Radiology MRI

9 days old neonate. Mother known with sinus thrombosis during pregnancy. This is T1 without contrast showing high signal of methemoglobine in sinus rectus, superior sagittal sinus and cavernous sinus - representing massive blood clots of sinus thrombosis.


SWI sequence is showing low signal of hemosiderine deposits in central veins. T2 sequence is showing clot filled occipital part of sagittal sinus. ToF MRV (flow based venous angio) shows corresponding flow defects, same on MRV MiP reconstruction.


DWI and ADC-map showing ischemia in the basal ganglia, corpus callosum and corona radiata frontally. Those ischemic changes can be reversible in case of sinus thrombosis (venous infarcts). Major risk are the possible brain hemorrhages - that are fortunately not present in this case.

Teaching point is to look very carefully at non-contrast T1 of neonate for possible high signal changes representing methemoglobine products, not only in dural sinus but also in the subarachnoidal spaces for pos…

This is MS patient with contrast enhancing plaque. Note on DWI sequence high signal as well as high on ADC - therefore no restriction but bright on DWI. DWI gives a clue to active plaques.


MS plaques showing highest signal on DWI are most suspect for activity - in my opinion. Therefore look at DWI (b1000) when reporting brain MRI of MS patients.

T1 GD+ sequences show multiple punctate and linear enhancing lesions in pons and medulla oblongata representing perivascular enhancing lymphatic tissue.


Enhancing punctate lesions are also present in corona radiata on both sides. FLAIR sequence showing corresponding white matter lesions that however present no significant oedema.

Findings represent CLIPPERS - Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids. Rare entity caused by infiltration of the brain with inflammatory cells in perivascular areas, mostly found in brainstem.

More comprehensive description of CLIPPERS in Radiopaedia

10 years old boy from parents being cousins to each other presents with progressive rigidity and dystonia. Initial MR showing significant bilateral atrophy in caudate nuclei and putamina with high signal on FLAIR and T2 consistent with gliosis.


Note striking symmetric atrophy of the putamina and caudate nuclei on T2 and IR.

Huntington disease (HD) is also known as Huntington chorea. HD is an autosomal dominant chronic hereditary neurodegenerative disorder with complete penetrance [Osborn]. 

Aggregates of huntingtin protein accumulate in axonal terminals, which eventually leads to the death of medium spiny neurons. Autopsy shows generalized cerebral atrophy with an average of 30% reduction in brain weight. Both the cortex and hemispheric WM are affected. The most characteristic gross abnormality is volume loss with rarefaction of the caudate nucleus, putamen, and globus pallidus [Osborn]. 

Microscopically, HD features neuronal loss with huntingtin nuclear inclusions, astrocytic gliosis, an…

Contrast enhanced T1 sequences showing large thrombi in the posterior parts of the superior sagittal sinus (SSS). However note that this young female patient in postpartum period is also presenting with classical signs of Intracranial Hypotension. There is general dura enhancement, swelling of hypophysis and slight sagging of the cerebellum. 



Transversal SWI and T2 show thrombus in SSS and swelling of the cortical veins. 



Sagittal and transversal FLAIR sequences show thrombus with higher signal that is obstructing (black ) flow-voids in SSS. 


It is believed that Intracranial Hypotension (that is most often caused by CSF leakage) is the reason for slowing down the venous blood flow in the dural sinus. However note that Dural Sinus Thrombosis (DST) is a very seldom complication of Intracranial Hypotension (2%). Most often does DST manifest as Intracranial Hypertension (20-40%).

Check my previous cases:
CSF Leakage - Intracranial Hypotension
Intracranial Hypotension
CSF Leakage Spine - MRI Prot…

Classic case of an incidental finding of a small Capillary Telangiectasia in the pons. Note low signal on SWI and diffuse subtle contrast enhancement on T1. Location is very typical but other locations are common. 


On T2 this small Capillary Telangiectasia is hardly visible, without any signs of oedema. There is a blush of enhancement on T1C+ coronal image.