Psychiatric Annals

CME Article 

Delirium Versus Dementia: A Diagnostic Conundrum in Clinical Practice

Ranji Varghese, MD; Muna Irfan, MD

Abstract

A common requested psychiatric consultation in a hospital setting is for evaluation of an elderly patient with observed changes in cognition and/or agitation. The underlying question is often whether the case represents delirium or preexisting dementia. In cases such as these, identifying the root cause can be a diagnostic quandary in that the patient may have underlying dementia and is inherently an unreliable source. When collateral information from people familiar with the patient is limited, behavioral observations, bedside mental status examination, historical information by medical and nursing staff, and diagnostic tests can be useful. This review attempts to assist the physician in differentiating a patient with delirium from a patient with an underlying dementing process. Additionally, the article reviews the epidemiology, predisposing and precipitating factors, clinical characteristics, diagnosis, and management of the patient who presents with observed changes in cognition and/or agitation. [Psychiatr Ann. 2017;47(5):239–245.]

Abstract

A common requested psychiatric consultation in a hospital setting is for evaluation of an elderly patient with observed changes in cognition and/or agitation. The underlying question is often whether the case represents delirium or preexisting dementia. In cases such as these, identifying the root cause can be a diagnostic quandary in that the patient may have underlying dementia and is inherently an unreliable source. When collateral information from people familiar with the patient is limited, behavioral observations, bedside mental status examination, historical information by medical and nursing staff, and diagnostic tests can be useful. This review attempts to assist the physician in differentiating a patient with delirium from a patient with an underlying dementing process. Additionally, the article reviews the epidemiology, predisposing and precipitating factors, clinical characteristics, diagnosis, and management of the patient who presents with observed changes in cognition and/or agitation. [Psychiatr Ann. 2017;47(5):239–245.]

Delirium and dementia continue to be highly prevalent and overlapping conditions in patients with advanced age. Similarities in their presentation can make diagnosis difficult. Considering the seriousness of delirium, accurate diagnosis and management is imperative.

Delirium

At its core, delirium is acute global brain failure with fluctuations in attentiveness and disorientation. According to the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-V),1 delirium is characterized by the following fundamental features:

  1. Disturbance in attention (decreased ability to direct, focus, sustain, and shift attention) and awareness

  2. The condition develops acutely (hours to days), reflects a change from baseline, and can fluctuate during the course

  3. Additional disturbance in cognition (memory deficit, disorientation, language, visuospatial ability, or perception) might be noted

  4. Not explained by another preexisting, evolving, or established neurocognitive disorder, and does not occur in the context of severely reduced level of arousal, such as coma

  5. Evidence from history, physical examination, or laboratory findings that the disturbance is caused by a medical condition, substance, or medication

Additional features may include (1) psychomotor behavioral disturbances such as hypoactivity, hyperactivity with increased sympathetic activity, and impairment in sleep duration and architecture; and (2) emotional disturbances, including fear, depression, euphoria, or perplexity.

Although delirium temporally arises acutely or subacutely, it can persist for several days. Often treatable and reversible, it is commonly unrecognized even by experienced practitioners in medical settings where it frequently presents, underscoring the importance of heightened vigilance for the vulnerable patient.

Morbidity and Mortality

Delirium can be associated with poor outcomes, depending on the severity. For example, pressure ulcers, aspiration pneumonia in the hypokinetic lethargic patient with delirium, or fall injuries in the hyperkinetic, agitated patient with delirium have been reported.2 Patients who recover from delirium report a decline in quality of life.3 Most striking, however, is the significant increase in mortality rates in elderly patients with delirium, estimated to be up to 30% while in the hospital and up to 40% during the course of 1 year from the onset of delirium.4

Epidemiology

Approximately 10% to 25% of elderly patients admitted to a hospital setting will present with features of delirium.2 An additional 30% of hospitalized elderly patients without delirium at admission will develop delirium during their hospital stay.5,6 Despite its frequency, even trained palliative care medical staff were able to correctly identify delirium only 44% of the time in one study.2

Clinical Symptoms

Although up to 45% of patients with delirium have psychomotor agitation or hyperkinetic delirium, the remainder will demonstrate hypokinetic or a mixed presentation.7 Compared to the disruptive, restless person with delirium, the hypokinetic patient does not express observable motor, behavioral, or neuropsychiatric symptoms. Thus, subtle, subsyndromal features such as paucity of speech or sleep-wake cycle changes can delay recognition and subsequent treatment. Delay in management is one of the factors contributing toward worse prognosis for a patient with hypokinetic delirium (Table 1).


            Clinical Characteristics and Neurobehavioral and Motor Symptoms of Delirium

Table 1.

Clinical Characteristics and Neurobehavioral and Motor Symptoms of Delirium

Predisposing Factors

Several risk factors have been identified for the development of delirium, with age older than 65 years being especially important.8 Furthermore, coexisting dementia also increases the propensity to develop delirium, as up to two-thirds of patients suffering from delirium also have underlying dementia.9

Illness severity and comorbid medical illnesses increase the risk for developing delirium. Use of anesthesia and opioids after surgery or inadequately treated surgery-related pain are frequent causes for the emergence of delirium.10

Polypharmacy, immobility, diminished activities of daily living, and impairments in vision or hearing are also statistically significant independent risk factors.10

There is no clear gender predilection for developing delirium.4

Conceptually, it may be helpful to identify those patients that carry a higher premorbid risk burden for developing delirium. The higher the vulnerability status, the higher the likelihood that a mild precipitant can lead to emergence of delirium. These can include treatable and reversible conditions such as bladder infections, dehydration, or electrolyte abnormalities. Conversely, in patients with a lower premorbid state for developing delirium, mild triggers are rarely the cause; thus, relatively serious medical concerns such as tumors or head trauma should be considered.

Precipitating Factors

Although numerous triggers for the development of delirium exist, stratifying them into metabolic, toxic, medication-related, and hypoxic or inflammatory insults to the central nervous system can be helpful (Table 2).


            Common Causes of Delirium

Table 2.

Common Causes of Delirium

Diagnosis

A detailed history and mental status examination are crucial in differentiating delirium from dementia. This is largely due to the tight association between the onset and timing of the presenting symptoms. Delirium presents in an acute or subacute fashion whereas dementia has a chronic, insidious, and progressive presentation. Although timing is an important beginning point of a decision tree for further diagnostic evaluation and management of the problem, it does not establish a cause.

In a case of delirium, inquiry should include a physical and neurological examination, vital signs, chest X-ray, electrocardiogram, basic electrolytes, complete blood count, hepatic and kidney function, glucose, and oxygen saturation. If applicable, drug levels in the urine and serum can point to toxicity. An electroencephalogram can be considered but is rarely warranted.

Equally important is an evaluation of the timing of any new medications or dose changes to existing medications. Temporal correlation of new onset changes in neuropsychiatric behavior to medication adjustment can prove pivotal in deciding about the focus of inquiry and using appropriate diagnostic tests.

One prospective study found a single etiology in approximately 55% of patients, with the remaining cases demonstrating several causes, leading to multifactorial delirium.11

In addition to laboratory and clinical examination, assessment and rating scales are useful in the assessment and monitoring of delirium after diagnosis has been made. The Confusion Assessment Method (CAM) assesses inattentiveness, disorganized thinking, alterations in the level of consciousness, and temporal correlation of the presentation.10 The CAM can also be helpful in identifying the presence of a delirium. The Memorial Delirium Assessment Scale provides a rating scale to follow the delirium in subsequent examinations.12 The Delirium Rating Scale is particularly useful in differentiating dementia, depression, and psychotic disorders.12 Further details of these scales can be found in the article by Trzepacz et al.12

Illustrative Case

An elderly woman residing in a transitional care facility due to a recent fall had been rehabilitating appropriately until approximately 2 to 3 days prior when staff observed changes in attention. The patient was found to be grabbing “the birds above my bed.” Because changes to baseline health status occurred over the short period of time, the investigation for an etiology should focus on recent changes to her health status. In this case, staff noted that urinary incontinence and fevers had begun 5 days previously. With this information, examination and diagnostic tests should then be prioritized to check for infectious causes. Therefore, urine cultures, blood cultures, and complete blood count with differential would be appropriate first steps. It should be noted that because delirium may have multiple etiologies, other triggers such as narcotic medications should also be explored. Thus, a comprehensive evaluation and continued inquiry for other precipitants would be recommended as treatment is started. Treatment should be followed and serial examination of the neuropsychiatric symptoms should be performed to determine effectiveness of therapy.

Management

With respect to the overall management of the patient with delirium, the overarching goal is to identify and treat the etiology causing the delirium while addressing the resulting neuropsychiatric symptoms. In a situation where specific etiology cannot be identified, treatment for the neuropsychiatric symptoms should commence anyway, especially in the case of hyperkinetic or agitated patients who are at high risk of falls and resulting injuries. Pharmacologic management of the agitated patient with delirium should include antipsychotic medications.2,7 In the case of hypoactive delirium, there is less evidence to support psychotropic medications.

Haloperidol has been successful in treating delirium, and its parenteral forms provide flexibility in administration. Other, less potent dopamine antagonists are useful when there are comorbid symptoms such as sleep disturbances or prolonged QTc. A QTc above 475 ms increases the risk for torsades de pointes and should warrant careful consideration of alternatives agents such as benzodiazepines. Atypical antipsychotics like quetiapine have less extrapyramidal adverse effects, which make them especially favorable in the elderly population.

In addition to pharmacotherapy, managing the patient's environment can help reduce distress, or at the least reduce and occasionally eliminate symptomatic medication management. Simple measures include optimizing the sleep environment and improving sleep hygiene. Including objects that are familiar to the patient can help orient the patient to their surroundings. Minimizing extraneous stimuli including noise or disruptions like unnecessary blood draws or vital signs are also helpful. Appropriate lighting and ensuring that hearing aids or eye glasses are being used to improve sensory integration are also important. From a safety standpoint, the patient should be in a room separate from other confused patients, closer to a nursing station, and a sitter should be used if needed. Mechanical restraints are not encouraged unless there are clear safety concerns.10

In summary, delirium poses a grave threat to vulnerable patients, can be exceedingly difficult to identify, is characterized by specific neuropsychiatric manifestations, and is often caused by multiple factors. Behavioral management and pharmacotherapy are the mainstay of treatment.

Dementia

Dementia is a frequent comorbidity with delirium, especially in the elderly population. Its presence can make the diagnosis of delirium challenging.

Dementias comprise a group of disorders that predominantly result in decline in the patient's level of functioning, with the cardinal feature being deficit in memory. This can include impairment of learning, retaining, and recapitulating new information. Additional features can include inability to express or comprehend verbal information, deficits in object identification in the absence of sensory dysfunction, visuospatial impairment, and difficulty in planning, reasoning, abstraction, judgement, and other executive functions. The criteria for major neurocognitive disorder as defined in DSM-51 are listed in Table 3.


            DSM-5 Criteria for Major Neurocognitive Disorder

Table 3.

DSM-5 Criteria for Major Neurocognitive Disorder

In people older than age 60 years, prevalence rates are between 4.5% and 7%, with Alzheimer's disease being the most common form.13

Risk Factors

Although vascular disease, genetic predisposition, presence of apolipoprotein E, and low education level increase the odds for developing dementia, advanced age is the leading risk factor.7

Types of Dementias

Classification of dementia requires a comprehensive discussion that is beyond the scope of this article; however, we will briefly review the types most commonly encountered in the clinical setting.

Alzheimer's disease. It is estimated that by age 85 years, 25% to 50% of people will have symptoms of AD, and by the year 2050, an estimated 10 to 11 million people in the United States will be diagnosed with AD.13

AD is characterized by gradual, progressive deterioration in memory as the initial presentation, with other cognitive domains such as visuospatial impairment and executive function being affected. Language and behavioral symptoms develop later in the course. The disease process is marked by overproduction and/or decreased clearance of amyloid beta peptides and aggregation of hyperphosphorylated tau, leading to neurofibrillary tangles in neurons. Deficits in recent memory retrieval, and dysfunction in executive planning and other prefrontal cortex duties are noted early in the course, whereas decline in gait, motor, and sensory systems occur as the disease process progresses.

Up to 60% of patients with AD will also have hyperkinetic or agitated behaviors, with up to 50% of patients having perceptual disturbances including hallucinations or delusional beliefs, which can be mistaken as delirium.7

Dementia with Lewy bodies. Dementia with Lewy bodies (DLB) is the second most-common neurodegenerative disorder.7 This progressive degenerative disorder has the following cardinal features: parkinsonian symptoms, visual hallucinations, and fluctuation in attention, concentration, and memory. Parkinsonian symptoms include resting tremor, rigidity, bradykinesia/akinesia, postural instability, and gait disturbances.

REM sleep behavior disorder is a pathognomonic symptom for synucleiopathies, including DLB. It is characterized by lack of muscle atonia during REM sleep leading to potentially violent dream-enactment behaviors.14,15

Dementia of Parkinson's disease is largely differentiated from DLB by the onset of parkinsonism prior to cognitive decline, with motor symptoms being the predominant symptom. In contrast, cognitive decline with visual hallucinations are the predominant symptoms in DLB with less prominent parkinsonian symptoms.16

Frontotemporal dementia. Frontotemporal dementia is a neurodegenerative disorder characterized by degeneration of the frontal and/or temporal lobes. Early changes in behavior, personality, and executive functioning are noted in the behavioral variant whereas aphasia occurs in the language variant.17

Vascular dementia. Cognitive decline can also occur with cerebrovascular disease, which is largely mediated by atherosclerosis leading to neuronal loss by microvascular changes, large vessel infarction, and subcortical white matter disease. Build-up of amyloid plaques within cerebral arterial walls can also lead to eventual rupture. In fact, a significant portion of patients with vascular dementia also have comorbid AD. The main pathophysiological causes of vascular dementia are large vessel strokes (macroangiopathy, arteriosclerosis), small vessel disease (microangiopathy, arteriolosclerosis), and microhemorrhages.18 The symptoms tend to be chronic, progressive, and rarely reversible.

Other dementias. Other irreversible progressive disease processes that lead to dementia include corticobasal degeneration, progressive supranuclear palsy, HIV-associated dementia, Huntington's disease, and others. Although the majority of dementias are progressive neurodegenerative disorders, decline in cognitive functioning due to other central nervous system disturbances such as brain trauma can also lead to permanent cognitive impairment.14,18

Assessment and Management

In diagnosing a case of dementia, collateral information from a reliable source, including family members or friends, is of paramount importance, as the person who suffers from dementia usually lacks insight into their deficits.The assessment should include information on the patient's daily activities, short- and long-term memory, changes in ability to perform routine tasks such as preparing meals, personal finances, difficulties in driving to familiar places, recalling recent conversations, and changes in the ability to track personal items such as wallets, keys, or purses.

Diagnostic tools. Along with history and physical examination, formalized and validated screening questionnaires can help with the diagnosis.16 The Mini-Mental State Examination is a validated screening questionnaire but has limitations in sensitivity for mild dementias. On the other hand, the Short Test of Mental Status improves on sensitivity for mild cognitive impairment, and the Montreal Cognitive Assessment has the added advantage of increasing accuracy.

Because of the limitations of the tools to distinguish subtypes of dementia, laboratory assessments, neuroimaging, and neuropsychometric testing can also be used. The evaluation includes potentially reversible etiologies such as liver function tests, serum vitamin B12, thyroid-stimulating hormone, HIV testing, rapid plasma reagin, arterial blood gases, and chest X-ray if indicated. Imaging is especially important in patients with a sudden decline in cognition. In clinical practice, a magnetic resonance imaging scan is often ordered but is not absolutely necessary in making the diagnosis.

Treatment

Considering that dementias are progressive and rarely reversible, treatment is focused on managing comorbid medical conditions, including irritants (such undertreated pain) or dehydration, which could lead to aggressive behaviors.

As with delirium, having a structured routine and familiarity in personal spaces is important. There is some scant evidence on group-based validation treatments.7

The goals of medication management are to slow the progression of the cognitive decline and to treat comorbid agitation and depressive syndromes that may evolve along the course. Acetylcholine esterase inhibitors, including donepezil, rivastigmine, and galantamine, are generally used in mild and moderate cases of AD and DLB. The N-methyl-D aspartate receptor antagonist, memantine, is generally reserved for moderate to more severe cases either alone or in conjunction with an acetylcholinesterase inhibitor.

The use of psychotropic antipsychotic medications to treat aggression and agitation is controversial, and no randomized controlled trials have been performed to adequately compare the usefulness of these medications. Moreover, there are no data to support one particular antipsychotic medication instead of another. However, the side-effect profile of these medications can help guide a decision. For instance, atypical antipsychotics with decreased predisposition for parkinsonism may be used instead of traditional first-generation antipsychotic medications that tend to have a higher rate for developing extrapyramidal symptoms. Adverse effects, including increased mortality, cerebrovascular events, and worsening of cognitive decline in using these medications support the idea that they should be used sparingly.

The use of antidepressant medications may also have some advantages in managing the evolution of depression or anxiety in the setting of cognitive decline. Superimposed mood or anxiety disorders can lead to agitation and aggression, highlighting the importance of early management. Antidepressants with less anticholinergic properties, such as the selective serotonin reuptake inhibitors, should be considered instead of the tricyclic antidepressants, which have higher anticholinergic properties.

Summary

It is often a diagnostic challenge to evaluate and manage acutely hospitalized patients in terms of whether delirium or an underlying dementing process led to clinical presentation. Such cases warrant a careful historical account from collateral sources regarding the onset, chronological course, and characterization of the symptoms. In addition, observations from ancillary staff concerning temporal fluctuations or fixed nature of deficits can shed light on the underlying pathophysiological process.

In the case of delirium, inquiry into the etiology must include more than one possible source and treatment should not be postponed. Serial examinations using validated rating scales can aid in assessing the progress of treatment. Treatment should also include nonpharmacological strategies that assist in orienting the patient, in addition to pharmacotherapy that can reduce agitation.

With regard to dementia, rarely does the process begin abruptly, and nor does it wax and wane. Most patients present with smoldering change in their mental status leading to specific cognitive deficits that tend to follow a predictable temporal course depending on the neurodegenerative disorder. The focus of treatment is to keep patients functional as long as possible while mitigating aggressive or injurious behaviors either through pharmacological or nonpharmacological management. The differentiating features are listed in Table 4.


            Distinguishing Features of Dementia Versus Delirium

Table 4.

Distinguishing Features of Dementia Versus Delirium

References

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Press; 2013.
  2. Fong TG, Tulabaev SR, Inouye SK. Delirium and elderly adults: diagnosis, prevention, and treatment. Nat Rev Neurol. 2009;5:210–220. doi:10.1038/nrneurol.2009.24 [CrossRef].
  3. Andrew MK, Freter SH, Rockwood K. Incomplete functional recovery after delirium in elderly people: a prospective cohort study. BMC Geriatr. 2005; 5:5. doi:10.1186/1471-2318-5-5 [CrossRef].
  4. Innouye SK. Delirium and older persons. N Engl J Med. 2006;354:1157–1165. doi:10.1056/NEJMra052321 [CrossRef].
  5. Levkoff SE, Evans DA, Liptzin B, et al. Delirium. The occurrence and persistence of symptoms among elderly hospitalized patients. J Arch Intern Med. 1992;152(2):334–340. doi:10.1001/archinte.1992.00400140082019 [CrossRef]
  6. Pompei P, Foreman M, Cassel CK, et al. Detecting delirium among hospitalized older patients. Arch Intern Med. 1995;155(3):301–307. doi:10.1001/archinte.1995.00430030095011 [CrossRef]
  7. Philbrick KL, Rundell JR, Netzel PJ, Levenson JL. Clinical Manual of Psychosomatic Medicine. 2nd ed. Arlington, VA: American Psychiatric Association Publishing; 2012:104–105.
  8. Ranhoff AH, Rozzini R, Sabatini T, Cassinadri A, Boffelli S, Trabucchi M. Delirium in a sub-intensive care unit for the elderly: occurrence and risk factors. Aging Clin Exp Res. 2006;18(5):440–445. doi:10.1007/BF03324841 [CrossRef]
  9. Bo M, Martini B, Ruatta C, et al. Geriatric ward hospitalization reduced incidence delirium among older medical inpatients. Am J Geriatr Psychiatry. 2009;17(9):760–768. doi:10.1097/JGP.0b013e3181a315d5 [CrossRef]
  10. Trzepacz PT, Breitbart W, Franklin J, Work Group on Delirium. Practice Guideline for the Treatment of Patients with Delirium. Washington, DC: American Psychiatric Association; 2010:20–21.
  11. Francis J, Martin D, Kapoor WN. A prospective study of delirium in hospitalized elderly. JAMA. 1990;263(8):1097–1101. doi:10.1001/jama.1990.03440080075027 [CrossRef]
  12. Trzepacz PT, Mittal D, Torres R, Kanary K, Norton J, Jimerson N. Validation of the Delirium Rating Scale-revised-98: comparison with the delirium rating scale and the cognitive test for delirium. J Neuropsychiatry Clin Neurosci. 2001;13(2):229–242. doi:10.1176/jnp.13.2.229 [CrossRef].
  13. Prince M, Bryce R, Albanese E, Wimo A, Ribeiro W, Ferri CP. The global prevalence of dementia: a systematic review and meta-analysis. Alzheimers Dement. 2013;9(1):63–75.e2. doi:10.1016/j.jalz.2012.11.007 [CrossRef].
  14. Holsinger T, Deveau J, Boustani M, Williams JW Jr, . Does this patient have dementia. JAMA. 2007;297(21):2391–2404. doi:10.1001/jama.297.21.2391 [CrossRef].
  15. Mahowald MW, Schenck CH. REM sleep behaviour disorder: a marker of synucleinopathy. Lancet Neurol. 2013;12(5):417–419. doi:10.1016/S1474-4422(13)70078-4 [CrossRef].
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  18. Love S. Neuropathological investigation of dementia: a guide for neurologists. J Neurol Neurosurg Psychiatry. 2005;76(Suppl 5):v8–v14. doi:10.1136/jnnp.2005.080754 [CrossRef].

Clinical Characteristics and Neurobehavioral and Motor Symptoms of Delirium

Neuropsychiatric symptoms <list-item>

Disorientation to time and place

</list-item><list-item>

Attention and concentration deficits <list-item>

Inability to focus or sustain attention

</list-item>

</list-item><list-item>

Short-term memory deficits <list-item>

Inability to recall recent events as a manifestation of impaired attention and registration

</list-item>

</list-item><list-item>

Fluctuations in consciousness

</list-item><list-item>

Disturbances in perception <list-item>

Can vary from visual hallucinations to illusions

</list-item><list-item>

Auditory disturbances less common

</list-item>

</list-item><list-item>

Executive dysfunction and disorganized thoughts <list-item>

Prefrontal cortical dysfunction including planning, complex cognitive tasks, and decision-making

</list-item><list-item>

Disorganized and tangential thoughts, whereas hypokinetic patients display paucity of thought

</list-item>

</list-item><list-item>

Language <list-item>

Disorganized speech such as rambling, mumbling

</list-item>

</list-item><list-item>

Visuospatial <list-item>

Disturbances in ability to construct simple geometric figures can suggest prefrontal and parietal involvement

</list-item>

</list-item><list-item>

Sleep wake disturbances <list-item>

Circadian rhythm disturbance

</list-item>

</list-item>
Motor symptoms <list-item>

Agitation, restless

</list-item><list-item>

Stuporous, withdrawn, hypokinetic

</list-item><list-item>

Mixed (fluctuating between stuporous and hyperkinetic agitated state)

</list-item>

Common Causes of Delirium

Etiologies Mechanisms
Metabolic derangement Electrolytes disturbances including hypo/hyperkalemia, hyponatremia Vitamins deficiencies such as thiamine, niacin, folate, vitamin B12 Organ dysfunction such as acute/chronic renal failure, liver failure Heart or lung failure Abnormalities in acid-base level such as acidosis/alkalosis Hormonal disturbances including hypo/hyperthyroidism, hypoglycemia or hyperglycemia
Hypoxic insult to CNS Blood loss, leading to decreased oxygen perfusion to CNS Hypoxic injury from drugs, trauma Hypotension
Infectious causes Systemic infections: urinary and respiratory tract infection, sepsis CNS infections: meningitis and/or encephalitis
Toxic etiologies Abuse/withdrawal of CNS active substances (alcohol) Toxins (lead, mercury, household pesticides, vapor organic solvents acuteor chronic exposure)
Medications Analgesics   Narcotics (opiates) Anticholinergic medications   Tricyclic antidepressants, atropine, scopolamine, antihistamines, anti-spasmodics Antibiotics, antimicrobials   Cephalosporins, isoniazid, amphotericin B, acyclovir, interferon Anticancer medications   Methotrexate, vinblastine, vincristine Cardiac medications   Clonidine, beta blockers, digitalis, methyldopa, quinidine, tocainide Corticosteroids Central acting agents   Benzodiazepines, benzodiazepine receptor agonists; anticonvulsants (valproic acid, phenobarbital, lithium)   Antiparkinsonian agents (L-dopa, amantadine) Stimulants   Ephedrine, cocaine, amphetamines

DSM-5 Criteria for Major Neurocognitive Disorder

<list-item>

Based on history and clinical assessment evidence of significant impairment in at least one of the following cognitive domains <list-item>

Learning and memory

</list-item><list-item>

Language

</list-item><list-item>

Executive function

</list-item><list-item>

Complex attention

</list-item><list-item>

Perceptual-motor function

</list-item><list-item>

Social cognition

</list-item>

</list-item><list-item>

Must be acquired representing significant decline in social functioning

</list-item><list-item>

Deficits must interfere with independence in everyday activities

</list-item><list-item>

In the case of neurodegenerative dementias such as Alzheimer's disease, the disturbances are typically of insidious onset and are progressive, based on evidence from the history or serial mental-status examinations

</list-item><list-item>

Disturbances are not occurring in context of delirium

</list-item><list-item>

Deficits are not accounted for by another mental disorder (eg, major depressive disorder, schizophrenia)

</list-item>

Distinguishing Features of Dementia Versus Delirium

Feature Delirium Dementia
Onset Abrupt or subacute Insidious
Course Fluctuates Progressive
Duration Days to weeks Permanent
Attention Impaired Impaired in late stages
Consciousness Fluctuates/impaired Alert/stable (can be impaired in dementia with Lewy bodies and terminalstages)
Reversibility Usually Often irreversible
Behavior Agitated or withdrawn (change from premorbid state) Impaired in late stages; can be apathetic to agitated depending on dementia
Orientation Impaired but can fluctuate Impaired in late stages
Memory Impaired (change from pre-morbid state) mainly due to inattentiveness Impaired, progressive
Perception Visual hallucinations predominate Auditory or visual hallucinations (depending on dementia process)
Speech Incoherent Word-finding difficulty
Thought Disorganized Impoverished
Sleep Sleep/wake reversed or disturbed hour to hour Fragmented sleep
Authors

Ranji Varghese, MD, is the Medical Director, Minnesota Regional Sleep Disorders Center, Hennepin County Medical Center; and an Assistant Professor of Neurology, University of Minnesota. Muna Irfan, MD, is the Site Director, Sleep Fellowship, Hennepin County Medical Center; and an Assistant Professor of Neurology, University of Minnesota.

Address correspondence to Ranji Varghese, MD, Minnesota Regional Sleep Disorders Center, Hennepin County Medical Center, 701 Park Avenue South - G8, Minneapolis, MN 55415; email: Ranji.Varghese@hcmed.org.

Disclosure: The authors have no relevant financial relationships to disclose.

10.3928/00485713-20170411-02

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