Altered mental status

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

An altered level of consciousness is any measure of arousal other than normal. Level of consciousness (LOC) is a measurement of a person’s arousability and responsiveness to stimuli from the environment. A mildly depressed level of consciousness or alertness may be classed as lethargy; someone in this state can be aroused with little difficulty. People who are obtunded have a more depressed level of consciousness and cannot be fully aroused. Those who are not able to be aroused from a sleep-like state are said to be stuporous. Coma is the inability to make any purposeful response. Scales such as the Glasgow coma scale have been designed to measure the level of stuporconsciousness.

An altered level of consciousness can result from a variety of factors, including alterations in the chemical environment of the brain (e.g. exposure to poisons or intoxicants), insufficient oxygen or blood flow in the brain, and excessive pressure within the skull. Level of consciousness may decline abruptly or slowly, or it may increase and decrease intermittently. Prolonged unconsciousness is understood to be a sign of a medical emergency. A deficit in the level of consciousness suggests that both of the cerebral hemispheres or the reticular activating system have been injured. A decreased level of consciousness correlates to increased morbidity (disability) and mortality (death). Thus it is a valuable measure of a patient’s medical and neurological status. In fact, some sources consider level of consciousness to be one of the vital sign.^[1]

• Altered mental status: Altered mental status is a collection of states with change in cognitive contain, vigilance, and attentiveness.
• Cognition: Cognition is a cortical function in which knowledge is gained by ones reasoning, or without the need for conscious reasoning (instincts) and perceptions.
• Vigilance: Vigilance is a calibration of awakeness. Vigilance is low in sleep and is higher person is awake.
• Mental content:Mental content is a capacity of a person to integrate past and present experiences to the stimuli to the external and internal world.
• Attention: Attention is an ability to choose and concentrate a stimuli from all mental content which is relevant to a given situation.^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Moises Romo, M.D., Pratik Bahekar, MBBS [2]

The description of altered mental status might have been employed as early as 30,000 years ago. Celsus was the first person to use the word delirium, adapted from phrenitis, the description of alteration in consciousness by Hippocrates. Procopius gave a detailed description of what now is known as hypoactive and hyperactive delirium. Altered mental status was poorly understood before 19th century and was merely seen as symptoms of intoxication or demonic possession. A chronic global ischaemia hypothesis due to atherosclerosis was suggested to be the causant all cognitive alterations, including psychiatric disorders, such as schizophrenia. New investigations are being developed to understand the neural and psychological mechanisms of consciousness, such as priming effects using subliminal stimuli, alterations in consciousness produced by trauma, illness, or drugs.

• The description of altered mental status might have been employed as early as 30,000 years ago, many times called “mystic state“.^[1]
• Celsus was the first person to use the word delirium (second century AD) to refer to a mental disorder that appeared after a head trauma or during fever;^[2] he then equally used the term phrenitis introduced by Hippocrates (500 BC) as a synonym of delirium.^[3]
• In year 542 AD, Procopius gave a detailed description of delirium either as violent with insomnia, excitement, shouting, and rushing off in flight (now hyperactive delirium) or drifted into coma, forgetting all those familiar to them (now hypoactive delirium).^[2]
• Acoording to data, “Conscious” and “consciousness” was first mentioned in English language back in 16th century; it is derived from the Latin (con- “together” +scio “to know”).^[4]
• Before the 18th century, dementia was called imbecility, morosis, fatuitas, anoea, foolishness, stupidity, simplicity, carus, idiocy, dotage, or senility, which was used to refer to the varying degree of behavioural deterioration.^[5]
• The modern concept of consciousness is attributed to the English physician and phylosopher John Locke, who published in 1690 his essay “Concerning Human Understanding”.^[6] Locke defined consciousness as “the perception of what passes in a man’s own mind“.^[1]
• The word dementia was introduced by Blancard in 1726 to refer to the extinction of the imagination and judgment;^[7] in 1765, the word was updated by Diderot as the abolition of the reasoning faculty.^[8]

• At the begining of the nineteenth century, studies like those from Rostan in 1823 atributed cognitive failure to softening of the brain, which was observed by post-mortem findings in old people who presented dementia features in life.^[7]
• In the 20th century, studies like those from North and Bostock in1925, found atherosclerotic changes in autopsies of many of the patients with dementia, which suggested for many years a ‘chronic global ischaemia’ hypothesis where all cognitive alterations were due to atherosclerosis, including disorders such as schizophrenia.^[9]
• New investigations are being developed to understand the neural and psychological mechanisms of consciousness, such as priming effects using subliminal stimuli, alterations in consciousness produced by trauma, illness, or drugs.

• Altered mental status was poorly understood before 19th century and was merely seen as symptoms of intoxication or demonic possession.^[10]
• Many times, individuals with altered mental status due to medical or psychiatric conditions were sentenced to torture, convictions, and death by courts such as the Holy Inquisition.
• Altered mental status has been described and mentioned in several books over time according to the understanding of the moment, such as the award winning “Delirium” by Laura Restrepo.

• The creativity and the work of famous paintings such as “The Starry Night” from Vincent van Gogh is well known to be influenced in someway by alterations in mental status; it is still not completly known if it may be due to the effects of absinthe, overmedication with digitalis, epilepsy or a manic depression.^[11]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Moises Romo, M.D., Pratik Bahekar, MBBS [2]

Altered mental status, despite its frequency, the term is vague and has several synonyms such as confusion, not acting right, confusional state, altered behavior, generalized weakness, lethargy, agitation, psychosis, disorientation, inappropriate behavior, inattention, and hallucination. Such lack of standardized terminology makes the assessment and appropriate management of patients with altered mental status difficult. It is important to ditinguish red flags, since acute altered mental status is a medical emergency. The first step in the evaluation of a patient with altered mental status is to establish the time course. Altered mental status may be classified as dementia, delirium, psychosis, and other neurological causes according to its origin.

• Altered mental status may be classified according to its origin into 4 major groups: dementia, delirium, psychosis, and neurologic causes.

• Dementia is a slow and progressive disorder characterized by cognitive decline beyond what might be expected from normal aging. Dementia involves memory and at least 1 of the other domains, including personality, praxis, abstract thinking, language, executive functioning, complex attention, social and visuospatial skills.^[1] Individuals usually present normal vital signs, normal level of conscioussness. Several diseases may cause dementia, being Alzheimer’s disease the most common.^[2]

• Delirium is an acute and relatively sudden (developing over hours to days) decline in attention, focus, perception, and cognition that usually appears in the elderly.^[3][4] The clinical presentation may vary from hyperactive or hypoactive psychomotor behavioral disturbances. Hypoactive delirium is oftenly missdiagnosed with other disorders such as depression; the rapidly fluctuating time course of delirium is used to help in the latter distinction.^[5]

• Psychosis is a generic psychiatric term for a mental state that results in a loss of contact with reality.^[6] Psychosis is a common characteristic to many psychiatric, neuropsychiatric, neurologic, neurodevelopmental, and other medical conditions.^[7] It caused most of the times by fluctuations of neurotransmitters such as dopamine, acetylcholine, gamma-amino-butyric acid (GABA), and glutamate, which ultimately results in in high levels of distress and deterioration of normal social functioning.^[8]

• Some focal neurological deficits can produce changes in perception, psychomotor skills or behavior. This group’s presentation vary widely depending on the localization and cause of impairment. Within this group there may be found subclassifications such as the levels of consciousness (confusional state, lethargy, obtundation, stupor, coma), vegetative state, locked-in syndrome, and brain death.^[9]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Moises Romo, M.D., Pratik Bahekar, MBBS [2]

Altered mental status is a state of a variety of diseases, hence, there is no single pathophysiology mechanism. Although, the neural science behind alertness, wakefulness, and arousal are not fully understood, it is known that the reticular formation plays an important role in these.

Altered mental status is a state of a variety of diseases, hence, there is no single pathophysiology mechanism. It is known that the reticular formation plays an important role in the state of alertness. We explain the most important subtypes of altered mental status:

While the pathogenesis of AD remains unclear, It is thought that dementia is the result of:

• Neuronal loss.^[1][2][3]
• Overproduction and/or decreased clearance of amyloid beta peptides.^[4][5][6]
• Accumulation of neurofibrillary tangles (tau proteins).^[7][8]
• Production of oxygen radicals and nitric oxide, and inflammatory processes.^[9]
• Decreased levels of cholinergic neurotransmission.

• Over-excitation of the glutamate neurotransmitter system via N-methyl-D-aspartate.

The pathogenesis of Parkinson’s disease is a depletion of dopamine due to the following mechanisms:

• Protein misfolding with decreased function and plasticity.^[10][11][12]
• Defective proteolysis with aggregation of this protein and neuronal death.^[13][14][15]
• Mitochondrial dysfunction with the following cell damage.^[16][17][18]
• Oxidative stress with the following neuronal damage.^[19][20]
• Iron metabolism with following increase of storage in the substantia nigra.^[21][22][23]
• Immunologic and inflammatory mechanisms due to infiltration of CD4+ T cells.^[24][25]

Delirium is caused by a broad spectrum of diseases and clinical problems. Among the hypothesis of delirium developement are:

• Neurotransmitter hypothesis. A decreased oxidative metabolism in the brain may cause a reduced cholinergic function, excess release of dopamine, norepinephrine, and glutamate, and both decreased and increased serotonergic and γ-aminobutyric acid activity may underlie the different symptoms and clinical presentations of delirium.^[26][27][28]
• Inflammatory hypothesis. Stress causes the release of cytokines which may directly damage the brain or affect neurotransmitter synthesis.^[29][30][31]

30-50 percent of early-onset Alzheimer’s dementia (AD) is associated with an autosomal dominant inheritance and consists of mutations in the following genes:^[32][33]

• Presenilin1 (PS1) gene, also called PSEN1 gene on chromosome 14 (20-30% cases)
• Presenilin 2 (PS2) gene, also called PSEN2 gene on chromosome 1 ( rare)

• Point mutations in amyloid beta A4 protein gene, also called amyloid precursor protein (APP) gene on chromosome 21 are associated in some cases of early onset (< 65 yr) familial AD cases

Late onset (Alzheimer’s dementia -AD2)

• Apolipoprotein 4 gene (APOE4) mutation is associated with late onset (>60 years) Alzheimer’s dementia (AD)^[34]
• p.Arg47His allelic variant in TREM2 gene^[35]

Some of specific genes involving in PD are:

• Glucocerebrosidase gene ^[36]
• SNCA-associated PD ^[37]
• LRRK2-associated PD ^[38]
• Parkin-associated PD ^[39]
• PINK1-associated PD ^[40]
• DJ-1-associated PD ^[41]

The genes that may be used as risk biomarkers for the developement of delirium are the following:

• Polymorphisms in the receptor DRD2 and dopamine transporter genes (rs6276, rs6277, and rs2734839)^[42]
• Homozygous AA genotype of rs393795 in the SLC6A3 gene^[43]
• APOE4 polymorphism^[44]
• Reduced expression of miRNA-124 which results in decreased Ku70^[45]

The most important conditions/diseases associated with altered mental status include:

• Stroke
• Metabolic imbalances
• Traumatic brain injury
• Fever
• Infections
• Lung diseases (e.g. cancer)
• Chronic or terminal illnesses
• Miocardial infarction

The most important characteristics of Alzheimer’s disease on gross pathology are:

• Temporal atrophy (especially in the hippocampus)
• Dilation of ventricles

The most important characteristics of Parkinson’s disease on gross pathology are:

There are no characteristic gross pathology findings in dementia.

The most important histopathological characteristics of Alzheimer’s disease are:

• Neurofibrillary tangles: Consists of tau, location in the hippocampus, cerebral cortex, hypothalamus. Dementia severity correlates better with neurofibrillary tangles number rather than senile plaque number
• Senile plaques or the neuritic plaques consists of two components which are A-beta amyloid which radiate from the center and the neurites with swollen axons. Senile plaques are considered to be more specific for alzheimer’s than neurofibrillary tangles
• Loss of neurons
• With or without cerebral amyloid angiopathy

The most important histopathological characteristics of Parkinson’s disease are:

• The pathologic hallmark of PD is the presence of lewy bodies, which are round cytoplasmic eosinophilic inclusions. The content of these bodies are mostly alpha synuclein and ubiquitin, but we can also find complement proteins, microflament subunits, and parkin substrate protein.^[46]

• The pathologic manifestations of apoptosis include condensation of chromatin and cytoplasm, fragmentation of cell and lysosome-mediated phagocytosis.^[47] Neuronal apoptosis occurs in normal individuals (0.5 percent of substantia nigra neurons) but in PD patients this can be as high as 2 percent.^[48][49]

There are no characteristic histopathological findings in delirium.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2] Kiran Singh, M.D. [3]

Life threatening causes of altered mental status include malignant hypertension, myocardial infarction, rabies and sepsis. Other common causes of altered mental status include alcohol withdrawal, dehydration, electrolyte disturbance and hypoglycemia.

• Carbon monoxide toxicity
• Heat stroke
• Hypothermia
• Malignant hypertension
• Myocardial infarction
• Rabies
• Sepsis

• Alcohol withdrawal
• Drug withdrawal
• Dehydration
• Electrolyte disturbance
• Encephalitis
• Epileptic seizures
• Hyperglycemia
• Hypoglycemia
• Meningitis
• Sepsis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

A lowered level of consciousness indicate a deficit in brain function. Level of consciousness can be lowered when the brain receives insufficient oxygen (as occurs in hypoxia); insufficient blood (as occurs in shock); or has an alteration in the brain’s chemistry.^[1] Metabolic disorders such as diabetes mellitus and uremia can alter consciousness. Hypo- or hypernatremia (decreased and elevated levels of sodium, respectively) as well as dehydration can also produce an altered LOC.^[2] A pH outside of the range the brain can tolerate will also alter LOC.^[3] Exposure to drugs (e.g. alcohol) or toxins may also lower LOC,^[1] as may a core temperature that is too high or too low (hyperthermia or hypothermia). Increases in intracranial pressure (the pressure within the skull) can also cause altered LOC. It can result from traumatic brain injury such as concussion. Stroke and intracranial hemorrhage are other causes. Infections of the central nervous system may also be associated with decreased LOC; for example, an altered LOC is the most common symptom of encephalitis.^[4] Neoplasms within the intracranial cavity can also affect consciousness, as can epilepsy and post-seizure states.^[3] A decreased LOC can also result from a combination of factors. A concussion, which is a mild traumatic brain injury (MTBI) may result in decreased LOC.

In patients with altered mental status, the emergency physician must also consider other neurologic diagnoses. In patients who appear unresponsive, locked-in syndrome should be considered and is caused by focal injury to the ventral pons secondary to an infarct, hemorrhage, or trauma. If secondary to an infarct, the distal basilar artery is usually occluded. Multiple sclerosis and central pontine myelinosis can also cause locked-in syndrome. Though the clinical presentation is variable, quadriplegia and anarthria is usually present, but vertical eye gaze and upper eyelid movement are usually retained. Despite having the outward appearance of being unresponsive, patients with locked-in syndrome have normal levels of consciousness and are fully aware of their surroundings. If locked-in syndrome is suspected, then prompt neuroimaging and neurology consultation are warranted. Patients with a suspected thromboembolic cause of locked-in syndrome should immediately go to interventional radiology for intra-arterial thrombolytic therapy, even if the symptoms have being ongoing for more than the traditional 3-hour window. Without emergent intervention, survival and neurological recovery for these patients can be poor.

Non-convulsive status epilepticus (NCSE) should also be considered in patients who have altered mental status, especially if no obvious cause for their mental status changes is found. This diagnosis should strongly be considered if the patient has a seizure history or had a seizure prior to arriving to the ED. One systematic review reported that NCSE occurred in 8% – 30% of patients with altered mental status (mean prevalence = 22%). This systematic review consisted of 5 studies that predominantly enrolled patients in the hospital setting. NCSE is an underrecognized and important form of altered mental status that can only be diagnosed with electroencephalography (EEG). If this cause of altered mental status is considered, then neurology consultation should be obtained promptly; the treatment of NSCE (benzodiazepine and anti-epileptic medications) is significantly different from other causes of altered mental status.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

The etiology of delirium (and other forms of acute brain dysfunction) involves a complex interplay between patient vulnerability (or predisposing) factors and precipitating factors. Patients who are highly vulnerable (e.g. 92 year old with severe dementia, poor functional status, and multiple comorbidities) will require a relatively benign insult to develop delirium. For these patients, a relatively benign insult such as a simple urinary tract infection or small dose of narcotic medication can precipitate delirium. Because elderly patients are more likely to have multiple vulnerability factors, they are more susceptible to becoming delirious compared with their younger counterparts. Nursing home patients are particularly vulnerable. For patients who are less vulnerable (e.g. 67 year old with no dementia, little comorbidity burden, and who is still functionally independent), higher doses of noxious stimuli such as severe sepsis are required to develop delirium. Consequently, when a patient with little or no vulnerability factors presents to the ED with delirium, stupor, or coma, the clinician should have more concern for an underlying life threatening illness. To develop stupor of coma, even higher doses of noxious stimuli are required.

A multitude of patient vulnerability factors for delirium have been identified in the hospital literature and can likely be extrapolated to stupor and coma. Dementia is the most consistently observed vulnerability factor for delirium regardless of clinical setting. A dose-response relationship seems to exist; as the severity of dementia worsens, the risk of developing delirium increases. Similarly, low education attainment also increases the patient’s susceptibility to developing delirium. Both dementia and education attainment may be indicative of poor cognitive reserve and reflect the inability of the brain to adequately compensate for any noxious or stressful physiological insult. Other commonly observed vulnerability factors for delirium include poor functional status, advanced age, home psychoactive medication use such as narcotics, benzodiazepines, and medications with anticholinergic properties, history of alcohol abuse, visual impairment, high comorbidity burden, and malnutrition. There are limited data from the ED setting, but one study identified dementia, premorbid functional impairment, and hearing impairment as risk factors for delirium in the ED.14 Another ED study also identified dementia as a risk factor for delirium. They also observed that patients with advanced age, or a past history of cerebrovascular disease and seizure disorder were more likely to be delirious in the ED.

Medications are important vulnerability and precipitating risk factors factor for delirium, because polypharmacy is highly prevalent in the older patient population. Clegg et al. performed a systematic review and observed that benzodiazepines, opioids, dihydropyridines (e.g. nifedpine), and antihistamines may increase the risk for delirium. Of the opioids, meperidine is probably the most deliriogenic. These medications, especially benzodiazepines and opioids, can also induce stupor and coma at higher doses.

Medications with anticholinergic properties are thought to be frequent causes of delirium. There are over 600 medications with anticholinergic properties, and of these, 11% are frequently prescribed to the older patients.80 Some examples of commonly prescribed medications with anticholinergic properties are diphenhydramine, promethazine, hydroxyzine, meclizine, lomotil, and heterocyclic antidepressants (e.g. amitriptyline, nortriptyline, doxepin). In acute stroke patients, Caerio et al. found that that patients on home medications with anticholinergic properties were more susceptible to developing delirium during hospitalization. In 278 older medical patients, Han et al. observed that anticholinergic medications were associated with increased delirium severity. However, the evidence linking medications with anticholinergic properties and delirium is not consistently observed. Agostini et al. observed a trend towards increase risk (relative risk = 2.1, 95%CI: 0.9 – 4.7) of developing delirium in older hospitalized patients when diphenhydramine was used.83 Luukkanen et al. found that older patients who used more than one medication with anticholinergic properties were more likely to have delirium in the unadjusted analysis (27.0% versus 16.7%, p-value = 0.05). However, this relationship became non-significant after adjusting for age, gender, and comorbidity. In 147 hospitalized older patients, Campbell et al. observed that anticholinergic medications were not associated with delirium that developed in the hospital. These discrepant observations may be a result of patient characteristics (stroke versus non-stroke, race, etc.,) or the method in which anticholinergic burden was measured. Despite these discrepant findings, the general consensus among geriatric and psychiatric experts is that medications with anticholinergic properties in older patients should be avoided, especially if safer alternatives exist.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

Delirium, stupor, and coma represent a broad spectrum of acute brain dysfunction and are associated with an impairment of consciousness. There are two interrelated domains of neurologic function that are related to consciousness:

1. Content
2. Level (also known as arousal) of consciousness.

The content of consciousness has many components such as orientation, perception, executive function, and memory, and is mediated at the cortical level. The level (or arousal) of consciousness signifies the patient’s wakeful state and reactivity to surrounding stimuli. This is mediated at the ascending reticular activating system located in the brainstem. Traditionally, terms such as lethargic, drowsy, or somnolent have been used to describe level or arousal of consciousness. Because these descriptors can have different meanings for different clinicians, using a structured arousal scale such as the Richmond Agitation Sedation Scale (RASS) may be a more reliable method to describe altered level of consciousness. This scale ranges from -5 (unresponsive to pain and voice) to +4 (extreme combativeness). As the patient’s level of consciousness becomes more disturbed, the concern for an underlying life threatening acute medical illness should similarly increase. Patients with acute brain dysfunction can not only fluctuate between different RASS scores, but can also transition between delirium, stupor, and coma.

Stupor and coma occurs in 5 to 9% of older ED patients and when present, are considered to be medical emergencies that require immediate evaluation. These two forms of acute brain dysfunction occur over a period of hours to days and represent the most severe disruptions in both the level and content of consciousness. Stupor (RASS −4) is a condition of deep sleep or similar behavioral unresponsiveness from which the patient can be aroused only with vigorous and continuous stimulation. Coma (RASS −5) is defined as a state of unresponsiveness in which the patient cannot be aroused with any stimuli.

Delirium is an acute disturbance of consciousness (i.e. attention) that is accompanied by an acute loss in cognition that is not better explained by a preexisting dementia. This form of acute brain dysfunction occurs in 8 to 10% of patients of older ED patients. Similar to stupor and coma, delirium occurs over a period of hours and days, and its course tends to wax and wane throughout the day. In contrast to stupor and coma, however, some elements of the level and content of consciousness are maintained in patients with delirium. The degree of impairment in the level of consciousness can be variable, ranging from moderate sleepiness (RASS −3) to extreme combativeness (RASS +4). Patients with delirium also have inattention which is considered a cardinal feature of delirium. The impairment of content of consciousness is similarly variable and leads to an acute loss in cognition. Examples of such impairments observed in delirious patients are disorganized thought, perceptual disturbances, and disorientation.

Delirium can be further classified into three psychomotor subtypes: hypoactive, hyperactive, and mixed. Hypoactive (RASS < 0) delirium is described as “quiet” delirium and is characterized by psychomotor retardation; delirious patients with this subtype can appear drowsy, somnolent, or even lethargic. Because the clinical presentation can be very subtle, hypoactive delirium is frequently undetected by health care providers,21 and is often attributed to other etiologies such as depression or fatigue. To the contrary, patients with hyperactive delirium (RASS > 0) have increased psychomotor activity and may appear restless, anxious, agitated, or combative. Hyperactive delirium is more easily recognized by health care providers. Mixed-type delirium exhibits fluctuating levels of psychomotor activity; the patient can exhibit hypoactive symptomatology at one moment and hyperactive symptomatology several hours or even seconds later. Hypoactive delirium and mixed-type delirium appear to be the predominant subtypes in older patients regardless of the clinical setting. In the ED specifically, hyperactive delirium is the least common subtype.

It is hypothesized that each psychomotor subtype has different underlying pathophysiological mechanisms. Though the mechanisms are unclear, it is hypothesized that each delirium subtypes has differential neurotransmitter activity (cholinergic, dopamine, serotonin, and gamma-aminobutyric acid). Each psychomotor subtype may also be cause by different etiologies. Delirium caused by an infection or metabolic derangement is more likely to be the hypoactive subtype, whereas delirium caused by alcohol or benzodiazepine withdrawal is more likely to be the hyperactive subtype. The psychomotor subtypes of delirium may also have a differential effect on clinical course and outcomes. In 225 older patients admitted to a post acute care facility, Kiely at al. observed that patients with hypoactive delirium had the highest 1-year mortality rate compared with the other subtypes.

Delirium is distinct from dementia, yet many clinicians use these terms interchangeably. It is important to note, however, that dementia is an important predisposing factor to delirium, and patients can have both conditions concurrently. As previously mentioned, the loss of cognition observed in delirium tends to occur rapidly, and its course tends to fluctuate throughout the day. The loss of cognition observed in dementia is usually gradual (over months to years), and its course tends to be stable. Patients with delirium also have inattention, which is considered the cardinal feature of delirium where as attention is usually preserved in patients with dementia. Altered level of consciousness, disorganized thinking, sleep-wake cycle disturbances, and perceptual disturbances are also commonly observed in delirium, whereas these characteristics are typically absent in dementia.

There are instances when the clinical features of delirium and dementia overlap, making them difficult to distinguish from each other. This is especially the case in patients with end-stage dementia, where they can exhibit symptoms of inattention, altered level of consciousness, disorganized thinking, sleep-wake cycle disturbances, and perceptual disturbances in the absence of delirium.34 When patients with end-stage dementia develop delirium, an acute change in mental status is still observed, and any pre-existing abnormalities in cognition and level of consciousness will likely worsen. For this reason, diagnosing delirium can be extremely challenging in patients with severe dementia and establishing their baseline mental status is critical to the diagnosis.

Delirium is classically thought of as reversible and is usually precipitated by an underlying medical illness. However, there are also a proportion of patients whose delirium is not transient, and their symptoms can persist for months or even years. Dementia is thought of as irreversible and not secondary to an underlying medical illness. However, there are circumstances in which dementia may be reversible. Hypothyroidism, normal pressure hydrocephalus, vitamin B12 deficiency, and depression are examples of illnesses that can cause reversible dementia or a dementia-like illness (pseudodementia). One meta-analysis comprised of 39 articles reported that 9% of dementia were potentially reversible, but only 0.6% of the dementia cases showed any improvement in cognition after the reversible cause was addressed.

Dementia with Lewy bodies is the second most common type of dementia (after Alzheimer’s) and deserves special mention because it can be very challenging to distinguish from delirium. Similar to delirium, the loss of cognition observed in dementia with Lewy bodies can be rapid, and it can fluctuate over several hours or days. Perceptual disturbances are also commonly observed in dementia with Lewy bodies. Patients with dementia with Lewy bodies, however, have Parkinsonian motor symptoms such as cog wheeling, shuffling gait, stiff movements, and reduced arm-swing during walking; these motor symptoms are usually absent in patients with delirium. Differentiating between dementia with Lewy bodies and delirium can be difficult in the ED and may require a detailed evaluation by a neurologist or psychiatrist.

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