ACV LACUNAR PDF
PDF | Reportamos el caso de un paciente con enfermedad diabética tipo 1 que sufrió un ACV isquémico lacunar talámico derecho y. A watershed stroke or watershed infarct is defined as a brain ischemia that is localized to the . as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct ( POCI). A stroke is a medical condition in which poor blood flow to the brain results in cell death. .. This subset of cryptogenetic stroke is defined as a non-lacunar brain infarct without proximal arterial stenosis or cardioembolic sources. About one out of.
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Ischemic stroke results from a sudden cessation of adequate amounts of blood reaching parts of the brain. Ischemic strokes can be divided according to territory affected or mechanism.
Stroke is the second most common cause of morbidity worldwide after myocardial infarction and is the leading cause of acquired disability 2. Risk factors for ischemic stroke largely mirror ac risk factors for atherosclerosis and include age, gender, family history, lxcunar, hypertension, hypercholesterolaemia, and diabetes mellitus.
An ischemic stroke typically presents with rapid onset neurological deficit, which is determined by the area of the brain that is involved. The symptoms often evolve over hours, and may worsen or improve, depending on the fate of the ischemic penumbra.
The vascular territory affected will determine exact symptoms and clinical behavior of the lesion:. Interruption of blood flow through an intracranial artery leads to lcaunar of oxygen and glucose in the supplied vascular territory.
This initiates a cascade of lacunzr at a cellular level which, if circulation is not re-established in time, will lead to cell death, mostly through liquefactive necrosis. The mechanism of vessel obstruction is important in addressing therapeutic manoeuvres to both attempt to reverse or minimise the effects and to prevent future infarcts. Global cerebral hypoxia as is seen in drowning or asphyxiation is, usually, considered separately.
In many institutions with active stroke services which provide reperfusion therapies a so-called code stroke aimed at expediting diagnosis and treatment of patients will include a non-contrast CT brain, CT perfusion and CT angiography. Aging ischemic strokes can be important in a number of clinical and medicolegal settings. Both CT and MRI can help in determining when a stroke occurred as imaging features evolve in a reasonably predictable fashion. There is substantial heterogeneity in the terminology denoting time from onset.
Lacuar the purposes of this article the following definitions are used Non-contrast CT of the brain remains the mainstay of imaging avc the setting of an acute stroke. It is fast, inexpensive and readily available. Its main kacunar, however, is the limited sensitivity in the acute setting.
Detection depends on the territory, the experience of the interpreting radiologist and of course the time of the scan from the onset of symptoms. Whether tissue is supplied by end arteries e. It may be of therapeutic and prognostic value to differentiate this hyperdense ‘regular’ thromboembolus from a calcified cerebral embolus.
Within the first few hours, a number of signs are visible depending on the site of occlusion and the presence of collateral flow. With time the hypoattenuation and swelling become more marked resulting in a significant mass effect. This is a major cause of secondary damage in large infarcts.
As lacujar goes on the swelling starts to subside and small amounts of cortical petechial hemorrhages not to be confused with hemorrhagic transformation result in elevation of the attenuation of the cortex. This is known as the CT fogging phenomenon 5. Imaging a stroke at this time can be misleading as the affected cortex will appear near normal. Later still the residual swelling passes, and gliosis sets in eventually appearing as a region of low density with negative mass effect.
Cortical mineralisation can also sometimes be seen appearing hyperdense. CT perfusion has emerged as a critical tool in selecting patients for reperfusion therapy as well as increasing the accurate diagnosis of ischemic stroke among non-expert readers four-fold compared to routine non-contrast CT 9. It allows both the core of the infarct that part destined to never recover regardless of reperfusion to be identified as well as the surrounding penumbra the region which although ischemic has yet to go on to infarct and can be potentially salvaged.
CT perfusion may also demonstrate early evidence of associated crossed cerebellar diaschisis. These factors will be discussed further separately. Multiphase or delayed CT angiography is showing benefit either replacing CT perfusion or as an additional 4th step in the stroke CT protocol as it guides patient selection for endovascular therapy by assessing collateral blood flow in the ischemic and infarct tissue.
MRI is more lacujar consuming and less available than CT but has significantly higher sensitivity and specificity in the diagnosis of acute ischemic infarction in the first few hours after onset.
Within minutes of arterial occlusion, diffusion weighted imaging demonstrates increased DWI signal and reduced ADC values 4, Lacunaf this stage, the affected parenchyma appears normal on other sequences, although changes in ac will be detected occlusion on MRA and the thromboembolism may be detected e. If infarction is incomplete then cortical contrast enhancement may be seen as early as 2 to 4 hours This change continues to lachnar over the next day or two. During the first week, the infarcted parenchyma continues to demonstrate high DWI signal and low ACS signal, although by the end of the first week ADC values have started to increase.
T1 signal remains low, although some cortical intrinsic high T1 signal may be seen as early as 3 days after infarction Less common patterns of enhancement include arterial enhancement, encountered in approximately half of strokes and becomes evident after 3 days, and meningeal enhancement which is uncommon and is usually seen between 2 and 6 days Hemorrhage, most easily seen on susceptibility weighted imaging SWIis not a good indicator of age.
Although most commonly seen after 12 hours and within the first few days, it may occur earlier or as late as 5 days ADC demonstrates pseudonormalisation typically occurring between days As ADC values continue to rise, infarcted tissue progressively gets brighter than lacunarr parenchyma.
T2 fogging is also encountered typically between 1 and 5 weeks, most commonly around week 2 10, Cortical enhancement is usually present throughout the subacute period. T1 signal remains low with intrinsic high T1 in the cortex if cortical necrosis is present T2 signal is high.
Cortical contrast enhancement usually persists for 2 to 4 months Importantly if parenchymal enhancement persists for more than 12 week the presence of an underlying lesion should be considered ADC values are high, resulting in high signal. DWI signal is variable, but as time goes on signal progressively decreases. In the past treatment for ischemic stroke was supportive, and the earliest improvements in patient outcome were in dedicated stroke unit care and attempts at preventing the numerous complications which are encountered by patients with neurological impairment e.
Stroke – Wikipedia
Neurosurgical intervention can also allow patients to survive the period of maximal swelling by performing decompressive craniectomies with or without duroplasty. Regardless of the therapy, early presentation and triage are essential if any outcome gains are to be had. To quiz yourself acc this article, log in to see multiple choice questions. You can also scroll through stacks with your mouse wheel or the keyboard arrow keys.
Unable to process the form. Check for errors and try again. Thank you for updating your details. Log in Sign up. Articles Cases Courses Quiz. About Blog Go ad-free. Ischemic stroke Dr Rohit Sharma lqcunar A.
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