Trismus and spasticity: is it neurological?

<h3></h3> A 35-year-old female diagnosed with cerebral palsy in childhood was admitted with a two- week history of worsening spasticity, decline in mobility, drowsiness, dysarthria and trismus. She had an intrathecal baclofen pump for her spasticity which was found to be non- functioning on review. However, it did not explain her trismus or reduced consciousness. Further investigations revealed severe refractory hypophosphataemia. Her imaging revealed generalised atrophy with diffuse, generalised white matter hyperintensity and thinning of the corpus callosum. (Subsequent genetic testing confirmed biallelic homozygous GJC2 mutation confirming autosomal recessive hypomyelinating leukodystrophy as the underlying neurological diagnosis). EEG was unremarkable. On close review it was revealed that she had an admission a few weeks earlier with anaemia when she had two infusions of Ferrous Carboxymaltose (FCM), a week apart. Although she only had mild symptoms of worsening mobility after the first infusion, she deteriorated rapidly after the second with the above symptoms. A diagnosis of FGF-23 induced hypophosphataemia was made which was triggered by FCM on a background of Vitamin D deficiency. She was treated with alfacalcidol and long-term phosphate with improvement in spasticity and trismus. The patient serves as a reminder that not all cases of spasticity are due to primary neurological causes.