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15.03.12 КТ головного мозга. И снова консультация!!!!

Уважаемые коллеги, снова нужна ваша помощь!  Ребенок не из нашей больницы, анамнез, как обычно, скудный. Мальчик, 3 года. В конце февраля была лакунарная ангина, в начале марта повторное повышение температуры, на фоне лихорадки - судороги. Сейчас слабость в правой верхней конечности. Анализ ликвора - повышение белка, цитоза нет. Контрастирование от руки.

 

                                                          натив                                                                         с контрастом

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 Гиральное накопление. Ой, я

 Гиральное накопление. Ой, я совсем в этом мало понимаю, Оля, но не может быть проявлением коркового энцефалита?

 
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Gyral Enhancement Superficial

Gyral Enhancement

Superficial enhancement of the brain parenchyma is usually caused by vascular or inflammatory processes and is only rarely neoplastic (Fig 11). Vascular causes of serpentine (gyral) enhancement include vasodilatation after reperfusion of ischemic brain, the vasodilatation phase of migraine headache, posterior reversible encephalopathy syndrome (PRES), and vasodilatation with seizures (1921). Serpentine enhancement from breakdown of the blood-brain barrier is most often seen in acutely reperfused cerebral infarction, subacute cerebral infarction, PRES, meningitis, and encephalitis. The primary distinction between vascular and inflammatory causes of the serpentine pattern of enhancement relies on correlation with clinical history and the region of enhancement. An abrupt onset of symptoms suggests a vascular cause, whereas a more indolent history and nonspecific headache or lethargy suggests inflammation or infection. Gyral lesions affecting a single artery territory are often vascular, whereas inflammatory lesions may affect multiple territories. The most common vascular processes affect the middle cerebral artery territory (up to 60% of cases). However, PRES lesions usually localize in the posterior cerebral artery territory (2127).

Figure 11a.  Cortical gyral enhancement. (a) Diagram illustrates gyral enhancement that is localized to the superficial gray matter of the cerebral cortex. There is no enhancement of the arachnoid, and none in the subarachnoid space or sulci. (b) Coronal gadolinium-enhanced T1-weighted MR image in a case of herpes encephalitis shows multifocal, intraaxial, curvilinear, cortical gyri-form enhancement that involves both temporal lobes. The enhancement is most prominent on the right but is also seen in the left insular region (arrows) as well as in the medial frontal lobes and cingulate gyrus (arrowhead).

Figure 11b.  Cortical gyral enhancement. (a) Diagram illustrates gyral enhancement that is localized to the superficial gray matter of the cerebral cortex. There is no enhancement of the arachnoid, and none in the subarachnoid space or sulci. (b) Coronal gadolinium-enhanced T1-weighted MR image in a case of herpes encephalitis shows multifocal, intraaxial, curvilinear, cortical gyri-form enhancement that involves both temporal lobes. The enhancement is most prominent on the right but is also seen in the left insular region (arrows) as well as in the medial frontal lobes and cingulate gyrus (arrowhead).

Herpes virus encephalitis produces superficial gray matter disease, changing signal intensity, and a breakdown of the blood-brain barrier to produce contrast enhancement in a cortical gyral pattern. Herpes encephalitis most often begins in the medial temporal lobes (uncus) and in the cingulate gyrus of the medial frontal and parietal lobes (Fig 11) (2224,28). Pathologic specimens often show petechial hemorrhage and inflammation in these same locations (Fig 12). The lesion distribution is consistent with the hypothesis that herpes virus infection follows the olfactory pathways from the nasal cavity into the brain. The corticalgyral enhancement in herpes encephalitis may lag behind the onset of signs and symptoms and may be suppressed by steroid medications; thus, the absence of enhancement does not exclude encephalitis.

Figure 12.  Herpes encephalitis. Photograph of a coronally sectioned gross specimen shows multiple petechial hemorrhages (arrowheads) and some granular atrophy of the insular cortex and the undersurface and medial temporal lobe. Scale is in centimeters.

Vascular gyral enhancement results from various mechanisms with variable time courses. The earliest enhancement can be caused by reversible blood-brain barrier changes when ischemia lasts for only several hours before reperfusion occurs (25,2931). Early reperfusion may also produce vasodilatation, with increased blood volume and shortened mean transit time. These features were first observed at conventional angiography; they were described as dynamic changes and were called “luxury perfusion” because of the increased blood flow (32). The increased blood flow is caused by autoregulation mechanisms, which are “tricked” by the increased tissue PCO2 that accumulates before reperfusion occurs. Ischemia or infarction may demonstrate gyral enhancement on both CT and MR images within minutes (with early reperfusion) (Fig 13). In the healing phases of cerebral infarction, from several days (5–7 days) to several weeks after the event, there will be vascular proliferation or hypertrophy (Fig 14). Contrast enhancement usually fades away between 4 weeks and 4 months after the stroke, and enhancement is usually replaced by brain volume loss (33). The vascular changes facilitate the breakdown and removal of the dead brain tissue and lead to the encephalomalacia and atrophy characteristic of old “healed” infarction. The imaging appearance of postictal states may mimic the findings of cerebral infarction in several features, including gyral swelling, increased signal intensity on T2-weighted images and decreased signal intensity on T1-weighted images, sulcal effacement, and gyral enhancement (21). Reperfusion, whether acute (eg, after thrombolysis) or subacute to chronic (“healing” infarction), is required to deliver contrast material to produce enhancement.

Figure 13a.  Cortical gyral enhancement in embolic cerebral infarction in a 65-year-old woman. (a) On an axial nonenhanced CT scan, the sulci in the right hemisphere are normally prominent; on the left, the parietal sulci are effaced within a wedge-shaped region of abnormal hypoattenuation. The gyral surface is actually slightly hyperattenuating due to reperfusion injury with secondary petechial hemorrhage in the infarcted cortex. (b) Axial contrast-enhanced CT scan shows cortical gyral enhancement. The same endothelial damage that allows red cells to extravasate also permits contrast material to escape the vascular lumen and enter the brain parenchyma.

Figure 13b.  Cortical gyral enhancement in embolic cerebral infarction in a 65-year-old woman. (a) On an axial nonenhanced CT scan, the sulci in the right hemisphere are normally prominent; on the left, the parietal sulci are effaced within a wedge-shaped region of abnormal hypoattenuation. The gyral surface is actually slightly hyperattenuating due to reperfusion injury with secondary petechial hemorrhage in the infarcted cortex. (b) Axial contrast-enhanced CT scan shows cortical gyral enhancement. The same endothelial damage that allows red cells to extravasate also permits contrast material to escape the vascular lumen and enter the brain parenchyma.

Figure 14a.  Cortical gyral enhancement in subacute thrombotic cerebral infarction. (a) Axial contrast-enhanced CT scan shows enhancement that is limited to the opercular surfaces, insula, and caudate nucleus head (all of which are gray matter). (b) Photograph of an axially sectioned gross specimen shows green staining, which is caused by bilirubin bound to serum albumin, and which outlines areas of the brain where the blood-brain-barrier is no longer intact. Note how the green stain is almost exclusively in the gray matter of the cortex (arrowheads), basal ganglia (*), caudate nucleus, and claustrum. In these areas, the healing process would have removed the infarcted tissue, resulting in encephalomalacia and atrophy, if the patient had not died (the jaundiced patient died 2 weeks after left internal carotid thrombosis caused infarction of the anterior and middle cerebral artery territories).

Figure 14b.

  Cortical gyral enhancement in subacute thrombotic cerebral infarction.

(a)

Axial contrast-enhanced CT scan shows enhancement that is limited to the opercular surfaces, insula, and caudate nucleus head (all of which are gray matter).

(b)

Photograph of an axially sectioned gross specimen shows green staining, which is caused by bilirubin bound to serum albumin, and which outlines areas of the brain where the blood-brain-barrier is no longer intact. Note how the green stain is almost exclusively in the gray matter of the cortex (arrowheads), basal ganglia (*), caudate nucleus, and claustrum. In these areas, the healing process would have removed the infarcted tissue, resulting in encephalomalacia and atrophy, if the patient had not died (the jaundiced patient died 2 weeks after left internal carotid thrombosis caused infarction of the anterior and middle cerebral artery territories).

 
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 Значит, исходя из анамнеза и

 Значит, исходя из анамнеза и "долгого" развития - воспаление.

 
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  Спасибо за ценную

 

Спасибо за ценную информацию! Да, я тоже написала о гиральном накоплении контраста. В заключении  - дифференцировать между  ангиоматозом и менингоэнцефалитом. Про ишемию думала, но такая площадь поражения у меня не уложилась в ишемию определенного сосудистого бассейна. А ведь если септическая ишемия, то могут быть разные бассейны?  И еще подскажите, как расценить участок повышения плотности на 7 сверху скане на нативе (рядом с задним рогом левого желудочка), как кровоизлияние или другое? 

 
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как кровоизлияние

как кровоизлияние

 
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 Мне кажется, что Оля

 Мне кажется, что Оля наиболее близка к истине. Ангиоматоз Штурге-Вебера не исключал бы, т.к. до контраста есть линейные участки повышения  плотности в коре, а характер усиления местами напоминает сосуды. Менингоэнцефалит или септическая ишемия подходят несколько больше. Участок повышенной плотности позади левого бокового желудочка не похож на кровь, ведь нет других признаков кровоизлияния и этот участок еще усиливается. Ведь повышенная плотность может бы при ишемии и воспалении в зонах гиперперфузии, полнокровия, что соответствует гиральному или узловому паренхиматозному типу контрастного усиления. Также обратите внимание, что в коре есть участки более повышенной плотности, чем позади желудочка, а изображения мозга достаточно шумные, что может давать ошибочное ощущение патологических участков повышенной плотности. То есть, я не согласен с нашим Кормчим - Марио ! ;)

 
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А я согласен с вашим не

А я согласен с вашим не согласием. Мы вчера разобрали немного это наблюдение в чате. 

 
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 Битва Титанов?!  

 Битва Титанов?!   Аргументируйте, плиз! (двойной умаляющий смайлик)

 
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Описывать скиалогию не буду,

Описывать скиалогию не буду, седьмой луч все описал. В чате я высказался за сосудистый генез феномена; такая презентация гиперденсности и гиперконтрастирования борозд описана при васкулитах (ангиит мелких ветвей), ангиоматоза, даже после приступа судорог (см. ниже). Сошлись на том что надо делать контроль КТ (а лучше МРТ), если нет развития клиники энцефалита.

Дифференциальный ряд gyral hyperdensities/contrast enhancement:

 

GYRAL ENHANCEMENT:
* Ischemia/Infarction (incl. seizures, migraines, etc.)
* Cerebritis/Encephalitis (e.g. Herpes)
Meningeal carcinomatosis (carcinomatous meningitis)
Meningitis - chronic > acute
AVM
Cortical vein thrombosis
Lymphoma
Meningioangiomatosis (NF2)

COMMENT: Sturge-Weber will be dense without contrast due to tram track calcification in cortex underlying a meningeal venous angioma

Наблюдение гиперденсного кортекса после судорог:

Hyperdensity on CT After Seizure: A Pitfall

  1. I. Hussain Bangash, MRCP

    1. Department of Pediatrics, Division of Pediatric Neurology Duke University Medical Center, Durham, NC
  1. Raymond S. Kandt, MD

    1. Department of Pediatrics, Division of Pediatric Neurology Duke University Medical Center, Durham, NC
  1. Bernard J. D'Souza, MD

    1. Department of Pediatrics, Division of Pediatric Neurology Duke University Medical Center, Durham, NC
  1. Ralph Heinz, MD

    1. Department of Radiology Duke University Medical Center, Durham, NC

Abstract

A 12-year-old boy had a hyperdense area corresponding to a gyral pattern on an enhanced CT brain scan within 12 hours of his last seizure. The hyperdense area disappeared on a subsequent enhanced CT scan after he was seizure free for about 48 hours. The hyperdense area was in a location (mesial frontal lobe) predicted by the interictal physical exam findings and the seizure type recorded on video-EEG monitoring. We postulate that the CT abnormality was due to transitory increase of regional cerebral blood flow and vascular permeability. (J Child Neurol 1987;2:276-278).

 
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 Большой пасиб! Книксен!

 Большой пасиб! Книксен!

 
 

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