Cerebral Palsy maybe/maybe not

It was a complication of parental Rh Factor incompatibility before the newer preventative measures were made standard procedure. It is reliably prevented. So, beware! Today, athetoid cerebral palsy probably occurs in the full term infant who undergoes a brief but profound anoxic event, implicating a brain region of high oxygen need. Athetosis is seldom manifest before two years after birth. This makes sense as a similar disorder is seen in carbon monoxide poisoning. Interestingly, the movement disorder of CO poisoning shows up many months after everybody has celebrated the good fortune of surviving. Babies with athetoid cerebral palsy often do not show the disorder until one to two years. They may be described as a bit floppy at birth, however. The thinking is that the damage may be to supportive cells that are woven like lace through the brain. Absent these cells, the unattended neuron elements then wither, late. Beware that most of what is written about athetoid as being this or that is just blindly repeated from old texts that were written before the bilirubin mess was fixed. Today’s athetosis isn’t what it was with yellow babies. Today we are far more likely to see bits of athetoid quality mixed with rigidity and spasticity. Whereas undoing athetoid movement is really not available (short of brain surgery), spasticity that aggravates athetoid reaction can be dealt with to reduce athetoid extremes.

Slowing neuron signal trains like this /\/\/\/\ to this __/\______/\______ helps.

Ethanol perineural injections that bugger myelin is used effectively to put speed bumps on those nerve paths which are eliciting aggravated athetoid activity.