TH and Allan-Herndon-Dudley syndrome: As we outline in Figure 10 and Figure 11, when there is a lack of TH due to a deficiency of the MCT8 and OATP1C1 transporters, the pyramidal neurons are no longer in the same healthy synaptic state as in a normal situation, so their output is very plausibly altered, producing the typical symptoms of upper motor neuron disease, which are present in AHDS patients as bilateral Babinski reflexes and hyperreflexia [90], and, in the patient with OATP1C1 deficiency, spasticity of the lower limbs and myoclonic-like movements [24].