EPS review
Started by Solideliquid
We can start with a DSM IV-TR diagnosis:
333.7 Neuroleptic-Induced Acute Dystonia
Abnormal positioning or spasm of the muscles of the head, neck, limbs, or trunk developing within a few days of starting or raising the dose of a neuroleptic medication (or after reducing a medication used to treat extrapyramidal symptoms).
There are also categories for:
333.99 Neuroleptic-Induced Acute Akathisia
333.82 Neuroleptic-Induced Tardive Dyskinesia
332.1 Neuroleptic-Induced Parkinsonism
333.7 Neuroleptic-Induced Acute Dystonia
Abnormal positioning or spasm of the muscles of the head, neck, limbs, or trunk developing within a few days of starting or raising the dose of a neuroleptic medication (or after reducing a medication used to treat extrapyramidal symptoms).
There are also categories for:
333.99 Neuroleptic-Induced Acute Akathisia
333.82 Neuroleptic-Induced Tardive Dyskinesia
332.1 Neuroleptic-Induced Parkinsonism
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Psyclops said:
Cogwheeling, or muscle regidity at rest is part of parkinsonism. Probably due to the neuroleptic D2 blockage resulting in to much acetylcholine.
You can give cogentin or another anti-cholinergic drug. Or even parkinsons drugs for it.
Although I wonder how giving something like Levodopa will interfere with a neuroleptic and or it's efficacy.
Solideliquid said:
Badly... hallucinations are a common side effect with sinemet... full blown psychosis in overdose.
Doc Samson said:
Can you explain the pathophys behind the others? (Akathesia, Dystonia, and TD)
Thanks Samson!
Solideliquid said:
I've seen cogwheeling in other degenerative brain d/o too - people were on thorazine (and yes we all know the shuffle) but I'll tell you what, I saw some SERIOUS cogwheeling as well. There are a few brain lesions that will present with cogwheeling too - although I can't tell you what the lesions are, probably SN infarct?
It's fairly common on inpatient units.Psyclops said:
Saw it today as a matter of fact - in an older patient in which we increased zydis. Saw a Pisa syndrome too in its classic etiology.
Poety said:Is this on a test Solid?
pathophys freak 😱 😀 😛
LOL I just don't want to be outdone by the med students...MUST rule with an iron fist! just kidding...
Thanks everyone, but I knew what casued it generally, being EPS and all. And I knew it could be treated with cogentin or another anti-cholinergic. What I was hoping to get is why it occurs in the "click, click, click" way, I find that so creepy.
Psyclops said:
Well, they're rigid, so its hard for them to move their limbs, so when you pull on their arm, its the resistance of the muscle. As you're tugging, you overwhelm their resistance and it gives in a little each time - wait, are you talking about the pathophys of this too? Like how the stretch receptors are responding IN the muscle?
I've never seen "clicking" I've only seen stepwise resistance in cogwheeling, with gradula release. Perhaps Sazi can answer.
SOLID: GET OVER IT IWTH THE MED STUDENTS
Don't you remember the interns? They're the ones with the "deer caught int he headlights" syndrome
Some neurology texts classify cogwheeling as a variation of tremor, with the manifestation visible upon testing - either by wrist rotating or flexion of the arm. Evidence for this comes from that fact that cogwheeling can be seen in tremors without muscle tone increase.
Essential tremor, for example, demonstrates this finding.
If you approach these symptoms (dystonia, cogwheeling) from a Parkinson's perspective, it becomes more evident that this is a phenomena associated with a drop in intracerebral dopamine (<50% of normal). Subsequent mismatch of dopamine/cholinergic activity then contributes to symptoms.
The pathophysiology (stretch receptors, golgi tendon organs, etc, flower spray, annulospiral end organs) of the various symptoms are difficult to ascertain due to the differences in anatomic distrubition and individual differences in postsynaptic receptors for dopamine (of which there are 4 types).
Essential tremor, for example, demonstrates this finding.
If you approach these symptoms (dystonia, cogwheeling) from a Parkinson's perspective, it becomes more evident that this is a phenomena associated with a drop in intracerebral dopamine (<50% of normal). Subsequent mismatch of dopamine/cholinergic activity then contributes to symptoms.
The pathophysiology (stretch receptors, golgi tendon organs, etc, flower spray, annulospiral end organs) of the various symptoms are difficult to ascertain due to the differences in anatomic distrubition and individual differences in postsynaptic receptors for dopamine (of which there are 4 types).
