Vascular hemichorea: a rare presentation of lacunar infarction. Residente de Medicina Interna. Cecilia Botta. Postgrado de Medicina Interna. Ex Residente de Medicina Interna. Elizabeth Marchissio.

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Become a Radiopaedia Supporter and go Ad-Free. Ischaemic stroke results from a sudden cessation of adequate amounts of blood reaching parts of the brain. Ischaemic 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 ischaemic stroke largely mirror the risk factors for atherosclerosis and include age, gender, family history, smoking, hypertension, hypercholesterolaemia, and diabetes mellitus.

An ischaemic 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 ischaemic penumbra.

The vascular territory affected will determine the exact symptoms and clinical behaviour of the lesion:. Interruption of blood flow through an intracranial artery leads to deprivation of oxygen and glucose in the supplied vascular territory. This initiates a cascade of events 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.

Ageing ischaemic 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. For the purposes of this article the following definitions are used 10 :. Non-contrast CT of the brain remains the mainstay of imaging in the setting of an acute stroke.

It is fast, inexpensive and readily available. Its main limitation, 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. Non-contrast CT has also been used historically to exclude patients from receiving thrombolysis based on the extent of hypoattenuation at presentation.

This criterion has, however, been removed from the American Heart Association guidelines Nonetheless, finding large areas of established infarction on acute non-contrast CT continues to play an important role in patient selection and management.

It may be of therapeutic and prognostic value to differentiate this hyperdense 'regular' thromboembolic focus 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. Early features include:. 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 time goes on the swelling starts to subside and small amounts of cortical petechial haemorrhages not to be confused with haemorrhagic 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 ischaemic 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 ischaemic 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. See CT perfusion. 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 ischaemic and infarct tissue. MRI is more time consuming and less available than CT but has significantly higher sensitivity and specificity in the diagnosis of acute ischaemic 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, At this stage, the affected parenchyma appears normal on other sequences, although changes in flow 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 increase over the next day or two. During the first week, the infarcted parenchyma continues to demonstrate high DWI signal and low ADC 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 Haemorrhage, most easily seen on susceptibility weighted imaging SWI , is 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 normal 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 weeks 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. Often described as an emerging application of point-of-care ultrasonography , the use of transcranial Doppler TCD sonography has been utilised for the diagnosis of intracranial vessel occlusion, as well as the differentiation between ischaemic and haemorrhagic stroke In the context of a CT negative for intracerebral haemorrhage and a clinically suspicious patient presentation, diagnostic criteria for occlusion of an insonated vessel are as follows 12 ;.

Sonographic monitoring of the complications of ischaemic stroke is also possible, including the detection of;. In the past treatment for ischaemic stroke was supportive, and the earliest improvements in patient outcome were in dedicated stroke unit care and attempt at preventing the numerous complications which are encountered by patients with neurological impairment e.

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.

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Once your system installs this update, you will not be able to upload new images. Please use another browser until we can get it fixed. On this page:. Quiz questions. Robbins and Cotran Pathologic Basis of Disease. Saunders Company. Read it at Google Books - Find it at Amazon. Edit article Share article View revision history Report problem with Article. URL of Article. Article information. Systems: Central Nervous System , Vascular.

Cases and figures. Case 1: "stroke" window Case 1: "stroke" window. Case 2 Case 2. Case 3: pontine Case 3: pontine. Case 4: haemorrhagic cerebral infarction Case 4: haemorrhagic cerebral infarction. Case 5 Case 5. Case 8: pontine infarct Case 8: pontine infarct. Case left thalamic lacunar infarct Case left thalamic lacunar infarct. Case acute midbrain infarction Case acute midbrain infarction. Case 15 Case


Brain Ischemia - Vascular territories

Lacunar stroke or lacunar infarct LACI is the most common type of ischaemic stroke , resulting from the occlusion of small penetrating arteries that provide blood to the brain's deep structures. Patients who present with symptoms of a lacunar stroke, but who have not yet had diagnostic imaging performed, may be described as suffering from lacunar stroke syndrome LACS. Much of the current knowledge of lacunar strokes comes from C. Miller Fisher 's cadaver dissections of post-mortem stroke patients.


Lacunar stroke

Notice the posterior extention. The infarction was the result of a dissection blue arrow. In unilateral infarcts there is always a sharp delineation in the midline because the superior vermian branches do not cross the midline, but have a sagittal course. This sharp delineation may not be evident until the late phase of infarction. In the early phase, edema may cross the midline and create diagnostic difficulties. Infarctions at pontine level are usually paramedian and sharply defined because the branches of the basilar arery have a sagittal course and do not cross the midline.



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