Showing posts with label hypoxic ischemic encephalopathy. Show all posts
Showing posts with label hypoxic ischemic encephalopathy. Show all posts

Thursday, June 16, 2011

Striatocapsular haemorrhage-MRI

13 yr old with movement disorders with history of hypoxia. MR shows bilateral, symmetrical linear altered  signal intensity with no restricted diffusion or blooming on susceptibility images. Possibly represents striatal haemorrhage sequelae in the external capsular area between lateral putamen and insular cortex. By Dr MGK Murthy, Mr Hamid and Dr Mukarab.



Teaching points

Striatocapsular haemorrhage is classfied by chung etal
type1-Anterior                                  in the region of artery of heubner
type2-Middle-                                   in the  region of medial lenticulostriatal  artery
type3-Posteromedial-                       in the region of Postero medial branches of  lateral lenticulostriatal artery
type4-Posterolateral-                        in the region of postero lateralbranches of lateral lentiuclostriate artery
type5-lateral-                                   Most lateral branches of lateral lenticulostriatal artery
type6-Massive 

Friday, October 15, 2010

Hypoxic ischemic encephalopathy-MRI

History : 4 day old neonate was delivered by LSCS after clinical fetal destress on account of meconium staining of the liquor. Apgar at birth reported normal with normal sugar levels presently, with history of seizures.MRI Brain shows two well defined dots of restricted diffusion seen in the parasagittal location of posterior parietal region predominantly involving the white matter, with not reaching upto the cortex, no significant basal ganglia or thalamic involvement, or cortical highlighting or diffuse white matter hyperintensity or gross structural abnormalities.

Hypoxic ischemic encephalopathy is now appropriatly reffered to as neonatal encephalopathy to encompase all the variants:

a) Commonest presentation for an acute hypoxia in term children usually leads to severe basal ganglia thalamic lesions ( BGT), predominantly an initially involving posterolateral lentiform nucleus and ventrolateral thalami. These are usually severe and lead to high mortality. The additional features amongst them diffuse cerebral edema, slit like ventricles and reduced extra-cerebral spaces.

b) The other uncommon variant is reffered to as parasagittal infarction which involves the deep white matter only at border zones of major arterial territories ( water shed ) some of these may present with full blown HIE as well. These occur usually in the presence of severe hypoglycemia and lead to microcephaly all though the neurodevelopmental outcome surprisingly good particularly for motor function because there is minimal or no involvement of BGT. These infants may also show more profound metabolic abnormalities such as prolonged conjugated hyperbilirubinemia, and recurrent hypoglysemia and developed marked cognitive and motor impairement.

c) Multifocal areas of infarction that do not appear to be in parasagittal distribution may be secondary to infections like herpes, varicella, and listeria, in which case contrast study would help. The CMV lesions may persist for years in white matter and not show atrophy, the key lies in the presence of subependymal cysts.






Case by Dr MGK Murthy, Sr Consultant Radiologist
Teleradiology Providers, Unit of Prime Telerad Providers (P) Ltd