Dementia with Lewy body (DLB) is one of the most common neurodegenerative diseases, characterized by fluctuating cognitive dysfunction, visual hallucinations and motor symptoms similar to Parkinson’s disease, often preceding motor symptoms. The main pathological feature is the Lewy body (LB), which is widely distributed in the cerebral cortex and brainstem.
In 1912, Frederick Lewy first identified an intracytoplasmic inclusion in the midbrain substantia nigra of patients with primary Parkinson’s disease (PD), which was also confirmed by other scholars and named LB. dementia patients were quite rare. It was not until the 1980s that new histochemical staining techniques became available that LB could be more easily detected, and more and more dementia patients were found to be associated with LB.
In 1961, Okazaki et al. first described the pathology and clinical manifestations of this type of dementia in detail and proposed the name DLB, and since then, other names for diseases related to DLB have emerged, such as diffuse Lewy body disease, cortical Lewy In 1995, the First International Working Conference on Lewy Body In 1995, the first International Working Conference on Dementia unified the name of the disease as dementia with Lewy bodies, or DLB (DLB has not been listed as a separate disease unit in ICD-10 and DSM-V).
Recent studies have concluded that DLB accounts for 15-20% of dementia in old age and is the 2nd most prevalent disease after Alzheimer’s disease (AD). There are few epidemiological investigations on the prevalence of DLB. Based on non-population-based studies, the prevalence of DLB accounts for 3.0% to 26.3% of all dementias in people over 65 years of age, similar to the autopsy findings of 15% to 25%. Based on a small number of demographic surveys, the prevalence of DLB ranges from 0.1% to 2.0% in people over 65 years of age and 5.0% in people over 75 years of age. DLB is usually rarely inherited in families.
The etiology and pathogenesis of DLB are not yet known. Some studies have confirmed that cholinergic and monoaminergic neurotransmitter impairment in DLB patients may be associated with cognitive impairment and extrapyramidal movement disorders. Genetic studies have revealed that some DLB patients and familial PD patients have mutations in the α-synuclein gene, and the gene product α-synuclein is a component of both Lewy bodies and age spots, which may presumably be related to the development of DLB; in addition, the APOEε4 gene may also be a risk factor for DLB.
Lewy bodies are widely distributed in the cerebral cortex and subcortical nuclei of DLB patients, and they are intracytoplasmic eosinophilic round vesicles. It is generally believed that Lewy bodies are the result of abnormal aggregation of α-synuclein from soluble to insoluble, and that factors affecting α-synuclein expression and metabolism may be associated with the development of DLB. In some DLB and familial PD, there are mutations in the α-synaptic nucleoprotein gene, resulting in the replacement of its position 5 threonine by alanine, causing abnormal aggregation of α-synaptic nucleoprotein from soluble to insoluble; neurofilaments are mainly abnormal aggregation of their trimeric subunits, affecting the function of microtubule proteins and causing neuronal function and damage. Electron microscopically Lewy bodies are osmiophilic granules mixed with helical tubules or double helical filaments. It has been reported in the literature that Lewy bodies are positive for ubiquitinated proteins and negative for tau proteins and β-amyloid, indicating a significant difference from the typical pathological changes of AD. There are more diseases with Lewy body pathological features, among which primary α-synucleinopathies mainly include DLB, primary Parkinson’s disease and multiple sclerosis, in addition to Lewy bodies can be found in the brains of AD patients.
Despite the increasing understanding of the disease, the relationship between DLB and PD and AD is fraught with controversy, especially since PD presents with dementia symptoms during disease progression, and many researchers believe that there is a spectrum of LB disease. LB is found in more than 40% of AD brains, and these patients are sometimes referred to as the LBD variant of AD (LBV-AD), suggesting an overlap between AD and DLB, making the diagnosis and treatment of the disease difficult. making the diagnosis and treatment of the disease difficult. At present, there are few studies on DLB in China. This consensus systematically describes the clinical characteristics, diagnosis and treatment of DLB with reference to the third DLB consensus authored by McKeith et al. and the diagnostic criteria for Lewy body cognitive dysfunction (NCDLB) published by DSM-5, combined with the latest research literature.
I. Clinical characteristics
1. Clinical symptoms: In recent years, more and more studies have been conducted on the prodromal phase of AD and PD. Some studies suggest that non-amnesic cognitive impairment, fluctuating cognitive impairment relatively rare, prodromal symptoms such as fast-acting sleep behavior disorder, visual hallucinations, depression, delirium, Parkinson’s syndrome-like manifestations, hyposmia, constipation and postural hypotension will exist before the appearance of typical DLB symptoms.
As the disease progresses, the typical clinical features of DLB gradually emerge, namely fluctuating cognitive decline, whose main characteristic symptoms include a decline in thinking and reasoning abilities, with multiple alternations between blurred consciousness and wakefulness within a day to several days, with attention, executive function and visuospatial deficits being the most severe; PD-like motor symptoms, which occur in about 50% of patients, include slow movement, trunk bowed posture, muscle tonus and balance disturbances; recurrent and vivid visual hallucinations; others include delusions, difficulties in processing visual information, dream abnormalities in fast-acting sleep, sleep disturbances, abnormalities in vegetative functions, and memory impairment of less severity than AD.
The following clinical symptoms help to distinguish DLB from AD: fluctuations in cognitive function with arousal and attentional changes, fluctuations evidenced by excessive daytime sleepiness (with adequate nocturnal sleep conditions) or daytime sleepiness of 2 h or more, prolonged gazing into the distance, episodes of disorganized speech, etc., and visual hallucinations. In addition, paraclinical amnesia is a prominent sign and symptom of AD and appears early in the disease, while DLB paraclinical amnesia is not prominent.A study by McKeith et al [8] concluded that DLB is better than AD on cognitive tests such as naming, short- or medium-term recall, and recognition, while AD is better than DLB in verbal fluency, visual perception, and executive function.DLB patients have better executive function and visual DLB patients have more impaired executive and spatial functions than AD, such as the stroop test and the digit breadth test.
Other symptoms that alert clinicians to the diagnosis of DLB (compared to AD) include: non-visual hallucinations, delusions, unexplained syncope, fast-acting eye sleep disorder, and psychotropic drug sensitivity.
2. Physical and cognitive examination: Patients have PD-like signs and symptoms but do not meet the diagnostic criteria for PD, have mild gait disturbances that cannot be explained by the patient’s old age and osteoarthrosis, resting tremor is less common than PD, and myoclonus is present before severe dementia. Orthostatic hypotension is more common in patients with DLB, even when dementia symptoms are not severe.
DLB usually exhibits cognitive impairment consistent with dementia. A study using the MMSE as a cognitive score showed that DLB:AD:AD+DLB was (15.6 ± 8.7) points: (10.7 ± 8.6) points: (10.6 ± 8.6) points, with relatively good cognitive tests in DLB, while at other times it became blurred and muted, and these fluctuations are characteristic of DLB. Memory extraction is more severely impaired relative to memory storage, and naming tests are relatively better than visuospatial tests (e.g., clock drawing and number transcription).
3. Laboratory tests: Laboratory tests cannot provide a basis for the diagnosis of DLB, but can indicate the risk of certain dementia types. Routine dementia tests include a full set of biochemical tests, routine blood tests, thyroid function, vitamin B12 levels, and, if necessary, syphilis, Lyme disease or AIDS-related tests. Cerebrospinal fluid is not routinely tested. recent studies of cerebrospinal fluid in DLB have found that cerebrospinal fluid tau is higher in AD patients than in DLB, LBV-AD is in between, and cerebrospinal fluid Aβ levels are higher than normal in DLB, LBV-AD and AD, but there is no difference between the three. the APOE allele assay can indicate the risk of AD.
4. Imaging examinations.
(1) MRI: cranial MRI helps to distinguish vascular dementia from DLB. patients with vascular dementia often have white matter ischemic lesions, while DLB does not. medial temporal lobe structures including hippocampal atrophy in DLB are less severe than in AD, but more severe than in normal controls; atrophy of the Nucleus Basalis of Maynert (NBM) and the nucleus accumbens in DLB Cortical atrophy in the middle and posterior cingulate gyrus, superior temporo-occipital lobe and orbital surface of the prefrontal lobe was more pronounced in DLB than in AD, whereas in AD it was in the parahippocampal gyrus, cingulate gyrus knee and temporal pole.
(2) SPECT/PET: SPECT or PET in DLB patients reveals reduced occipital blood flow or metabolism, whereas the occipital lobe is relatively preserved in AD patients; and FDG uptake in the occipital cortex is more significantly decreased in DLB compared with Parkinson disease dementia (PDD) (P<0.01). striatum in DLB fdg uptake is symmetrically reduced in pdd. striatal fdg uptake is reduced asymmetrically in pdd, with lower striatal fdg uptake contralateral to the first symptom than ipsilateral to the first symptom < span="">[10]. The detection of presynaptic dopaminergic function by SPECT and PET using dopamine transporter molecules as ligands (DAT) markers has been included as a suggestive feature for the diagnosis of likely DLB, and dopamine transporter abnormalities have a sensitivity of over 78% and specificity of over 90% for the diagnosis of DLB. Postmortem studies have confirmed that 123I-FP-CIT-SPECT has higher sensitivity (88%) and specificity (100%) for differentiating DLB from other non-DLB dementias, with a meta-analysis showing 86.5% sensitivity and 93.6% specificity.Lim et al. performed SPECT and PET on 14 patients with a clinical diagnosis of DLB and 10 patients with a clinical diagnosis of AD. PET, with SPECT using 123 I-beta-CIT as a tracer and PET using 18 F-FDG as a tracer, revealed a relatively intact middle and posterior part of the cingulate gyrus, called cingulate insularity. Both CIT-SPECT and FDG-PET can be used to aid in the diagnosis of DLB, and loss of dopaminergic transporters can diagnose DLB more accurately than perfusion or hypometabolism.
The distribution of amyloid in patients with clinically diagnosed DLB using Pit complex B as a tracer is similar to that of AD, with amyloid deposits seen in the frontal, parietal, precuneus, and posterior cingulate gyrus in DLB and less in patients with PD combined with dementia. These studies suggest that amyloid deposits may exacerbate dementia in DLB but have little impact on the nature of the disease, if not improved disease-specific treatments for AD and DLB emerge, a metabolic imaging approach to improve diagnostic accuracy is not necessary.
(3) 123I-MIBG myocardial imaging to detect myocardial sympathetic function has been used as a complementary diagnostic tool and supporting feature for the diagnosis and differential diagnosis of DLB with 98% sensitivity and 94% specificity to detect DLB and facilitate the diagnosis of early DLB with higher specificity compared to DAT imaging to differentially diagnose PD and PD-related diseases, therefore investigators recommend it as a complement to DAT imaging
5. Pathology: The characteristic pathology of Lewy body dementia is LB, which often coexists with AD-like pathology; LB is mainly present in the brainstem, limbic system, and neocortex; AD-like pathology is characterized by the presence of different degrees of senile plaques and neurogenic fiber tangles at different sites.
Highly likely DLB has diffuse LB and low or moderate AD-like pathology in the neocortex, or LB and low AD-like pathology in the limbic system. Moderately likely DLB has LB with predominant limbic system and moderate AD-like pathology, or LB with diffuse neocortex and high AD-like manifestations. Low-grade possible DLB has brainstem-dominant LB and either degree of AD-like manifestations, or limbic system-dominant LB and high AD-like manifestations.
6. Other: DLB has abnormalities on EEG, usually earlier than AD, but it cannot be used as a differential diagnosis yet. In some cases, neuropsychological examination can be used to distinguish DLB from AD or as a baseline for later evaluation.
II. Diagnosis of DLB and diagnostic criteria
In 1996, McKeith et al [20] first proposed diagnostic criteria for DLB, and in 2005, McKeith et al developed an expert consensus for DLB, see Table 1. 2013, DSM-5 published diagnostic criteria for Lewy body cognitive dysfunction (NCDLB) [6], see Table 2. the DSM-5 criteria classify NCDLB into mild (mild), i.e., mild cognitive The DSM-5 criteria classify NCDLB into mild (mild), i.e., mild cognitive impairment, and severe (major), i.e., dementia. The diagnosis of severe is necessitated by progressive cognitive impairment and is clinically characterized by three core symptoms of fluctuating cognitive dysfunction, PD-like dyskinesia, and visual hallucinations. cognitive dysfunction in DLB is characterized by early changes in complex attention and executive functioning, with fluctuations in hallucinations, depression, and paranoia occurring in a psychotic-like pattern, and symptoms of PD-like dyskinesia often appearing before or within a year after cognitive impairment. Parkinson’s signs need to be differentiated from neuroleptic-induced extrapyramidal symptoms. The supporting features of NCDLB are frequent recurrent falls and unexplained loss of consciousness, such as syncope and momentary seizures, and possible observation of vegetative dysfunction, such as upright hypotension and urinary incontinence. The diagnosis of mild NCDLB applies to patients who present at some stage of cognitive or functional impairment when the accompanying core or supporting points are not sufficient to meet the criteria for severe neurocognitive disorder (NCD). However, for all mild NCDs, there is often insufficient evidence for any single etiology, and this is when the use of an unspecified diagnosis is most appropriate.
The distinction between DLB and PDD is internationally controversial, and some experts recommend that the two types be diagnosed separately as distinct disorders. Pre-existing diagnoses are often based on a one-year time period, and it is believed that a diagnosis of PDD is more likely in those with motor symptoms of Parkinson’s disease followed by cognitive impairment one year after the onset of the disease. However, some scholars believe that since DLB and PDD have the same pathology and are different clinical types of the same disease related to α-synuclein, clinical diagnosis can only be defined by the time of motor impairment and cognitive impairment, which should be 2 subtypes of one disease.
(1) Essential features (necessary for the diagnosis of probable or likely DLB).
Dementia with progressive cognitive decline that interferes with normal social and work functioning.
Cognitive impairment is most prominent with attention, executive function, and visuospatial deficits; significant or persistent memory decline early in the disease is not required, but usually occurs during disease progression
(2) Core features (2 core features are required to diagnose likely DLB and one core feature is required for probable DLB).
Fluctuating cognitive dysfunction: manifested primarily by significant changes in attention and alertness over time
recurrent episodes of visual hallucinations with vivid images.
Spontaneous Parkinson’s syndrome
(3) Cue features (at least one core feature plus at least one cue feature is diagnostic of likely DLB, lack of core features, only one or more cue features can be considered diagnostic of likely DLB, no core features are diagnostic of likely DLB).
REM sleep behavior disorder.
High sensitivity to sedative drugs.
Reduced uptake of dopamine transporters in the basal ganglia region on PECT or PET
(4) Supporting features (usually present, but do not enhance diagnostic specificity).
Recurrent falls or syncope.
Transient, unexplained loss of consciousness.
Severe autonomic dysfunction, such as postural hypotension, urinary incontinence.
Other forms of hallucinations.
Systemic delusions.
Depression.
CT or MRI of the head suggesting relatively normal medial temporal lobe structures.
SPECT or PET suggestive of generalized hypometabolism in the occipital lobe.
myocardial imaging suggestive of reduced MIBG uptake.
EEG suggesting slow waves and transient sharp waves in the temporal lobe
(5) Unsupportive features.
Presence of focal neurological signs or brain imaging evidence of cerebrovascular disease.
Examination suggestive of other somatic or brain disorders that can cause similar clinical signs.
The presence of Parkinson’s syndrome-like manifestations only when the dementia is severe
(6) Chronological order of onset of symptoms.
In clinical practice, the most appropriate terminology should be chosen, and sometimes a general term such as Lewy body disease can be used, and the “1-year principle” is usually used to distinguish DLB from PDD, i.e. There are some studies that use other time intervals, but this makes inter-study comparisons difficult. In some clinicopathological studies or clinical trials, 2 clinical subtypes are usually included, called Lewy body disease or α-synucleinopathy.
The criteria apply to major or mild neurocognitive disorder; the type of neurocognitive disorder is characterized by an insidious onset and progressive development; the type of neurocognitive disorder is diagnosed as likely or probable Lewy body neurocognitive disorder by meeting one core and suggestive feature; likely major or mild Lewy body neurocognitive disorder with two core features, or one probable or possible Lewy body neurocognitive disorder with one core feature, or one or more core features.
(1) Core features.
Fluctuating cognitive dysfunction, characterized by altered attention and alertness.
Recurrent episodes of visual hallucinations with vivid content images.
Spontaneous Parkinson’s signs, following progressive cognitive decline.
(2) Suggestive features.
Meeting the criteria for rapid eye movement phase sleep behavior disorder.
Abnormal sensitivity to neuroleptics.
The above impairment cannot be better explained by other disorders, such as cerebrovascular disease, other neurodegenerative disorders, substance effects, or other psychiatric, neurological, or systemic disorders.
Differential diagnosis
In the diagnosis of DLB, depending on the symptoms and signs, it needs to be differentiated from a variety of diseases, such as AD, PDD, corticobasal degeneration, frontotemporal dementia, vascular dementia, hydrocephalus, cavernous syndrome, prion disease, progressive supranuclear palsy, and multisystem atrophy, etc. DLB should be clinically differentiated from AD and PDD. The differential diagnosis mainly relies on clinical manifestations, pathological features, etc. The neuropsychological cognitive scale is useful for the differential diagnosis of AD and DLB, which is mainly examined in terms of memory, language, attention and executive functions, with a later impact on visuospatial functions. The “1-year principle” in the diagnosis of DLB and PDD is an artificial time cut-off point to differentiate the two. If the “1-year principle” is not followed and the clinical manifestations are sometimes not completely distinguishable from each other. Most patients with PDD develop dementia in the middle to late stages of PD. Molecular imaging examinations such as PET-CT scans can be of great help in differentiating AD, PDD, and DLB. For example, 11C-PIB PET-CT labeled amyloid plaque molecular imaging suggests that the amyloid plaque load in the brain of PDD is significantly lower than that of DLB.
IV. Treatment of DLB
DLB as one of the neurodegenerative diseases, so far there is no evidence that the disease can be cured, but some drugs are clinically proven to control symptoms, improve patients’ quality of life and prolong life expectancy, and play a role in slowing down the progression of the disease, so DLB should be identified and diagnosed early, and comprehensive treatment should be carried out early so that the course of the disease can be scientifically managed throughout. The difficulty in swallowing can lead to malnutrition; the difficulty in movement and balance can lead to falls and fractures; the difficulty in swallowing and inability to move can lead to lung infection and heart failure, and most patients eventually die from these complications. The latter also includes aerobic functional exercise, scientific dietary and nutritional management, patient and caregiver education and care.
(i) Pharmacological treatment
The pharmacological management of DLB is complex and challenging for neurologists, psychiatrists, geriatricians and general hospital physicians. It usually employs multiple treatment modalities, or multiple pharmacological therapeutic targets. It generally includes symptomatic treatments such as anti-parkinsonian motor symptoms, anti-dementia treatment, anti-psychiatric symptoms and autonomic dysfunction. Since there are no effective drugs approved to cure DLB, the various drugs we apply now are only symptomatic treatments.
1. Anti-PD-like treatment of motor symptoms: levodopa monotherapy is often preferred for DLB, with improvement in about 50% of patients. The drug should be started in small doses and slowly increased to the dose required to relieve more than 50% of the symptoms and then maintained. Because such drugs are likely to cause disorders of consciousness and psychotic symptoms, they should be used with caution and preferably without anticholinergic drugs.
2, antipsychotic drug treatment: DLB visual hallucinations are the most common, but also often accompanied by delirium, anxiety, depression and behavioral abnormalities. Mild patients do not require treatment, and if medication is needed, cholinesterase inhibitors or atypical antipsychotics should generally be used. Open drug studies have confirmed that cholinesterase inhibitors improve psychiatric symptoms in DLB; whereas a randomized placebo-controlled clinical study only confirmed that cabalactam treatment reduces the frequency and extent of visual hallucinations and may even improve cognitive function. When atypical antipsychotics are needed, quetiapine, clozapine, and aripiprazole are usually used clinically. They are not recommended due to the high number of adverse drug reactions to typical antipsychotics and the fact that most patients have hypersensitivity reactions to these drugs, which may significantly aggravate their psychiatric symptoms. It should be noted that the long-term use of large amounts of atypical antipsychotics also has the potential for serious adverse effects, increasing the risk of heart and stroke and mortality, as well as worsening symptoms and cognitive impairment, and therefore should be used with clinical caution. After careful evaluation of the pros and cons, small to moderate doses can be applied, but the minimum course of treatment should be maintained under close supervision and requires consultation with the caregiver and, if necessary, the patient himself.
3. Anti-dementia drug therapy: The concentration of acetylcholine in the brain of DLB patients decreases. Compared with AD patients, DLB patients receive cholinesterase inhibiting drugs with better effect, and patients’ cognitive fluctuation will decrease, alertness will increase, and memory will improve.
Although there are no FDA-approved medications for the treatment of DLB patients, clinical studies have confirmed the clinical effectiveness of certain cholinesterase inhibitors. Randomized placebo-controlled studies suggest efficacy of esnon in the treatment of DLB, and there are also short-term and long-term open trials with consistent results. A series of open trials has shown that donepezil is also effective in the treatment of DLB. Only preliminary open trial results are available for galantamine. In the treatment of DLB with antidementia drugs, a rebound of neurological and psychiatric symptoms can occur if the treatment drug is abruptly stopped. Therefore, it is recommended that patients with DLB who are effectively treated with cholinesterase inhibitors should not easily stop the drug or switch to other cholinesterase inhibitors. Patients with apathy, anxiety, poor concentration, hallucinations, delusions, sleep disturbances and cognitive impairment improve to varying degrees after treatment. Overall, the three available cholinesterase inhibitors have similar effects, and the treatment dosage is larger than the AD dosage. The PD-like signs may worsen transiently in some patients during treatment, and although they do not affect the overall efficacy, they need to be observed with caution and discontinuation should be considered in case of severe motor symptoms. To avoid cholinergic-like adverse effects of cholinesterase inhibitors such as nausea, vomiting, loss of appetite, diarrhea and drowsiness, drug dose titration or administration with food is recommended. Cholinesterase inhibitors increase the risk of upright hypotension, falls, and syncope, inseparable from DLB’s own vegetative dysfunction, and should be noted and guarded against.
Memantine, a glutamate antagonist, has been approved by the FDA for the treatment of patients with moderate-to-severe AD, but has not been approved for the treatment of PDD and DLB. studies have concluded that memantine improves cognitive function and neuropsychiatric symptoms in DLB. In a multicenter, double-blind, placebo-controlled study of 72 patients with DLB or PDD treated for 24 weeks, patients treated with memantine had better overall clinical impression scores than placebo, and another study also showed that patients treated with the drug had better overall clinical impression scores on 2 important screening tools (memantine vs. placebo, 3.3 vs. 3.9), and neuropsychiatric scale scores (memantine vs. placebo, -4). meperidine vs. placebo, -4.3 vs. 1.7) when evaluated. There is relatively little clinical information on the treatment of DLB with memantine, and the few reports indicate an uncertain therapeutic effect and a risk of exacerbating delusions and hallucinations. Further clinical studies and validation are needed.
4. Mood abnormalities and sleep disorder treatment: DLB depressive symptoms are common, and there is a lack of clinically sound treatment options for this condition. Currently 5-hydroxytryptamine reuptake inhibitors (SSRI) and 5-hydroxytryptamine-norepinephrine reuptake inhibitors (SNRI) are recommended for the pharmacological treatment of depression, and tricyclic antidepressants and drugs with anticholinergic effects should be avoided. Sleep disorders such as RBD-related sleep behavior abnormalities can be treated with clonazepam 0.25 mg at bedtime, melatonin 3 mg and quetiapine 12.5 mg, etc. They should be gradually increased and monitored for efficacy and associated adverse effects. It has also been reported in the literature that melatonin 3 mg at bedtime is more effective in combination with clonazepam. Cholinesterase inhibitors may be helpful for sleep disorders. patients with DLB also often present with apathy and cholinesterase inhibitors are generally recommended.
(ii) Non-pharmacological support
1. Aerobic functional exercise: Some data show that cognitive stimulation training contributes to memory improvement and quality of life in patients with mild to moderate dementia. Physical therapy and aerobic exercise are helpful in maintaining the patient’s mobility. Aerobic functional exercise can also prevent and delay cognitive decline. At the same time, family members of DLB patients should be told to encourage patients to actively participate in aerobic functional exercise, but they must pay attention to safety.
2. Nutritional management: Patients with DLB can eat water normally in the early stage, and there are no special rules for diet, but in the late stage, patients often have swallowing difficulties and malnutrition, at this time, the patients’ recipes should be changed to soft food or semi-liquid food, and attention should be paid to supplementing high protein diet. For patients with severe swallowing difficulties and high risk of aspiration, gastrostomy should be performed early to ensure adequate nutrition.
3. Patient and caregiver education: It is preferred to educate patients, their spouses, family members and caregivers about the disease of DLB and mobilize the society to care for DLB patients.
V. Prognosis
DLB is an irreversible progressive neurodegenerative disease, the rate of progression varies from person to person, and is generally considered to be faster than the course of AD. DLB is often combined with the following conditions: severe patients may suffer from malnutrition due to dysphagia; patients are prone to bed sores due to prolonged bed rest; pulmonary infections due to dysphagia and dyskinesia, and patients eventually die from complications such as paralysis, malnutrition and infections.