Cognitive symptoms from steroids appear within the first few weeks of treatment, appear to be dose dependent, and may or may not be accompanied by steroid psychosis or other Cushing's-type symptoms.

The symptoms include deficits in

- verbal and non-verbal memory

- working memory

- attention

- sustained concentration

- executive function

- psychomotor speed

- academic or occupational performance.

These symptoms have been shown to improve within months to a year after discontinuing glucocorticoid medication, but residual impairments following prolonged steroid use can remain.

Steroid dementia syndrome describes the signs and symptoms of hippocampal and prefrontal cortical dysfunction, such as deficits in memory, attention, and executive function, induced by glucocorticoids. Dementia-like symptoms have been found in some individuals who have been exposed to glucocorticoid medication, often dispensed in the form of asthma, arthritis, and anti-inflammatory steroid medications. The condition reverses, but not always completely, within months after steroid treatment is stopped.

The term "steroid dementia" was coined by Varney et al. (1984) in reference to the effects of long-term glucocorticoid use in 1,500 patients. While the condition generally falls under the classification of Cushing's syndrome, the term "steroid dementia syndrome" is particularly useful because it recognizes both the cause of the syndrome and the specific effects of glucocorticoids on cognitive function. Further, the more precise terminology clearly distinguishes the condition from full-blown Cushing's syndrome, which is extremely broad regarding the causes (endogenous or exogenous, pituitary or adrenal) and the multitude of symptoms (ranging from skin disorders to osteoporosis), and from hypercortisolemia, which identifies neither the source nor the symptoms of excess circulatory cortisol.

Symptoms are not limited to but may include:

- Increased general confusion as natural light begins to fade and increased shadows appear.

- Agitation and mood swings. Individuals may become fairly frustrated with their own confusion as well as aggravated by noise. Individuals found yelling and becoming increasingly upset with their caregiver is not uncommon.

- Mental and physical fatigue increase with the setting of the sun. This fatigue can play a role in the individual's irritability.

- Tremors may increase and become uncontrollable.

- An individual may experience an increase in their restlessness while trying to sleep. Restlessness can often lead to pacing and or wandering which can be potentially harmful for an individual in a confused state.

Patients with psychoorganic syndrome often complain about headaches, dizziness, unsteadiness when walking, poor tolerance to the heat, stuffiness, atmospheric pressure changes, loud sounds, neurological symptoms.

The common reported psychological symptoms include:

- loss of memory and concentration

- emotional liability

- Clinical fatigue

- long term major depression

- severe anxiety

- reduced intellectual ability

The cognitive and behavioral symptoms are chronic and have little response to treatment.

Depending on lesion location, some patients may experience visual complications.

Sundowning, or sundown syndrome, is a neurological phenomenon associated with increased confusion and restlessness in patients with delirium or some form of dementia. Most commonly associated with Alzheimer's disease, but also found in those with other forms of dementia, the term "sundowning" was coined due to the timing of the patient's confusion. For patients with sundowning syndrome, a multitude of behavioral problems begin to occur in the evening or while the sun is setting. Sundowning seems to occur more frequently during the middle stages of Alzheimer's disease and mixed dementia. Patients are generally able to understand that this behavioral pattern is abnormal. Sundowning seems to subside with the progression of a patient's dementia. Research shows that 20–45% of Alzheimer's patients will experience some sort of sundowning confusion.

Pseudodementia is a phenotype approximated by a wide variety of underlying disorders (1). Data indicate that some of the disorders that can convert to a pseudodementia-like presentation include depression (mood), schizophrenia, mania, dissociative disorders, Ganser syndrome, conversion reaction, and psychoactive drugs (2). Although the frequency distribution of disorders presenting as pseudodementia remains unclear, what is clear is that depressive pseudodementia, synonymously referred to as depressive dementia(3) or major depression with depressive dementia (4), represents a major subclass of the overarching category of pseudodementia (4).

It has long been observed that in the differential diagnosis between dementia and pseudodementia, depressive pseudodementia appears to be the single most difficult disorder to distinguish from nosologically established "organic" categories of dementia(5), especially degenerative dementia of the Alzheimer type (6).

Depressive Pseudodementia is a syndrome seen in older people in which they exhibit symptoms consistent with dementia but the cause is actually depression.

Older people with predominant cognitive symptoms such as loss of memory, and vagueness, as well as prominent slowing of movement and reduced or slowed speech, were sometimes misdiagnosed as having dementia when further investigation showed they were suffering from a major depressive episode. This was an important distinction as the former was untreatable and progressive and the latter treatable with antidepressant therapy or electroconvulsive therapy or both. In contrast to major depression, dementia is a progressive neurodegenerative syndrome involving a pervasive impairment of higher cortical functions resulting from widespread brain pathology.

Pseudosenility also reversible dementia is a condition where older people are in a state of memory loss, confusion, or disorientation that may have a cause other than the ordinary aging process. Generally, the term "reversible dementia" is used to describe most cases. A more specific term "Pseudodementia" is referring to "behavioral changes that resembler those of the progressive degenerative dementias, but which are attributable to so-called functional causes".

The "New York Times" reports that illnesses such as the flu and hydrocephalus, as well as side-effects to common medications, can produce symptoms in the elderly that are difficult to distinguish from ordinary dementia caused by aging. However, if the real cause of the effects is caught early enough, the effects can be reversed. According to studies cited in Cunha (1990), approximate 10% to 30% of patients who have exhibited symptoms of dementia might have a treatable or reversible pathologic process to some extent.

Psychoorganic syndrome (POS) is a progressive disease comparable to presenile dementia. It consists of psychopathological complex of symptoms that are caused by organic brain disorders that involve a reduction in memory and intellect. Psychoorganic syndrome is often accompanied by asthenia.

Psychoorganic syndrome occurs during atrophy of the brain, most commonly during presenile and senile age (e.g. Alzheimer's disease, senile dementia). There are many causes, including cerebrovascular diseases, CNS damages to traumatic brain injury, intoxication, exposure to organic solvents such as toluene, chronic metabolic disorders, tumors and abscesses of the brain, encephalitis, and can also be found in cases of diseases accompanied by convulsive seizures. Psychoorganic syndrome may occur at any age but is most pronounced in elderly and senile age.

Depending on the nosological entity, the main symptoms of psychoorganic syndrome are expressed differently. For example, in atrophic cases such as Alzheimer's disease, the symptoms are more geared towards a memory disorder, while in Pick 's disease, mental disorders are more commonly expressed.

The history of disturbance in pseudodementia is often short and abrupt onset, while dementia is more often insidious. Clinically, people with pseudodementia differ from those with true dementia when their memory is tested. They will often answer that they don't know the answer to a question, and their attention and concentration are often intact, and they may appear upset or distressed. Those with true dementia will often give wrong answers, have poor attention and concentration, and appear indifferent or unconcerned.

Investigations such as SPECT imaging of the brain show reduced blood flow in areas of the brain in people with Alzheimer's disease, compared with a more normal blood flow in those with pseudodementia.

Alcohol-related dementia presents as a global deterioration in intellectual function with memory not being specifically affected, but it may occur with other forms of dementia, resulting in a wide range of symptoms. Certain individuals with alcohol-related dementia present with damage to the frontal lobes of their brain causing disinhibition, loss of planning and executive functions, and a disregard for the consequences of their behavior. Other types of alcohol-related dementia such as Korsakoff's Syndrome cause the destruction of certain areas of the brain, where changes in memory, primarily a loss of short term memory, are the main symptom. Most presentations of alcohol dementia are somewhere along the spectrum between a global dementia and Korsakoff's psychosis, and may include symptoms of both.

Individuals affected by alcohol-related dementia may develop memory problems, language impairment, and an inability to perform complex motor tasks such as getting dressed. Heavy alcohol abuse also damages the nerves in arms and legs, i.e. peripheral neuropathy, as well as the cerebellum that controls coordination thereby leading to the development of cerebellar ataxia. These patients frequently have problems with sensation in their extremities and may demonstrate unsteadiness on their feet.

Alcohol-related dementia can produce a variety of psychiatric problems including psychosis (disconnection from reality), depression, anxiety, and personality changes. Patients with alcoholic dementia often develop apathy, related to frontal lobe damage, that may mimic depression. People with alcoholism are more likely to become depressed than people without alcoholism, and it may be difficult to differentiate between depression and alcohol dementia.

Symptoms of OBS vary with the disease that is responsible. However, the more common symptoms of OBS are confusion; impairment of memory, judgment, and intellectual function; and agitation. Often these symptoms are attributed to psychiatric illness, which causes a difficulty in diagnosis.

The main symptom resulting from PCA is a decrease in visuospatial and visuoperceptual capabilities. Because the posterior region of the brain is home to the occipital lobe, which is responsible for visual processing, visual functions are impaired in PCA patients. The atrophy is progressive; early symptoms include difficulty reading, blurred vision, light sensitivity, issues with depth perception, and trouble navigating through space. Additional symptoms include apraxia, a disorder of movement planning, alexia, an impaired ability to read, and visual agnosia, an object recognition disorder. Damage to the ventral, or “what” stream, of the visual system, located in the temporal lobe, leads to the symptoms related to general vision and object recognition deficits; damage to the dorsal, or “where/how” stream, located in the parietal lobe, leads to PCA symptoms related to impaired movements in response to visual stimuli, such as navigation and apraxia.

As neurodegeneration spreads, more severe symptoms emerge, including the inability to recognize familiar people and objects, trouble navigating familiar places, and sometimes visual hallucinations. In addition, patients may experience difficulty making guiding movements towards objects, and may experience a decline in literacy skills including reading, writing, and spelling. Furthermore, if neural death spreads into other anterior cortical regions, symptoms similar to Alzheimer's disease, such as memory loss, may result. PCA patients with significant atrophy in one hemisphere of the brain may experience hemispatial neglect, the inability to see stimuli on one half of the visual field. Anxiety and depression are also common in PCA patients.

Movement Disorder

- Dystonia

- Parkinsonism

- Chorea

- Ocular flutter

- Motor tics

Psychiatric Symptoms

- Agitation

- Emotional lability

- Psychosis

- Depression

Associated symptoms

- Encephalopathy

- Sleep disorder

- Reduced consciousness

- Mutism

Alcohol-related dementia is a broad term currently preferred among medical professionals. Many experts use the terms alcohol (or alcoholic) dementia to describe a specific form of ARD, characterized by impaired executive function (planning, thinking, and judgment). Another form of ARD is known as wet brain (Wernicke-Korsakoff syndrome), characterized by short term memory loss and thiamine (vitamin B1) deficiency. ARD patients often have symptoms of both forms, i.e. impaired ability to plan, apathy, and memory loss. ARD may occur with other forms of dementia (mixed dementia). The diagnosis of ARD is widely recognized but rarely applied, due to a lack of specific diagnostic criteria.

On many non-medical websites, the terms wet brain and alcohol-related dementia are often used interchangeably, creating significant confusion. Additionally, the term alcohol-induced persistent dementia is another non-specific name that is sometimes used.

The symptoms of dementia vary across types and stages of the diagnosis. The most common affected areas include memory, visual-spatial, language, attention and problem solving. Most types of dementia are slow and progressive. By the time the person shows signs of the disorder, the process in the brain has been happening for a long time. It is possible for a patient to have two types of dementia at the same time. About 10% of people with dementia have what is known as "mixed dementia", which is usually a combination of Alzheimer's disease and another type of dementia such as frontotemporal dementia or vascular dementia. Additional psychological and behavioral problems that often affect people who have dementia include:

- Balance problems

- Tremor

- Speech and language difficulty

- Trouble eating or swallowing

- Memory distortions (believing that a memory has already happened when it has not, thinking an old memory is a new one, combining two memories, or confusing the people in a memory)

- Wandering or restlessness

- Perception and visual problems

- "Behavioral and psychological symptoms of dementia" (BPSD) almost always occur in all types of dementia. BPSDs may manifest as:

When people with dementia are put in circumstances beyond their abilities, there may be a sudden change to crying or anger (a ""catastrophic reaction"").

Psychosis (often delusions of persecution) and agitation/aggression also often accompany dementia.

As certain of pseudodementia remains potentially treatable, it is essential that they are distinguished from primarily dementia of the Alzheimer's type (DAT), and multi-infarct dementia (MID). For instance, pseudodementia associated with depression (DD) has been found as the most frequently appearing, while as many as 10% to 20% patients are misdiagnosed as primary degenerative dementia (PDD) or vice versa. A significant overlapping in cognitive and neuropsychological dysfunction in DD and PDD patients seemed to increase the difficulty in diagnosis. However, differences in the severity of impairment and quality of patients' responses could be observed, and DD patients exhibited a greater depressive symptomatology. Additionally, a test of antisaccadic movements may be used to differentiate DD from PDD patients. as PDD patients significantly display poorer performance on this test. A general comparison between aspects of DD and PDD is shown below.

In general, pseudodementia patients present a considerable cognitive deficits, including disorders in learning, memory and psychomotor performance. Substantial evidences from brain imaging such as CT scanning and positron emission tomography (PET) have also revealed abnormalities in brain structure and function.

In the first stages of dementia, the signs and symptoms of the disorder may be subtle. Often, the early signs of dementia only become apparent when looking back in time. The earliest stage of dementia is called mild cognitive impairment (MCI). 70% of those diagnosed with MCI progress to dementia at some point. In MCI, changes in the person's brain have been happening for a long time, but the symptoms of the disorder are just beginning to show. These problems, however, are not yet severe enough to affect the person’s daily function. If they do, it is considered dementia. A person with MCI scores between 27 and 30 on the Mini-Mental State Examination (MMSE), which is a normal score. They may have some memory trouble and trouble finding words, but they solve everyday problems and handle their own life affairs well.

Age: Children, Young Adult, Elderly

Sex: Both

Onset: Subacute

Clinical features NMDA Ab related patients in adult shows;

- Early features of higher cognitive dysfunction, confusion, behavioural changes, amnesia, dysphasia. Psychiatric: hallucinations, psychotic, agitation, depressive, anxiety, obsessive. Seizures: generalized, complex partial, simple partial.

- Late features: Spontaneous reduction in conscious level, Movement disorder: choreoathetoid (orofacial, upper limbs, lower limbs), parkinsonian, rigidity, myoclonus, oculogyric crises, opisthotonus, startle. Dysautonomia : tachy/brady-cardia, hyperhidrosis, persistent pyrexia, central hypoventilation, labile/high blood pressure, hypersalivation, pseudoobstruction, cardiac asystole.

NMDA Ab related patients in children and adolescent.

Commonly

- Behavioral or personality change, sometimes associated with

- Seizures and

- Sleep dysfunction;

- Severe speech deficits on admission

- Stereotyped movements,

- Autonomic instability

- Hypoventilation

Rarely

- Dyskinesias or dystonia;

Other Cases have similar presentation

- Disorientation,

- Hallucinations

- Confusion

- Memory loss

- Seizures: Partial temporal lobe. Pilomotor Status epilepticus

- Relative absence of cerebellar and brainstem sings

- Post partum psychosis

- Dyskinesias

Differentiating the different dementia syndromes can be challenging, due to the frequently overlapping clinical features and related underlying pathology. In particular, Alzheimer's dementia often co-occurs with vascular dementia.

People with vascular dementia present with progressive cognitive impairment, acutely or subacutely as in mild cognitive impairment, frequently step-wise, after multiple cerebrovascular events (strokes). Some people may appear to improve between events and decline after more silent strokes. A rapidly deteriorating condition may lead to death from a stroke, heart disease, or infection.

Signs and symptoms are cognitive, motor, behavioral, and for a significant proportion of patients also affective. These changes typically occur over a period of 5–10 years. Signs are typically the same as in other dementias, but mainly include cognitive decline and memory impairment of sufficient severity as to interfere with activities of daily living, sometimes with presence of focal neurologic signs, and evidence of features consistent with cerebrovascular disease on brain imaging (CT or MRI). The neurologic signs localizing to certain areas of the brain that can be observed are hemiparesis, bradykinesia, hyperreflexia, extensor plantar reflexes, ataxia, pseudobulbar palsy, as well as gait and swallowing difficulties. People have patchy deficits in terms of cognitive testing. They tend to have better free recall and fewer recall intrusions when compared with patients with Alzheimer's disease. In the more severely affected patients, or patients affected by infarcts in Wernicke's or Broca's areas, specific problems with speaking called dysarthrias and aphasias may be present.

In small vessel disease, the frontal lobes are often affected. Consequently, patients with vascular dementia tend to perform worse than their Alzheimer's disease counterparts in frontal lobe tasks, such as verbal fluency, and may present with frontal lobe problems: apathy, abulia, problems with attention, orientation, and urinary incontinence. They tend to exhibit more perseverative behavior. VaD patients may also present with general slowing of processing ability, difficulty shifting sets, and impairment in abstract thinking. Apathy early in the disease is more suggestive of vascular dementia.

Rare genetic disorders which result in vascular lesions in the brain have other patterns of presentation. As a rule, they tend to present earlier in life and have a more aggressive course. In addition, infectious disorders, such as syphilis, can lead to arterial damage, strokes, and bacterial inflammation of the brain.

Mild cognitive impairment (MCI), also known as incipient dementia and isolated memory impairment, is a neurological disorder that occurs in older adults which involves cognitive impairments with minimal impairment in instrumental activities of daily living. MCI involves the onset and evolution of cognitive impairments beyond those expected based on the age and education of the individual, but which are not significant enough to interfere with their daily activities. It may occur as a transitional stage between normal aging and dementia. Causation of the syndrome in and of itself remains unknown, as, therefore, do prevention and treatment.

The presenting symptom of dementia with Lewy bodies is often cognitive dysfunction, though dementia eventually occurs in all individuals with DLB. In contrast to Alzheimer's disease (AD), in which memory loss is the first symptom, those with DLB first experience impaired attention, executive function, and visuospatial function, while memory is affected later. These impairments present as driving difficulty, such as becoming lost, misjudging distances, or as impaired job performance. In terms of cognitive testing, individuals may have problems with figure copying as a result of visuospatial impairment, with clock-drawing due to executive function impairment, and difficulty with serial sevens as a result of impaired attention. Short-term memory and orientation to time and place remain intact in the earlier stages of the disease.

While the specific symptoms in a person with DLB may vary, core features include: fluctuating cognition with great variations in attention and alertness from day to day and hour to hour, recurrent visual hallucinations (observed in 75% of people with DLB), and motor features of Parkinson's disease. Suggestive symptoms are rapid eye movement (REM)-sleep behavior disorder and abnormalities detected in PET or SPECT scans. REM sleep behavior disorder (RBD) often is a symptom first recognized by the patient's caretaker. RBD includes vivid dreaming, with persistent dreams, purposeful or violent movements, and falling out of bed. Benzodiazepines, anticholinergics, surgical anesthetics, some antidepressants, and over-the-counter drug cold remedies may cause acute confusion, delusions, and hallucinations.

Tremors are less common in DLB than in Parkinson's disease. Parkinsonian features may include shuffling gait, reduced arm-swing during walking, blank expression (reduced range of facial expression), stiffness of movements, ratchet-like cogwheeling movements, low speech volume, sialorrhea, and difficulty swallowing. Also, DLB patients often experience problems with orthostatic hypotension, including repeated falls, fainting, and transient loss of consciousness. Sleep-disordered breathing, a problem in multiple system atrophy, also may be a problem.

One of the most critical and distinctive clinical features of the disease is hypersensitivity to neuroleptic and antiemetic medications that affect dopaminergic and cholinergic systems. In the worst cases, a patient treated with these medications could become catatonic, lose cognitive function, or develop life-threatening muscle rigidity. Some commonly used medications that should be used with great caution, if at all, for people with DLB, are chlorpromazine, haloperidol, or thioridazine.

Visual hallucinations in people with DLB most commonly involve perception of people or animals that are not there, and may reflect Lewy bodies or AD pathology in the temporal lobe. Delusions may include reduplicative paramnesia and other elaborate misperceptions or misinterpretations. These hallucinations are not necessarily disturbing, and in some cases, the person with DLB may have insight into the hallucinations and even be amused by them, or be conscious they are not real. People with DLB also may have problems with vision, including double vision, and misinterpretation of what they see, for example, mistaking a pile of socks for snakes or a clothes closet for the bathroom.

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.

Symptoms include mental deterioration, language disorder, transient ischemic attack, muscle ataxia, and impaired movements including change of walk, slowness of movements, and change in posture. These symptoms usually coincide with multiple falls, epilepsy, fainting, and uncontrollable bladder.

Because Binswanger’s disease affects flow processing speed and causes impaired concentration, the ability to do everyday tasks such as managing finances, preparing a meal and driving may become very difficult.

Posterior cortical atrophy (PCA), also called Benson's syndrome, is a form of dementia which is usually considered an atypical variant of Alzheimer's disease (AD). The disease causes atrophy of the posterior part of the cerebral cortex, resulting in the progressive disruption of complex visual processing. PCA was first described by D. Frank Benson in 1988.

In rare cases, PCA can be caused by dementia with Lewy bodies and Creutzfeldt–Jakob disease.

PCA usually affects people at an earlier age than typical cases of Alzheimer's disease, with initial symptoms often experienced in people in their mid-fifties or early sixties. This was the case with writer Terry Pratchett (1948-2015), who went public in 2007 about being diagnosed with PCA. In "The Mind's Eye", neurologist Oliver Sacks examines the case of concert pianist Lilian Kallir (1931–2004), who suffered from PCA.

Vascular dementia, also known as multi-infarct dementia (MID) and vascular cognitive impairment (VCI), is dementia caused by problems in the supply of blood to the brain, typically a series of minor strokes, leading to worsening cognitive decline that occurs step by step. The term refers to a syndrome consisting of a complex interaction of cerebrovascular disease and risk factors that lead to changes in the brain structures due to strokes and lesions, and resulting changes in cognition. The temporal relationship between a stroke and cognitive deficits is needed to make the diagnosis.