatments to help improve word-finding skills.

Although a person with anomia may find it difficult to recall many types of words such as common nouns, proper nouns, verbs, etc., many studies have shown that treatment for object words, or nouns, has shown promise in rehabilitation research. The treatment includes visual aids, such as pictures, and the patient is asked to identify the object or activity. However, if that is not possible, then the patient is shown the same picture surrounded by words associated with the object or activity. Throughout the process, positive encouragement is provided. The treatment shows an increase in word-finding during treatment; however, word identifying decreased two weeks after the rehabilitation period. Therefore, it shows that rehabilitation effort needs to be continuous for word-finding abilities to improve from the baseline. The studies show that verbs are harder to recall or repeat, even with rehabilitation.

Other methods in treating anomic aphasia include Circumlocution Induced Naming therapy (CIN), wherein the patient uses circumlocution to assist with his or her naming rather than just being told to name the item pictured after given some sort of cue. Results suggest that the patient does better in properly naming objects when undergoing this therapy because CIN strengthens the weakened link between semantics and phonology for patients with anomia, since they often know what an object is used for but cannot verbally name it.

Anomia is often burdensome on the families and friends of those suffering from it. One way to overcome this burden is computer-based treatment models, effective especially when used with clinical therapy. Leemann et al. provided anomic patients with computerized-assisted therapy (CAT) sessions, along with traditional therapy sessions using treatment lists of words. Some of the patients received a drug known to help relieve symptoms of anomia (levodopa) while others received a placebo. The researchers found that the drug had no significant effects on improvement with the treatment lists, but almost all of the patients improved after the CAT sessions. They concluded that this form of computerized treatment is effective in increasing naming abilities in anomic patients.

Additionally, one study researched the effects of using "excitatory (anodal) transcranial direct current stimulation" over the right temporo-parietal cortex, a brain area that seems to correlate to language. The electrical stimulation seemed to enhance language training outcome in patients with chronic aphasia.

As autotopagnosia is not a life-threatening condition it is not on the forefront of medical research. Rather, more research is conducted regarding treatments and therapies to alleviate the lesions and traumas that can cause autotopagnosia. Of all the agnosias, visual agnosia is the most common subject of investigation because it is easiest to assess and has the most promise for potential treatments. Most autotopagnosia studies are centered on a few test subjects as part of a group of unaffected or “controlled” participants, or a simple case study. Case studies surrounding a single patient are most common due to the vague nature of the disease.

Imaging studies have shown differing results which probably represents the heterogeneity of language problems than can occur in PNFA. However, classically atrophy of left perisylvian areas is seen.

Comprehensive meta-analyses on MRI and FDG-PET studies identified alterations in the whole left frontotemporal network for phonological and syntactical processing as the most consistent finding. Based on these imaging methods, progressive nonfluent aphasia can be regionally dissociated from the other subtypes of frontotemporal lobar degeneration, frontotemporal dementia and semantic dementia.

There is no curative treatment for this condition. Supportive management is helpful.

There is currently no known curative treatment for SD. The average duration of illness is 8–10 years, and its progression cannot be slowed. Progression of SD can lead to behavioral and social difficulties, thus supportive care is essential for improving quality of life in SD patients as they grow more incomprehensible.

Continuous practice in lexical learning has been shown to improve semantic memory in SD patients.

SD has no known preventative measures.

Currently, the specific causes for PPA and other degenerative brain disease similar to PPA are unknown. Autopsies have revealed a variety of brain abnormalities in people who had PPA. These autopsies, as well as imaging techniques such as CT scans, MRI, EEG, single photon emission computed tomography (SPECT), and positron emission tomography (PET), have generally revealed abnormalities to be almost exclusively in the left hemisphere.

Due to the progressive, continuous nature of the disease, improvement over time seldom occurs in patients with PPA as it often does in patients with aphasias caused by trauma to the brain.

In terms of medical approaches to treating PPA, there are currently no drugs specifically used for patients with PPA, nor are there any specifically designed interventions for PPA. A large reason for this is the limited research that has been done on this disease. However, in some cases, patients with PPA are prescribed the same drugs Alzheimer's patients are normally prescribed.

The primary approach to treating PPA has been with behavioral treatment, with the hope that these methods can provide new ways for patients to communicate in order to compensate for their deteriorated abilities. Speech therapy can assist an individual with strategies to overcome difficulties. There are three very broad categories of therapy interventions for aphasia: restorative therapy approaches, compensatory therapy approaches, and social therapy approaches. Rapid and sustained improvement in speech and dementia in a patient with primary progressive aphasia utilizing off-label perispinal etanercept, an anti-TNF treatment strategy also used for Alzheimer's, has been reported. A video depicting the patient's improvement was published in conjunction with the print article. These findings have not been independently replicated and remain controversial.

Visual agnosia is an impairment in recognition of visually presented objects. It is not due to a deficit in vision (acuity, visual field, and scanning), language, memory, or low intellect. While cortical blindness results from lesions to primary visual cortex, visual agnosia is often due to damage to more anterior cortex such as the posterior occipital and/or temporal lobe(s) in the brain. There are two types of visual agnosia: apperceptive agnosia and associative agnosia.

Recognition of visual objects occurs at two primary levels. At an apperceptive level, the features of the visual information from the retina are put together to form a perceptual representation of an object. At an associative level, the meaning of an object is attached to the perceptual representation and the object is identified. If a person is unable to recognize objects because they cannot perceive correct forms of the objects, although their knowledge of the objects is intact (i.e. they do not have anomia), they have apperceptive agnosia. If a person correctly perceives the forms and has knowledge of the objects, but cannot identify the objects, they have associative agnosia.

Broadly, visual agnosia is divided into apperceptive and associative visual agnosia.

Apperceptive agnosia is failure of object recognition even when the basic visual functions (acuity, color, motion) and other mental processing, such as language and intelligence, are normal. The brain must correctly integrate features such as edges, light intensity, and color from sensory information to form a complete percept of an object. If a failure occurs during this process, a percept of an object is not fully formed and thus it cannot be recognized. Tasks requiring copying, matching, or drawing simple figures can distinguish the individuals with apperceptive agnosia because they cannot perform such tasks.

Associative agnosia is an inability to identify objects even with apparent perception and knowledge of them. It involves a higher level of processing than apperceptive agnosia. Individuals with associative agnosia can copy or match simple figures, indicating that they can perceive objects correctly. They also display the knowledge of objects when tested with tactile or verbal information. However, when tested visually, they cannot name or describe common objects. This means that there is an impairment in associating the perception of objects with the stored knowledge of them.

Although visual agnosia can be general, there exist many variants that impair recognition of specific types. These variants of visual agnosia include prosopagnosia (inability to recognize faces), pure word blindness (inability to recognize words, often called "agnosic alexia" or "pure alexia"), agnosias for colors (inability to differentiate colors), agnosias for the environment (inability to recognize landmarks or difficult with spatial layout of an environment, i.e. topographagnosia) and simultanagosia (inability to sort out multiple objects in a visual scene).

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.

Semantic dementia (SD), also known as semantic variant primary progressive aphasia (svPPA), is a progressive neurodegenerative disorder characterized by loss of semantic memory in both the verbal and non-verbal domains. However, the most common presenting symptoms are in the verbal domain (with loss of word meaning). SD is one of the three canonical clinical syndromes associated with frontotemporal lobar degeneration (FTLD), with the other two being frontotemporal dementia and progressive nonfluent aphasia. SD is a clinically defined syndrome, but is associated with predominantly temporal lobe atrophy (left greater than right) and hence is sometimes called temporal variant FTLD (tvFTLD). SD is one of the three variants of Primary Progressive Aphasia (PPA), which results from neurodegenerative disorders such as FTLD or Alzheimer's disease. It is important to note the distinctions between Alzheimer’s Disease and Semantic dementia with regard to types of memory affected. In general, Alzheimer’s Disease is referred to as disorder affecting mainly episodic memory, defined as the memory related to specific, personal events distinct for each individual. Semantic dementia generally affects semantic memory, which refers to long-term memory that deals with common knowledge and facts.3

It was first described by Arnold Pick in 1904 and in modern times was characterized by Professor Elizabeth Warrington in 1975, but it was not given the name semantic dementia until 1989. The clinical and neuropsychological features, and their association with temporal lobe atrophy were described by Professor John Hodges and colleagues in 1992.

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

Disconnection syndrome is a general term for a number of neurological symptoms caused by damage to the white matter axons of communication pathways—via lesions to association fibers or commissural fibers—in the cerebrum, independent of any lesions to the cortex. The behavioral effects of such disconnections are relatively predictable in adults. Disconnection syndromes usually reflect circumstances where regions A and B still have their functional specializations except in domains that depend on the interconnections between the two regions.

Callosal syndrome, or split-brain, is an example of a disconnection syndrome from damage to the corpus callosum between the two hemispheres of the brain. Disconnection syndrome can also lead to aphasia, left-sided apraxia, and tactile aphasia, among other symptoms. Other types of disconnection syndrome include conduction aphasia (lesion of the association tract connecting Broca’s area and Wernicke’s), agnosia, apraxia, pure alexia, etc.

Diagnosis may be clinical if associated with dementia and other etiologies. In cases caused by stroke, MRI will show a corresponding stroke in the inferior parietal lobule. In the acute stage, this will be bright (restricted diffusion) on the DWI sequence and dark at the corresponding area on the ADC sequence.

Gerstmann syndrome is a neuropsychiatric disorder that is characterized by a constellation of symptoms that suggests the presence of a lesion in a particular area of the brain. (It should not be confused with Gerstmann-Sträussler-Scheinker syndrome, which is a transmissible spongiform encephalopathy.) Damage to the inferior parietal lobule of the dominant hemisphere results in Gerstmann's syndrome.

It is named for Josef Gerstmann.

There is much research that needs to be conducted on CCAS. A necessity for future research is to conduct more longitudinal studies in order to determine the long-term effects of CCAS. One way this can be done is by studying cerebellar hemorrhage that occurs during infancy. This would allow CCAS to be studied over a long period to see how CCAS affects development. It may be of interest to researchers to conduct more research on children with CCAS, as the survival rate of children with tumors in the cerebellum is increasing. Hopefully future research will bring new insights on CCAS and develop better treatments.

Many studies have shown that disconnection syndromes such as aphasia, agnosia, apraxia, pure alexia and many others are not caused by direct damage to functional neocortical regions. They can also be present on only one side of the body which is why these are categorized as hemispheric disconnections. The cause for hemispheric disconnection is if the interhemispheric fibers, as mentioned earlier, are cut or reduced.

An example is commissural disconnect in adults which usually results from surgical intervention, tumor, or interruption of the blood supply to the corpus callosum or the immediately adjacent structures. Callosal disconnection syndrome is characterized by left ideomotor apraxia and left-hand agraphia and/or tactile anomia, and is relatively rare.

Other examples include commissurotomy, the surgical cutting of cerebral commissures to treat epilepsy and callosal agenesis which is when individuals are born without a corpus callosum. Those with callosal agenesis can still perform interhemispheric comparisons of visual and tactile information but with deficits in processing complex information when performing the respective tasks.