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When you encounter "bradykinesia, limb stiffness", what else do you think of besides Parkinson's or Parkinson's syndrome? Let's take a look at today's case!
■ qualitative diagnosis:
According to older men, the disease is chronic-onset, slowly worsening, with damage to high-order cortical function, extrapyramidal and autonomic nerves, and manifests as
.
Neurodegenerative diseases are highly
likely to be considered.
In terms of treatment, nutritional nerves, blood activation and stasis, blood replenishment and qi are given, the patient has difficulty falling asleep at night, and the family members increase their sleep after giving clozapine on their own, until noon the next day, that is, the patient is particularly sensitive
to sedative drugs.
In summary, the diagnosis is probable dementia of Lewy bodies (DLB).
to sedative sleep medications.
1So what are the main clinical manifestations of DLB?
Fluctuating cognitive impairment: cognitive impairment often manifests as executive function and visuospatial dysfunction, while early impairment of recent memory function is less significant
.
Visuospatial dysfunction is often prominent, patients are likely to get lost in a familiar environment, and the clinical presentation of DLB fluctuates
relative to the progressive worsening course of Alzheimer's disease (AD).
Patients often present with sudden, transient cognitive impairment, during which cognitive function, orientation, language, visuospatial ability, attention, and judgment are reduced
.
It can last for minutes, hours or days, after which it recovers dramatically
.
Vivid visual hallucinations: 50%~80% of patients have visual hallucinations
in the early stages of the disease.
Visual hallucinations often appear at night, auditory hallucinations, olfactory hallucinations can also exist, and patients in the later stage cannot distinguish hallucinations, and they will be very excited about the denial of others
.
Parkinsonism: mainly includes bradykinesia, increased muscle tone, and resting tremor, which is often less pronounced
in DLB than in classic Parkinson's disease.
Other symptoms such as sleep disturbances, autonomic dysfunction, and personality changes
.
REM sleep behavior disorder is thought to be the earliest symptom of
DLB.
Autonomic dysfunction is common orthostatic hypotension, sexual dysfunction, constipation, urinary retention, sweating, less sweating, syncope, dry eyes, dry mouth, etc
.
Autonomic disturbances may result from
damage to the horn cells on the side of the spinal cord.
Personality changes are common such as increased aggression and depression
.
2What are the auxiliary tests to confirm the diagnosis?
Laboratory tests: there is no specific laboratory test for DLB, so the purpose of testing is to make the diagnosis
differential.
Tests are required to rule out other diseases
.
Imaging examination: MRI and CT have no typical manifestations, and SPECT and PET found that the occipital cortex metabolic rate of DLB patients decreased and the dopamine activity of the striatum was reduced, which had certain differential significance
.
Neuropsychological examination: suggestive of cognitive dysfunction, mainly manifested in visuospatial dysfunction
.
For example, ask the patient to draw a clock face, although the number, hour, minute and second hands on the clock face are readily available, but the relationship between them is completely confusing, the numbers may be concentrated on one side of the clock face, and the length of the hour and minute hands is disproportionate
.
Another example is the drawing of a three-dimensional hut, although the parts are complete, but the spatial relationship is wrong, and the patient completely ignores the perspective relationship (Figure 2).
Figure 2
3What about the latest diagnostic criteria[1]?
In 2017, McKeith et al.
revised the diagnostic criteria for DLB, as follows: 1.
Symptoms necessary to diagnose DLB:
(1) Progressive cognitive decline that significantly affects social or occupational function
.
(2) Cognitive function is most obvious
with attention, executive function and visuospatial function impairment.
(3) There can be no memory damage in the early stage of the disease, but as the course of the disease progresses, memory impairment becomes more and more obvious
.
2.
If the three core symptoms have two of the following three characteristics at the same time, it is diagnosed as likely DLB, and if only one is present, it is diagnosed as possible DLB
.
(1) Fluctuating cognitive dysfunction, the patient's attention and alertness change significantly
.
(2) Recurrent detailed shaped visual hallucinations
.
(3) Spontaneous symptoms
of parkinsonism.
(4) Rapid eye movement sleep phase behavior disorder (RBD).
3.
suggestive symptoms, with one or more core symptoms, and also have one or more suggestive symptoms, the diagnosis is likely DLB; The absence of core symptoms but the presence of one or more suggestive symptoms is a possible diagnosis of DLB
.
(1) Polysomnography (PSG) confirmed REM phase sleep disorder
.
(2) Abnormal cardiac 123I-MIBG scintigraphy
.
(3) SPECT or PET indicate a decrease
in dopaminergic activity in the basal nucleus.
4.
Supporting evidence (DLB patients often present but not diagnostically specific):
(1) Recurrent falls, fainting, or transient loss
of consciousness.
(2) Autonomic dysfunction (such as orthostatic hypotension, urinary incontinence).
(3) Hallucinations and illusions of other senses
.
(4) Systemic delusions
.
(5) Depression
.
(6) CT or MRI showed that the temporal lobe structure was intact
.
(7) SPECT/PET indicates a decrease
in the metabolic rate of the occipital cortex.
(8) M-iodobenzylguanidine (MIBC) scintillation scan showed a decrease
in myocardial uptake rate.
(9) EEG showed slow waves, and short bursts of sharp waves
appeared in the temporal lobe.
5.
Conditions that do not support the diagnosis of DLB:
(1) focal neurological signs or neuroimaging evidence
of stroke.
(2) Examination suggests other physical diseases or brain diseases
that can lead to similar clinical symptoms.
(3) The symptoms of
parkinsonism only appear when dementia is severe.
6.
Requirements for the order of occurrence of symptoms For Lewy body dementia, dementia symptoms generally appear earlier than or at the same time as Parkinsonism
.
Parkinson's disease dementia should be diagnosed in patients with well-defined Parkinson's disease
.
If a distinction between Parkinson's disease dementia and DLB is required, the "1-year nule" should be referenced, that is, DLB can be considered for dementia that occurs within 1 year of Parkinson's symptoms, and dementia that develops after 1 year should be diagnosed as Parkinson's disease dementia
.
4How to treat it[2]?
At present, there is no specific treatment, and the medication is mainly symptomatic
.
Improve cognition: At present, the efficacy is more certain, cholinesterase inhibitors, which can be used as the preferred drug, and there is also a certain effect
on improving dyskinesia.
Improve visual hallucinations: donepezil has a certain effect
.
Improve apathy, anxiety, hallucinations and delusions: lismine works
.
Improve psychiatric symptoms: newer atypical antipsychotics such as olanzapine, amazopine, and quetiapine can be used with caution and are relatively safe
.
Classical antipsychotics such as haloperidol and thioridazine can be used for AD, but are contraindicated for DLB
.
These drugs can exacerbate dyskinesia, leading to increased muscle tone throughout the body, and in severe cases, antipsychotic malignant syndrome can be life-threatening
.
Selective 5-HT receptor reuptake inhibitors have a certain effect
on improving mood.
Levodopa can add attention to hallucinations, and the effect on improving Parkinson's symptoms in DLB patients is not significant, so it should be used
with caution.
Summary:
DLB is an irreversible and progressive neurodegenerative disease that progresses at a rate that varies from person to person and is thought to be faster than the course
of AD.
DLB is often associated with malnutrition due to dysphagia in severe cases; Due to long-term bed rest, patients are prone to bedsores; Early diagnosis and treatment are critical
to the prognosis of patients who suffer from complications such as paralysis, malnutrition and infection, leading to lung infections due to dysphagia and dysatile movements.
References: [1] McKeith IG, Boeve BF, Dickson DW, et al.
, Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium.
Neurology.
2017 Jul 4; 89(1):88-100.
[2]Taylor J P,McKeith I G,Burn D J,et al.
New evidence on the management of Lewy body dementia[J].
Lancet Neurol,2020,19(2):157-169.
Where to see more dementia knowledge?
Come to the "Doctor Station" and take a look 👇
Patients are especially sensitive to sedative medications, what disease can you think of?
When you encounter "bradykinesia, limb stiffness", what else do you think of besides Parkinson's or Parkinson's syndrome? Let's take a look at today's case!
Case review
The patient, a 64-year-old male, was admitted to the hospital
mainly for "memory loss with visual hallucinations for 2 years and decreased exercise for 2 months".
The patient took "olanzapine, donepezil, memantine" for two months due to memory loss without obvious cause 2 years before admission, accompanied by episodic visual hallucinations, dizziness and sleep disorders, and the treatment effect was not good
.
Before February, he had decreased limb movement and slow movement, and came to our hospital for further diagnosis and treatment, and was admitted to our department
as "Parkinson's disease".
The patient has been mentally motivated since the onset of the disease, and the diet is OK
.
Poor sleep, normal urine and urine, no significant change in weight compared with before, no fever, sore throat, cough, diarrhea, loss of smell, taste and other symptoms in the past two weeks, no antipyretic drugs
.
In the past 5 years ago, there was trembling of the right limb, and the outer hospital was treated according to "Parkinson's disease", and oral "dopashydrazide tablets, pramipexole, selegiline" were not effective
.
At present, selegiline has been discontinued, and it was proposed to be diagnosed as "ankylosing spondylitis" in the outer hospital, and the current spinal stiffness and deformation
.
Family members complain that the patient has recently shown cognitive recourse in the morning, unresponsiveness in the afternoon, and poor
memory.
Personal or family history is not special
.
▌Physical examination:
Cardiopulmonary examination showed no obvious abnormalities
.
Blood pressure: sitting: 123/82mmHg, immediately after standing: 90/62mmHg, 1min: 95/65mmHg, 3min: 101/70mmHg
.
Clear speech, slow response, cognitive decline, mask face, double pupils are equal to circles, sensitive to light reflection, double eyeballs can move in all directions, no diplopia and nystagmus, bilateral frontal lines and nasolabial folds are symmetrical, the corners of the teeth are not biased, the tongue is centered, the head is turned and shrugged strongly
.
Limb muscle strength and muscle tone are normal, slow movement, bilateral rotation test, finger-nose test, heel knee tibia test slowed, but still accurate
.
Negative
pathological signs.
Negative
meningeal irritation.
▌Auxiliary inspection:
There were no obvious abnormalities
in blood analysis, coagulation pentamine, HIV+TP, thyroid function, biochemical whole items, blood homocysteine, folic acid, and vitaminB 12.
▌Neuropsychological scale:
Simple Mental Status Check Scale (MMSE): 14 points
.
Montreal Cognitive Assessment Scale (MoCA): 9 points
.
Activities of Daily Living Scale (ADL): 44 points
.
Hamilton Anxiety Scale (HAMA): 10 points
.
Hamilton Depression Scale (HAMD): 14 points
.
Clinical Dementia Rating Scale (CDR): 2 points
.
Non-contrast head CT showed no obvious abnormalities
.
The patient was previously diagnosed with "ankylosing spondylitis", and the spine is stiff and deformed, and the magnetic resonance coordination of the head is not good
.
Positioning, qualitative diagnosis?
■ qualitative diagnosis:
According to older men, the disease is chronic-onset, slowly worsening, with damage to high-order cortical function, extrapyramidal and autonomic nerves, and manifests as
.
Neurodegenerative diseases are highly
likely to be considered.
In terms of treatment, nutritional nerves, blood activation and stasis, blood replenishment and qi are given, the patient has difficulty falling asleep at night, and the family members increase their sleep after giving clozapine on their own, until noon the next day, that is, the patient is particularly sensitive
to sedative drugs.
In summary, the diagnosis is probable dementia of Lewy bodies (DLB).
The director asked a question
to sedative sleep medications.
1So what are the main clinical manifestations of DLB?
Fluctuating cognitive impairment: cognitive impairment often manifests as executive function and visuospatial dysfunction, while early impairment of recent memory function is less significant
.
Visuospatial dysfunction is often prominent, patients are likely to get lost in a familiar environment, and the clinical presentation of DLB fluctuates
relative to the progressive worsening course of Alzheimer's disease (AD).
Patients often present with sudden, transient cognitive impairment, during which cognitive function, orientation, language, visuospatial ability, attention, and judgment are reduced
.
It can last for minutes, hours or days, after which it recovers dramatically
.
Vivid visual hallucinations: 50%~80% of patients have visual hallucinations
in the early stages of the disease.
Visual hallucinations often appear at night, auditory hallucinations, olfactory hallucinations can also exist, and patients in the later stage cannot distinguish hallucinations, and they will be very excited about the denial of others
.
Parkinsonism: mainly includes bradykinesia, increased muscle tone, and resting tremor, which is often less pronounced
in DLB than in classic Parkinson's disease.
Other symptoms such as sleep disturbances, autonomic dysfunction, and personality changes
.
REM sleep behavior disorder is thought to be the earliest symptom of
DLB.
Autonomic dysfunction is common orthostatic hypotension, sexual dysfunction, constipation, urinary retention, sweating, less sweating, syncope, dry eyes, dry mouth, etc
.
Autonomic disturbances may result from
damage to the horn cells on the side of the spinal cord.
Personality changes are common such as increased aggression and depression
.
2What are the auxiliary tests to confirm the diagnosis?
Laboratory tests: there is no specific laboratory test for DLB, so the purpose of testing is to make the diagnosis
differential.
Tests are required to rule out other diseases
.
Imaging examination: MRI and CT have no typical manifestations, and SPECT and PET found that the occipital cortex metabolic rate of DLB patients decreased and the dopamine activity of the striatum was reduced, which had certain differential significance
.
Neuropsychological examination: suggestive of cognitive dysfunction, mainly manifested in visuospatial dysfunction
.
For example, ask the patient to draw a clock face, although the number, hour, minute and second hands on the clock face are readily available, but the relationship between them is completely confusing, the numbers may be concentrated on one side of the clock face, and the length of the hour and minute hands is disproportionate
.
Another example is the drawing of a three-dimensional hut, although the parts are complete, but the spatial relationship is wrong, and the patient completely ignores the perspective relationship (Figure 2).
Figure 2
3What about the latest diagnostic criteria[1]?
In 2017, McKeith et al.
revised the diagnostic criteria for DLB, as follows: 1.
Symptoms necessary to diagnose DLB:
(1) Progressive cognitive decline that significantly affects social or occupational function
.
(2) Cognitive function is most obvious
with attention, executive function and visuospatial function impairment.
(3) There can be no memory damage in the early stage of the disease, but as the course of the disease progresses, memory impairment becomes more and more obvious
.
2.
If the three core symptoms have two of the following three characteristics at the same time, it is diagnosed as likely DLB, and if only one is present, it is diagnosed as possible DLB
.
(1) Fluctuating cognitive dysfunction, the patient's attention and alertness change significantly
.
(2) Recurrent detailed shaped visual hallucinations
.
(3) Spontaneous symptoms
of parkinsonism.
(4) Rapid eye movement sleep phase behavior disorder (RBD).
3.
suggestive symptoms, with one or more core symptoms, and also have one or more suggestive symptoms, the diagnosis is likely DLB; The absence of core symptoms but the presence of one or more suggestive symptoms is a possible diagnosis of DLB
.
(1) Polysomnography (PSG) confirmed REM phase sleep disorder
.
(2) Abnormal cardiac 123I-MIBG scintigraphy
.
(3) SPECT or PET indicate a decrease
in dopaminergic activity in the basal nucleus.
4.
Supporting evidence (DLB patients often present but not diagnostically specific):
(1) Recurrent falls, fainting, or transient loss
of consciousness.
(2) Autonomic dysfunction (such as orthostatic hypotension, urinary incontinence).
(3) Hallucinations and illusions of other senses
.
(4) Systemic delusions
.
(5) Depression
.
(6) CT or MRI showed that the temporal lobe structure was intact
.
(7) SPECT/PET indicates a decrease
in the metabolic rate of the occipital cortex.
(8) M-iodobenzylguanidine (MIBC) scintillation scan showed a decrease
in myocardial uptake rate.
(9) EEG showed slow waves, and short bursts of sharp waves
appeared in the temporal lobe.
5.
Conditions that do not support the diagnosis of DLB:
(1) focal neurological signs or neuroimaging evidence
of stroke.
(2) Examination suggests other physical diseases or brain diseases
that can lead to similar clinical symptoms.
(3) The symptoms of
parkinsonism only appear when dementia is severe.
6.
Requirements for the order of occurrence of symptoms For Lewy body dementia, dementia symptoms generally appear earlier than or at the same time as Parkinsonism
.
Parkinson's disease dementia should be diagnosed in patients with well-defined Parkinson's disease
.
If a distinction between Parkinson's disease dementia and DLB is required, the "1-year nule" should be referenced, that is, DLB can be considered for dementia that occurs within 1 year of Parkinson's symptoms, and dementia that develops after 1 year should be diagnosed as Parkinson's disease dementia
.
4How to treat it[2]?
At present, there is no specific treatment, and the medication is mainly symptomatic
.
Improve cognition: At present, the efficacy is more certain, cholinesterase inhibitors, which can be used as the preferred drug, and there is also a certain effect
on improving dyskinesia.
Improve visual hallucinations: donepezil has a certain effect
.
Improve apathy, anxiety, hallucinations and delusions: lismine works
.
Improve psychiatric symptoms: newer atypical antipsychotics such as olanzapine, amazopine, and quetiapine can be used with caution and are relatively safe
.
Classical antipsychotics such as haloperidol and thioridazine can be used for AD, but are contraindicated for DLB
.
These drugs can exacerbate dyskinesia, leading to increased muscle tone throughout the body, and in severe cases, antipsychotic malignant syndrome can be life-threatening
.
Selective 5-HT receptor reuptake inhibitors have a certain effect
on improving mood.
Levodopa can add attention to hallucinations, and the effect on improving Parkinson's symptoms in DLB patients is not significant, so it should be used
with caution.
Summary:
DLB is an irreversible and progressive neurodegenerative disease that progresses at a rate that varies from person to person and is thought to be faster than the course
of AD.
DLB is often associated with malnutrition due to dysphagia in severe cases; Due to long-term bed rest, patients are prone to bedsores; Early diagnosis and treatment are critical
to the prognosis of patients who suffer from complications such as paralysis, malnutrition and infection, leading to lung infections due to dysphagia and dysatile movements.
References: [1] McKeith IG, Boeve BF, Dickson DW, et al.
, Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium.
Neurology.
2017 Jul 4; 89(1):88-100.
[2]Taylor J P,McKeith I G,Burn D J,et al.
New evidence on the management of Lewy body dementia[J].
Lancet Neurol,2020,19(2):157-169.
Where to see more dementia knowledge?
Come to the "Doctor Station" and take a look 👇
