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Head emergencies (Cerebral infarction (diminished blood flow which causes…
Head emergencies
Cerebral infarction
- diminished blood flow which causes irreversible damage of ischemic zone
- Main mechanisms include:
vessels occlusion (predominantly of atheromatosus origin)
embolism (due to myocardial infarction, valvular disease, cardiomyopathy)
arterial spam (in the course of subarachnoid hemorrhage)
- Depending on age: acute, subacute, chronic
- Another classification:
ischemic infarction (80%), hemorrhage
- STROKE is the clinical presentation of cerebral infarction.
- symptoms loss of: consciousness, muscle strength, feeling, speech, vision, other functions controlled by affected region
- CT:
within the first 12 hours are normal.
hyperdense artery sign
loss of outline of cortical sulci
loss of gray-white matter interfaces (obscuration of cortex-white matter border)
after 24 h – wedge-shaped low density area involving gray and white matter, confined to one vascular territory
mass effect is observed – compression of the adjacent structures (especially lateral ventricle) due to volume increase, contralateral midline shift and effacement of the sulci on the affected side
hemorrhagic transformation may occur (hyperdense foci)
- CT in subacute/chronic stage:
-after few days gyral enhancement after iv CM injection (CM is not administered routinely in patients with cerebral infarct)
-in chronic stage :
mass effect and contrast ehhancement disappear
marked hypodensity in the territory of the infarct
volume loss – increased size of ventricle and sulci adjacent to infarction
- MRI:
more sensitive than CT
more precisely depicts acute infarct
on T1WI:
-loss of gray-white matter interfaces
-gyral edema
-sulcal effacement
-contrast enhancement
on T2WI: high signal
mass effect
in chronic stage: mass effect and contrast enhancement disappear, area of infarct presents signal similar to CSF
- Diffusion-Weighted Imaging (DWI):
functional MR reflects diffusion of water molecules in the tissues (extracellular & extravascular)
used for microscopic movement of water molecules known as brownian motions
man value is to detect the region of restricted diffusion
provides: qualitative evaluation ---- DW images
quantitive evaluation ---- ADC map
Intracranial hemorrhage
- causes: Trauma, Arterial hypertension, Hemorrhagic infarction, Aneurysms and vascular malformations, Intratumoral hemorrhage (hemorrhagic focus within tumor makes difficult differetiation between neoplasm and hematoma), Perinatal hemorrhage (premature neonates)
- Location:
Parenchymal (predominantly caused by arterial hypertension, in those cases basal ganglia and thalamus are preferentially involved)
Subarachnoid (caused by bleeding from ruptured aneurysm, vascular malformation, traumatic origin- uncommon)
Subdural or epidural (mainly of traumatic origin)
- CT:
high density lesion
surrounding edema (peripheral hypodense zone)
mass effect
may rupture into the ventricular system
within a few weeks – density gradually decreases
- MRI:
used to visualize cerebral hematomas in subacute/chronic stage if CT findings are not typical
typical high signal of extracellular methemoglobin in subacute/early chronic hematomas (T1-, T2WI)
low signal of hemosiderin in chronic hematomas (especially on T2WI)
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Craniocerebral Trauma
Extracerebral hemorrhage
Epidural hematoma (EDH)
- Etiology: A fracture causes laceration of middle meningeal artery (90%) or dural venous sinus (10%)
- Location: between the inner skull and the dura, tends not to cross suture lines
95% supratentorial (frontotemporal, frontoparietal area)
5% posterior fossa
5% bilateral
IMAGING
- CT:
non-contrast CT is the study of choice
biconvex-shaped (lentiform) extracerebral mass,
2/3 hyperedense, 1/3 mixed:hyper/hypodense
in chronic stage – the density decreases
the brain adjacent to EDH is flat and displaced
- MRI:
intensity depends on age
ACUTE EDH- isointense on T1WI, hyperintense on T2WI,
SUBACUTE and EARLY CHRONIC EDH (6-21 days)- hyperintense on T1- and T2WI (high signal of extracellular methemoglobin)
CHRONIC EDH- hypointense on T1- and T2WI (low signal of hemosiderin)
Subdural hematoma (SDH)
- Etiology: tearing of cortical veins
- Location: between dura and arachnoid, can cross sutures
95% supratentorial (frontoparietal area, convexity, middle fossa)
15% bilateral
IMAGING
- CT:
crescentic extracerebral mass
acute SDH - 2/3 hyperdense, 1/3 mixed: hyper/hypodense
in subacute stage - may be nearly isodense with underlying cortex
in chronic stage - hypodense
- MRI: appearance of SDH varies with clot age (like in EDH)
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Intraaxial lesions
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Cortical contusions
- punctate or linear hemorrhages that occur along gyral area.
- Etiology: brain striking on an osseous ridge or dural fold, may also be associated with a depressed skull fracture.
- Location:
frontal and temporal lobes
cortex around Sylvian fissure
parasagittal region
- CT:
initial findings may be subtle or absent,
early findings: low density lesions, often mixed with hyperdense foci of hemorrhage,
24-48 h after injury CT reveals more lesions than on initial scans.
- MRI: more sensitive than CT in detecting cortical contusions
hyperintense foci on T2WI are seen,
hyperintense lesions on T1WI are identified as hemorrhagic foci
Brainstem injury
- Etiology: forces that cause disruption of small perforating blood vessels
- CT: often normal, sometimes hemorrhagic foci in dorsolateral part of brainstem are revealed
- MRI: more sensitive than CT, should be method of choice in assessment of brainstem lesions
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- Imaging of emergencies concerning Central Nervous System is based on:
-Plain film: if fracture is suspected and no signs of brain damage are observed
-CT: short time, high sensitivity in detection of acute bleeding, good demonstration of bony injury
-MRI: not used in „acute cases”, acute blood poorly visible
-DSA: to detect the source of intracranial hemorrhage
- Emergencies and life-threatening conditions concerning the brain:
Craniocerebral Trauma
Cerebral infarction
Intracranial hemorrhage
Intracranial hypertension
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