Glutamate and glycine levels are extremely high in the CSF with shaken baby syndrome⁽³⁾. In experimental acute subdural hematoma in the infant rat, glutamate in extracellular fluid in the cortex increases more than 7 times over the basal level⁽⁴⁾. The pathogenesis of brain parenchymal injuries is unknown but it seems to be related to increased release of glutamate from the pre-synaptic terminal with traumatic stimuli, and decreased re-uptake of glutamate from the synapse with hypoxia or ischemia. Widespread parenchymal injury may be related to the distribution of predominant NMDA receptors in the cortex in neonates and infants. Histologic similarities are observed between child abuse victims and infants with hypoxic ischemic encephalopathy. However, a history of apnea suggesting hypoxic-ischemic injury is found in only 57% of shaken babies. Diffuse axonal injury is rare (3/53) in neuropathological studies ⁽⁵⁾.

The distribution of widespread parenchymal injury is not related to vascular territories or the location and size of acute subdural hematomas on CT and MRI (Figures 2 and 3). DWI is useful in detecting cytotoxic edema due to excitotoxic brain injury. The severity of DWI abnormality correlates with patients' outcome ⁽⁶⁾. MRS shows decreased NAA (decreased neuronal activity), increased lactate (metabolic acidosis) and increased glutamate/glutamine (increased extracellular glutamate) ⁽⁷⁾. Neuroprotective effects by several kinds of selective glutamate receptor antagonists are reported in animal studies ^(8-10).

Figure 2. A 6-month-old boy with shaken baby syndrome

A. T2WI shows bilateral subdural fluid collection and no apparent abnormalities in the brain parenchyma.

B. Sagittal T1WI shows an acute subdural hematoma as a small linear hyperintensity located in the occipital area (arrow).

C,D. DWI clearly shows the extent of parenchymal abnormality as hyperintense lesions with decreased ADC in bilateral fronto-parieto-occipital white matter. This distribution is not related to the location of the acute subdural hematoma and is similar to that of hypoxic-ischemic encephalopathy.

E. MRS (TE 30 ms, PRESS) shows an increased glutamate/glutamine peak (Glx) that may represent increased glutamate release or decreased glutamate re-uptake.

Figure 3. A 2-month-old boy with shaken baby syndrome

A. On T2WI, the gray-white matter delineation is unclear and multiple intraparenchymal hemorrhages are noted probably due to shearing injury (arrows).

B,C. DWI shows diffuse and extensive hyperintensity in the gray and white matter with decreased ADC that represents cytotoxic edema presumably resulting from excitotoxic injury. Only the right frontal lobe is relatively spared (arrow).