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Conductive deafness

Read in Chinese(Traditional)

   

[Intro]

outer or middle ear disease caused by hearing impairment as conductive deafness.

[Cause]

Lewy body dementia is caused by what the?

(a) causes

cause is unknown so far, the researchers found that the nervous system of α-synuclein (& alpha ;-synuclein) is the main component of Lewy body structure, part of the DLB and the existence of familial parkinson's disease α-synuclein gene mutation, so that by the soluble α-synuclein into insoluble, abnormal aggregation, speculated that α-synuclein mutations may be related to the pathogenesis of DLB ​​and PD. DLB few familial tendency, but the japanese have been reported in patients with familial DLB. Although there are reports that some patients with DLB and AD patients had Apo Eε4 alleles increased, but the exact genetic mechanisms to be studied.

(B) the pathogenesis

pathogenesis is unclear, experiments confirmed that, DLB patients with cholinergic and monoamine neurotransmitter systems are damaged, the brain cortex, forebrain Meynert nucleus and caudate nucleus and other parts of the choline acetyltransferase (ChAT) levels decreased significantly, and the basal ganglia area dopamine metabolite homovanillic acid (HVA) concentrations decreased by dopamine physical abnormalities, putamen 5-ht and norepinephrine concentrations were significantly reduced damage to the neurotransmitter systems decline in cognitive function in patients with DLB and extrapyramidal movement disorders and so on.

1. the cerebral cortex and brainstem dispersed and associated axonal Lewy body disease, major change is the pathological features associated with lesions including senile plaques, neurofibrillary tangles, sponge-like vacuolar degeneration and substantia nigra, locus coeruleus and Meynert nucleus regional neuron loss. Lewy body from Lewy (1912) first described the typical lewy bodies found in the brainstem substantia nigra and locus coeruleus, also located in the vagus nerve dorsal nucleus, Meyrnert basal ganglia and hypothalamus of nuclear and other monoamine neurons, located in the cerebral cortex of the Lewy body no dense core granules, irregular fibers around the core, known as the pale body (pale body), may be the predecessor of Lewy body; cortical lewy bodies are mainly distributed in the limbic system, temporal Ye Xingren nuclear and parahippocampal areas, cingulate and so on. he staining shows Lewy body 3 ~ 25μm in diameter, round or oval, eosinophilic cytoplasm was uniformly red, dense granules messy arrangement constitutes 1 ~ 10nm core. Electron microscope, the center of osmiophilic granules mixed with a spiral (helical tube) or double helical filaments (paired helical filaments), the core around the loose arrangement of fibers surrounding the uniform composition, pale stained halo (halo), with associated antibody response to Lewy body staining. Lewy body is called the synapse synapse Lewy body (intra-neuritic Lewy body), lewy bodies were located in the cytoplasm of nerve cells, axons can also be found within the nerve cells outside the Lewy body (extracellular Lewy body), no typical halo, HE stain lightly stained pink, electron microscope, arranged by the loose irregular filamentous structures. immunohistochemistry lewy bodies found in the pan with a large number of well-established (ubiquitin), α-synuclein, complement proteins, microtubules and actin protein (tubulin), etc., but no tau protein and amyloid protein. In all of the Lewy body dementia related to cerebral cortical atrophy is not obvious, showing mild frontal lobe atrophy; Alzheimer disease Louis obvious visible body the middle temporal lobe atrophy, and have more amyloid senile plaques and neurofibrillary tangles. Other patients with dementia with lewy bodies seen in the substantia nigra pigmented cell loss, no senile plaques and neurofibrillary tangles, tau protein antibody staining helps to distinguish between two different types of pathological changes.

immunohistochemical study tips, Lewy body of the crystal protein (crystallin), ubiquitin and α-synuclein labeled positive, he staining Lewy body-color light and easy to display, with ubiquitin immunohistochemistry can clearly show the good. Routine immunohistochemical staining has not been found in Lewy body tau protein, tau protein can be used immunohistochemical staining of different neurons in Lewy body and tau protein staining small spherical neurofibrillary tangles. Lewy body-related axonal changes (Lewis-related-neurites, LRN) is a neurofilament degeneration, he staining is generally difficult to observe LRN, but can clearly show the ubiquitin staining, LRN more common in the hippocampus, amygdala, Meynert nucleus and dorsal vagal nuclear and so on. Lewy body dementia may also have different levels of the brain of AD pathological changes, such as senile plaques, neurofibrillary tangles, neuronal demyelination and spongy degeneration.

2. Lewy body dementia present histological type, there are two ways

(1) according to Lewy body distribution can be divided into the brain stem type, transition type (transitional type) and diffuse. ① brain stem type: lewy bodies are mainly restricted to the brain stem, the equivalent of Parkinson disease; ② diffuse: Lewy body extensively involving the cerebral cortex, japanese scholars stressed the light microscope prefrontal, cingulate gyrus, temporal lobe and insular cortex, etc. site, found at 100 times magnification of more than 5 Lewy body before diagnosis of this type; ③ transition type: 100 times in lewy bodies within the field of vision less than five, but European and american scholars to master the more flexible conditions.

(2) based on the combined AD pathology is divided into common type and Pure. ① common type: In addition to a large number of Lewy body disease, yet the merger senile plaques, neurofibrillary tangles, etc., cortical atrophy and neuron loss is not serious; ② Pure: not only Lewy body-like changes associated with AD. Clinical and pathologic studies have shown that about 75% of the ordinary type of DLB ​​patients with memory disorders, psychiatric symptoms onset, followed by progressive dementia increased, and the remaining 25% of patients with Parkinson's syndrome, or shy-drager syndrome onset; Pure DLB younger age of onset, early Parkinson's syndrome have significant performance, followed by dementia.

[Sign]

early symptoms of Lewy body dementia What?

1. Lewy body dementia more than old age, disease, only a small number of young patients, the slow progress. The main clinical manifestations of dementia, extrapyramidal movement disorders and mental disorders, three groups of symptoms. Mainly dominated by dementia, mild symptoms of Parkinson's disease, a few cases the contrary, the symptoms may fluctuate.

2. DLB cognitive dysfunction in patients with cognitive decline overall, cortical dementia and AD are, there are similarities, often memory loss, disorientation lack of onset However, less early memory impairment, there is volatility, there may aphasia, apraxia and agnosia. Some patients have features of subcortical dementia, such as lack of concentration, decreased alertness and less fluent in other languages. Progress in Alzheimer's ability to appear as the lack of space, have frontal release symptoms such as a strong grip and groping reflexes. cognitive dysfunction may have fluctuations in a few weeks or even a day can have significant changes, abnormal alternating with the normal state, the performance when the light weight or no law.

3. extrapyramidal movement disorders and Parkinson's syndrome often seen in patients with DLB performance, such as muscle rigidity, and bradykinesia reduce such movement, tremor rare. extrapyramidal symptoms may occur simultaneously with cognitive impairment, may have appeared. Two sets of symptoms have appeared within one year have diagnostic significance, generally poor response to levodopa treatment. Department of DLB ​​and AD are due to the insidious onset, slow progress, the exact time of onset is difficult to estimate, should be a comprehensive analysis of medical history and symptoms, signs, not simply confined to a certain time period. DLB patients also appear myoclonus, autonomic dysfunction, dystonia, dysphagia, and sleep disorders, such as frequent falls, syncope, or transient loss of consciousness.

4. psychiatric symptoms often psychiatric symptoms, characterized by 80% of patients with visual hallucinations, vivid content, complete, and often quiet people, objects and animals, specific images, the patient can be seen vividly described the scene, and firmly believe, may have delusions, delirium, agitation and other psychiatric disorders, was significantly volatility. Stability of the nerve is very sensitive to antipsychotic agents is different from other types of dementia DLB features, but prone to side effects or increase the existing extrapyramidal movement disorders, cognitive decline, and even lethargy, and coma. There are reports of serious side effects of drugs can increase the mortality rate three times DLB, side effects and gender, age, extent of disease, drug type and dose. One case of DLB ​​patients treated with conventional doses of stable sleep aids coma.

fluctuations of cognitive impairment, visual hallucinations and parkinson's disease patients, DLB should be considered possible. International use of more diagnostic criteria are:

1.DLB is a prerequisite for the clinical diagnosis of cognitive dysfunction, affecting the social and working ability. Although there is no obvious disease, early memory impairment, with the progress of the disease may increase, there are obvious obstacles to the attention of the frontal cortex function and visuospatial impairment.

2. have the following symptoms in two to three clinically diagnosed possible (clinical probable) DLB, with a clinical suspect (clinical possible) DLB ① volatility cognitive dysfunction, with varying degrees of attention and vigilance disorders; ② repeated attacks of the contents of the specific image of the visual hallucinations; ③ the same time or after the occurrence of Parkinson's syndrome movement disorders.

3. support for DLB diagnostic criteria ① repeated falls; ② syncope; ③ transient loss of consciousness; ④ sensitive nerve stabilizer; ⑤ various forms of delirium and other forms of illusion .

4. does not support the DLB diagnostic criteria ① prompt focal neurological signs of stroke and neuroimaging evidence; ② clear clinical symptoms by other medical or neurological disease to explain.

[Aftertreat]

Lewy body dementia ate?

[Prevent]

conductive hearing loss should be how to prevent?

prevent conductive hearing loss: 1

[Treat]

Lewy body dementia treatment of Attention?

(a) treatment

DLB currently no effective therapy, treatment principles and AD is similar to the following drugs can improve some of the symptoms.

1. cholinesterase inhibitors such as donepezil (Aricept), rivastigmine (Exelon) and the cortex can improve cognitive function and behavioral disorders, also activation of nerve cells can be used to improve brain circulation agents and drugs.

2. dopamine, such as levodopa / benserazide (Madopar), levodopa / carbidopa (Pa Jinning), and dopamine receptor agonists such as pergolide (pergolide) and so can improve symptoms of Parkinson's syndrome, the symptomatic treatment of Parkinson's syndrome, delirium and hallucinations easy to make heavier, starting dose should be small, careful dosage.

3. depression can be selective 5-ht reuptake inhibitors such as citalopram, fluoxetine, etc., such as visual hallucinations with a new antipsychotic risperidone (Lee piperazine ketone), olanzapine (olanzapine) with good results; DLB patients sensitive nerve stabilizer and antipsychotic drugs should be used with caution.

(b) the prognosis

patients with poor prognosis, duration of 5 to 10 years, died of complications.

Lewy body dementia, Chinese medicine treatment methods

No information

western Lewy body dementia treatment

No information

[Examine]

conductive hearing loss should be how?

check the external auditory canal and tympanic membrane; the tuning fork examination and pure tone threshold audiometry to identify the nature and extent of deafness. Of children and uncooperative adults, but also an objective audiometry, such as acoustic impedance audiometry, auditory brainstem response audiometry and ECoG and so on.

how simple hearing and vestibular function test method?

hearing and vestibular function tests are many ways in recent years This research and clinical work has made great progress. However, the general primary health care units, due to limitations, there can not have advanced and sophisticated inspection equipment for the inspection difficult, as patients and their families has become even more powerless, and so a simple means of checking.

hearing test: can watch the sound test. Before the medication, hearing test with a watch in the medication process, but also with a watch with a hearing test. Pay attention to put the location of the table, each should be placed in the same direction, and not the table should be close to the skin or bones in the ear the top of the watch should be a certain distance from the ear. So hear is the sound conduction through the air, or sound through bone conduction, hearing can not accurately reflect the actual situation. In the trial, if it is found after treatment than before treatment to hearing loss, cochlear system should consider the possibility of poisoning.

vestibular function tests: gait posture by standing still and observation, to determine the balance function of the head. The first choice of static standing posture standing feet together, then both feet to stand around the dislocation, the last first with one foot standing, which is the most difficult. If the balance function is normal, by the standing can be maintained for more than 10 seconds, if the balance dysfunction, the stand is difficult to maintain, will soon be dumped to the side, side to side or forward backward. observation of gait posture, walking test can be taken, that those who turn a blind eye to be examined along a straight line to walk forward. normal landing can be done in the linear feet on both sides, there will be no normal walking is significantly skewed, unsteady gait, like a drunken reeling. Generally walk ten steps, walking is enough to distinguish between stable or not. This check, should be examined to understand whether there are physical defects, polio sequelae, hemiparesis, in patients with poor mental development is not suited to this test method. Vestibular function tests done, should open its eyes to be checked, first standing and walking, if the performance of a standing posture and gait are more stable, or difficult to distinguish between stable or not, turn a blind eye if the patient standing and walking, to learn more about balance.

[Diff]

conductive deafness What are the symptoms easily confused?

should pay attention to and identification of deafness.

check the external auditory canal and tympanic membrane; the tuning fork examination and pure tone threshold audiometry to identify the nature and extent of deafness. Of children and uncooperative adults, but also an objective audiometry, such as acoustic impedance audiometry, auditory brainstem response audiometry and ECoG and so on.

how simple hearing and vestibular function test method?

hearing and vestibular function tests are many ways in recent years This research and clinical work has made great progress. However, the general primary health care units, due to limitations, there can not have advanced and sophisticated inspection equipment for the inspection difficult, as patients and their families has become even more powerless, and so a simple means of checking.

hearing test: can watch the sound test. Before the medication, hearing test with a watch in the medication process, but also with a watch with a hearing test. Pay attention to put the location of the table, each should be placed in the same direction, and not the table should be close to the skin or bones in the ear the top of the watch should be a certain distance from the ear. So hear is the sound conduction through the air, or sound through bone conduction, hearing can not accurately reflect the actual situation. In the trial, if it is found after treatment than before treatment to hearing loss, cochlear system should consider the possibility of poisoning.

vestibular function tests: gait posture by standing still and observation, to determine the balance function of the head. The first choice of static standing posture standing feet together, then both feet to stand around the dislocation, the last first with one foot standing, which is the most difficult. If the balance function is normal, by the standing can be maintained for more than 10 seconds, if the balance dysfunction, the stand is difficult to maintain, will soon be dumped to the side, side to side or forward backward. observation of gait posture, walking test can be taken, that those who turn a blind eye to be examined along a straight line to walk forward. normal landing can be done in the linear feet on both sides, there will be no normal walking is significantly skewed, unsteady gait, like a drunken reeling. Generally walk ten steps, walking is enough to distinguish between stable or not. This check, should be examined to understand whether there are physical defects, polio sequelae, hemiparesis, in patients with poor mental development is not suited to this test method. Vestibular function tests done, should open its eyes to be checked, first standing and walking, if the performance of a standing posture and gait are more stable, or difficult to distinguish between stable or not, turn a blind eye if the patient standing and walking, to learn more about balance.

[Disease]

conductive deafness related diseases

heart boils ear - ear syndrome in children dwarf - retinal atrophy - ear deaf ear syndrome, hereditary presbycusis sore ear fistula ear fungus disease of congenital deafness sudden deafness kidney carbuncle knock deafness tinnitus ear ear ear eczema boils


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