Additional symptoms related to CPM:
I’ve previously described movement issues like dystonia, Parkinson like tremors, other tremors, and random jerking movements, but this is something I have not heard about previously, choreic.
I had no idea what the word meant or what it is related to before a few days ago, so please feel free to add any input you might have about it.
The dictionary definition is: “An involuntary spasmodic twitching or jerking in muscle groups not associated with the production of definite purposeful movements.”
- Review: Neurology and medicine
Dystonia and chorea in acquired systemic disorders
Metabolic aetiologies of dystonia and chorea
|Osmotic demyelination syndrome (central pontine myelinolysis)|
Literature also seems to suggest that these reasons that these choreic movements occur is because of injury the putanem or basal ganglia. It suggests that there is a decreased amount of GABA, and there there are issues with Dopamine and glutamate.
Frankly, folks, I simply can’t read through this very detailed information from the following journal link, but it goes into great explanation why both dystonia and chorea are found in a variety of brain damage injuries, including CPM/EPM, Huntington’s disease, and many others.
Here is the quote:
As discussed earlier, dystonia and chorea most commonly result from striatal dysfunction, and hypoxia-ischaemia has been shown to alter several neurotransmitter systems in the striatum. Glutamate is the main neurotransmitter in cortical neurons projecting to the striatum and may contribute excitotoxic injury. Hypoxia-ischaemia has been shown to increase striatal extracellular glutamate, and decrease glutamate transporter concentrations. Direct lesioning of the globus pallidus with excitatory amino acids in monkeys produces cocontraction of opposing muscle groups on reaching, as in dystonia.9Extracellular dopamine concentrations rise and concentrations of dopamine metabolites fall after hypoxia-ischaemia.710Dopamine may also potentiate the excitotoxic properties of glutamate, and depleting the striatum of dopamine before hypoxia-ischaemia decreases the degree of striatal injury. In the neonatal rat model of cerebral hypoxia-ischaemia, striatal D1 and D2 dopamine receptor numbers fluctuate until 9 to 11 weeks after injury, at which time the D1 receptor number has returned to normal but the reduction in D2 receptors persists.11 Hypoxia-ischaemia also results in areas of complete loss of preproenkephalin mRNA in the dorsal striatum of the rat brain.12 Enkephalin, together with GABA, is an inhibitory neurotransmitter in the projections from the putamen to the external pallidum. Hypoxic-ischaemic necrosis of medium sized spiny striatal neurons may be responsible for decreased concentrations of the inhibitory neurotransmitter, GABA. By contrast, the striatal cholinergic system remains relatively preserved or even upregulated after hypoxia-ischaemia, as evidenced by an increase in cholinergic fibres and cell bodies, and an increase in acetylcholine release.13This is interesting in that anticholinergic medications often ameliorate dystonic movements.
J Neurol Neurosurg Psychiatry 1998;65:436-445 doi:10.1136/jnnp.65.4.436
- Review: Neurology and medicine
I will try to add more to this post in the future if I can, but right now, I can’t. Please feel free to leave questions or suggestions as you like.
Have a great night 🙂
- You Have Dystonia? (dystoniamuse.com)
- Essential Tremor and Receiving Social Security Disability (socialsecurityhome.com)
- Huntington’s Chorea and Receiving Social Security Disability (socialsecurityhome.com)
- Hereditary Tremor and Receiving Social Security Disability Benefits (socialsecurityhome.com)