CT scan or MRI can confirm dementia via observation of ventricular dilation and cortical substance degeneration.

Pick's disease can be confirmed via CT scan or MRI with atrophy of frontal and temporal lobe roots.

Alzheimer's is a disease confirmed by atrophy of the parietal and temporal lobe ganglia along with changes in the cortical ganglia found in a CT scan or MRI.

Along with occupational and environmental evaluation, a neurological exam, ECHO, EEG, CT-San, and X-ray of the brain may be conducted to determine disorder. Neuroimaging that detects cerebral atrophy or cardiovascular subcortical alterations can help point to psychoorganic syndrome. Strong CNS lesions are detected in POS patients. However, this is found to be difficult as many psychiatric disorders, like dementia, have common diagnosis.

Diagnosing POS is an ongoing and developing in the medical and psychiatric industry. Exact diagnosis is difficult due to many symptoms mirroring other psychological disorders in the older aged patients.

Treatment of OBS varies with the causative disorder or disease. It is important to note that it is not a primary diagnosis and a cause needs to be sought out and treated.

An organic brain syndrome (OBS), also known as an organic brain disease/disorder (OBD), an organic mental syndrome (OMS), or an organic mental disorder (OMD), is a syndrome or disorder of mental function whose cause is alleged to be known as organic (physiologic) rather than purely of the mind. These names are older and nearly obsolete general terms from psychiatry, referring to many physical disorders that cause impaired mental function. They are meant to exclude psychiatric disorders (mental disorders). Originally, the term was created to distinguish physical (termed "organic") causes of mental impairment from psychiatric (termed "functional") disorders, but during the era when this distinction was drawn, not enough was known about brain science (including neuroscience, cognitive science, neuropsychology, and mind-brain correlation) for this cause-based classification to be more than educated guesswork labeled with misplaced certainty, which is why it has been deemphasized in current medicine.

"Acute" organic brain syndrome is (by definition) a recently appearing state of mental impairment, as a result of intoxication, drug overdose, infection, pain, and many other physical problems affecting mental status. In medical contexts, "acute" means "of recent onset". As is the case with most acute disease problems, acute organic brain syndrome is often temporary, although this does not guarantee that it will not recur (happen again) or progress to become chronic, that is, long-term. A more specific medical term for the "acute" subset of organic brain syndromes is delirium.

"Chronic" organic brain syndrome is long-term. For example, some forms of chronic drug or alcohol dependence can cause organic brain syndrome due to their long-lasting or permanent toxic effects on brain function. Other common causes of chronic organic brain syndrome sometimes listed are the various types of dementia, which result from permanent brain damage due to strokes, Alzheimer's disease, or other damaging causes which are not reversible.

Though OBS was once a common diagnosis in the elderly, until the understanding of the various types of dementias it is related to a disease process and is not an inevitable part of aging. In some of the older literature, there was an attempt to separate organic brain syndrome from dementia, but this was related to an older world view in which dementia was thought to be a part of normal aging, and thus did not represent a special disease process. The later identification of various dementias as clear pathologies is an example of the types of pathological problems discovered to be associated with mental states, and is one of the areas which led to abandonment of all further attempts to clearly define and use OBS as a term.

Blood tests, cerebrospinal fluid examination by lumbar puncture (also known as spinal tap), brain imaging studies, electroencephalography (EEG), and similar diagnostic studies may be used to differentiate the various causes of encephalopathy.

Diagnosis is frequently clinical. That is, no set of tests give the diagnosis, but the entire presentation of the illness with nonspecific test results informs the experienced clinician of the diagnosis.

Research efforts are focusing on prevention in identifying early signs from relatives with associated disorders similar with schizophrenia and those with prenatal and birth complications. Prevention has been an ongoing challenge because early signs of the disorder are similar to those of other disorders. Also, some of the schizophrenic related symptoms are often found in children without schizophrenia or any other diagnosable disorder.

Treating the underlying cause of the disorder may improve or reverse symptoms. However, in some cases, the encephalopathy may cause permanent structural changes and irreversible damage to the brain. These permanent deficits can be considered a form of stable dementia. Some encephalopathies can be fatal.

Locked-in syndrome can be difficult to diagnose. In a 2002 survey of 44 LIS patients, it took almost 3 months to recognize and diagnose LIS after the patient had suffered the incident (i.e., a stroke or an injury) that had caused his/her LIS. Locked-in syndrome may mimic loss of consciousness in patients, or, in the case that respiratory control is lost, may even resemble death. Patients are also unable to actuate standard motor responses such as withdrawal from pain; as a result, testing often requires making requests of the patient such as blinking or vertical eye movement.

Brain imaging may provide additional indicators of locked-in syndrome, as brain imaging provides clues as to whether or not brain function has been lost. Additionally, an EEG can allow the observation of sleep-wake patterns indicating that the patient is not unconscious but simply unable to move.

The same criteria are used to diagnose children and adults. Diagnosis is based on reports by parents or caretakers, teachers, school officials, and others close to the child.

A professional who believes a child has schizophrenia usually conducts a series of tests to rule out other causes of behavior, and pinpoint a diagnosis. Three different types of exams are performed: physical, laboratory, and psychological. Physical exams usually cover the basic assessments, including but not limited to; height, weight, blood pressure, and checking all vital signs to make sure the child is healthy. Laboratory tests include electroencephalogram EEG screening and brain imaging scans. Blood tests are used to rule out alcohol or drug effects, and thyroid hormone levels are tested to rule out hyper- or hypothyroidism. A psychologist or psychiatrist talks to a child about their thoughts, feelings, and behavior patterns. They also inquire about the severity of the symptoms, and the effects they have on the child's daily life. They may also discuss thoughts of suicide or self-harm in these one-on-one sessions. Some symptoms that may be looked at are early language delays, early motor development delays and school problems.

Many of persons with childhood schizophrenia are initially misdiagnosed as having pervasive developmental disorders (autism spectrum disorder, for example).

The diagnosis is typically made clinically with magnetic resonance imaging of the brain often revealing hyperintensities on "T"-weighed imaging. Three patterns have been described: superior frontal sulcus, dominant parieto-occipital, and holohemispheric watershed.

The treatment of PRES dependent on its cause. Anti-epileptic medication may also be appropriate.

Although the brain and spinal cord are surrounded by tough membranes, enclosed in the bones of the skull and spinal vertebrae, and chemically isolated by the blood–brain barrier, they are very susceptible if compromised. Nerves tend to lie deep under the skin but can still become exposed to damage. Individual neurons, and the neural networks and nerves into which they form, are susceptible to electrochemical and structural disruption. Neuroregeneration may occur in the peripheral nervous system and thus overcome or work around injuries to some extent, but it is thought to be rare in the brain and spinal cord.

The specific causes of neurological problems vary, but can include genetic disorders, congenital abnormalities or disorders, infections, lifestyle or environmental health problems including malnutrition, and brain injury, spinal cord injury or nerve injury. The problem may start in another body system that interacts with the nervous system. For example, cerebrovascular disorders involve brain injury due to problems with the blood vessels (cardiovascular system) supplying the brain; autoimmune disorders involve damage caused by the body's own immune system; lysosomal storage diseases such as Niemann-Pick disease can lead to neurological deterioration. The National Institutes of Health recommend considering the evaluation of an underlying celiac disease in people with unexplained neurological symptoms, particularly peripheral neuropathy or ataxia.

In a substantial minority of cases of neurological symptoms, no neural cause can be identified using current testing procedures, and such "idiopathic" conditions can invite different theories about what is occurring.

Traditionally, genetic abnormalities in neurodevelopmental disorders were detected using karyotype analysis, which found 5% of relevant disorders. , chromosomal microarray analysis (CMA) has replaced karyotyping, because of its greater diagnostic yield in about 20% of cases, detecting smaller chromosome abnormalities. It is the first line genomic test.

New descriptions include the term Copy-number variants (CNVs), which are losses or gains of chromosomal regions greater than 1 kb in length. CNVs are mentioned with the chromosomal band(s) they involve and their genome sequence coordinates. CNVs can be nonrecurrent and recurrent.

With CMA costs of testing have increased from 800 US$ to 1500$. Guidelines from the American College of Medical Genetics and Genomics and the American Academy of Pediatrics recommend CMA as standard of care in the US.

A widely accepted treatment for the syndrome of subjective doubles has not been developed. Treatment methods for this disease sometimes include the prescription of antipsychotic drugs, however, the type of drug prescribed depends on the presence of other mental disorders. Antipsychotic drugs (also known as neuroleptics) such as risperidone, pimozide, or haloperidol may be prescribed to treat the underlying psychiatric illness.

In addition to drug therapy, interpersonal counseling has also been suggested as a method to ease relations between the patient and his/her suspected doubles. However, the relationship between the patient and his/her double is not always negative.

Recovery from this syndrome is situational, as some drug therapies have been effective in some individuals but not others. Patients may live in a variety of settings, including psychiatric hospitals, depending on the success of treatment. With successful treatment, an individual may live at home. In many of the reported cases, remission of symptoms occurred during the follow-up period.

This disorder can be dangerous to the patient and others, as a patient may interrogate or attack a person they believe to be a double. Inappropriate behavior such as stalking and physical or psychological abuse has been documented in some case studies. Consequently, many individuals suffering from this disorder are arrested for the resulting misconduct (see the case of Mr. B in #Presentation).

A neurological disorder is any disorder of the nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms. Examples of symptoms include paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be assessed by neurological examination, and studied and treated within the specialities of neurology and clinical neuropsychology.

Interventions for neurological disorders include preventative measures, lifestyle changes, physiotherapy or other therapy, neurorehabilitation, pain management, medication, or operations performed by neurosurgeons. The World Health Organization estimated in 2006 that neurological disorders and their sequelae (direct consequences) affect as many as one billion people worldwide, and identified health inequalities and social stigma/discrimination as major factors contributing to the associated disability and suffering.

It is extremely rare for any significant motor function to return. The majority of locked-in syndrome patients do not regain motor control, but devices are available to help patients communicate. However, some people with the condition continue to live much longer, while in exceptional cases, like that of Kerry Pink and Kate Allatt, a full spontaneous recovery may be achieved.

In a recent analysis (Susac et al., 2003), MRI images from 27 patients fulfilling the diagnostic criteria of Susac's syndrome were reviewed. Multifocal supratentorial lesions were present in all patients. Most lesions were small (3 to 7 mm), though some were larger than 7 mm. All 27 patients had corpus callosum lesions. These all had a punched-out appearance on follow up MRI. Though most commonly involving white matter, many patients also had lesions in deep grey matter structures, as well as leptomeningeal enhancement. Multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM) can mimic the MRI changes seen in patients with Susac's syndrome. However, the callosal lesions in Susac's syndrome are centrally located. In comparison, patients with MS and ADEM typically have lesions involving the undersurface of the corpus callosum. Deep gray matter involvement commonly occurs in ADEM but is very rare in MS. Leptomeningeal involvement is not typical of either MS or ADEM. What this means is that if 10 lesions are found in the brain of an MS patient, a lesion may be found in the corpus callosum. If you have 10 lesions in a Susac patient, more than half will be in the corpus callosum.

A concern about this illness is that it mimics multiple sclerosis when looking at the vision loss and brain lesions. If close attention is not paid to the retina of a patient with vision loss and brain lesions, their symptoms may be mistaken for MS instead of Susac's syndrome. This may account for the low prevalence of the illness. There is also a pathological similarity between the endotheliopathy in Susac's syndrome with that seen in juvenile dermatomyositis.

Early and aggressive treatment is important to prevent irreversible neurological damage, hearing loss, or vision loss. Medications used include immunosuppressive agents and corticosteroids such a prednisone, or intravenous immunoglobulins (IVIG). Other drugs that have been used are mycophenolate mofetil (Cellcept), azathioprine (Imuran), cyclophosphamide, rituximab, and anti-TNF therapies.

Hearing aids or cochlear implants may be necessary in the event of hearing loss.

Education, and a "watch and wait" strategy, are the only treatment needed for many, and the majority of individuals with tics do not seek treatment; treatment of tic disorders is similar to treatment of Tourette syndrome.

About half of parents of children with ASD notice their child's unusual behaviors by age 18 months, and about four-fifths notice by age 24 months. According to an article, failure to meet any of the following milestones "is an absolute indication to proceed with further evaluations. Delay in referral for such testing may delay early diagnosis and treatment and affect the long-term outcome".

- No babbling by 12 months.

- No gesturing (pointing, waving, etc.) by 12 months.

- No single words by 16 months.

- No two-word (spontaneous, not just echolalic) phrases by 24 months.

- Any loss of any language or social skills, at any age.

The United States Preventive Services Task Force in 2016 found it was unclear if screening was beneficial or harmful among children in whom there is no concerns. The Japanese practice is to screen all children for ASD at 18 and 24 months, using autism-specific formal screening tests. In contrast, in the UK, children whose families or doctors recognize possible signs of autism are screened. It is not known which approach is more effective. Screening tools include the Modified Checklist for Autism in Toddlers (M-CHAT), the Early Screening of Autistic Traits Questionnaire, and the First Year Inventory; initial data on M-CHAT and its predecessor, the Checklist for Autism in Toddlers (CHAT), on children aged 18–30 months suggests that it is best used in a clinical setting and that it has low sensitivity (many false-negatives) but good specificity (few false-positives). It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders. Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture. Although genetic screening for autism is generally still impractical, it can be considered in some cases, such as children with neurological symptoms and dysmorphic features.

Accurately assessing for a specific Depressive Disorder diagnosis requires an expenditure of time that is deemed unreasonable for most primary care physicians. For this reason, physicians often use this code as a proxy for a more thorough diagnosis. There is concern that this may lead to a "wastebasket" mindset for certain disorders. In addition reimbursement through Medicare may be lower for certain non specific diagnosis.

Neurodevelopmental disorders are in their multitude associated with widely varying degrees of difficulty, depending on which there are different degrees of mental, emotional, physical, and economic consequences for individuals, and in turn families, groups and society.

While infection with rubella during pregnancy causes fewer than 1% of cases of autism, vaccination against rubella can prevent many of those cases.

Anumonye reported treatment success with lorazepam; others found benefit with antidepressants and relaxation exercises.