Cortical Laminar Necrosis in an Infant with Severe Traumatic Brain Injury

Abstract

An unconsciousness 12-month-old male infant was brought into the emergency room after car accident. On arrival, the patient's physical condition was unremarkable except for his neurological examination. Neurological examination revealed that pupils were equal (4 mm/4 mm) but not reactive to light and all extremities showed extension to nail bed pressure. Initial brain computed tomography (CT) showed severe brain swelling, intraventricular hemorrhage (IVH) and left parietal bone fracture (Fig. 1). His intracranial pressure (ICP) was expected to be critically high, so we performed external ventricular drainage on right Kocher's point. The initial pressure was 25 cm H2O and serous, slightly bloody fluid was drained. During the supportive medical management in ICU, there was no event and the pa- INTRODUCTIONCortical laminar necrosis (CLN) is defined as the breaking down of a definite cell layer, especially in layers 3 and 5, in the cerebral cortex 1) , which seen as laminar high-signal on T1-weighted images, was described in Sawada et al. 10) and by Nabatame et al. 7) , and was thought to indicate the presence of methemoglobin, but pathological study revealed no hemorrhage 11) . High intensity cortical lesions are observed on T1-weighted magnetic resonance image (MRI) in brain infarcts 7,10) , which can be CLN, hemorrhagic infarcts or a combination of the two 11) . Though the imaging pattern of CLN in conventional imaging is the same for both entities, the pathophysiological mechanisms leading to its formation are entirely different. Infarction results from occlusion of intracranial artery whereas hypoxic insult causes selective neuronal loss affecting the most vulnerable regions of brain 3,5) . CLN represents to neuronal ischemia accompanied by gliosis and layered deposition of fat-laden macrophages 11) . CLN has been identified in conditions with energy depletion and metabolic changes, including hypoxia, epilepsy, hypoglycemia, hyponatremia, and mitochondrial disorders 9) . Here, we report a 12 month-old male infant who suffered diffuse brain injuries following car accident and showed CLN. Cortical laminar necrosis appears as hyperinense lesions with a laminar pattern on T1 weighted magnetic resonance (MR) imaging, without signs of hemorrhage or calcification on T2 weighted MR imaging or computed tomography. It has been reported to be associated with hypoxia, metabolic disturbances, drugs, and infections. We present a 12 month-old male infant who suffered diffuse brain injuries following car accident and showed laminar necrosis of cortex.

Advanced magnetic resonance imaging of cortical laminar necrosis in patients with stroke

“…The DWI abnormalities are usually reversible after 2-4 weeks and they were associated with poor outcome in previous series. 3,4,10,11,19 Advanced MRI techniques including ASL were performed in four patients in our study. Hypoperfusion areas were noted in three out of four patients imaged with ASL.…”

“…The DWI abnormalities are usually reversible after 2–4 weeks and they were associated with poor outcome in previous series. 3,4,10,11,19…”

Confounding Imaging Findings in Subacute-Chronic Cerebral Infarction

“…They are visualized in MRI as cortical curvelined hyperintensities that follow the gyri pattern in T1 sequences without contrast and FLAIR. This hypersignal in T1 is caused by the accumulation of macromolecules, lipid-laden macrophages and no for the presence of blood or calcium [21]. It can be mistaken with the presence of blood in the infarct.…”

“…Laminar cortical necrosis is due to unequal destruction of the neocortex with preservation of some layers and impairment of others (layers 3-5), accompanied by gliosis [21], and appearing during the late subacute and chronic stages of cerebral infarct. It occurs when the influx of oxygen and glucose are inadequate for maintaining regional cerebral metabolism as in cerebral infarct, hypoxia, cerebral hipoperfusion and hipoglicemia or due to an increased demand (status epilepticus) [22].…”