Shaken Baby Syndrome (SBS)
Shaken Baby Syndrome (Shaken Baby Syndrome) develops as a result of aggressive shaking of an infant, even without visible signs of external physical trauma. Although the isolated role of shaking is sometimes debated, most experts recognize this mechanism as primary.
The biomechanics of injury involve impacts of the brain tissue against the inner surface of the skull, leading to contusions. In addition, repetitive movements cause shearing injuries (shearing injuries). They are most frequently localized in the subcortical zone at the gray-white matter junction. MRI is the preferred diagnostic method because it visualizes these changes significantly better than CT.
Classic radiological signs of SBS:
- Subarachnoid hemorrhage.
- Contusions, lacerations, or tears of the brain parenchyma.
- Diffuse cerebral edema.
- Spinal subdural hematomas (according to recent data, occur in approximately 40% of cases).
Cerebral edema and outcomes in SBS
Cerebral edema is a crucial diagnostic criterion for shaken baby syndrome. It is hypothesized to be secondary and to develop against the background of hypoxic-ischemic injury. The edema is typically massive, most pronounced in the parieto-occipital lobes, while the basal ganglia, cerebellum, and brainstem remain relatively spared.
The prognosis in severe edema is extremely unfavorable. The brain tissue undergoes rapid destruction, and marked atrophy is visualized on scans within just 2–3 weeks. The ultimate outcome is multicystic encephalomalacia and microcephaly, accompanied by severe motor and cognitive deficits.
On serial MRI scans (T1-weighted images), shortening of the relaxation time in the cortex can be observed due to cortical laminar necrosis and parenchymal infarction. Chronic subdural collections show a slightly higher signal than cerebrospinal fluid due to high protein content from previous hemorrhage.
Hydrocephalus: pathophysiology and classification
The term hydrocephalus (Hydrocephalus) is used to describe conditions accompanied by enlargement of the ventricular system. The primary goal of imaging diagnostics is to differentiate forms requiring surgical treatment from ventriculomegaly, which occurs passively due to primary brain underdevelopment or atrophy.
The underlying pathology is an imbalance between CSF production (by the choroid plexuses) and its absorption (primarily by the brain tissue, and to a lesser extent by the arachnoid granulations). CSF flow is directed from the lateral ventricles to the third, and then to the fourth ventricle, and heavily depends on cerebrovascular pulsation.
Two main forms are distinguished:
- Communicating (extraventricular obstructive) hydrocephalus.
- Non-communicating (intraventricular obstructive) hydrocephalus.
Clinical and radiological presentation of hydrocephalus
Clinical manifestations vary drastically depending on the child's age:
- In children under 2 years of age (with open fontanelles), progressive macrocephaly dominates. Frontal bossing, thinning of the cranial vault, suture diastasis, and tension of the anterior fontanelle are noted. The «sunsetting» sign, abducens nerve palsy, and lower extremity spasticity (resulting from stretching of the corticospinal tracts) are characteristic.
- In older children (sutures closed), the skull is rigid. There is no macrocephaly; symptoms of intracranial hypertension predominate: morning vomiting, headache, papilledema, and altered level of consciousness.
Signs of intraventricular obstruction on imaging:
- Dilatation of the temporal horns, disproportionate to the size of the lateral ventricles.
- Enlargement of the third ventricle recesses with downward bulging of its floor.
- Periventricular (transependymal) interstitial edema.
- Effacement of the subarachnoid spaces, basal cisterns, and major sulci.
Briefly: answers to topical questions
What anatomical structures are part of the choroid plexuses of the lateral ventricles and what is their CSF production rate?
Choroid plexuses are located within the brain ventricles and are most prominent in the lateral ventricles. According to sources, they are represented by venous vascular plexuses and covered by ependyma; CSF secretion is carried out by the ependyma of the choroid plexuses. The rate of CSF production is not specified in the provided sources.
To memorize the symptoms of hydrocephalus in infants, use the «Head-Eyes-Legs» rule: Head (macrocephaly, bulging fontanelle, suture diastasis), Eyes («sunsetting» sign, abducens nerve palsy), Legs (spasticity due to stretching of the corticospinal tracts).
Class and exam questions
Which parts of the brain are least affected in shaken baby syndrome?
In massive cerebral edema associated with SBS, the basal ganglia, brainstem, and cerebellum generally remain relatively spared.
Why do children with hydrocephalus develop lower extremity spasticity?
This occurs due to the mechanical stretching of the corticospinal tracts that wrap around the enlarged brain ventricles.
What developmental pathology frequently causes hydrocephalus in infants?
Among congenital causes, Dandy-Walker malformation (Dandy-Walker) and Chiari II malformation (Chiari II) are common, especially after surgical repair of lumbosacral myelomeningocele.
What else to study on this topic
- Pathophysiology of cerebrovascular pulsation and CSF flow.
- MRI semiotics of white matter shearing injuries.
- Radiological presentation of cortical laminar necrosis on T1-weighted images.
- Congenital Dandy-Walker and Chiari II malformations.
- Differential diagnosis of macrocephaly: exclusion of craniosynostosis.
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