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What is Lewy Body Dementia?
Dementia is a clinical syndrome characterized by a chronic and progressive decline in higher mental functions, severe enough to interfere with a person’s social relationships, independence, and ability to carry out everyday activities and work.
Dementia is never a congenital condition, meaning it is never present from birth (unlike intellectual disability). Instead, it is an acquired condition that, in the vast majority of cases, develops in older age, typically starting around 60 years of age. This is the reason why, for decades, doctors and the general public used the generic and now outdated term “senile dementia” to describe any type of cognitive decline in the elderly.
Unlike other neurodegenerative disorders that share overlapping symptoms and clinical signs, dementia does not involve an altered level of consciousness or a primary loss of attention. These two features are what distinguish true dementia from a generic confusional state or delirium, which is usually acute, fluctuating, and reversible.
Lewy body dementia (LBD) is a progressive neurodegenerative disease characterized by the gradual loss of neurons in specific areas of the central nervous system. Over time, this neuronal loss produces a clinical picture of dementia along with measurable cerebral atrophy, that is, a visible reduction of brain tissue volume on imaging.
As with all dementias, the hallmark feature of Lewy body dementia is a decline in memory, which is accompanied by a cluster of other characteristic disturbances, including:
- Aphasia: a disorder of language that affects both comprehension and expression, whether spoken or written
- Apraxia: the loss of the ability to perform previously learned, purposeful motor tasks, even very simple ones such as brushing teeth or getting dressed
- Agnosia: the inability to recognize familiar objects, people, sounds, or places despite intact sensory function
- Impairment of executive function, meaning difficulties with planning, organizing, problem-solving, and multitasking
- Behavioral changes, including apathy, agitation, or disinhibition
- Mood alterations, such as depression, anxiety, or emotional instability
Lewy body dementia belongs to the group of dementias that are unfortunately irreversible, because they are caused by ongoing neurodegeneration, that is, the progressive and permanent death of nerve cells. According to most epidemiological estimates, it is the third most common cause of dementia after Alzheimer’s disease and vascular dementia, but it stands out because its symptoms tend to appear earlier and evolve more rapidly than in other neurodegenerative dementias.
Over time, the disease severely compromises the patient’s quality of life, eventually leading to a complete loss of independence in daily activities such as eating, dressing, walking, and personal hygiene. Because the disease combines cognitive, motor, psychiatric, and autonomic symptoms, it is often more disabling and more difficult to manage than other forms of dementia, both for the patient and for the family caregivers involved in daily care.
What Happens Inside the Brain
To understand Lewy body dementia, it helps to know what actually happens at the cellular level. The disease takes its name from abnormal protein deposits called Lewy bodies, first described by the German neurologist Friedrich Lewy in the early twentieth century while studying patients with Parkinson’s disease.
These abnormal deposits accumulate inside neurons, disrupting their normal communication and function, and eventually leading to cell death. As neurons die, the brain regions involved gradually shrink, a process known as atrophy. The areas most commonly and earliest affected include the brainstem, particularly the substantia nigra, as well as the limbic system and, as the disease progresses, the cerebral cortex, the outer layer of the brain responsible for memory, perception, thought, and language.
This is why Lewy body dementia produces such a broad and variable symptom picture: it does not affect a single, isolated brain region but rather a network of structures responsible for movement, cognition, mood, perception, and even basic autonomic functions such as blood pressure regulation and digestion.
Lewy body dementia is closely related, both biologically and clinically, to Parkinson’s disease. In fact, both conditions belong to a broader family of disorders called “synucleinopathies”, so named because they are caused by the abnormal accumulation of a protein called alpha-synuclein. The main clinical difference lies in the timing: in Parkinson’s disease, movement symptoms typically appear years before cognitive decline, while in Lewy body dementia, cognitive and motor symptoms tend to emerge close together, often within the same year.
Prognosis and Disease Course
The long-term prognosis of Lewy body dementia is unfortunately unfavorable. As with other neurodegenerative dementias, there is currently no cure, and the disease follows a progressive course.
Over time, cognitive decline is inevitable and is accompanied by a wide range of additional psychiatric and neurological complications, including worsening hallucinations, increasingly severe motor impairment, and greater dependence on caregivers for basic daily activities.
One of the most frequent and dangerous complications of Lewy body dementia is difficulty walking and loss of balance, which leads to a marked increase in the frequency of falls. These falls often result in fractures, head trauma, and hospitalizations, and are frequently a direct or indirect cause of death in affected patients. In addition, the presence of significant autonomic dysfunction, including blood pressure instability, swallowing difficulties, and increased susceptibility to infections such as pneumonia, further worsens the overall prognosis.
Predicting life expectancy in Lewy body dementia is difficult, and the data currently available in the medical literature are limited compared with more common conditions such as Alzheimer’s disease. Survival can be measured either from the onset of the first symptoms or from the time of formal diagnosis, and these two figures can differ significantly, since diagnosis is often delayed by several years due to the complexity of the clinical picture.
A widely cited 2017 systematic review estimated survival as follows:
- From the onset of symptoms: between 5.5 and 7.7 years
- From the time of diagnosis: between 1.9 and 6.3 years, which is generally shorter than the survival typically seen in Alzheimer’s disease
It is important to underline that these are population averages, and individual prognosis can vary considerably depending on the age at onset, the presence of coexisting medical conditions, the severity of motor symptoms, the quality of medical and caregiving support, and how quickly complications such as falls, infections, or severe behavioral disturbances develop. Some patients maintain a relatively stable quality of life for several years with appropriate multidisciplinary support, while others experience a much faster decline.
Causes
Lewy body dementia has a characteristic and specific neuropathological picture that distinguishes it from other types of dementia, to the point that it is now recognized as a distinct disease entity rather than simply a variant of Alzheimer’s disease or Parkinson’s disease.
Lewy bodies are abnormal clumps, or inclusions, that form inside nerve cells (neurons). They can be visualized under the microscope thanks to their ability to take up specific histological stains, a property referred to as “PAS positivity” (Periodic Acid-Schiff staining).
These inclusions are intracytoplasmic aggregates of a protein normally found at neuronal synapses, called alpha-synuclein. In healthy neurons, alpha-synuclein plays a role in regulating the release of neurotransmitters, the chemical messengers that allow nerve cells to communicate with one another. In Lewy body dementia, this protein misfolds and clumps together, initially accumulating in the substantia nigra, a brainstem structure that is also central to the pathology of Parkinson’s disease, and then progressively spreading to other regions of the brain, including the limbic system and the cerebral cortex.
Despite decades of research, the underlying cause that triggers the abnormal folding and accumulation of alpha-synuclein remains unknown. Current scientific hypotheses point to a combination of genetic predisposition, age-related cellular vulnerability, oxidative stress, mitochondrial dysfunction, and possibly environmental exposures, but no single definitive cause has been identified. Unlike some other neurodegenerative diseases, Lewy body dementia is only rarely linked to a clearly inherited genetic mutation, and most cases are considered sporadic, meaning they occur without a clear family history.
Risk Factors
As with other forms of dementia, the risk of developing Lewy body dementia can be influenced by a combination of factors, which can be divided into two categories: non-modifiable and modifiable.
Non-modifiable risk factors:
- Advancing age, since the disease is rare before the age of 50 and becomes increasingly common after 60
- Female sex, although some studies also report a higher prevalence in men, and data on sex differences remain somewhat inconsistent
- A family history of neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, or other forms of dementia
Modifiable risk factors:
- Smoking
- Exposure to environmental toxins, such as certain pesticides and industrial chemicals
- Diabetes
- Hormonal factors, including estrogen levels
- Cardiovascular risk factors such as obesity, high blood pressure, and high cholesterol or triglycerides
- Low educational attainment, which is thought to reduce so-called “cognitive reserve”, the brain’s ability to compensate for age-related changes and early neurodegeneration
While modifiable risk factors cannot guarantee prevention of Lewy body dementia, addressing them through a healthy lifestyle, including regular physical activity, a balanced diet, smoking cessation, and good management of cardiovascular health, is strongly recommended by major health organizations as part of a broader strategy to support overall brain health and reduce the risk of cognitive decline in general.
Symptoms
The clinical picture of Lewy body dementia typically begins with an onset phase, often referred to as the stage of “early symptoms”, which is usually dominated by a subtle deterioration of memory and noticeable changes in personality. Importantly, patients themselves are frequently unaware of these changes, and it is common for the affected person to deny or minimize their symptoms, a phenomenon known as anosognosia.
Like other dementias, including Alzheimer’s disease, Lewy body dementia is a chronic, slowly progressive illness, which means that early symptoms tend to develop gradually and can go unnoticed for a long time, sometimes being mistaken for normal aging, stress, or depression.
From a neurological point of view, Lewy body dementia can present with a remarkably varied array of clinical signs. These generally fall into four main domains: memory, behavior, psychiatric symptoms, and higher cortical functions.
Early Symptoms
Memory disturbances
Memory problems in Lewy body dementia can involve several different types of memory simultaneously:
- Fixation memory, meaning difficulty remembering recent facts, events, or conversations
- Working memory, with a tendency to forget what one was doing just moments earlier, for example losing track of a task midway through
- Semantic memory, involving an inability to recall basic general knowledge or the meaning of common words
It is worth noting that, unlike Alzheimer’s disease, memory loss is not always the very first or most prominent symptom in Lewy body dementia. In many patients, visual hallucinations, fluctuating attention, or parkinsonian motor signs appear before significant memory problems become evident, which is one reason the disease is so often misdiagnosed in its early stages.
Behavioral disturbances
Patients often develop apathy and a marked lack of interest in previously enjoyed activities. Disinhibition may also occur, leading to disorganized, socially inappropriate, or even antisocial behavior. A particularly characteristic symptom is the so-called “catastrophic reaction”, an intense emotional outburst that occurs when the patient suddenly becomes aware, even briefly, of their own cognitive or functional deficits.
Psychiatric symptoms
A reduction in mood is common, ranging from mild sadness to a more or less severe depressive episode. Personality changes may progress toward frankly delusional thinking, and patients may experience detailed, vivid visual hallucinations, often described as seeing people, animals, or objects that are not actually present.
Advanced Symptoms
As the disease progresses and cerebral atrophy spreads to involve a larger portion of the cerebral cortex, additional and more severe symptoms typically emerge:
- Aphasia: a language disorder characterized by the inability to produce or understand spoken or written language
- Apraxia: a disorder of voluntary movement characterized by the inability to carry out coordinated, purposeful actions, such as brushing one’s teeth, combing one’s hair, or tying shoelaces, even though muscle strength and coordination are otherwise preserved
- Agnosia: a perceptual disorder characterized by the inability to recognize objects, familiar people, or well-known places, despite normal functioning of the sense organs involved
- Impaired executive function, with growing difficulty in planning, organizing, and making decisions
- Disorganized thinking, which becomes impoverished and incoherent, with a marked reduction in the ability to reason abstractly or analyze information
- Mood alterations, with a persistent tendency toward generalized “sadness” for most of the day and, in many cases, full-blown depression. Paradoxically, in the most advanced stages of the disease, this depressive tone can sometimes appear to normalize, likely reflecting a further loss of emotional awareness rather than genuine improvement
- Visuospatial disturbances, including difficulty judging distances, navigating familiar environments, or correctly interpreting what is seen
- Disorientation in time and space, meaning affected individuals may fail to recognize their own home, or may develop the belief that they have been kidnapped or are being held somewhere against their will. These situations are frequently accompanied by other delusional ideas or agitated behavior, which can be extremely distressing for both patients and family members
As the disease advances further, the combined burden of all these symptoms progressively erodes the patient’s quality of life, ultimately resulting in a complete loss of autonomy. In the final stages, patients become entirely dependent on caregivers for every aspect of daily living, including feeding, mobility, personal hygiene, and communication.
Diagnosis
Diagnosing Lewy body dementia is notoriously challenging, largely because its clinical presentation overlaps substantially with other forms of dementia, particularly Alzheimer’s disease and Parkinson’s disease dementia. It is important for patients and families to understand that a fully definitive diagnosis can, strictly speaking, only be confirmed through a neuropathological examination after death, based on a detailed microscopic study of brain tissue samples showing the presence of Lewy bodies. During life, doctors rely on a combination of clinical criteria and diagnostic tests to reach what is called a diagnosis of “probable” or “possible” Lewy body dementia.
Clinical history and neurological examination
When consulting a neurologist, the diagnostic process begins with a thorough clinical evaluation, including a detailed medical history aimed at exploring:
- The timing of symptom onset and how they have evolved
- The specific type and combination of symptoms reported by the patient and, crucially, by family members or caregivers, who often notice changes the patient is not fully aware of
- The degree of impairment in the patient’s quality of life, which helps determine whether the disease is in an early or advanced stage
- The presence of other psychiatric, neurological, infectious, or toxic conditions that can produce symptoms resembling dementia
- Current medication use, since several drugs can cause or worsen cognitive symptoms, particularly in older adults
- Family history of neurological or psychiatric disease
Following the history, a complete neurological examination is essential to identify the specific signs associated with dementia, including memory testing, assessment of language and praxis, evaluation of gait and balance, and screening for parkinsonian features such as tremor, rigidity, and slowness of movement.
Differential diagnosis
Because many of these symptoms can also be caused by other conditions, a careful differential diagnosis is essential. Conditions that must be considered and excluded include:
- Other neurological or psychiatric disorders capable of producing memory deficits and related symptoms, such as major depressive disorder or other types of dementia
- Cerebrovascular events, including stroke or cerebral hemorrhage
- Long-term effects of alcohol use
- Metabolic disturbances, such as thyroid dysfunction or vitamin deficiencies
- Chronic subdural hematoma
- Brain tumors
- Normal pressure hydrocephalus
- Other neurodegenerative diseases, such as Parkinson’s disease, Huntington’s disease, prion disease, and progressive supranuclear palsy
- Infections, particularly tertiary syphilis and HIV-related cognitive impairment
Laboratory and imaging investigations
After the clinical evaluation, the diagnostic process typically continues with laboratory tests and imaging studies, including:
- Blood tests: routine blood work can help rule out electrolyte imbalances or hormonal abnormalities, such as hypothyroidism, that can mimic or contribute to a dementia-like clinical picture
- Cerebrospinal fluid (CSF) analysis: performed through a lumbar puncture, this test allows a small sample of spinal fluid to be collected and analyzed, which can be useful for excluding Alzheimer’s disease based on specific biomarkers
- Brain MRI or CT scan: these imaging studies allow physicians to assess the degree of brain atrophy and widening of the cortical sulci, both typical findings in dementia, and to rule out tumors or other structural brain abnormalities. Unfortunately, unlike some other forms of dementia, Lewy body dementia does not show a single, highly specific structural abnormality on routine MRI or CT imaging, which is one of the reasons diagnosis remains challenging
- PET scan with fluorodeoxyglucose (FDG-PET): a nuclear medicine technique that uses a radiolabeled tracer to evaluate glucose metabolism in different regions of the brain, often showing a characteristic pattern of reduced metabolism in the occipital lobes in Lewy body dementia
- Dopamine transporter imaging (DaTscan): an additional nuclear medicine test, increasingly used in specialized centers, that can detect reduced dopamine transporter activity in the brain, supporting the diagnosis when parkinsonian features are present
Cognitive screening
The diagnostic workup usually concludes with a standardized cognitive screening tool, most commonly the “Mini Mental State Examination” (MMSE), a structured questionnaire administered to the patient that produces a numerical score reflecting overall cognitive status. A score below 24 out of 30 is highly suggestive of dementia, although additional, more detailed neuropsychological testing is often needed to characterize the specific pattern of cognitive impairment and support a more precise diagnosis.
It is worth mentioning that internationally recognized consensus criteria, most notably those developed and periodically updated by an international panel of experts on dementia with Lewy bodies, are used by specialists to classify the diagnosis as “probable” or “possible”, based on the combination of core clinical features (fluctuating cognition, recurrent visual hallucinations, REM sleep behavior disorder, and spontaneous parkinsonism) together with supportive biomarkers such as those described above.
Characteristics and Differences from Other Dementias
From an anatomical standpoint, the defining feature of this disease is the presence of Lewy bodies within brain tissue, a finding that, as noted, can only be confirmed with certainty during a post-mortem autopsy examination.
Beyond the general symptom pattern shared by all dementias, Lewy body dementia is distinguished by several specific and clinically important features:
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Parkinsonism: patients frequently develop signs similar to those seen in Parkinson’s disease, including tremor, slowness of movement (bradykinesia), muscle rigidity, and difficulty maintaining balance and walking normally. Unlike classic Parkinson’s disease, tremor at rest may be less prominent, while gait instability and rigidity tend to be more pronounced.
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Visual hallucinations: a particularly distinctive feature of these hallucinations is their striking realism and richness of detail, often resembling vivid, dream-like scenes involving people, children, or animals. Hallucinations involving smell, hearing, or touch are considerably rarer than visual ones.
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Fluctuating attention and cognition: patients can lose focus and awareness within moments, seemingly “drifting off” during a task they were performing just a short time earlier. The same fluctuation can occur unexpectedly in the middle of a conversation, with the person suddenly appearing confused, drowsy, or unresponsive, only to become lucid again shortly afterward. These fluctuations can vary from hour to hour or even day to day, and represent one of the most characteristic and clinically useful features for distinguishing Lewy body dementia from Alzheimer’s disease.
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REM sleep behavior disorder: many patients act out their dreams during sleep, sometimes talking, shouting, or making sudden movements, occasionally injuring themselves or their bed partner. This symptom is now recognized as one of the earliest and most specific warning signs of Lewy body dementia, and it can precede the onset of cognitive symptoms by several years.
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Frequent falls: these individuals experience a notably high frequency of accidental falls while walking, often leading to serious complications such as hip fractures, pelvic fractures, and head trauma.
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Sphincter incontinence: a disorder characterized by the involuntary loss of stool and gas from the anus (fecal incontinence) and involuntary loss of urine (urinary incontinence).
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Autonomic dysfunction: beyond incontinence, patients frequently experience other signs of autonomic nervous system failure, including orthostatic hypotension (a drop in blood pressure upon standing, which can cause dizziness or fainting), constipation, and swallowing difficulties.
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Hypersensitivity to neuroleptic medications: this is, without question, the single most specific and clinically important feature of this form of dementia. Even at very low doses, antipsychotic (neuroleptic) medications can trigger a severe and potentially life-threatening extrapyramidal reaction in these patients, characterized by muscle spasms, worsening confusion, marked sedation, rigidity, tremor even at rest, and further memory impairment. Whenever a physician encounters a case of dementia in which a marked extrapyramidal reaction develops after the administration of a neuroleptic drug, Lewy body dementia should always be strongly suspected. Because of this risk, it is essential that any new medication, particularly antipsychotics, is prescribed and monitored only by a physician experienced in managing this condition.
Treatment
As with other neurodegenerative dementias, there is currently no definitive cure for Lewy body dementia that can reverse the disease or restore lost neurons. This unfortunately explains the poor long-term prognosis once the disease reaches an advanced stage.
The therapeutic approach is essentially medical and pharmacological, aimed at slowing the progression of symptoms and controlling them for as long as possible, while also addressing the significant burden the disease places on patients and their families.
Medication challenges
In addition to the already limited number of effective treatment options, Lewy body dementia is characterized by a marked intolerance to neuroleptic (antipsychotic) medications, even at very low doses, as previously discussed. This intolerance significantly complicates the management of behavioral and psychiatric symptoms, since these medications, which are commonly used in other forms of dementia to control agitation, delusions, or hallucinations, can cause severe adverse reactions in patients with Lewy body dementia.
For this reason, when antipsychotic treatment is genuinely necessary, physicians increasingly turn to a specific class of drugs with a more favorable safety profile, most notably low-dose quetiapine, which has a comparatively weaker but safer pharmacological effect on the extrapyramidal system. These medications can partially help control psychiatric symptoms such as delusional thinking and depression, but they must always be used cautiously, at the lowest effective dose, and under close medical supervision.
Cholinesterase inhibitors
Cholinesterase inhibitors, a class of medications also used in Alzheimer’s disease, have shown a certain degree of benefit in Lewy body dementia, particularly in improving cognitive fluctuations, attention, and even some hallucinations. However, this benefit is generally most evident in the earlier stages of the disease and tends to diminish over time as neurodegeneration progresses. Some patients also experience improvement in alertness and reduced apathy with these medications, although individual response can vary considerably.
Managing motor symptoms
For the parkinsonian motor symptoms, such as rigidity and slowness of movement, doctors may cautiously consider medications used in Parkinson’s disease, such as levodopa. However, these drugs must be used carefully, since they can sometimes worsen hallucinations or psychiatric symptoms, requiring a delicate balance between improving mobility and avoiding a worsening of cognitive or behavioral symptoms.
Supportive and non-pharmacological therapy
Given these significant pharmacological limitations, non-pharmacological supportive care takes on even greater importance in Lewy body dementia, offering a realistic and valuable opportunity to preserve an acceptable quality of life for as long as possible.
Supportive therapy is generally based on several complementary approaches:
- Occupational therapy, which helps patients maintain independence in daily activities for as long as possible and adapts the home environment to reduce fall risk and improve safety
- Behavioral therapies, aimed at managing agitation, anxiety, and disruptive behaviors through structured routines and environmental modifications rather than medication alone
- Cognitive therapies, including cognitive stimulation exercises designed to support memory, attention, and reasoning skills for as long as possible
- Sensory training, which can help patients better process visual and auditory information and may reduce the distress associated with hallucinations
- Physical therapy, focused on maintaining mobility, balance, and muscle strength, which is particularly important given the high risk of falls associated with this condition
A multidisciplinary team, typically involving a neurologist, geriatrician, psychiatrist, physical therapist, occupational therapist, and social worker, is generally considered the most effective approach to managing the complex and evolving needs of patients with Lewy body dementia throughout the course of the disease.
Living with Lewy Body Dementia: Advice for Patients and Caregivers
Because Lewy body dementia combines cognitive, motor, and psychiatric symptoms, caring for a loved one with this condition can be particularly demanding. The following practical suggestions, drawn from guidance provided by major dementia care organizations, can help improve daily management and safety:
- Fall prevention: remove tripping hazards at home, install grab bars in bathrooms, ensure adequate lighting, particularly at night, and consider a physical therapy evaluation to assess gait and balance.
- Managing hallucinations: rather than directly contradicting the patient, caregivers are often advised to respond calmly, avoid arguing about the reality of what the person is seeing, and gently redirect attention, since hallucinations in Lewy body dementia are frequently vivid but not necessarily distressing to the patient.
- Medication safety: always inform every healthcare provider, including emergency room staff, dentists, and specialists, about the diagnosis of Lewy body dementia before any new medication is prescribed, given the serious risk of neuroleptic sensitivity.
- Sleep management: since REM sleep behavior disorder is common, consider protective measures in the bedroom, such as removing sharp objects from the nightstand and, if needed, discussing specific sleep medications with the treating physician.
- Routine and structure: maintaining a consistent daily schedule can help reduce confusion and agitation, since predictability tends to be reassuring for patients with fluctuating cognition.
- Caregiver support: caring for someone with Lewy body dementia is physically and emotionally demanding. Seeking support from dementia caregiver support groups, respite care services, and mental health professionals is strongly encouraged to prevent caregiver burnout.
Frequently Asked Questions
Is Lewy body dementia the same as Alzheimer’s disease?
No. Although both are progressive neurodegenerative dementias and can share some overlapping symptoms, they are caused by different underlying processes (alpha-synuclein aggregation in Lewy body dementia versus amyloid plaques and tau tangles in Alzheimer’s disease) and have distinct clinical features, particularly the early presence of visual hallucinations, fluctuating cognition, and parkinsonism in Lewy body dementia.
Is Lewy body dementia the same as Parkinson’s disease dementia?
The two conditions are closely related and share the same underlying pathology, but they are generally distinguished based on timing: if cognitive decline appears before or within one year of the onset of motor symptoms, the diagnosis is typically Lewy body dementia; if dementia develops more than a year after a well-established diagnosis of Parkinson’s disease, it is usually classified as Parkinson’s disease dementia.
Can Lewy body dementia be prevented?
There is currently no proven way to completely prevent Lewy body dementia, since its exact cause remains unknown. However, adopting a heart-healthy lifestyle, avoiding smoking, managing cardiovascular risk factors, staying mentally and physically active, and pursuing higher educational and cognitive engagement throughout life may help reduce overall dementia risk.
How is Lewy body dementia diagnosed with certainty?
A fully certain diagnosis can only be made after death, through microscopic examination of brain tissue confirming the presence of Lewy bodies. During life, doctors rely on a combination of clinical criteria, cognitive testing, and imaging studies to reach a diagnosis of “probable” or “possible” Lewy body dementia with a high degree of confidence.
Sources and Bibliography
- Mioni R., Lopiano L., Durelli L., Mauro A., Chiò A. Il Bergamini di Neurologia. Libreria Cortina, Torino.
- Mueller C., Ballard C., Corbett A., Aarsland D. The prognosis of dementia with Lewy bodies. The Lancet Neurology, 2017.
- National Institute on Aging. What Is Lewy Body Dementia? Causes, Symptoms, and Treatments.
- Mayo Clinic. Lewy Body Dementia: Symptoms and Causes.
- Lewy Body Dementia Association (LBDA). Diagnostic Criteria for Dementia with Lewy Bodies.
- McKeith I.G. et al. Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium. Neurology, 2017.
- NHS. Symptoms of Lewy Body Dementia.
- Alzheimer’s Association. What Is Lewy Body Dementia?
