A 41-year-old female with history of migraine presented to the ED with acute onset of aphasia. In addition to the aphasia, there was numbness and tingling in the right arm and face. Patient demonstrated expressive aphasia and was not able to answer questions posed in the ED. Gadolinium MR perfusion images demonstrated decreased relative cerebral blood flow (top) in the left parietal/occipital lobes and increased time-to-peak (bottom) in the contralateral cerebellar hemisphere. Although crossed cerebellar diaschisis (CCD) is seen mostly on radiotracer studies (hypometabolism on PET studies), it was nicely demonstrated in our patient. CCD occurs more often after supratentorial infarctions but has been reported in the setting of migraine. This phenomenon occurs immediately after brain injury due to the large number of functional connections between cerebrum and cerebellum. In reverse CCD, the brain abnormality is due to injury of the cerebellum. Because of the limited number of slices on perfusion MR studies, particularly when using ASL techniques, it is important to keep in mind that the cerebellum may be involved in several supratentorial abnormalities and needs to be included in the study.  I would be interested in finding out if anyone else has seen this type of migraine-associated CCD.

Does anyone know what this mass could be? It was biopsied 2 years ago and pathology reported it as  “normal brain tissue”.

As you can see, the lesion is hyperintense on T2, hypointense on T1 and does not enhance.  No calcifications are present and no there is no restricted diffusion .

The patient is 25  year old and has loss of short term memory and seizures.

Any input into the nature of the mass is welcome.

1.  I have  a sample with some ADC values obtained in 1,5 T and others obtained in 3T ( same b value). Can I use the ADC values for statistics or do you think that they cannot be compared?

2.  Are the ADC values obtained using a diffusion sequence  the same that the ADC values obtained in a DTI sequence with 12 directions?

Thank you in advance.

The paper describes a small series of patients who were outside of the traditional stroke therapy window, but underwent endovascular therapy anyway. The majority of the patients had small DWI abnormalities in the setting of significant neurological symptoms (NIHSS greater than 8), a circumstance that has been termed a clinical-diffusion mismatch. Of those who underwent successful revascularization, all had significant clinical improvement, and none had intracerebral hemorrhage. The data makes physiological sense. Patients with major artery occlusions, severe neurological symptoms and small diffusion abormalities must have excellent collateral circulation that is sustaining neuronal viability despite synaptic dysfunction that produces the neurological syndrome.

If the findings described by Janjua et al. are confirmed, it begs the question of how many potential patients may fit the clinical-diffusion mismatch criteria.  The number may be quite large as data from another paper by Copen et al. that was also recently ePublished (Existence of the Diffusion-Perfusion Mismatch within 24 Hours after Onset of Acute Stroke: Dependence on Proximal Arterial Occlusion Radiology. 2009 Jan 21. [Epub ahead of print]).  Copen et al. found that well over half of all patients with a proximal anterior circulation occlusion had relatively small diffusion abnormalities. 

Janjua and his co-authors have made an exceptional contribution to stroke research and I believe are lighting the path towards improved care of patients with the most severe strokes.