thrombus expansion
Introduction
Introduction One of the clinical manifestations of multiple cerebral infarction during thrombus expansion, multiple cerebral infarction refers to multiple ischemic softening infarction in the brain, also known as multiple brain softening. In addition to common convulsions, sensations and language barriers, dementia may also occur. Doctors refer to this type of dementia as multi-infarct dementia (ie, arteriosclerotic dementia). Multiple cerebral infarction occurs in men aged 5O to 60 years. Hypertension and arteriosclerosis are the main causes. The more lesions in this disease, the higher the incidence of dementia, and bilateral infarction is more prone to dementia than unilateral. Therefore, we should actively prevent the recurrence of cerebral infarction.
Cause
Cause
Cause of thrombosis
Cerebral infarction is a severe stenosis or occlusion of the cerebral blood vessels, which leads to blockage of cerebral blood flow and ischemia and necrosis of the brain tissue. It accounts for about 50%-60% of all acute cerebrovascular diseases. There are many causes of cerebral infarction, mainly cerebral vascular occlusion and brain blood circulation disorders.
After acute occlusion of the cerebral vessels, cerebral edema gradually appeared in the first 4h-6h ischemic area. After 12h, the brain cells began to necrosis, but the infarct area was difficult to distinguish from normal brain tissue. From 24h to 5th, cerebral edema reached a peak and the collateral circulation began to build up. From the second week onwards, cerebral edema gradually reduced, but tissue necrosis and liquefaction in the infarct area were more obvious. Although a more adequate collateral circulation has been established, some patients may have thrombolysis and revascularization, and the blood vessel wall of the infarct area may be hemorrhagic due to ischemic injury, which may form a hemorrhagic infarction.
Examine
an examination
Related inspection
Angiography
Thrombosis expansion
1. CT manifestations: (1) acute phase: generally the first 5 days after onset as an acute phase. The increase of water in the lesion area caused two effects on the CT image. One was the density of the lesion area, and the density difference between the cortex and the medulla. In the early stage, the density reduction was generally not significant, and it was mostly wedge-shaped, which was consistent with the blood supply range of the affected artery. Boundary blurring; the other is the effect of mass effect or mass caused by the increase of water volume in the lesion area. The light manifestation is swelling of brain tissue in the lesion area, cerebral sulcus and brain oil disappear, and the heavy performance is the midline structure. The contralateral displacement, the so-called intracranial sputum, is related to the area of cerebral infarction. The larger the area, the more significant the occupancy effect. The above two effects generally reach the extreme on the 3rd and 5th day after the onset of the disease.
It should be pointed out that the early changes in CT in the early cerebral infarction take 3-6 hours at the earliest, and the typical performance after the late 24 hours or more. If there is a typical clinical manifestation of cerebral infarction and CT is negative, CT should be reviewed in a short period of time to avoid missed diagnosis.
(2) Subacute phase: refers to the 6th to 21st day after the onset, the edema is obviously absorbed, and the occupancy effect is weakened or disappeared. In most cases, it is also low-density, and the boundary is clearer than the acute phase; however, a small number of patients exhibit equal-density lesions, which are difficult to detect, the so-called "fog" effect, because the average effect of some different density components in the lesion area is mixed together. (Low-density substances such as water, lipids, and cavities are mixed with high-density components such as blood, calcification, and iron). An enhanced scan at this time is very helpful for diagnosis. After injection of contrast agents, typical cerebral infarction is characterized by enhanced brain recurrence, and the cerebral gyrus of the cerebral cortex in the infarct area and the nucleus of the basal ganglia are enhanced.
(3) Chronic phase: 21 days later, the ischemic necrosis of brain tissue is cleared by phagocytic cells, leaving a cavity containing cerebrospinal fluid, combined with gliosis, the lesion area is still low density, similar to cerebrospinal fluid, the boundary is clear, but the volume is reduced The performance of the affected side of the ventricle is enlarged, the subarachnoid space including the brain fissure, the ditch, the deepening of the pool, and the atrophy of the cortex.
(4) lacunar infarction: most of them are located in the basal ganglia or deep brain white matter in the cerebral hemisphere, and the lesion size is below 1.5 cm. Generally, there is no occupancy effect such as pressure displacement of the ventricular system.
(5) Hemorrhagic infarction: CT features are characterized by scattered, uneven high-density hemorrhage on the background of low-density infarction. Unlike hematoma, its density is not as high as hematoma, and it is not as uniform as a hematoma.
2. MRI performance:
After 1 hour of cerebral ischemia, the water content of brain tissue can increase, which causes changes in MRI signals. MRI shows that cerebral infarction is superior to CT. Ischemia mainly affects the T1 and T2 relaxation times, ie both are prolonged. In the early stage of ischemia, a large number of water molecules accumulate, and the leakage of macromolecular substances with the blood-brain barrier has not yet occurred, and the prolongation of T1 and T2 is most obvious. At this time, on the T1-weighted image, the ischemic region is a low signal and the T2-weighted image is a high signal. T2-weighted images are more sensitive to showing infarction. With the development of infarction, vasogenic edema begins to occur and protein infiltrates into the ischemic area, so the elongation of Tl and TZ is not as long as in the early stage, which affects the change of signal intensity. MRI is important for the detection of cerebral infarction in the early posterior fossa. Because CT examination often has artifacts and the effect is not good, and early treatment is closely related to prognosis.
MRI is very sensitive to subacute hemorrhage in the infarct zone, T1 weighted image in the T of the original cerebral infarction; a thin high signal zone appears in the weighted signal reduction zone, and the T2 weighting shows a uniform high signal intensity change. The development of cerebral infarction is as follows: the mass effect disappears, then shrinks and leaves a softening foci. The softening lesion showed a prolonged relaxation of T1 and T2. T1 showed a low signal and T2 showed a high signal. Compared with the acute cerebral infarction, the edge of the brain softening lesion was clearer.
Diagnosis
Differential diagnosis
Thrombosis should be distinguished from the following symptoms
Brain abscess: healthy brain tissue has certain resistance to bacteria. Experiments have shown that inoculation of pathogenic bacteria into the brain is difficult to cause brain abscess. Brain damage, brain tissue necrosis caused by infarction, and postoperative residual dead space are beneficial to the formation of brain abscess. Most of the brain abscesses are secondary to extracranial infections, and a small number of cases are caused by open brain injury or post-craniotomy infection.
Brain abscess refers to the formation of purulent encephalitis, chronic granuloma and brain abscess caused by purulent bacterial infection, and a small part can also be caused by fungal and protozoal invasion into brain tissue.
