Step 1: The presence of dementia syndrome should be considered first
The main reliance is on a detailed history to understand the patient’s past intelligence and when the decline in intelligence began, including work, learning and memory abilities; as well as a patient and careful mental examination, especially for memory, calculation, comprehension, common sense and judgment. Short-range memory impairment (i.e., inability to learn new knowledge) is demonstrated by the patient’s inability to retell three objects after five minutes; long-range memory impairment (i.e., inability to recall knowledge already acquired in the past) is demonstrated by the patient’s inability to recall his or her past experiences (e.g., what happened yesterday, place of birth, occupation) or some general knowledge (e.g., current or past heads of state, well-known major holidays).
A diagnosis of dementia is then made according to the diagnostic criteria for dementia as follows.
1.Intelligence deficit which is severe enough to interfere with work and study and daily life: mild (work and study and social skills are reduced, but still maintain the ability to live independently), moderate (except for eating, dressing and urination and defecation can take care of themselves, the rest of life depends on others’ help) and severe (personal life is completely unable to take care of itself).
2. Evidence of short-range memory deficits, with frequent forgetting of recent events.
3. At least one of the following symptoms is present
(1) Significantly diminished ability to make abstract generalizations, such as difficulty interpreting idioms and proverbs, reduced mastery of vocabulary, inability to understand words of abstract meaning, and difficulty generalizing common features of similar things.
(2) Significantly diminished judgment, inability to make correct judgments about differences between similar things.
(3) Other disorders of higher cortical functions, such as aphasia, dysfluency, dyscognition, difficulty in calculation and composition, etc.
The second step is to identify the cause of the disease, i.e., its primary disease
There is a wide variety of diseases that can cause dementia, and the etiological diagnosis must take into account these etiologies in conjunction with the medical history, physical and neurological examination, laboratory tests and various ancillary diagnostic techniques to avoid missing any treatable cases of dementia. Some of the different etiologies of dementia are briefly described below for the reference of etiologic diagnosis.
1. Alzheimer’s disease or Alzheimer’s disease (AD)
This disease has a latent onset and is a chronic progressive brain degeneration caused by dementia, mainly manifesting three groups of symptoms such as transverse dementia, extrapyramidal movement disorders and psychiatric disorders. It is characterized by fluctuating cognitive decline, which can vary considerably within weeks or even within a day. The early stage is characterized by general cognitive decline with memory impairment, memory deficits (typical first signs), calculation deficits, time and place orientation deficits (e.g., disorientation), language and naming deficits, decreased social competence, and inability to manage normal work or family finances. Late cognitive decline is more pronounced, psychiatric symptoms are prominent and have eccentric behavior, abnormal social functioning is evident, seizure extrapyramidal symptoms (myotonicity, motor retardation, etc.), diaphoresis, positive cone system symptoms (Babinski sign, etc.).
2, vascular dementia (vasculardementia) used to be called cerebral arteriosclerotic dementia
This disease has the following clinical features.
(1) A history of recurrent stroke or cerebral blood supply deficiency, often showing a fluctuating course or stepwise deterioration, intellectual impairment mostly in the form of patchy deficits, and intellectual decline up to the level of dementia.
(2) VD executive function is more impaired compared to AD; time and place orientation, event or semantic memory is less impaired.
(3) May exhibit indifference to expression, oligophrenia, anxiety, depression, or euphoria.
(4) There are often positive neurological signs due to focal brain damage, which can be differentiated from AD.
(5) Dementia manifestations are related to the site of vascular lesions.
Multiple infarcts have a rapid onset, with phased progression or recurrent focal neuropsychological and pathological damage, such as cognitive dysfunction such as near-memory impairment and reduced computational power, hemiparesis, hemianesthesia and cone fasciculation signs. Cognitive dysfunction in internal carotid artery infarction with aphasia (dominant hemisphere infarction), transient blackness or Horner’s sign on the side of the lesion, contralateral hemiparesis & hemianesthesia, etc. Anterior cerebral artery infarction with volitional deficit, disuse, transcortical motor aphasia, memory loss, etc., with contralateral lower extremity paralysis and sensory impairment, urinary incontinence, etc. Cognitive dysfunction in middle cerebral artery infarction with severe aphasia (damage to the dominant hemisphere), dyslexia, dysgraphia and dyscalculia, contralateral hemiparesis, hemianesthesia, visual field deficits and cone fasciculation signs. Posterior cerebral artery infarction memory and cognitive dysfunction with loss of recognition, loss of reading (without loss of writing), visual field deficits and brainstem damage symptoms Infarcts in the thalamic region have impaired attention and memory with aphasia (dominant hemisphere impairment), motor and sensory deficits of varying degrees. Cavernous infarcts often have a history of hypertension, memory loss, psychomotor slowing, emotional apathy or depression with dyskinesia, Parkinson’s syndrome and pseudobulbar palsy. Small subcortical artery lesions with memory loss, psychomotor bradykinesia and euphoria with ataxia, pseudobulbar palsy, urinary incontinence and Parkinson’s syndrome (mostly without tremor). The dominant venous sinus lesions include aphasia, dyslexia, dysgraphia, word memory impairment, visuospatial impairment, inability to discriminate between left and right, finger loss, and dyscalculia.
3.Frontotemporal dementia (Pick)
This disease is characterized by frontotemporal lobe atrophy, and is a relatively common neurodegenerative dementia (accounting for 1/4 of all dementia patients), with a peak incidence of 60 years old and more women. The disease has an insidious onset and progresses slowly; early personality and affective changes are apparent, such as irritability, irritability, stubbornness, apathy and depression, and fragmentary delusions; Kluver-Bucy syndrome may appear, showing retardation, apathy, visual loss, etc.; atypical cognitive dysfunction, with marked speech impairment, spatial orientation preservation, and mild memory impairment. Neurological signs, primitive reflexes in the early stage, cone bundle signs and extrapyramidal signs in the late stage.
4. Lewy body dementia
Onset in old age, progressive course; dementia, fluctuating cognitive dysfunction, large changes within weeks or even 1 day, early cortical symptoms (aphasia, dysfunction and dyscognition), memory impairment is not obvious; Parkinson’s syndrome, myotonic and motor retardation, poor response to levodopa treatment; psychiatric symptoms: vivid visual hallucinations (80%), delusions, delirium, etc.; may be accompanied by myoclonus, dystonia Myoclonus, dystonia, swallowing disorder, sleep disorder, and autonomic dysfunction, etc.
5.Huntington’s disease and other subcortical disorders
This disease often starts at the age of 30-40 years, and is a delayed-onset autosomal dominant disorder. It is now possible to diagnose the disease with genetic markers before the onset of the disease. Chorea-like movements often appear first, and psychiatric symptoms are progressive, usually presenting as recurrent schizophrenic-like psychosis. There is a high incidence of suicide and severe dementia. A small number of patients may not develop chorea-like movements, which can be difficult to differentiate from AD in terms of symptoms and course, but typical cases with chorea-like movements and a positive family history are not difficult to diagnose. Other subcortical disorders (e.g., Parkinson’s disease, Wilson’s disease, supranuclear palsy) may also produce dementia. There are some signs that can help distinguish dementia from cortical dementia. Cortical appearance gives the impression of being awake, alert, and appearing younger than one’s actual age, while subcortical lines appear frail, improperly dressed, and confused; normal cortical movements, gait, and movements, while subcortical movements are slow, panicky, dance-like, or ataxic, with tremors, dance-like, and twisting spasms; cortical standing posture is straight, while subcortical lines are stooped and Wilson’s disease is a less common cause of dementia and needs to be considered especially when young patients have basal ganglia and cerebellar symptoms.
6.Jakob-Creutzfeldt disease
This disease is a rare form of dementia caused by a specific lentivirus. The pathological and anatomical features are spongiform encephalopathy. The clinical presentation is a slow onset, vague neurological-like symptoms followed by progressive dementia. The age of onset is 40 to 50 years, and the disease progresses rapidly, often entering severe dementia in about a year and dying from complications. The exact diagnosis depends on the pathological anatomy.
7.Normal pressure hydrocephalus
Normal pressure hydrocephalus (norma-lpressure hydrocephalus) mainly manifests clinically as a triad of progressive dementia, gait instability and urinary incontinence. CT and MRI scans show enlarged ventricles without significant cortical atrophy. Early administration of short-circuit shunt surgery can provide varying degrees of relief of psychoneurological symptoms.
8.Brain tumor
Rapidly developing brain tumors, such as astrocytoma, are prone to obvious disorders of consciousness; slowly growing brain tumors, such as meningioma, are less likely to cause mental disorders, and only personality disorders and dementia syndrome occur in later stages. The clinical diagnosis is based on focal neurological signs and signs of increased intracranial pressure.
9. Paralytic dementia
It is a chronic meningoencephalitis caused by the invasion of syphilis spirochetes into the human brain. The incubation period from syphilis infection is 6 to 12 years on average. The age of onset is mostly 30-50 years old, more men than women. If left untreated, the disease enters a state of severe dementia after 3 to 5 years. Neurological examination reveals signs such as coarse tremor of the lips, tongue, eyelids and fingers, dysarthria, ataxia, hyperactive tendon reflexes, pupil narrowing, marginal irregularity and unequal size on both sides, loss of response to light and presence of modulatory response (A-Roche pupil); the latter is diagnostic. Laboratory tests: increased cerebrospinal fluid cell count and increased protein content. Serum and cerebrospinal fluid syphilis serology tests are positive, and now the fluorescent syphilis spirochetal antibody adsorption test (FTA-ABS test) is commonly used clinically to examine the cerebrospinal fluid more specifically for neurosyphilis. Treatment is based on penicillin, if early treatment, 1/3 of patients can recover, 1/3 of patients can get different degrees of progress.
10.AIDS
It is a newly discovered disease in the last decade or so, and most people do not necessarily produce symptoms after infection. HIV (human immunodeficiency virus, HIV) is pro-neurological, so there are more neurological symptoms, which may include brain tumor symptoms, encephalitis symptoms, peripheral nerve symptoms, etc. There are two types of psychiatric symptoms caused by HIV: organic symptoms due to brain tissue damage, mainly cognitive impairment; and psychogenic symptoms due to this incurable disease, mainly anxiety and depression. AIDS-induced dementia can be caused by direct infection of the central nervous system by HIV, or by intracranial lesions and infections due to immune dysfunction (e.g., toxoplasmosis, lymphoma) and indirect effects due to systemic diseases, such as sepsis, hypoxemia, and electrolyte imbalance. This disease presents as a subcortical dementia in the early stages of infection and is quite difficult to distinguish from many functional disorders.
11. Carbon monoxide toxic dementia
In about 10% of patients with severe carbon monoxide poisoning, after a week to three months of normal mental clarity (pseudo-healing period) following recovery from a coma, a severe blurred-consciousness-dementia syndrome suddenly develops. The patient develops disorientation, bizarre behavior, and garbled speech, which progresses in a short period of time to loss of work and life skills, difficulty in comprehension, incontinence, and finally dementia. Neurological examination may include gait instability, ataxia, cogwheel-like increase in muscle tone or decerebrate ankylosis, hyperactive tendon reflexes and positive cone cord signs. The skin is prone to sweating, blistering, and poor peripheral circulation, which can easily lead to decubitus ulcers.
12.Other system disorders
Many metabolic and endocrine disorders can cause brain dysfunction. For example, hypothyroidism can produce cretinism in children, often accompanied by mental retardation, and mucinous edema in adults, who may present with apathy, slow movement, difficulty thinking, memory loss and lethargy. Early treatment with thyroxine often leads to recovery. Primary parathyroidism, which resolves rapidly with treatment, may occasionally lead to dementia. Pituitary insufficiency, adrenal insufficiency (Addison’s disease), and hyperadrenalism (Cushing’s disease) usually lead to depression or other affective disorders, and less often to dementia, but should be considered in the differential.
Hepatic encephalopathy due to chronic liver failure and chronic uremic encephalopathy can both lead to dementia. Dialysis dementia can occur in patients with kidney disease treated with dialysis for many years, possibly due to aluminum toxicity caused by dialysis fluid or common acid preparations, which may be relieved by stopping the intake of aluminum salts.
Cardiac arrhythmias and chronic pulmonary disorders lead to dementia through persistent hypoxia. Inflammatory lesions of the cerebral vessels due to collagen-vascular disease may also produce dementia. When signs of collagenous disease, such as increased sedimentation rate, proteinuria, or tubular patterns in the urine, are found and the diagnosis is still not confirmed, steroid testing may be indicated.
Sarcoidosis may sometimes present as dementia alone, but is usually accompanied by other symptoms of meningeal lesions. Steroid treatment may improve dementia.
Nutritional deficiencies can also lead to dementia. Dementia, dermatitis, and diarrhea are the classic triad of niacin deficiency-induced pellagra. Due to vitamin B12 deficiency, blood malignancy and other neurological dysfunctions, such as peripheral neuropathy and spinal and lateral column lesions, often precede the onset of dementia. The above symptoms of vitamin B12 deficiency are also seen in patients with folic acid deficiency, as collected by Medical Education|Net.