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Congenital Fibrosis of the Extraocular Muscles

FIXME

  • Non-progressive hereditary strabismus syndrome belonging to the congenital cranial dysinnervation disorders (CCDDs), characterized by congenital restrictive ophthalmoplegia with or without ptosis.
  • Prevalence ~1/250,000–1/230,000
  • Maldevelopment of the oculomotor (CN III) and trochlear (CN IV) nuclei/nerves and their axons, with secondary changes in the innervated muscles. This leads to a secondary fibrosis.
  • Congenital non-progressive external ophthalmoplegia with severe limitation of vertical gaze (usually upgaze) and variable limitation of horizontal gaze.
    • Fixed infraduction (eyes fixed downward) in classic CFEOM1;
    • CFEOM2 characteristically shows bilateral large-angle exotropia;
    • CFEOM3 often unilateral/asymmetric involvement.
  • Aberrant eye movements (e.g., convergent movement on attempted upgaze) and, in CFEOM2, poorly reactive pupils (pupillary involvement is absent in CFEOM1).
  • Marcus Gunn jaw-winking phenomenon and other signs of aberrant dysinnervation
  • Ptosis (uni- or bilateral) from levator palpebrae superioris dysfunction, with compensatory chin-up head posture to see beneath the lids and better position the infraducted eyes.
  • Absent binocular vision/poor stereopsis, refractive errors, amblyopia, and poor visual acuity.
  • Neuroimaging (MRI): hypoplasia of extraocular muscles and hypoplastic oculomotor nerves; trochlear, abducens, and optic nerves may also be hypoplastic.
  • Predominantly in CFEOM3
    • facial paralysis and dysmorphism, vocal cord paralysis, intellectual/social disability,
    • Kallmann syndrome (hypogonadotropic hypogonadism with anosmia)
      • progressive peripheral sensorimotor axonal polyneuropathy
      • congenital joint contractures, gait anomalies
      • cyclic vomiting
      • epilepsy.
    • CFEOM3 with polymicrogyria
      • Microcephaly and intellectual disability
  • Tukel syndrome: bilateral postaxial oligodactyly/oligosyndactyly of the hands.
  • Progressive cerebellar ataxia
  • Arthrogryposis multiplex congenita.

A congenital cranial dysinnervation disorder caused by abnormal development of ocular motor neurons and their axons, altering either motor neuron specification or nerve growth/guidance.

  • CFEOM1: heterozygous KIF21A mutations (chromosome 12q12; kinesin motor protein affecting axonal transport) — autosomal dominant.
  • CFEOM2: homozygous PHOX2A/ARIX mutations (11q13; homeodomain transcription factor required for CN III/IV development) — autosomal recessive.
  • CFEOM3: KIF21A or β-/α-tubulin isotype genes TUBB3 (16q24), TUBB2B (6p25), or TUBA1A — autosomal dominant, with variable expressivity.
    • Tukel syndrome is CFEOM3 with ulnar hand anomalies.

Germline mosaicism is common in apparently sporadic CFEOM1 (presumed rate ~38%), which can mimic recessive inheritance and is important for genetic counseling.

Feature CPEO CFEOM
Nature of disorder Mitochondrial myopathy of extraocular muscle Congenital cranial dysinnervation disorder (neurogenic; abnormal CN III/IV/VI development with secondary muscle fibrosis)
Onset Adult, typically 18–40 yrs; ptosis first sign Congenital / present at birth
Course Slowly progressive over years Non-progressive (rare exceptions)
Symmetry / gaze Generally symmetric, diffuse limitation of all directions; superior rectus often prominently involved Fixed characteristic pattern — CFEOM1: eyes fixed in infraduction, absent upgaze; CFEOM2: large-angle exotropia
Ptosis Common, may be uni- or bilateral, progressive Congenital, typically bilateral; chin-up head posture
Diplopia Usually absent (<30%) due to gradual symmetric onsetAbsent; binocular vision typically never develops
Pupils Spared Spared in CFEOM1; poorly reactive in CFEOM2
Inheritance / genetics Single large-scale mtDNA deletion (~50%, sporadic); also nuclear mtDNA-maintenance genes (POLG, RRM2B, TWNK) and mtDNA point mutations Mendelian: CFEOM1 (AD, KIF21A); CFEOM2 (AR, PHOX2A); CFEOM3 (AD, TUBB3/TUBB2B/TUBA1A/KIF21A)
Systemic/associated features “CPEO-plus”: retinopathy, ataxia, neuropathy, deafness, cardiac conduction block, diabetes (Kearns-Sayre) Usually isolated; CFEOM3 may have developmental/CNS anomalies (e.g., Tukel syndrome)
Muscle biopsy Ragged-red / COX-negative fibers; mitochondrial abnormalities Not a mitochondrial biopsy diagnosis; muscle shows fibrosis/denervation changes
Orbital MRI Mild EOM atrophy with fatty/spongiform T1 signal EOM hypoplasia + hypoplastic ocular motor nerves