eMedicine Specialties > Neurology > Behavioral Neurology and Dementia

Confusional States and Acute Memory Disorders

Author: Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Coauthor(s): Daniel H Jacobs, MD, Associate Professor of Neurology, University of Central Florida College of Medicine
Contributor Information and Disclosures

Updated: Jan 11, 2008

Introduction

Background

Delirium, also referred to as encephalopathy, or an acute confusional state, is defined as a transient disorder of cognition and attention accompanied by disturbances of the sleep-wake cycle and psychomotor behavior.¹ The key feature of delirium is the inability to maintain a coherent stream of thought or action, along with an impairment in attention and/or arousal. Patients cannot keep attention focused, and this attentional disorder underlies many of the other cognitive deficits. Delirious patients are distractible, may be hypersensitive to stimuli, and cannot prioritize important from irrelevant environmental sounds or sights. A mother's ability to hear only the cry of her baby and ignore the street noises, creaking floors, plumbing noises, or music from next door, is an example of the type of focused attention that is impossible in delirium.

Most patients with delirium have associated cognitive deficits such as altered perception (including hallucinations, illusions, and delusions, such as thinking that IV tubing is a snake or misinterpreting shadows on the ceiling as animals); memory loss (especially distorted memories, approximate answers, and misidentification of people or places); language deficits (especially writing); disorientation; difficulty with calculations, abstraction, insight, and judgment; and mood disorders, which can include fear, elation, anxiety, or depression. Some patients have relatively preserved orientation, language, and other cognitive function but simply cannot maintain focus on a conversation, talking about irrelevant details such as the sound of a beeper or a pattern on the wall.

Central to delirium is an alteration of consciousness, either alert and agitated, or somnolent, along with psychomotor abnormalities such as restlessness, agitation, and sleep-wake cycle disturbance. Another common set of associated symptoms in delirium are autonomic disturbances such as tachycardia, hypertension, fever, sweating, and piloerection. 

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR)² defines delirium as the following:

• Disturbance of consciousness (ie, reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention
• A change in cognition (such as memory deficit, disorientation, language disturbance) or the development of a perceptual disturbance that is not better accounted for by a preexisting, established, or evolving dementia
• The disturbance develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day.
• Evidence from the history, physical examination, or laboratory findings shows that the disturbance is caused by the direct physiological consequences of a general medical condition.

Delirium has been subdivided into 4 motoric subtypes, based on the alteration of level of consciousness.

• Hypoactive delirium with low psychomotor behavioral activity
• Hyperactive delirium with high psychomotor activity
• Mixed delirium with features of both hypo- and hyperactivity
• Delirium without psychomotor behavioral changes

Hypoactive delirium has in the past been less recognized than the hyperactive variety, but recent evidence indicates that it is much more common than the hyperactive variants, especially in intensive care patients.

Delirium is distinguished from dementia, which consists of a nonacute, usually progressive cognitive deficit usually reflecting deficits of multiple cognitive functions (negative symptoms in the Hughlings Jackson sense) and usually much less associated with the psychomotor, autonomic, and level of consciousness alterations (positive symptoms) that characterize delirium. 

Pathophysiology

Delirium is a syndrome, or a symptom complex, rather than a disease; the pathophysiology of delirium depends largely on the etiology of the syndrome. The syndrome can be attributed to numerous causes including, but not limited to, the following.

• Pulmonary disease (eg, hypoxia)
• Other abnormal systemic metabolic conditions such as hepatic or renal dysfunction
• Endocrine disorders such as thyroid or adrenal hypofunction or hyperfunction
• Ingestion of toxins or side effects of single or multiple interacting medications or withdrawal from alcohol or drugs
• Electrolyte imbalances, especially abnormalities in sodium, BUN, creatinine, glucose, calcium, magnesium, and phosphorus
• Nutritional deficiencies such as thiamine, cobalamin, or niacin
• Sepsis or systemic infections including simple urinary tract infections and CNS infections such as meningitis or encephalitis related to infection with HIV, herpes simplex, and West Nile virus
• Seizures or postictal states
• Inflammatory or autoimmune conditions such as paraneoplastic disorders, Hashimoto encephalopathy, and vasculitis
• Acute structural lesions such as cerebral infarctions or hemorrhages.

An overlap exists with acute psychiatric disorders (especially acute mania).

Patients with preexisting dementia can deteriorate into delirium with seemingly minor stressors such as urinary tract infections, traumatic injuries, or even environmental change. Focal CNS disorders in strategic locations can also cause delirium. Strokes are frequent causes of delirium. Lesion loci associated with acute confusional states include the basal forebrain (eg, infarction as complication of surgery to repair an anterior communicating artery aneurysm), the caudate nucleus, and thalamic lesions that affect Papez circuit (anterior nucleus, fornix, mammillothalamic tract), and hippocampal lesions, such as acute posterior cerebral artery territory strokes or herpes simplex encephalitis.

In addition, Wernicke aphasia and mirror-image lesions of the Wernicke area affecting the right hemisphere can also present with acute confusion or agitation, as can some thalamic lesions causing aphasia. Strokes are more likely to be associated with delirium when they occur in elderly patients with preexisting cerebral atrophy and also when they are accompanied by seizures. Multifocal strokes in embolic conditions, vasculitis, or hypoxic-ischemic encephalopathy are also frequent causes of delirium.

Frequency

United States

• Delirium is an extremely common condition. 
• Acute encephalopathies develop in 30-50% of hospitalized patients older than age 70; since nearly half of hospital populations are elderly, a conservative estimate is that approximately 10% of hospitalized patients on medical or surgical units have delirium at any given time. In addition, delirium often follows surgical procedures.
• Delirium has been associated with longer hospital stays, increased mortality, and also a risk of nearly 50% of permanent neurocognitive impairment in survivors.
• Delirium is estimated to affect more than 2 million persons in the United States each year, and the excess hospital cost associated with delirium exceeds $4 billion.

As the population of older Americans increases, the frequency and cost of delirium are likely to increase. Several studies have investigated risk factors for the development of delirium during hospitalization. Perhaps the easiest to use is provided by Inouye and colleagues for patients older than age 70.³ Five independent risk factors were preexisting dementia or cognitive impairment, vision impairment, functional impairment, high comorbidity, and use of physical restraints. Rates for low risk (0-1 factors), intermediate risk (2-3 factors), and high risk (4-5 factors) were 4%, 18%, and 63%, respectively. Other studies have found the presence of fractures, infections, and use of sedative or narcotic analgesic drugs to be predictors of delirium.

International

Delirium is common throughout the world. A review by Brown and Boyle in the British Medical Journal estimated that a fourth of hospitalized patients older than age 65 develop delirium during hospitalization.⁴

Mortality/Morbidity

Delirium is associated with high rates of mortality and morbidity, especially if undiagnosed. Inouye estimated in-hospital mortality of more than 20%, and mortality within a year of 35-40%.⁵ Ely and colleagues also found that delirium was an independent predictor of both mortality and longer hospital stays.⁶  The morbidity and mortality rates depend heavily on the patient's reason for admission and associated medical illnesses.

Race

Available studies on risk factors for delirium have not identified race as a specific predictor of delirium. 

Sex

A recent study of delirium in older patients admitted to a general internal medicine service found male gender to be an independent risk factor for delirium, along with several other factors.⁷ Most studies of delirium have not reported gender as a major predictor.

Age

• Virtually all studies of delirium have found age to be a predictor of acute confusional states. Aging changes in the brain, and especially preexisting cognitive deficits or strokes, render the nervous system more sensitive to toxic or metabolic insults, such as medication side effects, electrolyte imbalances, endocrine disorders and renal or hepatic failure, and infections, among many other conditions.
• Elderly patients may have exaggerated responses to over-the-counter and prescription medications with anticholinergic activity. These include diphenhydramine (Benadryl, Tylenol PM), bladder antispasmodics such as oxybutynin, and atropine sulfate (eg, Lomotil). Thioridazine (Mellaril), a prescription antipsychotic medication, and tricyclic antidepressants such as amitriptyline (Elavil) also have anticholinergic activity. These drugs may cause exaggerated adverse effects, including sundowning. Other medications implicated in delirium are narcotic analgesics, benzodiazepines, theophylline, and antiparkinson medications.

Clinical

History

Patients presenting with an acute confusional state should be evaluated first with a careful history, taken from a reliable person who knows the patient well (if possible), and a physical examination. The history should include details of prior illnesses, a complete medication list, and a historical baseline level of function. It also should include the temporal course of the changes in mental status.

• The context of the syndrome is especially important—the location of the patient when the condition was first noticed, eg, the intensive care unit, nursing home, or psychiatric ward.
• Underlying or past medical conditions such as diabetes, hypertension, and prior strokes should be documented. 
• The historian should ascertain whether the patient has suffered confusional episodes before and whether he or she recovered. Preexisting cognitive deficits or dementia are potent risk factors for the development of delirium in association with illness, hospitalization, or surgery.
• The features of confusion should be elucidated. Is the patient wakeful and alert, or sleepy; agitated, or calm; aphasic, or with normal language and speech?
• Alcohol and substance abuse history should be documented.
• All medications currently being administered to the patient should be reviewed, as well as reconciliation with home medications. Withdrawal from sedative or hypnotic drugs such as benzodiazepines can mimic alcohol withdrawal or delirium tremens.
• If the patient is unable to communicate verbally, the examiner should evaluate whether he or she can communicate with eye blinking and vertical eye movements (ie, locked-in syndrome). The examiner should also look for evidence of subtle seizures, such as eye blinks, facial twitches, or automatisms.
• The physician must also look for signs such as fever, confusion, and seizures (as in herpes encephalitis), or stiff neck and fever (as in meningitis or subarachnoid hemorrhage). These are true medical emergencies. One should also determine whether systemic diseases with neurologic ramifications have been diagnosed. For a few specific examples, eosinophilia and asthma might suggest Churg-Strauss syndrome; peripheral neuropathy and renal disease might suggest polyarteritis nodosa; hemoptysis might suggest Wegener granulomatosis.
• Careful review of laboratory studies is imperative, especially the complete blood count, electrolytes, BUN, creatinine, glucose, liver function tests, thyroid function tests, and urinalysis. Brain imaging (CT or MRI scanning) is mandatory in any patient with focal abnormalities on neurologic examination.

Physical

The examination should be complete enough to consider diseases of virtually any organ system. The neurologic examination should look especially at disorders of higher function, such as aphasia or neglect. Other focal neurologic findings such as eye movement and other cranial nerve abnormalities, motor, sensory, and cerebellar findings should be noted.

• Examine the general behavior and comment on level of arousal, alertness, and agitation.
• Patients with delirium, in addition to their "negative" symptoms and signs of deficient cognitive functions, have "positive" symptoms such as agitation, restlessness and hyperactivity, delusional thinking, hallucinations, and anxiety.
• Patients with delirium, unlike those with dementia, frequently have autonomic abnormalities such as tachycardia, hypertension, fever, sweating, and piloerection.
• Examine vital signs, neck stiffness, airflow, lungs, heart, and any abnormal movements such as tremor, myoclonus, tonic-clonic activity, or asterixis.
• Specific neurologic signs should also be sought carefully. These include a detailed examination of higher functions; because the higher functions examination is hierarchical, wakefulness and arousal should be tested first.
• Language should be tested carefully, including the ability to name, repeat, comprehend, read, write, and utter spontaneous speech. Aphasia is frequently mistaken for confusion by emergency department staff.
• Hemispatial attention should be checked (attention to left side is abnormal in focal disorders of right hemisphere) by asking the patient to draw, point to people in the room, or read. If not specifically sought, the neglect syndrome will be missed.
• Look for subtle movements of the face or eyes that are indicative of seizures.
• Eye movements to command should be checked if the patient appears unable to communicate (ie, locked-in syndrome).
• Extinction with double simultaneous stimulation (visual, auditory, tactile, or somatosensory) may be features of the neglect syndrome. Assess whether the patient can recognize his or her illness. Anosognosia is defined as the denial or neglect of illness, commonly occurring after right hemisphere injuries.
• The cranial nerve, motor, sensory, and cerebellar examinations should be geared toward discovering other neurologic signs that can help with localization or uncover an underlying condition. Specific examples of examination findings and their significance follow.
  • The cranial nerve examination should include funduscopic examination. Subhyaloid hemorrhages may be seen in cases of subarachnoid hemorrhage or trauma, and papilledema or absent venous pulsations may indicate increased intracranial pressure.
  • The visual fields should be checked with finger counting or response to threat, to discover subtle visual field defects or visual neglect/extinction.
  • Facial symmetry usually can be assessed, as can gag reflex. A swallow test may be needed to determine if the patient can handle oral food or medication.
  • Motor examination may show a subtle hemiparesis (eg, pronator drift, subtle proximal or distal unilateral weakness).
  • Focal long-tract signs (eg, hyperreflexia, Babinski sign), unilateral dyscoordination (ie, cerebellar lesion), and crossed sensory findings (eg, Brown-Sequard syndrome, brainstem lesion) can be the key to diagnosis of a focal lesion. 
  • Evaluating whether the patient can walk is crucial. Cerebellar hemorrhages and infarctions may be missed unless gait testing is performed.

Causes

Potential causes of delirium are numerous. A good clinician is thorough and systematic in the evaluation.

Intoxication

• Intoxicants can include prescription and over-the-counter medications, as well as alcohol and illicit drugs. Although these causes often are suspected in the emergency department (ED), they may be unsuspected in other settings (eg, postoperative delirium tremens in closet alcoholics).
• Iatrogenic toxicity can occur in patients taking prn (as needed) sedatives, especially elderly patients, or can be due to unsuspected drug interactions. Antipsychotic medications, for example, may worsen memory in patients with underlying Lewy body disease, a type of progressive dementia.
• Anticholinergic medications cause acute confusion and amnesia. Scopolamine patches, antidepressants such as amitriptyline, antispasmodics for irritable bowel syndrome, medications for neurogenic bladder such as oxybutynin, or tranquilizers such as haloperidol all have anticholinergic effects.
• Prescription medicines may be used inappropriately. Prednisone, dexamethasone, and other corticosteroids can cause paradoxical confusion, as can a host of other medications.
• Polypharmacy is a major cause of delirium. Patients may receive antidepressant or antianxiety medications from a psychiatrist, sleep aids from an internist, and anticholinergic medications from a urologist or gastroenterologist, and these drugs may be additive in their cognitive effects. Narcotic analgesics are also factors in many postoperative delirium cases.

Alcohol

• Confusional states due to alcohol are sufficiently important, complex, and common to merit their own category.
• The discussion of alcoholic dementia overlaps with that of nutritional dementia, traumatic dementia, epileptic dementia, vascular dementia, and toxic dementia due to illegal drugs, as these conditions tend to exist in the same patients.
• Alcohol withdrawal leads to the prototypic delirium, delirium tremens.
• Patients with alcoholism are typically malnourished and are at risk for Wernicke-Korsakoff disease, which includes confusion and memory loss, eye movement abnormalities, and ataxia. Administration of thiamine is essential to prevent permanent deficits. 
• The CT scans may show atrophy and hemorrhage due to thiamine deficiency, orbitofrontal or temporal contusions that may be signatures of prior trauma, or subdural hematomas. EEG results may be significant for seizure activity.
• Closet alcoholics can present with delirium tremens several days after admission to the hospital. Various electrolyte imbalances are common.

Metabolic, nutritional, and endocrine disorders

• Organ failure syndromes
• Azotemia
• Chronic lung disease with hypercarbia or hypoxia
• Hepatic failure
• Hyperammonemia (Asterixis may be a clue to hyperammonemia.)
• Nutritional deficiencies
• Pellagra
• Wernicke-Korsakoff syndrome (thiamine deficiency)
• Vitamin B-12 deficiency
• Endocrine syndromes
• Hypothyroidism or hyperthyroidism
• Cushing syndrome
• Hyperparathyroidism
• Diabetic ketoacidosis
• Metabolic disorders
• Hyponatremia
• Hypercalcemia
• Hypoglycemia or hyperglycemia

Focal brain lesions

• Focal brain lesions occasionally cause acute confusion. Subdural hematomas, strokes, cerebral hemorrhages, and mass lesions such as brain tumors or abscesses may be found on CT and MRI scans. Contrasted scans are more sensitive for mass lesions. If the confusion is due to increased intracranial pressure, as in a subdural hematoma, arousal may be most affected, and the patient may be sleepy. If the confusion is due to a stroke, it may be related to misdiagnosed aphasia, though delirium has been reported frequently with infarctions in specific vascular territories, especially the posterior cerebral artery, the anterior cerebral artery territory, or the inferior division middle cerebral artery (left hemisphere stroke with Wernicke aphasia or the homologous area of the right hemisphere).
• Deep lesions of the caudate nucleus, thalamus, or basal forebrain have also been associated with delirium and amnesia.
• Strokes are more likely to be associated with delirium if the patient is elderly, has coexistent cortical atrophy on imaging studies, or has associated seizures.
• Brain tumors often develop slowly, allowing the brain to compensate; therefore, they are somewhat less likely to present as acute confusional states. Seizures, infections, or medication effects can induce delirium in patients with a brain tumor.

Infections

• Urinary tract infections and pneumonias are common infections that cause confusion in debilitated, nursing home, and other elderly patients.
• Meningitis and encephalitis are causes of delirium. The association of delirium with fever or stiff neck should trigger evaluation for these conditions with urgent brain imaging and lumbar puncture. Chronic meningitis is not the exclusive domain of the immunosuppressed; in fact, cryptococcal meningitis, tuberculous meningitis, and carcinomatous meningitis may occur even with minimal symptoms like mild headache and confusion. Diabetics and elderly patients may have bacterial meningitis with minimal fever. Elderly nursing home residents may have Listeria meningitis that responds to ampicillin rather than third-generation cephalosporins. Patients from areas of endemic tuberculosis may be susceptible to tuberculous meningitis.
• Syphilis used to be a common cause of delirium. In the current era, HIV and related opportunistic infections, West Nile encephalitis, herpes simplex encephalitis, and Lyme disease are common infectious causes of delirium.

Epilepsy

• Epileptic seizure states can present as confusion. Patients may have nonconvulsive status epilepticus, a condition that can be easily diagnosed and treated. Two principal types of nonconvulsive status epilepticus have been recognized: absence status and complex partial status epilepticus. Both types may occur in patients without a history of prior seizures. These types are differentiated by the EEG findings. In absence epilepsy, spike-and-wave discharges are seen at a rate of 3 per second. In complex partial status epilepticus, the more common type, a focal discharge pattern may be seen.
• In younger patients, the Landau-Kleffner syndrome is a potentially treatable epileptic condition. Landau-Kleffner syndrome involves acquired aphasia with a convulsive disorder in previously healthy children who acutely or progressively lose language function. Patients typically have a severe comprehension defect, especially involving an auditory agnosia. The seizures in Landau-Kleffner patients usually respond to anticonvulsive therapy, but the language disorder often persists.

Developmental disorders

• Occasionally, a patient with an underlying developmental disorder persisting into adulthood, or a metabolic disease commonly presenting in adulthood may present with confusion. These conditions are much more common in children, and adult neurologists typically experience difficulty in diagnosing developmental disorders in children. For more information on the many metabolic diseases affecting the nervous system, the interested reader is referred to textbooks of child neurology.
• Developmental disorders are particularly prevalent in institutionalized patients, and tragically, only a few of the diseases are treatable. To cite just a few examples, adrenoleukodystrophy, metachromatic leukodystrophy (MLD), and cerebrotendinous xanthomatosis may present in adults. Adrenoleukodystrophy and MLD can be diagnosed by a characteristic pattern of demyelination on MRI. Cerebrotendinous xanthomatosis should be suspected in an individual with an abnormal gait and xanthomas of the Achilles tendons, eyelids, and patellae, due to deposition of cholestanol in the central and peripheral nervous systems. This disorder can be treated.
• Inflammatory conditions in the CNS include the rare, but treatable, conditions of CNS vasculitis and Hashimoto encephalopathy. Of note, patients with known lupus often have strokes due to nonbacterial thrombotic endocarditis (NBTE), hypercoagulable states related to antiphospholipid antibody, hypertension, or CNS dysfunction due to antibodies to neuronal tissues (antineuronal antibodies with ribosomal p protein, with CNS appearing normal on light microscopy). More often than not the coexistence of lupus and encephalopathy leads to a diagnosis other than vasculitis.
• Certain patterns of disease that suggest CNS vasculitis occur in conjunction with specific vasculitides. Their importance is related in part to the specificity of the respective treatments. Polyarteritis nodosa, a disease of small- and medium-sized blood vessels, often affects the heart and kidneys. Neurologic disease includes peripheral neuropathies, seizures, visual loss (due to involvement of optic structures), subarachnoid hemorrhage, and stroke. The survival rate is markedly better in patients who receive the therapeutic combination of cyclophosphamide (Cytoxan) and corticosteroids than in those who receive corticosteroids alone or no treatment (5-year survival rates, 18% in untreated patients; 55% in those treated with corticosteroids alone and 79% in those with combined treatment).
• Churg-Strauss syndrome includes asthma, eosinophilia, vasculitic neuropathy, and, rarely, CNS disease.
• Wegener granulomatosis, a systemic necrotizing granulomatosis, involves the upper and lower respiratory tracts, glomeruli, peripheral nerves, and cranial nerves. Patients often have circulating antineutrophilic cytoplasmic antibodies (ANCA). The disease once was considered fatal within 4-6 months in untreated patients and within 11 months in those treated with prednisone. Long-term survival is now routine in patients treated with the combination of prednisone and cyclophosphamide. Trimethoprim-sulfamethoxazole may decrease the relapse rate in some patients.
• Isolated CNS vasculitis can present with headaches, encephalopathy, and multifocal signs. Isolated CNS vasculitis should be diagnosed only according to strict criteria, including recurrent, multifocal vascular disease, exclusion of a systemic inflammatory of infectious process, angiography supportive of the diagnosis, and brain biopsy to exclude infection or neoplasia. Without the presence of these criteria, the diagnosis can be considered speculative. Therapy with cyclophosphamide and prednisone may result in long-term remission or cure.
• Hashimoto encephalopathy is a condition characterized by severe encephalopathy, seizures, and high circulating titers of antithyroid antibodies. The disorder likely reflects antibody-mediated inflammation in the CNS, since most patients with the condition are clinically euthyroid. EEG findings may be moderately abnormal, and the patient may respond to corticosteroid therapy.

Dementia

• Underlying dementia is present in many patients with delirium, but it should be a diagnosis of exclusion. Dementia, unlike delirium, is not readily reversible with correction of an underlying toxic, metabolic, or infectious disorder. Like delirium, dementia involves a loss of cognitive functions such as language, perception, attention, and memory. Unlike delirium, however, dementia is usually defined as a progressive or permanent state. Dementia usually lacks the alteration of consciousness, psychomotor abnormalities, and autonomic disturbances that are so common in delirium. 
• Dementia, once thought to be monolithic and more or less untreatable, can often be further fractionated and diagnosed by clinical examination and laboratory testing. Research is continuing into imaging characteristics and biological markers for specific dementias such as Alzheimer disease, frontotemporal dementia, and Creutzfeldt-Jakob disease.
• Visual hallucinations and a paradoxical response to antipsychotic medications make Lewy body disease, rather than Alzheimer disease, the likely diagnosis. Prominent behavioral or language disturbance increases the possibility of Pick disease or frontotemporal dementia. Marked apraxia of one hand makes the diagnosis of corticobasal ganglionic degeneration more likely.
• Presence of abnormal eye movements (especially vertical eye movements) may indicate progressive supranuclear palsy, although the physician should not forget to consider thiamine deficiency or Whipple disease in this situation.
• Again, dementias can underlie or accompany delirium. The diagnosis usually does not require lumbar puncture, except in the case of Whipple disease or suspected infectious illnesses such as chronic meningitis.

Vascular dementia

• Vascular dementia refers to dementia that is due to strokes. The strokes may be cortical and have localizing features, depending upon what part of the cortex is involved.
• Vascular dementia also refers to dementia due to multiple subcortical strokes, which are caused by extensive disease of the smallest caliber blood vessels.
• This has been known by multiple names, including Binswanger disease, état lacunaire, leukoaraiosis (referring to the radiographic or MRI appearance of white matter rarefaction), and others.
• Notably, the presence of subcortical strokes, even extensive ones, does not preclude Alzheimer disease.
• Clinically, patients with Binswanger disease have not only the radiographic characteristics but also distinct presenting features. These may include gait abnormalities and difficulties with memory, such as 3-word recall, and frontal lobe tests, such as the Thurstone or the go, no go paradigm.
• Typically, such patients do not have cognitive features such as anomia, apraxia, agnosia, and neglect, as are seen with cortical lesions.
• Some cases are associated with severe hypertension or elevation of the fibrinogen level.

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