Subcortical dementia

Introduction In general, multiple cerebral infarction dementia, thalamic dementia, and Binswanger disease are mostly in the subcortical nucleus and white matter, and the symptoms are mostly in the subcortical dementia range. Large-area cerebral infarction dementia and infarct dementia in the watershed area involve both cortex and subcortical, and the clinical symptoms and signs are cortical and subcortical mixed dementia.

Cause

(1) Causes of the disease

At present, there are five main pathophysiological factors leading to vascular dementia:

1. Cerebral artery occlusion leads to multiple infarction and reduction of brain tissue volume: atherosclerotic stenosis and occlusion occur repeatedly in the beginning of the internal carotid artery or middle cerebral artery, resulting in multiple large infarcts in the cerebral hemisphere. The lesion, or the watershed infarction of the frontal and temporal lobes, significantly reduces the volume of brain tissue. It is generally considered that when the volume of the infarct is more than 80-100 ml, the clinical manifestation of cognitive dysfunction due to severe neuronal loss and brain atrophy which performed.

2. Ischemia and hypoxia-low perfusion: important parts of the cerebral cortex involved in cognitive function and brain tissue sensitive to ischemia and hypoxia, long-term deficiency due to small vessel disease caused by hypertension and small arteriosclerosis The bloody hypoperfusion state causes delayed necrosis of neurons in this site and progressive cognitive dysfunction. Patients with clinically common vascular dementia may have near memory loss, mood or personality changes after repeated transient ischemic attacks. Foreign scholars have found that cognitive dysfunction in patients with cardiovascular disease, the number of patients with a history of heart failure or arrhythmia, the incidence of dementia is significantly higher than the same age group of controls.

3. Subcortical white matter lesions: glassy degeneration in the wall of small arteries in the white matter, fibrous hyperplasia and thickening of the wall, and extensive diffuse demyelination of white matter, which affects the cortical and subcortical connections. The most common type of cognitive dysfunction is Binswanger's disease, followed by autosomal dominant brain artery disease (CADASIL) with subcortical infarction and leukoencephalopathy.

4. Hemorrhagic lesions: subdural hematoma and subarachnoid hemorrhage including extracranial hemorrhage, hemorrhagic hematoma in the cerebral hemisphere, direct destruction and indirect compression of the brain parenchyma, and obstruction of the cerebrospinal fluid circulation pathway, clinically emerging Different degrees of dementia performance.

5. Various types of inflammatory cerebrovascular diseases: including non-specific vasculitis, as well as tuberculosis, syphilis, fungi, parasites, etc. can be the cause of cerebral vascular dementia. In addition, blood diseases, carbon monoxide poisoning, and central nervous system de-sheathing diseases can occasionally cause cerebral ischemia or cerebral infarction, and then symptoms of dementia. Wallin et al. have proposed a non-multiple infarction cerebral blood dementia with neurotransmitter defects, which is worth noting.

(two) pathogenesis

The distribution of lesions in cerebral vascular dementia has the following characteristics:

1 lesions multiple, the total volume of infarcts to reach a certain extent.

2 large individual lesions are more common on the left side; 3 lesions are more common in the frontal, temporal and thalamus.

4 cerebral ventricular white matter is also often damaged. From the perspective of functional positioning, the damage in these areas is closely related to the clinically occurring intellectual obstacles.

The function of the cerebral cortex is extremely complex. Through intensive cellular synaptic connections, various information is analyzed, integrated, and reacted at any time. Once the brain tissue is damaged, especially the bilateral cortical damage, it is bound to affect this fine advanced neurological function, and various intellectual obstacles appear. However, the cerebral cortex is highly compensatory. Only when the damage reaches a certain level, it loses compensatory ability and clinical symptoms appear.

The left cerebral hemisphere is the dominant hemisphere in the right hand. It plays a leading role in advanced neurological activities such as language and abstract thinking. Once a large lesion occurs, it is not difficult to understand that it will show the decline of intelligence and form dementia.

The cerebral cortex has specific neurological functions in the subcortical and various regions. Closely related to mental activities such as frontal lobe, temporal lobe, thalamus, etc., often closely related to intelligence. The frontal cortex can be linked to the subcortex via three loops:

1 The lateral dorsolateral prefrontal cortex and its subcortical to caudate nucleus, globus pallidus, thalamus. The lesions may have slower slogan and design fluency, learning and memory dysfunction, and abnormal exercise procedures.

2 The frontal lobe to the caudate nucleus may have personality changes in the lesions, manic, irritating and impulsive.

3 the medial frontal lobe to the ligament, the ventral side of the striatum. The lesions are silent, non-satisfied, blinking but unable to speak spontaneously. The answer to the question is often monosyllabic and urinary incontinence. In short, the frontal lobe, especially the lesions of the prefrontal and temporal surfaces, may be manic, silent, linguistic and dysfunctional, lack of motive force, inattention, memory impairment, and constitute dementia syndrome.

The temporal lobe, especially the hippocampus, participates in the memory loop (hippocampus--papillary-thalamic nucleus-cingular gyrus), bilateral hippocampus or dominant hemisphere hippocampal lesions, which may have significant memory impairment, especially near-memory loss. Lost and lost, careless. The temporal lobe lesions can also have various sensory disturbances, such as scent, scent, and visual distortion, or become bigger and smaller, dreamy, familiar or "unfamiliar", and may also have psychomotor excitement, self-injury, and injury. Unconscious chewing, exercise, groping and other automatic diseases. Most of the above symptoms are intermittent and can also occur continuously.

The thalamus can be roughly divided into three groups:

1 prenucleus, mainly related to the olfactory pathway. The fiber from the hippocampus passes through the papillary body from the dome to the hypothalamus, and then from the nipple thalamus to the anterior nucleus of the thalamus, and then to the cingulate. This loop is related to the famous Papez loop.

2 lateral nucleus, subdivided into two parts of the dorsal and abdomen, the anterior ventral nucleus receives the fibers from the globus pallidus, and is the relay station of the extrapyramidal system. The posterior ventrolateral nucleus and the posteromedial nucleus receive the spinal thalamus bundle, the medial collateral and the trigeminal The fibers of the mound are re-issued to the central posterior cortex.

3 The medial nucleus, which is divided into the dorsal medial nucleus and the central nucleus, receives fibers from other thalamic nuclei, and then sends fibers to the frontal lobes. Lesions of the bilateral medial dorsal nucleus may present with obvious mental symptoms such as memory loss, apathy, personality changes, and lethargy. Forgotten by thalamic lesions, there are not only recall obstacles, but also recognition abiliy obstacles. A common lesion of thalamic dementia is a focal lacunar infarction of the medial nucleus of the thalamus. Mostly bilateral lesions, occasionally a single lesion on the left side.

White matter lesions (shown as low density on CT and high on MRI), especially lesions of the paraventricular white matter are often associated with intelligence. The white matter near the anterior horn of the lateral ventricle is mostly composed of projection fibers from the frontal lobe. The lesions are mainly the extension of the frontal lobe lesions, and there are clinically intelligent disorders. White matter lesions beside the posterior horn of the lateral ventricle often show visuo-construction, attention, finger-motor-speed, and latency extension of the tactile resolution.

an examination

Related inspection

Cranial CT examination of blood, normal body, skin sensation

1. Clinical symptoms: Clinical symptoms can be divided into two categories, one is the mental symptoms that constitute dementia, and the other is the neurological symptoms of brain damage secondary to vascular disease.

In the psychiatric symptoms that constitute dementia, memory loss is an early core symptom, including near memory, far memory, and immediate memory, but the earliest appearance is the loss of near memory, and the far memory impairment occurs later. As memory declines, attention deficits gradually appear, and computational power, orientation power, and comprehension decline to varying degrees. Some authors have observed that the most common are time-oriented, computational, near-memory, spontaneous writing, and reduced transcription. The real mental symptoms are relatively small. The detection of memory and intelligence is currently in the form of scales such as memory quotient (MQ), Hasegawa Intelligence Scale (HDS), and Simple Intelligence Scale (MMSE). If the patient is unable to complete the test due to illness, he or she can take a social questionnaire, such as the Clayton Royal Behavioral Scale (CRBRS), to indirectly understand the patient's intelligence. When evaluating the results of these scales, the subject's condition, age, education level, psychological state, and the environment at the time of testing, the technical proficiency of the tester, etc. should be fully considered. It should be particularly emphasized that the low value of the scale is not necessarily dementia and must be considered comprehensively. If necessary, repeat the test.

Due to brain damage caused by vascular disease, various related neuropsychiatric symptoms may occur depending on the site. In general, lesions located in the left cerebral hemisphere cortex (dominant hemisphere) may have symptoms such as aphasia, misuse, loss of reading, loss of books, miscalculation, etc. Cortical lesions located in the right cerebral hemisphere may have visual spatial dysfunction; The lesions of the lower nucleus and its conduction bundle may have corresponding movements, sensations, and extrapyramidal disorders. Symptoms of strong crying, strong laughing pseudobulbaric palsy, and sometimes hallucinations and self-talk may occur. Psychic symptoms such as stupor, silence, and apathy. The above symptoms and signs are often developed stepwise in patients with multiple cerebral infarction dementia. The onset can be sudden or concealed. After each episode, some neuropsychiatric symptoms can be left, superimposed again and again, until the intelligence is fully degraded and becomes dementia. . A large area of cerebral infarction dementia is more acute, and the condition is serious. Fortunately, survivors will have serious neurological symptoms and signs, such as convulsions, bedridden, aphasia, loss of life ability, and more dementia. The incidence of subcortical arteriosclerotic encephalopathy is more concealed, and the dyskinesia is also mild. The condition can be relatively stable for a long time, but the condition can be aggravated rapidly after one stroke, and the intelligence is significantly reduced and progressively deteriorated.

Thalamic dementia is mainly characterized by mental symptoms such as forgetting, abnormal mood, and lethargy. Due to brain stem lesions, vertical eye gaze and other midbrain and pons symptoms may occur. In general, the symptoms of exercise are not obvious and are not persistent.

Infarct dementia in the watershed area is rare in clinical practice, mainly relying on imaging diagnosis, and abnormal images appear in the vicinity of the cerebral artery by CT or MRI. Clinically, there are many cases of hypothalamic cerebral vascular perfusion after various reasons, such as long-term shock, hypotension is not corrected, cardiac insufficiency, inappropriate use of antihypertensive drugs. The clinical symptoms can be light or heavy, depending on the brain area of the lesion. The bilateral lesions are more severe, and a few are shown as dementia.

In general, multiple cerebral infarction dementia, thalamic dementia, and Binswanger disease are mostly in the subcortical nucleus and white matter, and the symptoms are mostly in the subcortical dementia range. Large-area cerebral infarction dementia and infarct dementia in the watershed area involve both cortex and subcortical, and the clinical symptoms and signs are cortical and subcortical mixed dementia.

2. Clinical type

Cerebrovascular dementia can be roughly divided into five clinical types, namely, multi-infarct dementia, large-area cerebral infarction dementia, subcortical arteriosclerotic encephalopathy, thalamic dementia, and infarct dementia in watershed.

(1) multi-infarct dementia: multi-infarct dementia is the most common type, due to dementia caused by most cerebral infarction, clinically often have hypertension, arteriosclerosis, recurrent cerebrovascular disease, and stay after each episode Underneath more or less neurological and psychiatric symptoms, accumulated less and more, and eventually became a comprehensive serious mental decline.

(2) large area of cerebral infarction dementia: often due to occlusion of the main cerebral artery (such as middle cerebral artery, basilar artery, etc.), causing large area of cerebral infarction, severe brain edema, and even cerebral palsy. Most patients may die in the acute phase, and a small number of surviving patients have different levels of neuropsychiatric disorders, including dementia and loss of work and life.

(3) Subcortical arteriosclerotic encephalopathy: As early as 1894, Otto Binswanger mentioned that some patients with dementia had severe cerebral arteriosclerosis and subcortical white matter atrophy in the process of studying paralytic dementia. The author called chronic progressiveness. Chronic progresstive subcortical encephalitis; In 1962, Olszewski was renamed subcortical ateriosclerotic encephalopathy, now known as Binswanger disease. The disease is difficult to diagnose due to life, and has not caused clinical attention for a long time. Now the diagnostic methods are continuously improved, especially the progress of imaging. It is possible to obtain the correct diagnosis of Binswanger disease by CT or MRI. Although there is still a question about whether this type of dementia is an independent type, this type of dementia is one of the types of cerebrovascular dementia regardless of its clinical or pathological characteristics.

(4) Thalamic dementia: Thalamic dementia refers to dementia caused by focal infarction or lesion of bilateral thalamus (occasionally one side of the thalamus), which is rare in clinical practice. Thalamic dementia refers to dementia caused by focal lesions of the simple thalamus, and does not include thalamic lesions present in multiple cerebral infarction.

(5) Watershed infarct dementia: Watershed infarct dementia, also known as Borderzone infarct dementia, refers to long-term low perfusion at the junction of the anterior, middle, and posterior arteries. Causes severe ischemia or even infarction, leading to brain dysfunction. Dementia can occur clinically, and can be diagnosed by imaging before birth, which is rare.

At present, there is a lack of accepted diagnostic criteria for cerebral vascular dementia. According to the classification of mental and behavioral disorders published by ICD-10, the diagnosis points of F01 vascular dementia are as follows: the premise of diagnosis is dementia, and the damage of cognitive function is often not On average, there may be signs of memory loss, intellectual impairment, and focal neurological damage, and self-knowledge and judgment can be maintained. Sudden onset or staged degeneration, as well as focal neurological signs and symptoms make the diagnosis more likely. In some cases, only CT or final neuropathology can be used to confirm the diagnosis. Related features are hypertension, carotid murmur, emotional instability with transient depression, crying or bursting laughter, transient turbidity or convulsions, often exacerbated by further infarction, and personality remains relatively intact, but some patients may appear Obvious personality changes, such as apathy, lack of control or original personality characteristics, such as self-centered, paranoid or irritating.

The American Psychiatric Association proposed the following diagnostic criteria for multiple cerebral infarction dementia in 1979:

1. Dementia.

2. Symptoms are progressive in a progressive process with patchy defects in the early stage.

3. Focal neurological symptoms and syndromes (deep reflex hyperactivity, high stretch reflex, pseudobulbar palsy, abnormal gait, weakness of the extremities, etc.).

4. Evidence of cerebrovascular disease that is clearly associated with the disease can be found in medical history, physical examination or laboratory examination.

Recently (1992), the Center for Diagnosis and Treatment of Alzheimer's Disease, California, USA, also proposed a diagnostic criterion for ischemic vascular dementia that corresponds to Alzheimer's disease. According to the symptoms, signs and imaging findings, and if necessary, combined with pathology, different diagnostic conclusions, including "affirmative", "probable", "Possible", and "hybrid". In particular, the so-called mixed dementia may be due to Probable IVD and Possible Alzheimer's or definite IVD and hypothyroidism.

At present, there is no recognized standard for the diagnosis of cerebral vascular dementia in China, but the clinical diagnosis may include 3 points: 1 must be definitely dementia; 2 must have cerebrovascular disease related to the onset of dementia, and have imaging confirmed; 3 except other The cause of dementia was the use of Hachinski's ischemic score in the identification of Alzheimer's disease.

Because there is no consensus on the diagnosis of cerebral vascular dementia, coupled with the popularity of CT examination, some authors believe that the diagnosis is too wide, can not rely solely on multiple cerebral infarction or paraventricular white matter lesions to diagnose cerebrovascular dementia or Binswanger disease. Some authors believe that cerebrovascular dementia is not necessarily infarcted, and chronic progressive ischemic cerebrovascular disease may also have dementia, which is considered to be insufficiently diagnosed. Is the diagnosis too wide or too strict? It may be that different authors lack a consensus on cerebral vascular dementia, which shows that a recognized diagnostic criteria is urgently needed. The diagnosis of cerebral vascular dementia should have a strict differential diagnosis. The differential diagnosis includes two aspects, one is to identify whether there is dementia, and the other is to distinguish the difference from other types of dementia.

Differential diagnosis

Senile dementia

Alzheimer's disease and vascular dementia are the most common causes of dementia in the elderly. They can occur alone or in combination. Cerebrovascular disease also often exacerbates senile dementia. Therefore, the differential diagnosis of the survival period of both is more difficult, and the final diagnosis requires pathological examination. The identification of senile dementia and vascular dementia using the Hachinski ischemic scale is clinically simple and has certain accuracy. That is, 1 or 2 points for each clinical feature, 7 points or more for vascular dementia, and 4 points or less for vascular dementia.

Hachinski identification score table: There are main contents of the Hachinski ischemic scale, plus CT scan, those with a total score of less than 2 points can consider senile dementia, 3 to 4 points can be diagnosed with vascular dementia, more than 4 points can be Diagnosis of vascular dementia.

In addition, the Rortra-Sanchey improved score method has certain discriminative significance for senile dementia, vascular dementia and mixed dementia. That is, 6 points or more is vascular dementia, and 3 points or less is senile dementia, and mixed dementia is between the two.

2.Pick disease

It is a rare type of senile dementia, accounting for 1% to 7% of necropsy brain specimens. It usually occurs before the age of 65. Gradually, personality changes such as loss of self-control, no trimming, apathy, wandering behavior and appetite are repeated. Stereotyped language, the past skilled skills are degraded, but the memory and computational power damage is less severe, and the symptoms appear relatively late. Neuroimaging showed CT or MRI of the characteristic frontotemporal atrophy. SPECT examination revealed a significant reduction in cerebral blood flow in the frontotemporal region. Neuropathological examination revealed a swollen and lightly stained cell in the frontal cortex, Pick cells, a silver-containing inclusion body in the cytoplasm, Pick body, and microfilament and microtubule aggregation observed under an electron microscope. .

3. Parkinson's disease is an extrapyramidal disease in the elderly over 60 years old. The clinical manifestations are characterized by tremor, rigidity and exercise reduction. 30% of patients may have severe dementia during the course of the disease, showing volatility recognition. Knowing dysfunction and paroxysmal visual hallucinations, some patients may have symptoms and signs of unilateral limb dyskinesia, and no characteristic changes in neuroimaging. However, some patients may have cerebrovascular disease at the same time.

4.Creutzfeldt-Jacob disease

For subacute spongiform encephalopathy caused by chronic infection of prion (Prion), early clinical manifestations are progressive dementia and speech disorder, combined with mental and behavioral abnormalities, hand and foot pulsation and myoclonus, late dysphagia, Quadriplegia and disturbance of consciousness, the average duration of disease is 6 to 12 months. 80% of patients showed characteristic changes in EEG in the late stage of the disease, and high-amplitude spine-slow integrated waves periodically distributed on the slow-wave background with an interval of 0.5 to 2 s. Head CT or MRI showed no characteristic changes except mild brain atrophy. Brain biopsy and neuropathology are also required to determine the diagnosis before birth.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.