Parkinson's disease in the elderly
Introduction
Introduction to Parkinson's disease in the elderly Parkinson's disease (PD), also known as Paralysisagitans (Shakingpalsy), was first described by British scholar James Parkinson (1817) and is a common neurodegenerative disease in the elderly. The main lesions are in the substantia nigra and striatum. Tremor, muscle rigidity and decreased exercise are the main clinical features of this disease. basic knowledge The proportion of illness: 0.002% Susceptible people: the elderly Mode of infection: non-infectious Complications: fracture
Cause
The cause of Parkinson's disease in the elderly
Ageing (40%):
One of the most common causes, the prevalence of PD varies with age, with an estimated 0.35% for 40 years, 1% for 60 years, 2% for 85 years, and 1 out of every 40 normal people. Development of Parkinson's syndrome, some studies have shown a special correlation between PD and aging, aging process and reduction of glutathione peroxidase and catalase in PD; increased monoamine oxidase with age, iron, copper, calcium accumulation Melanin aggregation, increased with age, the incidence of high incidence of 61 to 70 years old, and then decreased, and its substantia nigra, striatum dopamine neurons degeneration, pigment particles and nerve cells lost, PD group Significantly heavier than the normal age group, the activity of tyrosine hydroxylase (TH) and dopamine decarboxylase decreased gradually, and the dopamine content of the striatum decreased progressively. After 50 years old, it was significantly lower than normal people of the same age, regardless of the aging process and PD. Whether in the living body or in autopsy, the content of dopamine in the striatum decreased, and the striatum dopamine receptor (DA-R) decreased year by year. In recent years, studies have shown that DA-R has several subtypes. Amino acid sequence and three-dimensional The spatial structure is clear, DA-R is different according to the distribution site, the concentration is different and the effect is different. DA-R itself is a macromolecular protein, which is regulated by various neurotransmitters, regulatory substances, hormones and certain drugs in the brain, PD When the nigrostriatal degeneration, dopaminergic neurons are lost, dopamine release is reduced, DA-R and D1, D2 receptors are in the denervation supersensitivity receptor density increase, D2 is the main excitatory Super sensitive, increased by 20% to 90%, levodopa decreased D2 receptor by 30% to 60%, the phenomenon of receptor increase disappeared, and late-sensitivity appeared, while the positron emission tomography developed by fludopa was applied. Scanning (PET) confirmed that dopaminergic neuron function decreased with age and was proportional to the number of deaths of substantia nigra cells. Although the dopamine transmitter decreased with age, the elderly patients only showed a small number of physiological Dopaminergic neuron degeneration is not enough to cause the disease. In fact, only the dopaminergic neurons in the substantia nigra are reduced by more than 50%, and the striatal dopaminergic transmitter is reduced by more than 80%. Symptoms of the disease usually occurs between 51 to 60 years, by age reasoned that if aging is the only cause of it, this time not yet reached the levels of dopamine in a sufficient extent, therefore, aging precipitating factor only PD disease.
Genetic factors (20%):
Through a detailed investigation of the family of PD patients, it has been widely recognized in terms of etiology that at least part of the disease is derived from genetic factors, and more importantly, it is recognized that the disease may have a long time before the symptoms, ie Subclinical status, so when the first patient in the family appears, and other family members appear to be sub-clinical, it is easily overlooked, resulting in the illusion of low family morbidity. Current research indicates that 20% to 25% of patients are at least One first-degree relative has PD, and the genetic mechanism has not yet been concluded. It is difficult to distinguish between clinical PD and sporadic cases. Most studies concluded that the most common PD is autosomal dominant. Inheritance, individual reports are multi-gene transmission methods. Data on quantitative genetic studies indicate that the coincidence of monozygotic twins is not as high as expected by hereditary diseases, and the coincidence rate of single-oval twins is 6.1% (82%). There were 5 pairs in the pair), the coincidence rate of double-oval twins was 4.6% (three pairs of 66 pairs), and there was no significant difference between the two, but some scholars noticed that among the twins, there may be a symptom between them. Long intervals, multiple tracking showed that the clinical symptoms were inconsistent for more than 23 years between the twins. To improve the diagnostic sensitivity, PET studies found that 45% of the monozygotic twins and 29% of the double-oval twins were consistent ( Bum, 1992), confirmed autologous inheritance of PD by autopsy, accompanied by reduced spread, both parents transmitted the disease, recent studies suggest that the mother may pass the mitochondrial genetic disease, because the egg contains mitochondria, PD patients The striatum genome has a large fragment deletion, and part of the deletion fragment gene encodes a complex I subunit, which is a component of the mitochondrial respiratory chain, but lacks a large family report showing a linear mitochondrial inheritance through a familial primary The combination of Essential Tremor (ET) and PD to study genetic factors also supports genetic factors associated with the pathogenesis of PD. Genetics may play a role in the pathogenic cause of PD through several mechanisms, such as obstructing dop- able neurons. Normal development, delayed or accelerated cell death or interfere with normal protective mechanisms, although genetic factors may not be the single major factor, but The susceptibility of transmission may play an important role. Studies have found that genetically determined damage from normal detoxification metabolism may increase susceptibility to environmental toxicants, such as cytochrome P45 O2 D6 gene may be one of PD susceptibility genes, a few families PD Closely related to the synaptic protein (-synuclein) gene and the Par Kin gene mutation, monoamine oxidase B (MAO-B) is another possible enzyme associated with PD. It is involved in the catabolism of dopamine and can produce free radical damage neurons, PD patients. MAO-B was significantly increased in platelets, and it was found that plasma levels of cysteine in PD patients increased, and sulfide levels decreased. In short, hypersensitivity to chemicals may be several unexplained neurological diseases, including PD. Risk factors, these may involve intra-neuronal absorption mechanisms, as well as chemical defense systems involving detoxification or activation of toxin precursors, some enzyme systems present in the brain, involved in the metabolism of foreign bodies, and any defect in the link may be Produces hypersensitivity to chemicals.
Environmental poisons (10%):
People have long noticed that manganese poisoning, carbon monoxide poisoning, phenothiazine, butyrylbenzene drugs can produce PD symptoms. It has been reported that pesticides, herbicides, industrial pollution and water pollution are related to the occurrence of PD, and the current cause of PD. Understanding of learning and pathogenic factors, many from the study of MPTP Parkinson's syndrome, MPTP is a chemical substance 1-methyl-4 phenyl-1,2,3,6-tetrahydropyridine, which is given to monkeys. The resulting PD model has been successful, and it has been shown that the blue spot of the monkey, the hypothalamus is damaged, and the inclusion bodies of neurons similar to the lewy body appear. Regarding the mechanism of MPTP poisoning, it has been clarified that MPTP itself is not an actual toxin. But it acts as a toxin precursor, a lipophilic molecule that has a high affinity for the melanin of the substantia nigra in the brainstem, easily passes through the blood-brain screen, and is rapidly converted by MAO-B into The toxic metabolite 1-methyl-4-phenylpyridine (MPP+), a dopamine transporter that mediates the absorption of MPP+ into the dopaminergic nerve endings, concentrates on the mitochondrial matrix, causing the depletion of NADHCOQ1 reductase (complex I) and ATP, Eventually leading to nerves Death, the current neurotoxic substances in the external environment are being researched and explored. Some evidence does not support the role of environmental factors in PD. Although some areas have a high prevalence, there is no obvious positive signs of clustering. The prevalence of this disease has been stable, so the above substances can not be the main cause of this disease with environmental factors.
Infection (10%):
A-type encephalitis is a frequent occurrence of PD. Some authors believe that PD is associated with viral infection. The researchers tested herpes simplex virus (HSV) and cytomegalovirus (CMV) in PD patients. In 1981, Marttile and Coworker applied trace indirect blood. The clotting reaction method was used to determine the titers of HSV-II type, type III and CMV in blood and cerebrospinal fluid. It was found that the effect of HSV-II type antibody in blood was several times higher than that of the control group. It is believed that PD is related to certain symptoms of viral infection, but The titer of HSV-II antibody in cerebrospinal fluid did not increase, so its significance was not certain. Later experiments confirmed that there was no significant difference in the titer of HSV antibody between blood and cerebrospinal fluid between PD patients and normal people. Therefore, PD was considered to be unrelated to viral infection. Later, some authors studied the antibody titers of various neurotropic viruses and failed to confirm the causal relationship.
Oxidative stress and free radical formation (10%):
The metabolism of living matter is inseparable from oxygen. The metabolism of cells requires energy to be gradually reduced. The whole process occurs in the mitochondria. Many other enzymes, such as tyrosine hydroxylase, monoamine oxidase, NADPH-cytochrome P450 degrading enzyme. And xanthine oxidase is also an intermediary for the production or utilization of reactive oxygen species. Reductive oxygen has a positive effect in many normal biological processes, but excessive formation can damage nerve cells. Similarly, in the process of dopamine metabolism, oxidation The reaction is an important component, not only through the monoamine oxidases B and A, but also through the intermediates or by-products produced by the automatic oxidation to neurometamin, including hydrogen peroxide, superoxide anion (02-) and Hydroxyloxide (OH-), in which OH-free radicals are most toxic to cells, the latter two are collectively called free radicals, which can interact with lipid membranes of cells to cause peroxidation of fat, and free radicals in PD patients. Increase, fat peroxidation can cause cell membrane damage and lead to cell death, all oxidation reactions require electron transport, in the presence of iron In the presence of aluminum and copper, oxygen accepts electrons to produce 02- and OH-, and in the oxidation reaction, dopamine oxides in the substantia nigra cells, polymerized into melanin and iron to form a Ferento reaction, there will also be OH formation, due to free radicals. The increase, causing the accumulation of lipid peroxides, and the accumulation of iron, both of which cause neuronal degeneration, iron can easily form free radicals, neuromelanin is an iron ion reservoir, iron in PD patients Compared with the control group, the ratio is increased by 40% to 50%, and mainly ferric iron, while the bound ferritin is reduced, and the granulating effect of ferritin allows the iron to pass through the receptor and increase the oxidative stress. This observation is coupled with the change in the load of iron in the experimental model. It is also found that iron can cause defects in mitochondrial complex I in the brain of PD patients, but lacks experimental basis, and causes nerves related to oxidative stress and free radical hypothesis. Metadenature is still in dispute in PD.
In conclusion, PD is not caused by a single factor. There may be multiple factors involved. Genetic factors may increase the susceptibility to disease, but only through the combination of environmental factors and aging, through oxidative stress, mitochondrial failure and other factors. Such mechanisms lead to massive degeneration of the substantia nigra dopaminergic neurons and cause disease.
Pathogenesis
Pathology
The main pathological changes in PD patients are pigmentation of the substantia nigra, loss of neurons and gliosis, especially in the dense zone of the substantia nigra and blue plaques; neuronal degeneration also occurs in the dorsal nucleus of the vagus nerve and no name, black visible to the naked eye. The color and the color of the blue spot are pale, pale, showing the substantia nigra under the microscope, the number of pigmented neurons in the dense band is reduced, the remaining neurons are degenerated, the pigment particles are reduced or broken, and are visible in the blue spot and the substantia nigra neurons. Lewy body, lewy body is a circular eosinophilic inclusion body, diameter 3 ~ 25nm, it has a dense particle core, 1 ~ 8nm (nano), there are loosely arranged fiber components around the core, presented as "halo ", immunohistochemical studies confirmed that the lewy body contains ubiquitin, calbindin, complement protein, microfilament subunit, tubulin and microtubules of proteins 1 and 2, but does not contain Tan protein - The gene of the synuclein is an important component of the lewy body. Others are also found in the cerebral cortex, the putamen, the hypothalamus, the innominate, the dorsal nucleus of the vagus nerve and the sympathetic ganglia, but to a lesser degree. In addition, the brain of the PD patient is still pale. body (pale body), especially in the black and blue spots, but the number is less than the lewy body, so there is no diagnostic reliability.
2. Biochemical pathology
There are multiple dopamine (DA) transmitter pathways in the brain, the most important is the substantia nigra-striatum pathway. DA and acetylcholine (Ach) act as two important neurotransmitter systems in the striatum, and their functions are mutually antagonistic. Maintaining balance plays an important role in basal ganglia loop activity. PD patients have degeneration of DA neurons, and DA reduction causes Ach system hyperfunction, resulting in excessive basal ganglia output, excessive inhibition of thalamic-cortical feedback activity, and facilitation of cortical motor function. The effect is weakened, so there are motor symptoms such as increased muscle tone and decreased movement. In recent years, the DA content of the midbrain-marginal system and the midbrain-cortex system has been gradually reduced, which may cause mental decline, behavioral emotional abnormalities, and speech disorder. Activity disorder, the degree of DA transmitter reduction is consistent with the severity of the patient's symptoms. The early stage of the lesion is increased by the rate of DA renewal and the DA receptor is deficient after hypersensitivity. The clinical symptoms are not obvious (subclinical status) or do not appear. Disease progression can produce typical Parkinson's symptoms and decompensation. In recent years, there have been new perspectives on other transmitters and enzymes in the basal ganglia, but its clinical significance. Can not be determined, described as follows:
(1)-aminobutyric acid (-GABA): an inhibitory transmitter of the central nervous system that controls extrapyramidal impulses in the basal ganglia, which is decarboxylated by glutamate decarboxylase (GAD). The experiment proved that the activity of GAD in PD patients was 50% lower than that in the normal control group, and the low concentration of GABA in the cerebrospinal fluid of PD patients was poor in the treatment of levodopa, and it was prone to "on-off" phenomenon.
(2) Methyl enkephalin: endorphins, endorphins can promote the transformation of dopamine receptors in the new striatum, frontal and limbic systems, and mainly act on dopamine D2 receptors, enkephalin Regulates the relationship between enkephalin and dopamine, and relieves the inhibition of leucine enkephalin on the dopaminergic system, which may play a role in anti-PD.
(3) Glutathione (GSH): It can scavenge oxidants and some free radicals produced during dopamine metabolism, and protect the substantia nigra, striatum of dopaminergic neurons from oxidants and free radicals. When the GSH is reduced in the substantia nigra, the scavenging effect is small, and when the dopamine neurons are damaged, PD occurs.
(4) Somatostatin (SS): a polypeptide consisting of 14 amino acids, widely distributed in the cerebral cortex of the basal ganglia. The SS content in the cerebrospinal fluid of PD patients was significantly reduced, but the treatment of PD with SS did not confirm the efficacy, while substance P, Cholecystokinin is also reduced, the meaning is unknown.
(5) Dopamine-B-hydroxylase (DBH): The change of this enzyme in PD has been reported differently because it can be used as a parameter to measure the activity of dopaminergic energy. Therefore, the significance of ascending and descending for clinical treatment has not been determined.
(6) Tyrosine hydrolase: It has a balanced relationship with dopamine and is reduced with the loss of dopamine. It is the rate-limiting enzyme for dopamine synthesis and is also a marker of cell loss.
In recent years, studies have shown that dopamine receptors (DA-R) have several types, common amino acid sequences, and the structure is clear. DA-R has different effects depending on the distribution site, and the effect is different. Kabalian (1976) based on DA-R for adenosine The association of the regulation of acid cyclase activity is divided into D1, D2, receptor, D1 receptor activation, adenylate cyclase activity, and cAMP level; D2 receptor activation inhibits gland The activity of nucleoside cyclase, Seeman (1981) is divided into D1, D2, D3, D4 according to the characteristics of radioligand and DA-R binding. Later studies added D5. The name used now is D1, which is divided into A. B type; A = past D1, B = D5; D2 is divided into ABC subtype, A = past D2, B = D3, C = D4, according to DA-R reaction to different drugs is divided into dopamine receptors, Antipsychotic drug receptors, dopamine agonists, dopamine inhibitors, etc. PD responds to drug therapy mainly at D2 receptors, and phenothiazine drugs inhibit D1 and D2 receptors. Role, but mainly affects the D2 receptor, bromocriptine has different effects on D1 and D2 receptors, is an inhibitor on D1, is an agonist on D2, left The therapeutic mechanism of dextrodazole and bromocriptine is not exactly the same, and the combination of the two drugs can obtain better therapeutic effects.
Prevention
Elderly Parkinson's disease prevention
The etiology and pathogenesis of PD are still unclear. Primary prevention is difficult to implement. The focus is on secondary and tertiary prevention. In secondary prevention, intervention measures are taken according to genetic causes. Relatives of PD patients, especially first-degree relatives, are susceptible populations. The focus is on early detection, early diagnosis, early treatment, and the patient often has a long period of pre-symptomatic period before the onset of the disease, that is, the subclinical state, the patient may feel the inflexibility of exercise, which is obviously slower than before, and is easily considered Aging and neglect, through regular visits, check the changes of related enzymes and hormone levels in the body, if necessary, do positron emission tomography (PET) to check whether the early function of the striatum is damaged, such as protective, preventive treatment, interference with the cause, Pathological mechanism, which interferes with the death of nerve cells, prevents or at least slows the progression of the disease, and is aimed at prevention of grade III prevention, prevention of comorbidities, loss of viability in advanced patients, prolonged bed-infection and accidental fractures, etc. Medical methods (see rehabilitation) are guided through the community or rehabilitation center to guide medication and training, regular follow-up, Door service, assisted by family members as guardians, computer network management in conditional areas, remote areas can also be guided through follow-up, questionnaires and other communication methods, the ultimate goal is to delay the progress of the disease, effectively control, prevent complications .
Complication
Elderly patients with Parkinson's disease complications Complications
Can be complicated by stiffness, movement disorders, infections and accidental fractures.
Symptom
Symptoms of Parkinson's disease in the elderly Common symptoms Mental disorders, snoring ability, two hands, tremor, limb involuntary tremor, fatigue, limb tremor, depression, stuttering dementia
The onset age of this disease is between 40 and 70 years old. The onset peak is before 50 to 60 years old. There are more men than women. The young family cases have also been reported. Trauma, depression, overwork, cold can induce the disease, and onset. Concealed, slowly progressing, often with less movement, dullness or posture change as the first symptom, gradually intensified, mainly with resting tremor, increased muscle tone, slow exercise or slow movement, autonomic dysfunction.
Symptom
(1) Early symptoms: The earliest symptoms of patients are often difficult to detect and are easily overlooked. Some people call it a subclinical state. The patient's activities are inflexible, less moving, and the spine is gradually appearing. The limbs are not easy to bend. The stride becomes smaller, the sound of the front rushing voice becomes smaller, the neck, back, shoulders and buttocks are painful, fatigued, and the cleft palate is slightly widened and gazing.
(2) Typical symptoms:
1 Tremor (tremor): often the first symptom, accounting for 80% of PD, characterized by resting tremor, active movement is not obvious, mostly from the distal end of one side of the upper limb (finger), and then gradually extended to the ipsilateral lower limb and contralateral The upper and lower limbs, the lower jaw, the lips, the tongue and the head are generally affected at the end. The tremor is coarse and the frequency is 4-8 times/s (4-8 Hz). It can be temporarily controlled but not persistent, and the excitement and fatigue are aggravated. It disappears during sleep, and the index finger of the thumb and flexion is pill-rolling. The younger one has multiple unilateral or first-onset symptoms. The elderly are almost bilateral, allowing the patient to move sideways. A fist or a loose fist can cause tremors on the other side of the limb. This test helps to detect early mild tremor. On the EMG, the rhythmic release is consistent with the alternating activities of the synergistic muscles and antagonist muscles. In the middle, there are still small irregular irregular stretching tremors of the fingers, and the electromyogram lacks the characteristics of alternating action potentials. 15% of PD patients have no tremors throughout the course of the disease, and some patients can incorporate posture. Quiver.
2rigidity: The rigidity of PD patients is due to the increase of extrapyramidal muscle tone, the muscle tension of agonist muscles and antagonist muscles is increased, and the resistance of passive joints is always increased, similar to curved soft lead tubes. Feeling, it is called "lead tube-like tonic"; if some patients have tremor, they can feel intermittent pauses in uniform resistance when flexing their limbs, such as gears rotating, called "gear-like rigidity" (cogwheel rigitidy), due to increased muscle tone and imbalance, often exhibits abnormal posture: head tilting forward, body forward bending, upper limb forearm adduction, elbow flexion, wrist straight, metacarpophalangeal joint flexion special posture In the elderly patients, muscle rigidity can cause joint pain, which is caused by the increase of muscle tension and the blood supply of the joint is blocked. Some clinical trials can help to find slight muscle rigidity.
A. Let the patient move the contralateral limbs to make the muscles of the tested limbs more pronounced.
B. When the patient is in the supine position and quickly withdraws the pillow under his head, the head is often slowly dropping (Head dropping test).
C. Have the patient place the elbows on the table, make the double forearms perpendicular to the tabletop, and let the arms and wrist muscles relax as much as possible. Normally, the wrist and the forearm are about 90° flexed. In patients with sickness, the wrist joints remain more or less in a straight position. If the road sign is erected on the railway, it is called a road sign phenomenon.
3 brady akinesia (brady akinesia): is a characteristic symptom of basal ganglia dysfunction in PD, when it is severe, it can not be exercised, showing various slow movements, such as tying shoelaces, dressing, shaving, brushing, etc. Slow or difficult Less facial expressions, reduced or even disappeared blinking movements, called "mask face", difficult to start, ability to overcome inertia, stop exercising difficulties, change the posture of the movement, once the pace of the footsteps, the feet rubbed Line, called "small gait", the faster and faster, the lack of accompanying swinging of the arms, the front of the trunk, can not stop immediately, called "flush gait", in the event of obstacles, squatting or pausing steps, with small steps With the head and torso turning around, the language barrier can be expressed as low pronunciation, unclear articulation, stuttering or repeated language, called flush language, trembling when writing, distorting, uneven spacing, and getting smaller and smaller. Known as "lower case", these characteristic dysplasia can also be manifested as difficulty in swallowing, slow chewing, can be expressed as nervousness or excitement, and suddenly all actions stop, like freezing, called The freezing effect is short-lived. On the contrary, there is an abnormal movement (kinesia paradoxia), which is a temporary release of the less-moving phenomenon and normal activity. In rare cases, such as the emergency state, there is also a significant effective movement, called contradiction. Exercise, on-off phenomenon, sudden activity can not be free from sudden activities, special signs can be repeatedly tapped on the upper edge of the eyebrow to induce blinking (myerson), both eyes upward gaze and Convergence movement is limited, that is, eye movement crisis, more common in encephalitis and drug-induced Parkinson's syndrome.
4 autonomic dysfunction: common salivary secretion caused by excessive salivation, excessive secretion of sebaceous glands and increased sweating, so that the skin, especially facial skin oily, low blood pressure is prone to orthostatic hypotension, but rarely fainting, to the elderly patients See, biochemical examination found that tyrosine content decreased plasma renin and aldosterone levels are low, but normal blood sodium, suggesting that the surrounding sympathetic nerve defects, patients can be intractable constipation, urinary incontinence, urine, urinary incontinence, etc. The pathological basis is vagus dorsal nucleus damage and sympathetic dysfunction.
5 mental disorders: common depression, usually mild to moderate, rare suicide, about 40% of PD patients have depression in their course of disease, characterized by anorexia, sleep disorders and lack of libido, followed by dementia, which is in PD The incidence rate is 12% to 20%, and the risk of dementia among the first-degree relatives is extremely high. Other symptoms are apathy, slow thinking, slow, and personality changes can be seen in loneliness and autism.
2. Signs
(1) Early characteristic signs are reduced blink rate. Usually, the frequency of blinking in healthy people is 15-20 times/min, while that in PD patients can be reduced to 5-10 times/min.
(2) Typical signs:
1 "striatum hand": flexion of the metacarpophalangeal joint, the proximal interphalangeal joint is straight, the distal interphalangeal joint is flexed; and the foot deformity can also occur.
2myerson: The blinking of the nose or the eyebrow does not inhibit the blinking reaction.
3 Oculogyric crisis: the tonic convulsions between the two eyeballs, usually in the two eyeballs are common, side and lower vision are rare, repeated attacks, often combined with neck, mouth and tendon.
4 opening and closing disability: involuntary lifting muscle inhibition and orbicularis muscle inhibition.
(3) atypical signs: knee reflex variation is large, can be normal, difficult to lead, can also be active, limited to single-measure PD patients, bilateral knee reflex symmetry, buckling reflex, lower forehead and forehead reflex Rarely increased.
Examine
Elderly patients with Parkinson's disease
1. routine laboratory inspection
Generally in the normal range, individual may have hyperlipidemia, diabetes, abnormal electrocardiogram and other changes.
2. Blood cerebrospinal fluid examination
It can detect the decrease of dopamine level, the high metabolite concentration of vanillic acid, the decrease of serotonin metabolite and -hydroxyindole acetic acid content, the decrease of dopamine -hydroxylase, the decrease of somatostatin in cerebrospinal fluid and the -aminobutyric acid Level reduction, etc.
3. Molecular biology examination
Biochemical detection using high performance liquid chromatography (HPLC) can detect the decrease of HVA content in cerebrospinal fluid and urine. Genetic testing can be found in a few familial PD patients by Southern blot, PCR, DNA sequence analysis, etc. .
4. Brain CT, MRI examination
Generally, there is no characteristic observation. Older patients may have different degrees of brain atrophy, ventricle enlargement, some patients with cerebral lacunar infarction, and individual basal ganglia calcification. Recently, some scholars have proved that PD patients with MRI have high white matter in T1-weighted images. Signal, and appears in the anterior portion of the center of the semi-oval and the white matter around the anterior horn of the lateral ventricle.
5. Functional imaging detection
Using PET or SPECT with specific radionuclide assays, such as 6-18 fluoro-levodopa (6-FD) to study the metabolism of dopamine, information on the density and affinity of dopamine receptors can be obtained, and dopamine in the brain of PD patients is found. The metabolic function is significantly reduced. The absorption index of the striatum is less than normal before the onset of clinical symptoms. The early hypersensitivity (compensation period) of D2 dopamine receptor activity can be found in the early stage of the disease, and the low sensitivity (decompensation period) in the later stage. And the reduction of dopamine transmitter synthesis is valuable for early diagnosis, differential diagnosis and disease progression monitoring, but it is expensive and has not been widely used in clinical practice.
Diagnosis
Diagnosis and identification of elderly patients with Parkinson's disease
diagnosis
Typical tremor paralysis diagnosis is not difficult, according to typical tremor, rigidity, exercise reduction and other symptoms, combined with sputum-like action, lead tube or gear-like muscle rigidity, mask face, lower case, gait gait and other signs, generally Make a diagnosis.
Differential diagnosis
1. Infection: There may be tremor paralysis syndrome after encephalitis, but its onset can occur at any age. If there is a clear history of encephalitis, it can help identify.
2. Poisoning: more common in manganese or carbon monoxide poisoning, patients often have a history of carbon monoxide poisoning or long-term manganese exposure, and later tremors, tonic and other symptoms.
3. Drugs: Certain drugs, such as phenothiazines, block the synaptic transmission of dopamine and cause tremors, tonics, etc. In addition, as reserpine can block the storage of dopamine at the axon end, metabolites of methyldopa Competing with dopamine receptors, these drugs can produce symptoms of tremor paralysis syndrome, and the history of medication and symptom recovery after withdrawal can be identified.
4. Trauma: Concussion, brain contusion and other traumatic brain injury can cause symptoms of tremor paralysis syndrome, and its history of trauma can be identified.
5. Arteriosclerosis: Mostly due to cerebral arteriosclerosis or multiple cerebral infarction, its clinical manifestations include the symptoms of Parkinson's syndrome, but also the primary symptoms such as dementia.
