In terms of the specific rehabilitation of visuoperceptual disorders such as Bálint's syndrome, the literature is extremely sparse. According to one study, rehabilitation training should focus on the improvement of visual scanning, the development of visually guided manual movements, and the improvement of the integration of visual elements. Very few treatment strategies have been proposed, and some of those have been criticized as being poorly developed and evaluated.

Three approaches to rehabilitation of perceptual deficits, such as those seen in Bálint's syndrome, have been identified:

1. The adaptive (functional) approach, which involves functional tasks utilising the person's strengths and abilities, helping them to compensate for problems or altering the environment to lessen their disabilities. This is the most popular approach.

2. The remedial approach, which involves restoration of the damaged CNS by training in the perceptual skills, which may be generalised across all activities of daily living. This could be achieved by tabletop activities or sensorimotor exercises.

3. The multicontext approach, which is based on the fact that learning is not automatically transferred from one situation to another. This involves practicing of a targeted strategy in a multiple environment with varied tasks and movement demands, and it incorporates self-awareness tasks.

The validity of Bálint's syndrome has been questioned by some. The components in the syndrome's triad of defects (simultanagnosia, oculomotor apraxia, optic ataxia) each may represent a variety of combined defects.

As autotopagnosia arises from neurological and irreversible damage, options regarding symptom reversal or control are limited. As of April 2010, there are no known specific treatments for autotopagnosia.

No medications or pharmaceutical remedies have been approved by the U.S. Food and Drug Administration to treat or cure autotopagnosia. There have been cases in which extensive rehabilitation has been beneficial following restitution, repetitive training to correct the impaired function, and compensation of other skills to make up for the deficit. Rehabilitation is not a definitive treatment and only shows signs of slight improvement in a small percentage of autotopagnosia patients. The condition of the disease can be monitored with continued neurological examination and using a CT scan to note the progression of the parietal lesion.

Simultanagnosia (or simultagnosia) is a rare neurological disorder characterized by the inability of an individual to perceive more than a single object at a time. This type of visual attention problem is one of three major components (the others being optic ataxia and optic apraxia) of Bálint's syndrome, an uncommon and incompletely understood variety of severe neuropsychological impairments involving space representation (visuospatial processing). The term "simultanagnosia" was first coined in 1924 by Wolpert to describe a condition where the affected individual could see individual details of a complex scene but failed to grasp the overall meaning of the image.

Simultanagnosia can be divided into two different categories: dorsal and ventral. Ventral occipito-temporal lesions cause a mild form of the disorder, while dorsal occipito-parietal lesions cause a more severe form of the disorder.

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.

Patients with simultanagnosia, a component of Bálint's syndrome, have a restricted spatial window of visual attention and cannot see more than one object at a time in a scene that contains more than one object. For instance, if presented with an image of a table containing both food and various utensils, a patient will report seeing only one item, such as a spoon. If the patient's attention is redirected to another object in the scene, such as a glass, the patient will report that they see the glass but no longer see the spoon. As a result of this impairment, simultanagnosic patients often fail to comprehend the overall meaning of a scene.

In addition, patients note that one stationary object may spontaneously disappear from view as they become aware of another object in the scene.

Simultanagnosic patients often exhibit a phenomenon known as "local capture" where they only identify the local elements of stimuli containing local and global features. However, recent studies have demonstrated that implicit processing of the global structure can occur. With the appropriate stimulus conditions, explicit processing of the global form may occur. For example, a study performed with Navon hierarchical letters, which are large letters composed of smaller ones, revealed that the use of smaller and denser Navon letters biased the patient towards global processing.

Adie's syndrome is not life-threatening or disabling. As such, there is no mortality rate relating to the condition; however, loss of deep tendon reflexes is permanent and may progress over time.

The usual treatment of a standardised Adie syndrome is to prescribe reading glasses to correct for impairment of the eye(s). Pilocarpine drops may be administered as a treatment as well as a diagnostic measure. Thoracic sympathectomy is the definitive treatment of diaphoresis, if the condition is not treatable by drug therapy.

Amnesia can result from a side-effect of prescription or non-prescription drugs. Both substance use and alcohol can cause both long-term and short-term memory loss, resulting in blackouts.

The most commonly used group of prescription drugs which can produce amnesia are benzodiazepines, especially if combined with alcohol, however, in limited quantities, triazolam (Halcion) is not associated with amnesia or memory impairment.

Since Usher syndrome results from the loss of a gene, gene therapy that adds the proper protein back ("gene replacement") may alleviate it, provided the added protein becomes functional. Recent studies of mouse models have shown one form of the disease—that associated with a mutation in myosin VIIa—can be alleviated by replacing the mutant gene using a lentivirus. However, some of the mutated genes associated with Usher syndrome encode very large proteins—most notably, the "USH2A" and "GPR98" proteins, which have roughly 6000 amino-acid residues. Gene replacement therapy for such large proteins may be difficult.

There is no cure for Williams syndrome. Suggestions include avoidance of extra calcium and vitamin D, as well as treating high levels of blood calcium. Blood vessel narrowing can be a significant health problem, and is treated on an individual basis.

Physical therapy is helpful to patients with joint stiffness and low muscle tone. Developmental and speech therapy can also help children and increase the success of their social interactions. Other treatments are based on a patient's particular symptoms.

The American Academy of Pediatrics recommends annual cardiology evaluations for individuals with Williams syndrome. Other recommended assessments include: ophthalmologic evaluations, an examination for inguinal hernia, objective hearing assessment, blood pressure measurement, developmental and growth evaluation, orthopedic assessments on joints, muscle tone, and ongoing feeding and dietary assessments to manage constipation and urinary problems.

Behavioral treatments have been shown to be effective. In regards to social skills it may be effective to channel their nature by teaching basic skills. Some of these are the appropriate way to approach someone, how and when to socialize in settings such as school or the workplace, and warning of the signs and dangers of exploitation. For the fear that they demonstrate cognitive-behavioral approaches, such as therapy, are the recommended treatment. One of the things to be careful of with this approach is to make sure that the patients' charming nature does not mask any underlying feelings.

Perhaps the most effective treatment for those with Williams syndrome is music. Those with Williams syndrome have shown a relative strength in regards to music, albeit only in pitch and rhythm tasks. Not only do they show a strength in the field but also a particular fondness for it. It has been shown that music may help with the internal and external anxiety that these people are more likely to be afflicted with. Something of note is that the typical person processes music in the superior temporal and middle temporal gyri. Those with Williams syndrome have a reduced activation in these areas but an increase in the right amygdala and cerebellum.

People affected by Williams syndrome are supported by multiple organizations, including the Canadian Association for Williams Syndrome and the Williams Syndrome Registry.

Treatment of Aicardi syndrome primarily involves management of seizures and early/continuing intervention programs for developmental delays.

Additional comorbidities and complications sometimes seen with Aicardi syndrome include porencephalic cysts and hydrocephalus, and gastro-intestinal problems. Treatment for porencephalic cysts and/or hydrocephalus is often via a shunt or endoscopic of the cysts, though some require no treatment. Placement of a feeding tube, fundoplication, and surgeries to correct hernias or other gastrointestinal structural problems are sometimes used to treat gastro-intestinal issues.

Mirhosseini–Holmes–Walton syndrome is a syndrome which involves retinal degeneration, cataract, microcephaly, and mental retardation. It was first characterized in 1972.

There is evidence that this syndrome has a different mutation in the same gene as Cohen syndrome.

Amnesia is desirable during surgery, since a general anaesthetic should also give the person amnesia for the operation. Sedatives such as benzodiazepines, which are commonly used for anxiety disorders, can reduce the encoding of new memories, particularly in high doses (for example, prior to surgery in order for a person not to recall the surgery). Amnesiac drugs can be used to induce a coma for a child breathing using mechanical ventilation, or to help reduce intracranial pressure after head trauma.

Researchers are currently experimenting with drugs which induce amnesia in order to improve understanding of human memory, and develop better drugs to treat psychiatric disorders and memory related disorders. People with Alzheimer's disease and other forms of dementia are likely to benefit. By understanding the ways in which amnesia-inducing drugs interact with the brain, researchers hope to better understand the ways in which neurotransmitters aid in the formation of memory. By stimulating rather than depressing these neurotransmitters, memory may improve.

The use of a drug to erase traumatic or unwanted memories used to be referred to as "science fiction." Holmes et al. (2010) commented that the media misrepresented two recent studies as research on "erasing" traumatic memories, but showed the fear response associated with stressful memory could be greatly reduced whilst the factual memory of the trauma remained intact. Similarly, Brunet et al. (2008) found that the people with chronic Posttraumatic Stress Disorder who were treated with propranolol for a single day had a reduced response to existing trauma while retaining memory of the trauma. In the process of remembering, the memory needs to be restored in the brain. By introducing an amnesia-inducing drug during this process, the memory can be disrupted. While the memory remains intact, the emotional reaction is dampened, making the memory less overwhelming. Researchers believe this drug will help patients with post-traumatic stress disorder be able to better process the trauma without reliving the trauma emotionally. This has raised legal/ethical concerns should drugs be found to have altered the memory of traumatic events that occur in victims of crimes (e.g. rape), and whether it is therapeutically desirable to do so.

A syndrome is a set of medical signs and symptoms occurring together, constitutes a particular disease or disorder. The word derives from the Greek σύνδρομον, meaning "concurrence". In some instances, a syndrome is so closely linked with a pathogenesis or cause that the words "syndrome", "disease", and "disorder" end up being used interchangeably for them. This is especially true of inherited syndromes. For example, Down syndrome, Wolf–Hirschhorn syndrome, and Andersen syndrome are disorders with known pathogeneses, so each is more than just a set of signs and symptoms, despite the "syndrome" nomenclature. In other instances, a syndrome is not specific to only one disease. For example, toxic shock syndrome can be caused by various toxins; premotor syndrome can be caused by various brain lesions; and premenstrual syndrome is not a disease but simply a set of symptoms.

If an underlying genetic cause is suspected but not known, a condition may be referred to as a genetic association (often just "association" in context). By definition, an association indicates that the collection of signs and symptoms occurs in combination more frequently than would be likely by chance alone.

Syndromes are often named after the physician or group of physicians that discovered them or initially described the full clinical picture. Such eponymous syndrome names are examples of medical eponyms. Recently, there has been a shift towards naming conditions descriptively (by symptoms or underlying cause) rather than eponymously, but the eponymous syndrome names often persist in common usage.

In medicine a broad definition of syndrome is used, which describes a collection of symptoms and findings without necessarily tying them to a single identifiable pathogenesis. The more specific definition employed in medical genetics describes a subset of all medical syndromes.

Williams syndrome (WS) is a developmental disorder that affects many parts of the body. Facial features frequently include a broad forehead, short nose, and full cheeks, an appearance that has been described as "elfin". Mild to moderate intellectual disability with particular problems with visual spatial tasks such as drawing and fewer problems with language are typical. Those affected often have an outgoing personality and interact readily with strangers. Problems with teeth, heart problems, especially supravalvular aortic stenosis, and periods of high blood calcium are common.

Williams syndrome is caused by a genetic abnormality, specifically a deletion of about 27 genes from the long arm of one of the two chromosome 7s. Typically this occurs as a random event during the formation of the egg or sperm from which a person develops. In a small number of cases it is inherited from an affected parent in an autosomal dominant manner. The different characteristic features have been linked to the loss of specific genes. The diagnosis is typically suspected based on symptoms and confirmed by genetic testing.

Treatment includes special education programs and various types of therapy. Surgery may be done to correct heart problems. Dietary changes or medications may be required for high blood calcium. The syndrome was first described in 1961 by New Zealander John C. P. Williams. Williams syndrome affects between 1 in 7,500 to 1 in 20,000 people at birth. Life expectancy is less than that of the general population mostly due to the increased rates of heart disease.

The prognosis varies widely from case to case, depending on the severity of the symptoms. However, almost all people reported with Aicardi syndrome to date have experienced developmental delay of a significant degree, typically resulting in mild to moderate to profound intellectual disability. The age range of the individuals reported with Aicardi syndrome is from birth to the mid 40s.

There is no cure for this syndrome.

There is no medical treatment for either syndrome but there are some recommendations that can help with prevention or early identification of some of the problems. Children with either syndrome should have their hearing tested, and adults should be aware that the hearing loss may not develop until the adult years. Yearly visits to an ophthalmologist or other eye care professional who has been informed of the diagnosis of Stickler or Marshall syndrome is important for all affected individuals. Children should have the opportunity to have myopia corrected as early as possible, and treatment for cataracts or detached retinas may be more effective with early identification. Support for the joints is especially important during sports, and some recommend that contact sports should be avoided by those who have very loose joints.

If the Hirschsprung's disease is treated in time, ABCD sufferers live otherwise healthy lives. If it is not found soon enough, death often occurs in infancy. For those suffering hearing loss, it is generally regressive and the damage to hearing increases over time. Digestive problems from the colostomy and reattachment may exist, but most cases can be treated with laxatives. The only other debilitating symptom is hearing loss, which is usually degenerative and can only be treated with surgery or hearing aids.

Treatment for the disease itself is nonexistent, but there are options for most of the symptoms. For example, one suffering from hearing loss would be given hearing aids, and those with Hirschsprung’s disorder can be treated with a colostomy.

Many professionals that are likely to be involved in the treatment of those with Stickler's syndrome, include anesthesiologists, oral and maxillofacial surgeons; craniofacial surgeons; ear, nose, and throat specialists, ophthalmologists, optometrists, audiologists, speech pathologists, physical therapists and rheumatologists.

One case of Cohen Syndrome, in a Palestinian boy from Tul-Karem, was reported in the Israeli monthly Kol Israel BeAsakim (in Hebrew) in the December 2007 issue. Over the past several years there have been approximately 50 new cases worldwide. There are population groups with this condition in Australia, the UK and the US. It still seems to go undiagnosed leaving the number of cases less than 500.

Usher syndrome, also known as Hallgren syndrome, Usher-Hallgren syndrome, retinitis pigmentosa-dysacusis syndrome, or dystrophia retinae dysacusis syndrome, is an extremely rare genetic disorder caused by a mutation in any one of at least 11 genes resulting in a combination of hearing loss and visual impairment. It is a leading cause of deafblindness and is at present incurable.

Usher syndrome is classed into three subtypes according to onset and severity of symptoms. All three subtypes are caused by mutations in genes involved in the function of the inner ear and retina. These mutations are inherited in an autosomal recessive pattern.

Left untreated, tabes dorsalis can lead to paralysis, dementia, and blindness. Existing nerve damage cannot be reversed.