Periventricular Leukomalacia: Most Strongly Supported Finding
The diagnosis of periventricular leukomalacia (PVL) with scissoring gait most strongly supports bilateral lower limb spasticity (Answer B), as this represents the characteristic motor phenotype of spastic diplegia that directly results from PVL's preferential injury to descending motor pathways serving the lower extremities.
Understanding the Clinical Presentation
The scissoring gait pattern observed when this patient is held upright is a pathognomonic sign of bilateral lower limb spasticity, specifically indicating spastic diplegia 1. This occurs because PVL preferentially damages periventricular white matter where descending corticospinal tract fibers to the lower extremities are most densely concentrated 2, 3.
Why Bilateral Lower Limb Spasticity is Most Strongly Supported
- Direct pathophysiologic mechanism: PVL causes ischemic injury to periventricular white matter, specifically targeting the corticospinal tracts that control lower extremity motor function 2, 3
- Spastic diplegia is the hallmark outcome: PVL is explicitly recognized as being "associated with serious neurodevelopmental sequelae, especially spastic diplegia" 4
- The scissoring sign is diagnostic: This specific motor pattern directly demonstrates the bilateral lower limb spasticity that defines the clinical syndrome 1
Evaluating the Other Answer Choices
Static Motor Delay (Answer A)
While cerebral palsy from PVL does involve static (non-progressive) motor impairment, this descriptor is too broad and non-specific 1. The term "static motor delay" doesn't capture the specific spastic phenotype that PVL produces. The question asks what is "most strongly supported," and bilateral lower limb spasticity is far more specific and directly linked to the pathophysiology 1, 2.
Prematurity (Answer C)
This represents backward reasoning. While PVL is indeed "the predominant form of brain injury" in premature infants 2, and prematurity is a major risk factor for developing PVL 1, the presence of PVL does not "support" prematurity as a diagnosis. The patient either was or was not premature—this is historical fact, not something supported by current findings 1. Additionally, PVL can occur in term infants with hypoxic-ischemic injury 5.
Periventricular White Matter Changes on MRI (Answer D)
This is circular reasoning. The question states that "MRI reveals periventricular leukomalacia"—this IS the periventricular white matter change 2, 4. You cannot use a finding to support itself 6. The question is asking what the diagnosis of PVL supports, not what supports the diagnosis of PVL.
Clinical Implications for Severity and Prognosis
The presence of bilateral cystic PVL on MRI predicts nonambulant cerebral palsy (GMFCS III-V), while noncystic PVL is more likely to result in ambulant cerebral palsy 1. The bilateral nature of the lower limb involvement, as evidenced by scissoring, suggests:
- HINE scores <50 at 3-12 months would indicate likely bilateral CP 1
- Bilateral cystic PVL specifically predicts more severe motor impairment 1
- Early intervention with CP-specific therapies should be initiated immediately 1
Common Pitfalls to Avoid
Do not confuse the temporal relationship between prematurity and PVL: Prematurity is a risk factor that precedes PVL development, but finding PVL does not retrospectively "support" a diagnosis of prematurity 1, 2. The clinical history either documents prematurity or it doesn't.
Do not mistake "static" for "non-specific": While cerebral palsy is indeed a static encephalopathy, the specific motor phenotype (bilateral lower limb spasticity) is what PVL characteristically produces and is therefore most strongly supported 1, 4.
Recognize that PVL has specific motor topography: The periventricular location of injury preferentially affects lower extremity motor pathways, making bilateral lower limb spasticity the expected and most strongly supported finding 2, 3.