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

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.

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.

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.

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.

Logopenic progressive aphasia (LPA) is a form of primary progressive aphasia. It is defined clinically by impairments in naming and sentence repetition. It is similar to conduction aphasia and is associated with atrophy to the left posterior temporal cortex and inferior parietal lobule. It is suspected that an atypical form of Alzheimer's disease is the most common cause of logopenic progressive aphasia.

Although patients with the logopenic variant of PPA are still able to produce speech, their speech rate may be significantly slowed down due to word retrieval difficulty. Over time, they may experience the inability to retain lengthy information, causing problems with understanding complex verbal information. Some additional behavioral features include irritability, anxiety and agitation.

Compared to other forms of primary progressive aphasia, the logopenic variant has been found to be associated with cognitive and behavioral characteristics. Studies have shown that patients with the logopenic variant perform significantly worse on tests of calculation than other primary progressive aphasia patients. Several logopenic variant patients, especially those with Alzheimer’s disease pathology, have also been found to perform poorly on memory tasks.

Logopenic progressive aphasia is caused by damage to segregated brain regions, specifically the inferior parietal lobe and superior temporal regions. Difficulties in naming are produced from the thinning of the inferior parietal lobe. Damage to the dorsal pathways creates language deficiency in patients that is characteristic of logopenic progressive aphasia.

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.

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.

The two main categories of visual agnosia are:

- Apperceptive visual agnosia, impaired object recognition. Individuals with apperceptive visual agnosia cannot form a whole percept of visual information.

- Associative visual agnosia, impaired object identification. Individuals with associative agnosia cannot give a meaning to a formed percept. The percept is created, but it would have no meaning for individuals who have an associative agnosia.

MRI is often done to diagnose PSP. MRI may show atrophy in the midbrain with preservation of the pons giving a "hummingbird" sign appearance.

PSP is frequently misdiagnosed as Parkinson's disease because of the slowed movements and gait difficulty, or as Alzheimer's disease because of the behavioral changes. It is one of a number of diseases collectively referred to as Parkinson plus syndromes. A poor response to levodopa along with symmetrical onset can help differentiate this disease from PD. Also, patients with the Richardson variant tend to have an upright or arched-back posture as opposed to the stooped-forward posture of other Parkinsonian disorders, although PSP-Parkinsonism (see below) may show the stooped posture. Early falls are characteristic, especially with Richardson-syndrome.

Currently there is no single diagnosis test for MS that is 100% sensitive and specific. To have such a thing would require a standardised definition of the disease, which currently does not exist. The most commonly used definition, based in the McDonald criteria, focuses in the presence and distribution of the lesions, not in the underlying condition that produces them. Therefore, even twins with the same underlying condition can be classified different

Silent MS has been found in autopsies before the existence of MRI showing that the so-called "clinical definitions" cannot be applied to around 25% of the MS cases. Currently a distinction is made between "silent" and subclinical.

In absence of attacks, sometimes a radiological finding suggestive of demyelination (T2 hyperintensities) can be used to establish a pre-diagnosis of MS. This is often named "Radiologically Isolated Syndrome" (RIS). Cases before the first attack or CIS are subclinical in the sense that they do not produce clinical situations.

If a second radiological event appears without clinical consequences, the clinical situation is named "Silent MS" (Okuda criteria).

It has been noted that some aspects of the MS underlying condition are present in otherwise healthy MS patients' relatives, suggesting a wider scope for the "silent MS" term.

In these cases Interleukin-8 is a risk for clinical conversion. It has also been proposed that always exists a subclinical phase in the beginning of every MS case, during which the permeability of the BBB can be used for diagnosis

It is also under investigation wether MS has a prodrome, i.e. a stage in which the disease exists with non-specific symptoms. Some reports point to a prodrome of several years for RRMS and decades for PPMS.

Variant Creutzfeldt–Jakob disease (vCJD) or new variant Creutzfeldt–Jakob disease (nvCJD) is a transmissible spongiform encephalopathy which was identified in 1996 by the National CJD Surveillance Unit in Edinburgh, Scotland. It is always fatal and is caused by prions, which are mis-folded proteins. Over 170 cases of vCJD have been recorded in the United Kingdom, and around 30 cases in the rest of the world. The fact that the epidemiology of the disease coincided with an epidemic of bovine spongiform encephalopathy led to the hypothesis that consumption of BSE-infected beef caused the disease. It is a different disease from Sporadic and Familial Creutzfeldt–Jakob disease, though it is believed to be caused by the same pathogenic agent, a mis-folded protein, known as a prion.

Despite the consumption of contaminated beef in the UK being reckoned to be quite high, vCJD has infected a comparatively small cohort of people. One explanation for this can be found in the genetics of patients with the disease. The human PRNP protein which is subverted in prion disease can occur with either methionine or valine at amino acid 129, without any apparent difference in normal function. Of the overall Caucasian population, about 40% have two methionine-containing alleles, 10% have two valine-containing alleles, and the other 50% are heterozygous at this position. Only a single vCJD patient tested was found to be heterozygous; most of those affected had two copies of the methionine-containing form. Additionally, for unknown reasons, those affected are generally under the age of 40. It is not yet known whether those unaffected are actually immune or only have a longer incubation period until symptoms appear.

Abdominal ultrasound is of some benefit, but not diagnostic. Features that suggest posterior urethral valves are bilateral hydronephrosis, a thickened bladder wall with thickened smooth muscle trabeculations, and bladder diverticula.

Voiding cystourethrogram (VCUG) is more specific for the diagnosis. Normal "plicae circularis" are variable in appearance and often not seen on normal VCUGs. PUV on voiding cystourethrogram is characterized by an abrupt tapering of urethral caliber near the verumontanum, with the specific level depending on the developmental variant. Vesicoureteral reflux is also seen in over 50% of cases. Very often the posterior urethra maybe dilated thus making the abrupt narrowing more obvious. the bladder wall may show trabeculations or sacculations or even diverticuli.

Diagnosis can also be made by cystoscopy, where a small camera is inserted into the urethra for direct visualization of the posteriorly positioned valve. A limitation of this technique is that posterior valve tissue is translucent and can be pushed against the wall of the urethra by inflowing irrigation fluid, making it difficult to visualize. Cystoscopy may also demonstrate the bladder changes.

Centers in Europe and Japan have also had excellent results with cystosonography, although it has not been approved for use in the United States yet.

Based on studies conducted in the United States, the prognosis for individuals with ALECT2 amyloidosis is guarded, particularly because they are elderly and their kidney disease is usually well-advanced at the time of presentation. End-stage renal disease develops in 1 out of 3 patients and has a median renal survival of 62 months. A suggested prognostic tool is to track creatinine levels in ALect2 patients. The attached Figure gives survival plotss for individuals with LECT2 renal amyloidosis and serum creatinine levels less than 2 mg/100 ml versus 2 mg/100 ml or greater than 2 mg/100 ml. The results show that afflicted individuals with lower creatinine levels have a ~four-fold higher survival rate.

If suspected antenatally, a consultation with a paediatric surgeon/ paediatric urologist maybe indicated to evaluate the risk and consider treatment options.

Treatment is by endoscopic valve ablation. Fetal surgery is a high risk procedure reserved for cases with severe oligohydramnios, to try to limit the associated lung underdevelopment, or pulmonary hypoplasia, that is seen at birth in these patients. The risks of fetal surgery are significant and include limb entrapment, abdominal injury, and fetal or maternal death. Specific procedures for "in utero" intervention include infusions of amniotic fluid, serial bladder aspiration, and creating a connection between the amniotic sac and the fetal bladder, or vesicoamniotic shunt.

There are three specific endoscopic treatments of posterior urethral valves:

- Vesicostomy followed by valve ablation - a stoma, or hole, is made in the urinary bladder, also known as "low diversion", after which the valve is ablated and the stoma is closed.

- Pyelostomy followed by valve ablation - stoma is made in the pelvis of the kidney as a slightly "high diversion", after which the valve is ablated and the stoma is closed

- Primary (transurethral) valve ablation - the valve is removed through the urethra without creation of a stoma

The standard treatment is primary (transurethral) ablation of the valves. Urinary diversion is used in selected cases, and its benefit is disputed.

Following surgery, the follow-up in patients with posterior urethral valve syndrome is long term, and often requires a multidisciplinary effort between paediatric surgeons/ paediatric urologists, pulmonologists, neonatologists, radiologists and the family of the patient. Care must be taken to promote proper bladder compliance and renal function, as well as to monitor and treat the significant lung underdevelopment that can accompany the disorder. Definitive treatment may also be indicated for the vesico-ureteral reflux.

There has too little experience on the treatment of LECT2 amyloidosis to establish recommendations other than offering methods to support kidney function and dialysis. Nonetheless, it is important to accurately diagnose ALECT2-based amyloid disease in order to avoid treatment for other forms of amyloidosis.

Penetrating karatoplasty and endothelial keratoplasty can be used as treatments for severe cases of ICE [2,8]. Because glaucoma and elevated intraocular pressure are often present in ICE patients, long term follow up may be needed to ensure adequate intraocular pressures are maintained [2,7]

The disease is chronic and often progresses slowly. Prognosis is generally poor when associated with glaucoma [1,2].

Mutations in the GM2A gene cause GM2-gangliosidosis, AB variant. This condition is inherited in an autosomal recessive pattern.

The GM2A gene provides instructions for making a protein called the GM2 activator. This protein is required for the normal function of beta-hexosaminidase A, a critical enzyme in the nervous system that breaks down a lipid called GM2 ganglioside. If mutations in both alleles at this locus disrupt the activity of the GM2 activator, beta-hexosaminidase A cannot perform its normal function. As a result, gangliosides accumulate in the central nervous system until they interfere with normal biological processes. Progressive damage caused by buildup of gangliosides leads to the destruction of nerve cells.

GM2-gangliosidosis, AB variant is extremely rare. In contrast with both Tay-Sachs disease and Sandhoff disease, in which many mutant polymorphic alleles have been discovered, including pseudodeficiency alleles, very few GM2A mutations have been reported. When AB variant is reported, in often occurs with consanguineous parents or in genetically isolated populations.

GM2A is expressed in many tissues, and the GM2 activator protein has been reported to have other cellular functions. Because AB variant is so rarely diagnosed, it is likely that most mutations of GM2A are fatal at the embryionic or fetal stage of development in homozygotes and genetic compounds, and thus are never observed clinically.

Whether MTHFR deficiency has any effect at all on all-cause mortality is unclear. One Dutch study showed that the MTHFR mutation was more prevalent in younger individuals (36% relative to 30%), and found that elderly men with MTHFR had an elevated mortality rate, attributable to cancer. Among women, however, no difference in life expectancy was seen. More recently, however, a meta-analysis has shown that overall cancer rates are barely increased with an odds ratio of 1.07, which suggests that an impact on mortality from cancer is small or zero.

Courses of treatment for children with is dependent upon the severity of their case. Children with OHS often receive physical and occupational therapy. They may require a feeding tube to supplement nourishment if they are not growing enough. In an attempt to improve the neurological condition (seizures) copper histidine or copper chloride injections can be given early in the child’s life.

However, copper histidine injections have been shown ineffective in studies of copper metabolic-connective tissue disorders such as OHS.