Case of a 2 days old neonate with bilateral subdural hematomas, mainly infratentorial. Note high signal on the coronal T1, low on GRE, high signal with level on T2 and same level on T1 sequences. Signal characteristics represent early subacute hematomas with methemoglobin still in the red blood cells. I would like to use this case as a reminder of signal changes of intracranial hematomas on MRI.
The table above shows how we stage (name) hematomas according to time. Important observation is that the very early (hyperacute) hematomas contain Oxyhemoglobin and are difficult to see (isodense to brain) on T1 sequences. Same with Deoxyhemoglobin. Then after about 3 days we start to see high signal of Methemoglobin on T1. That continues to be high on T1 even when Methemoglobin is released from the hemolyzed Red Blood Cells, but then we start to see it as high even on T2. Late remains of the hemorrhage on MR can be seen as a rim of Hemosiderin deposits - that is just black. Gradient Echo (T2*) (GRE) sequences show hemorrhage as black since it is a sort of susceptibility artefact. It also exaggerates the volume of bleeding ("blooming artefact").
You may also check:
Neonatal Intraventricular Hemorrhage
Hemorrhagic Choroid Plexus Cyst
Late Subacute Hemorrhage on DWI
Hemorrhagic Brain Metastases
23 December 2010
10 December 2010
Oculomotor Infarct
This 40 years old patient has experienced acute oculomotor nerve paresis. A 1.5T MRI has revealed a micro infarct (about 2mm) in location of the oculomotor nerve nucleus in the mesencephalon. Note high signal on DWI (B1000), low signal on ADC and high on T2 (B0) of the Diffusion Weighted Images (DWI) and coronal FLAIR. This case illustrates how sensitive can DWI be even in small infarcts.
Above drawing courtesy of Bartleby.
Fig. 710 Anatomy of the Human Body by Henry Gray
This is also a great opportunity to remind the location of the oculomotor nerve nucleus in mesencephalon (8'). Note that mesencephalon here is "facing down" compared to MRI. Well seen structures on the MRI are Red Nucleus, Substantia Nigra and Cerebral Aqueduct.

Cranial Nerves Nuclei
Drawing titled: Brain stem human sagittal section - by Patrick J. Lynch, medical illustrator
Courtesy Wikipedia
Also note location of the other Cranial Nerves Nuclei in the brainstem that are nicely depicted in the above drawing.
Above drawing courtesy of Bartleby.
Fig. 710 Anatomy of the Human Body by Henry Gray
This is also a great opportunity to remind the location of the oculomotor nerve nucleus in mesencephalon (8'). Note that mesencephalon here is "facing down" compared to MRI. Well seen structures on the MRI are Red Nucleus, Substantia Nigra and Cerebral Aqueduct.

Cranial Nerves Nuclei
Drawing titled: Brain stem human sagittal section - by Patrick J. Lynch, medical illustrator
Courtesy Wikipedia
Also note location of the other Cranial Nerves Nuclei in the brainstem that are nicely depicted in the above drawing.
09 December 2010
Carotis Segments
Images from MR Angiography (MRA) with Time of Flight (ToF) source sequence on the left and reconstructed Maximum Intensity Projection (MIP) showing stenoses in the Internal Carotid Artery (ICA). This patient has a stent in the distal carotid artery that beginns in petrous and ends in cavernous segment. Presence of the stent can influence images of this ToF a non-contrast MRA. You can see stenosis (arrow). In such case I would recommend CTA. I would like to use this case for a short reminder of the terminology concerning ICA segments.
It is easier in CTA since we have reference anatomy points but just in case of the above MIP the typical curves can help. Here are the names of the Internal Carotid Artery Segments:
C1 = cervical
C2 = petrous
C3 = lacerum
C4 = cavernous
C5 = clinoidal
C6 = ophthalmic
C7 = communicating
Location of the markers corresponds with beginning of the segments (except for C1).
As we see our patient has stenosis in the C3 and C4 segments. Also note that there is hypoplastic A1 segment on the right (origin marked with arrowhead) as anatomic variant.
However when reporting the locations of stenosis I also like to give their descriptive names, not only numbers.
See also interesting publication from Medscape
Aneurysms of the Petrous Internal Carotid Artery: Anatomy
It is easier in CTA since we have reference anatomy points but just in case of the above MIP the typical curves can help. Here are the names of the Internal Carotid Artery Segments:
C1 = cervical
C2 = petrous
C3 = lacerum
C4 = cavernous
C5 = clinoidal
C6 = ophthalmic
C7 = communicating
Location of the markers corresponds with beginning of the segments (except for C1).
As we see our patient has stenosis in the C3 and C4 segments. Also note that there is hypoplastic A1 segment on the right (origin marked with arrowhead) as anatomic variant.
However when reporting the locations of stenosis I also like to give their descriptive names, not only numbers.
See also interesting publication from Medscape
Aneurysms of the Petrous Internal Carotid Artery: Anatomy
08 December 2010
Superficial Siderosis
Note extensive hemosiderine deposits superficially around brainstem, cerebellum - seen on first T2 images as well as deposits round basal ganglia and on the brain surface on the GRE (Gradient Echo) images.
Note extensive superficial hemosiderine deposits at cerebellum surface and brainstem on above GRE images.
Above coronal, sagittal, axial T1 and coronal FLAIR sequences show extensive cerebellar atrophy - that is also characteristic to Superficial Siderosis.
Note also extensive Superficial Siderosis of the spinal cord as well as it's atrophy.
Superficial Hemosiderosis (Superficial Siderosis) of the central nervous system results from chronic iron deposition in neuronal tissues associated with cerebrospinal fluid. Residues of blood are penetrating the pia mater and deposit in the superficial layers of the cerebral cortex. Superficial cortical hemosiderosis is defined as linear residues of blood in the superficial layers of the cerebral cortex. It has been shown in animal models with experimental siderosis that repeated bleeding in the subarachnoid space leads to deposition of hemosiderin in the subpial layer of the brain. When observing low signal deposits of hemosiderine it is important to note if it is located in the subarachnoidal space or superficially at the surface of the central nervous system. Superficial Siderosis is an effect and not a cause. One of the proposed causes is Cerebral Amyloid Angiopathy (CAA).
See also interesting article from AJNR:
Subarachnoid Hemosiderosis and Superficial Cortical Hemosiderosis in Cerebral Amyloid Angiopathy - J. Linn
Note extensive superficial hemosiderine deposits at cerebellum surface and brainstem on above GRE images.
Above coronal, sagittal, axial T1 and coronal FLAIR sequences show extensive cerebellar atrophy - that is also characteristic to Superficial Siderosis.
Note also extensive Superficial Siderosis of the spinal cord as well as it's atrophy.
Superficial Hemosiderosis (Superficial Siderosis) of the central nervous system results from chronic iron deposition in neuronal tissues associated with cerebrospinal fluid. Residues of blood are penetrating the pia mater and deposit in the superficial layers of the cerebral cortex. Superficial cortical hemosiderosis is defined as linear residues of blood in the superficial layers of the cerebral cortex. It has been shown in animal models with experimental siderosis that repeated bleeding in the subarachnoid space leads to deposition of hemosiderin in the subpial layer of the brain. When observing low signal deposits of hemosiderine it is important to note if it is located in the subarachnoidal space or superficially at the surface of the central nervous system. Superficial Siderosis is an effect and not a cause. One of the proposed causes is Cerebral Amyloid Angiopathy (CAA).
See also interesting article from AJNR:
Subarachnoid Hemosiderosis and Superficial Cortical Hemosiderosis in Cerebral Amyloid Angiopathy - J. Linn
Abscess and Subdural Empyema
Patient previously operated for bilateral Subdural Hematomas (SDH) presented in febrile state with seizures. CT revealed peripherally enhancing cavity with surrounding edema parieto-temporally. Also noted were hyperdense SDH frontally and parietally with suspected leptomeningeal enhancement (arrows).
MRI confirmed CT findings showing enhancing, fluid filled cavity with surrounding edema and subdural fluid collections showing high signal on FLAIR (last image) and leptomeningeal enhancement (third image). Note mass effect on the coronal image.
Diffusion Weighted Imaging presented restricted diffusion of the fluid in the cavity showing high signal on DWI sequence and low signal on ADC map. This type of diffusion restriction in the fluid cavity is very suggestive for abscess.
More cranially has DWI shown also restricted diffusion in the subdural fluid collections that indicate empyemas. With note that hematoma can also show restricted diffusion, high signal on FLAIR and leptomeningeal enhancement, the whole spectrum of findings in this patient have been evaluated. Conclusion from the radiology and clinical investigation was: Brain Abscess with Infected Subdural Hematomas - Empyemas. Patient was operated using stereotactic neurosurgery based on MRI T1 MPRAGE sequence (not shown). During operation a flow of pus under pressure was noted from the abscess cavity. This case presents value of Diffusion Weighted Imaging in distinguishing between abscess and tumor. Tumor with necrotic fluid cavity generally shows no restriction on DWI.
MRI confirmed CT findings showing enhancing, fluid filled cavity with surrounding edema and subdural fluid collections showing high signal on FLAIR (last image) and leptomeningeal enhancement (third image). Note mass effect on the coronal image.
Diffusion Weighted Imaging presented restricted diffusion of the fluid in the cavity showing high signal on DWI sequence and low signal on ADC map. This type of diffusion restriction in the fluid cavity is very suggestive for abscess.
More cranially has DWI shown also restricted diffusion in the subdural fluid collections that indicate empyemas. With note that hematoma can also show restricted diffusion, high signal on FLAIR and leptomeningeal enhancement, the whole spectrum of findings in this patient have been evaluated. Conclusion from the radiology and clinical investigation was: Brain Abscess with Infected Subdural Hematomas - Empyemas. Patient was operated using stereotactic neurosurgery based on MRI T1 MPRAGE sequence (not shown). During operation a flow of pus under pressure was noted from the abscess cavity. This case presents value of Diffusion Weighted Imaging in distinguishing between abscess and tumor. Tumor with necrotic fluid cavity generally shows no restriction on DWI.
07 December 2010
Contrast Perfusion MRI
Above color maps are from MRI Dynamic Susceptibility Contrast Perfusion (DSCP) study of the patient with follow-up after resection and radiotherapy of the parieto-occipitally located Anaplastic Astrocytoma eight years ago. There is no recurrent tumor - only gliosis. Sometimes DSCP can help in characterization of the enhancement pattern of rest or recurrent tumor to differentiate if from radiation necrosis. This case has no contrast enhancement. Reason for this blog post is to mention this interesting MRI technique that I hope to expand on in the future.
What we see are the color maps representing:
TTP (Time To Peak) - that shows the regional distribution of arrival time of the bolus in the tissue
CBF (Cerebral Blood Flow)
CBV (Cerebral Blood Volume)
MTT (Mean Transit Time)
Above are T2, FLAIR and contrast enhanced T1 sequences from the same region as presented on the Perfusion maps. Note gliosis, tissue atrophy and lack of enhancement.
Images from 3 Tesla scanner.
What we see are the color maps representing:
TTP (Time To Peak) - that shows the regional distribution of arrival time of the bolus in the tissue
CBF (Cerebral Blood Flow)
CBV (Cerebral Blood Volume)
MTT (Mean Transit Time)
Above are T2, FLAIR and contrast enhanced T1 sequences from the same region as presented on the Perfusion maps. Note gliosis, tissue atrophy and lack of enhancement.
Images from 3 Tesla scanner.
06 December 2010
Persistent Hypoglossal Artery
Large Persistent Hypoglossal Artery (PHA) is seen traversing the hypoglossal canal.
Note origin of this large vessel (Persistent Hypoglossal Artery marked with arrow) that is from distal Internal Carotid Artery (ICA) (arrow head) and located posteriorly to it.
3D reconstructions with mandible partially removed show PHA (arrow) as a large vessel posterior to ICA. Also note how it feeds the basilar artery after exiting from the hypoglossal canal. This case is very interesting not only due to persistent vessel but also that PHA is the only feeding vessel for the basilar artery since both vertebral arteries are hypoplastic and there are no posterior communicating arteries.
Interesting article form RadioGraphics:
Normal Variants of the Cerebral Circulation at Multidetector CT Angiography - Simon J. Dimmick
Note origin of this large vessel (Persistent Hypoglossal Artery marked with arrow) that is from distal Internal Carotid Artery (ICA) (arrow head) and located posteriorly to it.
3D reconstructions with mandible partially removed show PHA (arrow) as a large vessel posterior to ICA. Also note how it feeds the basilar artery after exiting from the hypoglossal canal. This case is very interesting not only due to persistent vessel but also that PHA is the only feeding vessel for the basilar artery since both vertebral arteries are hypoplastic and there are no posterior communicating arteries.
Interesting article form RadioGraphics:
Normal Variants of the Cerebral Circulation at Multidetector CT Angiography - Simon J. Dimmick
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