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Electrophysiological and 99mTc-HMPAO-SPECT studies in Menkes disease

L Sztriha1, M Janáky, J Kiss

  • 1Department of Paediatrics, FMHS, UAE University, Al Ain, United Arab Emirates.

Insights

Menkes kinky hair disease, a genetic disorder, affects brain development. Neuroimaging in two brothers revealed distinct patterns of reduced and increased cerebral blood flow, highlighting disease variability.

Area of Science:

  • Neurology
  • Medical Genetics
  • Pediatric Neurology

Background:

  • Menkes kinky hair disease (MKD) is a rare X-linked recessive disorder caused by mutations in the copper-transporting ATPase gene ATP7A.
  • It is characterized by copper deficiency in various tissues, leading to neurological dysfunction, connective tissue abnormalities, and characteristic hair changes.
  • Early diagnosis and management are crucial for improving outcomes, though the prognosis remains poor.

Observation:

  • Two brothers diagnosed with Menkes kinky hair disease presented with typical clinical and laboratory findings.
  • The older sibling (11 months) exhibited abnormal electroencephalogram (EEG), absent visual evoked potentials (VEPs), and abnormal brainstem auditory evoked potentials (BAEPs).
  • Neuroimaging (99mTc-HMPAO-SPECT) in the older sibling showed reduced regional cerebral blood flow (rCBF) in frontal and right temporal regions.

Findings:

  • The younger sibling, followed from birth, developed seizures and a hypsarrhythmia-like EEG.
  • Abnormal BAEPs with prolonged latencies were noted at 12 months, and VEPs disappeared by 18 months.
  • Unexpectedly, 99mTc-HMPAO-SPECT revealed left parietal hyperperfusion in the younger sibling, contrasting with the older brother's findings.

Implications:

  • These findings highlight the variable neuroimaging presentation of Menkes kinky hair disease, particularly in regional cerebral blood flow.
  • The contrasting patterns of hypoperfusion and hyperperfusion underscore the complex pathophysiology of MKD.
  • Further research into the underlying mechanisms of altered cerebral blood flow in MKD is warranted for potential therapeutic targets.

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