Teaching Plan Name:Yu Guang-hui Academic Year:2012-2013 Term:2 Date:2013.4.1 Period:5-6 Textbook Radiology Saution (international students) Content CNS3 Teaching hours 2 Objectives To introduce Cerebrovascular Diseases Key points CT&MRI imaging Points difficult to understand Content for self study CT、MRI anatomy Teaching multimedia Related knowledge Medical imaging technique,anatomy,pathology,medicine,surgery Teaching methods Heuristic method ldiscuss Outlines requirements and time allocation intracerebral haematoma A hematoma is the inevitable consequence of the rupture of a blood5min vessel,either artery,vein or capillary Classical intracerebral hematoma results from rupture of the periphera lenticulostriate arteries in the region of the extemal capsule The typical clinical presentation is of a sudden fulminating headache. hemiplegia and impairment of consciousness deepening into coma An intracerebral haematoma is considered acute within the first few days 10min Subacute haematoma is usually between a week and a fortnight old After two weeks it is considered to be chronic The density or signal characteristics of the haematoma examined with 15min CT or MR respectively vary with the age of the haematoma Evolution of hematoma and intensity of MRI 10min
Teaching Plan Name: Yu Guang-hui Academic Year: 2012-2013 Term: 2 Date: 2013.4.1 Period: 5-6 Textbook Radiology Specialty and Stratification 2010MBBSAutumn (international students) Content CNS3 Teaching hours 2 Objectives To introduce Cerebrovascular Diseases Key points CT&MRI imaging Points difficult to understand Basic patterns of abnormalities Content for self study CT、MRI anatomy Teaching equipment multimedia Related knowledge Medical imaging technique, anatomy, pathology, medicine, surgery Teaching methods Heuristic method \discuss Outlines, requirements and time allocation intracerebral haematoma ⚫ A hematoma is the inevitable consequence of the rupture of a blood vessel, either artery, vein or capillary ⚫ Classical intracerebral hematoma results from rupture of the peripheral lenticulostriate arteries in the region of the external capsule ⚫ The typical clinical presentation is of a sudden fulminating headache, hemiplegia and impairment of consciousness deepening into coma ⚫ An intracerebral haematoma is considered acute within the first few days Subacute haematoma is usually between a week and a fortnight old ⚫ After two weeks it is considered to be chronic ⚫ The density or signal characteristics of the haematoma examined with CT or MR respectively vary with the age of the haematoma ⚫ Evolution of hematoma and intensity of MRI 5min 10min 15min 10min
TIWI T2WI ferrohemoglobin iso- iso- ferrohemoglobin iso- hypo- methemoglobin akaryocyte hyper- hypo- membranolysis hyper hyper- hemosiderin hypo- hypo- Cerebral Infarction The main causes of infarction are atherosclerotic occlusion of large vessels 5min embolic occlusion ofdistal vessels,vasculitis and arterial spasm The common clinical presentation is stroke The role of immediate CT is two-fold:diagnose or exclude any other cause 10min mainly haemorhage and to recognize the extent of ischemia Three phases may be identified:acute,subacute and chronic 10min In the acute%of scans may be considered normal within the first few hours Some subtle early signs may be detected 10min A.loss of grey-white matter interface B.obscuration of the lentiform nucleus C.hyperdensity of the middle cerebral artery In about 15-20%of cases hemorrhagic foci detected after 24-48 hours On 10min MRI Less than2 hours,amostno abnomalities are seen except amid thickening of the cortex DWI The cortico-subcortical reduced diffusion is well seen T2WI 12 hours later Hyperintensity in the infarcted area,due tocytotoxicedema
T1WI T2WI ferrohemoglobin iso- isoferrohemoglobin iso- hypomethemoglobin akaryocyte hyper- hypomembranolysis hyper- hyperhemosiderin hypo- hypoCerebral Infarction ⚫ The main causes of infarction are atherosclerotic occlusion of large vessels, embolic occlusion of distal vessels, vasculitis and arterial spasm ⚫ The common clinical presentation is stroke ⚫ The role of immediate CT is two -fold: diagnose or exclude any other cause , mainly haemorrhage ; and to recognize the extent of ischemia ⚫ Three phases may be identified: acute, subacute and chronic ⚫ In the acute phase :about 60% of scans may be considered normal within the first few hours ⚫ Some subtle early signs may be detected : A．loss of grey-white matter interface B．obscuration of the lentiform nucleus C．hyperdensity of the middle cerebral artery ⚫ In about 15-20% of cases hemorrhagic foci detected after 24-48 hours On MRI ⚫ Less than 2 hours，almost no abnormalities are seen except a mild thickening of the cortex ⚫ DWI The cortico-subcortical reduced diffusion is well seen ⚫ T2WI 12 hours later Hyperintensity in the infarcted area, due tocytotoxic edema 5min 10min 10min 10min 10min
Carotid cavernous aneurysm 15min Develops within the dural outpouching of the cavemous sinus Most frequently aneurysms reach a significant size and become large or giant The clinical presentation is that of a cavemous sinus syndrome with involvement of the oculomotor nerves,diplopia and trigeminal neuralgia CT and MRI show a space-occupying lesion in the parasellar region .On CT the lesion is usually isointense and enhances following contrast injection .On MRI shows the flow void of circulating blood,thus reducing the differential diagnostic problems.Thrombosed components with paramagnetic signals such as T2 shortening of hemosiderin and T1 shortening of methemoglobin are easily seen Cerebral angiography remains the gold standard and when performed it should aim at verifying cross-collateral circulation following compression of the affected carotid as well as tolerance of occlusion.Development of intracranial stents will probably allow preservation of the parent artery
Carotid cavernous aneurysm ⚫ Develops within the dural outpouching of the cavernous sinus ⚫ Most frequently aneurysms reach a significant size and become large or giant ⚫ The clinical presentation is that of a cavernous sinus syndrome with involvement of the oculomotor nerves, diplopia and trigeminal neuralgia ⚫ CT and MRI show a space-occupying lesion in the parasellar region ⚫ On CT the lesion is usually isointense and enhances following contrast injection ⚫ On MRI shows the flow void of circulating blood, thus reducing the differential diagnostic problems. Thrombosed components with paramagnetic signals such as T2 shortening of hemosiderin and T1 shortening of methemoglobin are easily seen Cerebral angiography remains the gold standard and when performed it should aim at verifying cross-collateral circulation following compression of the affected carotid as well as tolerance of occlusion. Development of intracranial stents will probably allow preservation of the parent artery. 15min