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Children with irreversible brain damage associated with hypothyroidism and multiple intracranial calcifications
Junko Arii1, Yuzo Tanabe, Michiko Makino
1Chiba Rehabilitaiton Center, Department of Pediatrics, Graduate School of Medicine, Chiba University, Chiba-shi, Japan. junko-a@muf.biglobe.ne.jp
Insights
Children with later-onset hypothyroidism can experience irreversible brain damage, including motor and intellectual impairments. This study highlights the need to re-evaluate thyroid function in children with specific neurological symptoms and intracranial calcifications, even after normal newborn screening.
Area of Science:
- Pediatric Neurology
- Endocrinology
- Developmental Neuroscience
Background:
- Neonatal screening effectively detects congenital hypothyroidism, preventing severe developmental issues.
- However, hypothyroidism developing after the neonatal period may present later with neurological deficits.
- The long-term neurological consequences of childhood-onset hypothyroidism are not fully elucidated.
Observation:
- Three children presented with decelerated linear growth, lower limb spasticity, and mild intellectual impairment.
- All patients had normal neonatal thyroid-stimulating hormone (TSH) screening results.
- Brain imaging revealed multiple calcifications in the basal ganglia and subcortical areas.
Findings:
- Childhood-onset hypothyroidism, despite normal neonatal TSH screening, can lead to irreversible neurological damage.
- The observed neurological symptoms, including motor disturbances and intellectual deficits, resemble cerebral palsy.
- Intracranial calcifications in a specific distribution may be a marker of hypothyroidism-induced metabolic derangement.
Implications:
- Re-evaluation of thyroid function is crucial for diplegic patients with unexplained intracranial calcifications, particularly if neonatal screening was normal.
- Early diagnosis and treatment of postnatal hypothyroidism may mitigate or prevent severe neurological sequelae.
- This underscores the importance of considering acquired hypothyroidism in the differential diagnosis of pediatric neurological disorders.
Abstract:
Children who develop clinical hypothyroidism in early childhood have various degrees of irreversible brain damage, albeit less severe than cases detected by neonatal screening test for hypothyroidism in the first months of the life. We report three patients with hypothyroidism of childhood onset after a normal neonatal thyroid-stimulating hormone screening who showed deceleration in linear growth, spasticity in the lower limbs with deformity, mild intellectual impairment, and multiple calcifications in the basal ganglia and subcortical areas. The neurologic symptoms were not progressive but were irreversible in spite of thyroxine treatment. Motor disturbances commonly observed in postnatal-onset hypothyroidism are similar to those of cerebral palsy. Specific distribution of intracranial calcifications may result from metabolic derangement as a result of hypothyroidism, although the mechanism of calcification is not fully understood. We emphasize the need to re-evaluate thyroid function in diplegic patients with specific intracranial calcifications but normal neonatal thyroid-stimulating hormone screening.