Brain injury in hypoxia

Taught by: Dr. Rangan Srinivasaraghavan

Compiled to pdf Dr. Pavitra Viswanathan
Effect dependent on two aspects

• Gestation age
• Severity of hypoxic event

Key fact 1-Importance of Diving reflex

Acute and severe asphyxia limits the oxygen supply to the whole brain, resulting in damage to the
regions of high metabolic activity and higher density of glutamate receptors, i.e. basal ganglia and
thalamus.

In the case of sub-acute, mild hypoxia there is enough time to direct the blood into these important
areas, so they are not injured

Key fact 2 -pattern of injury and watershed areas

The pattern of brain injury on MRI in children with cerebral palsy is related to the gestational age of
occurrence.

• Typical preterm brain injury- Periventricular leukomalacia and post-haemorrhagic

porencephaly.Periventricular leucomalacia usually occurs between 28-34 weeks of gestation and
is caused by an ischaemic process in the watershed zone that exists in the periventricular white
matter of the immature brain.
• After about 34 weeks of gestation, subcortical and cortical areas are the most vulnerable
regions of the brain for hypoxic-ischaemic insult- resulting lesions include subcortical injury,
multicystic encephalamalacia and gliosis

The watershed region changes with child’s

gestation

In the preterm brain, ventriculopetal

penetrating arteries supply the periventricular
regions by extending inward from the surface
of the brain. Thus, hypoperfusion results in a
periventricular border zone of white matter
injury.

In the full-term, ventriculofugal vessels also

extend into the brain from the lateral
ventricles and the intervascular watershed
zone moves away from periventricular region
to a parasagittal location. This results in
Preterm periventricular white matter injury subcortical white matter and parasagittal
cortical injury during hypotension.
Late preterm- Subcortical white matter

Term- cortical n subcortical region

Scenario 1:

Preterm 32 weeker

Difficult perinatal period

What will be clinical and radiological picture if this child sustains brain injury?

Radiological: Bilateral, symmetrical periventricular gliosis, uneven external outlines of the lateral
ventricles, thinning of the white matter layer

Periventricular White matter thin= leukomalacia

Clinical picture:

Children with PVL develop spastic CP involving the lower limbs (diplegia), quadriplegia (tetraplegia –
with more pronounced symptoms in the lower limb)

Epilepsy may be seen

Mental retardation-usually mild in the case of PVL

Associated CVI- optic radiation is affected

Scenario 2:

Term child good weight

Cord prolapse or prolonged second stage

Acute severe asphyxia

What will be clinical and radiological picture?

Radiological picture:

Acute and severe hypoxia in term infants results in damage to the gray matter, especially the basal
ganglia and thalamus- Called Selective neuronal necrosis

Extensive multicystic involvement of white matter quite often accompanied by necrotic cavities within
the basal ganglia and thalamus is typical for a prolonged and severe hypoxia.

So it causes multicystic encephalomalacia and also basal ganglia n thalamus involvement

Clinical picture in term asphyxia

Severe spastic quadriplegic form of the cerebral palsy, with choreoathetotic symptoms

secondary microcephaly, mental retardation, and pseudobulbar symptoms

They are commonly accompanied by epilepsy

Scenario 3
In children with chronic low grade mild hypoxia like IUGR

What will be clinical and radiological picture?

Radiological Pattern: subcortical region involvement ll be predominant

Region affected: Parasagittal region

They ll have Parasagittal gliosis

Parasagittal brain injury is characteristic for mild or moderate, subacute hypoxia. It is located on the
border of the vascular territories – parasagitally, bilaterally and includes the cerebral cortex and the
adjacent white matter

Clinical Picture

Clinically this causes mild spasticity.. pyramidal tract lesions.. no extrapyramidal symptoms
Scenario 4:
Term child with Rh incompatibility and high bilirubin

Post exchange.. 2 times done

What will be clinical and radiological picture?

Pathogenesis

Unconjugated hyperbilirubinemia is the aetiology of kernicterus, especially when total bilirubin levels
exceed 35 mg/dL.

Unconjugated bilirubin, or ‘free bilirubin’, can cross the immature blood-brain barrier when the
concentration exceeds the normal albumin binding capacity and normal conjugating capacity of the
liver.

Radiological picture

As a result, this unconjugated bilirubin deposits symmetrically in the brain, with a predilection for globus
pallidi, subthalamic nuclei, hippocampus (especially CA2-CA3), putamen, thalamus, and cranial nerve
nuclei (especially of CN III, IV, and VI)

Black line is posterior limb of internal

capsule. T2 hyperintensity anterior to
it s seen. This s globus pallidi region.

MRI findings in Hyperbilirubinemia

assoc brain injury is

T2-weighted hyperintensities in the

globus pallidi.. it can be mild to
severe

Clinical feature:

Dyskinetic CP

The neurologic manifestations of kernicterus evolve with time

- during the early periods of infancy and consist of hypotonia, hyper-reflexia, and delayed acquisition of
motor milestones

- Later on, the extrapyramidal manifestations (dystonia, chorea-athetoid movement, etc.) appear
Hypoglycemic brain injury

Both asymptomatic and symptomatic Hypoglycemia children need to be followed up carefully

Pattern of brain injury in Hypoglycemia:

Parieto occipital injury with gliosis

Clinical Manifestations:

Epilepsy- West syndrome

Cerebral visual insufficiency and related behaviours

Microcephaly

NOT MUCH TONE ABNORMALITIES

Why occipital region is most affected in Hypoglycemia?

It s believed to be due to Hypoglycemia assoc excitotoxic damage - early infancy parieto occipital region
high degree of axonal migration and synapse formation s happening.. so these regions more prone
Summary of CP clinical imaging correlation

1. Quadriplegia spasticity with dystonia with microcephaly with pseudobulbar palsy

a. Acute profound asphyxia could be likely
b. Multicystic encephalomalacia with basal ganglia thalamic lesions may be seen
c. Quadriplegia- spasticity/ Diplegia- spasticity with or without vision concerns
2. Preterm brain injury causing PVL
a. Chronic mild hypoxia causing PVL n subcortical involvement
b. MRI- Periventricular leukomalacia with prominent ventricles with squaring of ventricles
or parasagittal gliosis
3. Dyskinetic CP with or without hearing loss
a. Neonatal jaundice with encephalopathy
b. MRI- T2 weighted HI in globus pallidi