Interesting consult...

Started by Doc Samson
Get help with your application

Use all the free resources available to you from SDN: articles, guides, expert advising, forums discussions, and school research.

Browse articles Compare schools My application plan Read Interview Feedback
Practice for interviews Ask an Advisor
Doc Samson

Doc Samson

gamma irradiated
Verified Member
Physician
15+ Year Member
I'll skip most of the details for the sake of confidentiality, but long story short:

Late 40's male with advanced Hep C, on methadone maintenance, presents with s/s of tardive dyskinesia. No history of neuroleptic exposure.

Questions?
 
How many years on methadone maintenance?

Some evidence has shown than >3yrs of exposure to methadone has effects on prolactin levels. Since prolactin normally is under tonic inhibitory control by dopimineregic factors & possibly dopamine itself...perhaps the duration of methadone exposure has "induced" (could that be the correct phrase) an altered movement disorder, particularly in view of the possibly altered metabolism of methadone by the hepatic disorder.

I have no specific evidence to suggest that this is a direct side effect of the drug...but long term methadone exposure definitely changes a variety of hormonal & neurohormonal balances over time.

Just a thought....
 
Please be more specific when you say s/s of tardive dyskinesia.

What specifically is the patient doing? Is it pure tongue movements or is there blinking as well? Other body parts other than head/face?

Ddx includes Meige's syndrome, rabbit syndrome, even Huntington's. More details, please 😀

Also:
Carlson KR. A syndrome resembling tardive dyskinesia which results from chronic methadone treatment. Psychopharmacology Bulletin. 14(4):76-7, 1978 Oct.

Of course the article is too old for electronic access...
 
Doc Samson said:
I'll skip most of the details for the sake of confidentiality, but long story short:

Late 40's male with advanced Hep C, on methadone maintenance, presents with s/s of tardive dyskinesia. No history of neuroleptic exposure.

Questions?
Click to expand...

Is this the old, long-term-methadone, then dyskinesia following amphetamine trick?

Someone challenged this guy with a stimulant for his interferon-induced depression and came up with TD?
 
Doc Samson said:
I'll skip most of the details for the sake of confidentiality, but long story short:

Late 40's male with advanced Hep C, on methadone maintenance, presents with s/s of tardive dyskinesia. No history of neuroleptic exposure.

Questions?
Click to expand...

Isn't this the time when you come back with another tidbit to the puzzle?

Got any more you can share???

I'm waiting on pins and needles😀 .
 
Sorry for the delay folks... 20 consults called in before 8:30 this morning.

Anyway... asking for more history is always a great response when you're getting pimped:

In terms of the exam:
Choreoathetoid movements of the upper extremeties bilaterally. Marked adventitious orobuccolingual movements. Speech is hypophonic and nasal. All of this new in the past ~8 weeks. No new meds.

Pt has been on Methadone 50 mg daily x 7 years. Is the star of the program, gets all his doses as take homes, no positive tox screens since starting tx.

Reglan, for all intents and purposes, is a neuroleptic. Hasn't taken it.

I found the same article by Carlson... it's about rhesus monkeys.
 
Can I ask you another question (sorry - not a med student🙁 )?

How are LFT's - any change in the last 8-12 weeks?

Are serum proteins the same as in the recent past?

Has renal function changed in the recent past?

I may be inappropriate in entering your thread...but, I do love a drug related question.

Oh...and sorry about your morning. But.....its getting close to the holidays🙁 ....in my area....our mhu gets busy this time of year until after New Years.
 
sdn1977 said:
Can I ask you another question (sorry - not a med student🙁 )?

How are LFT's - any change in the last 8-12 weeks?

Are serum proteins the same as in the recent past?

Has renal function changed in the recent past?

I may be inappropriate in entering your thread...but, I do love a drug related question.

Oh...and sorry about your morning. But.....its getting close to the holidays🙁 ....in my area....our mhu gets busy this time of year until after New Years.
Click to expand...

LFTs chronically elevated, but stable. No change in serum proteins, coags, or renal function. Always happy when other disciplines take an interest in our patients.
 
Doc Samson said:
I think we can call this thread officially hijacked.
Click to expand...

I don't know what they're talking about - perhaps me & my interest...sorry again!!!!

Can I ask one more question? Is there any possibility this gentlemen could have another source of methadone?

Could he be self medicating the development of td which does indeed take place after long term methadone tx....thus the no change in tox screen?

That may be my last question (I can't promise though🙄 )

Thank you for your indulgence!😀
 
Goodness...then...I'm stumped, without doing a complete literature search.

I await your diagnosis with anticipation......🙂

(Am I a bit sick that I think this revolves around his methadone metabolism in light of his liver issues????)
 
sdn1977 said:
Goodness...then...I'm stumped, without doing a complete literature search.

I await your diagnosis with anticipation......🙂

(Am I a bit sick that I think this revolves around his methadone metabolism in light of his liver issues????)
Click to expand...

Nope... that's the same wrong tree I was barking up, even getting that article about rhesus monkeys from the library.

Imaging anyone?
 
Anasazi23 said:
Dentate nucleus degeneration?


How do you know it just isn't opiate-induced choreoform movement disorder?
Click to expand...

I thought it was, until I saw the MRI. Increased uptake in the caudates and lentiform nuclei bilaterally. Read as "concerning for Creutzfeld Jacob Dz" but, of course, ""correlate with clinical exam." He does not have CJD.
 
Now you get into more complicated differentials. Elevated LFTs, as we know, are not indicitive of Hep C infection, but can be a marker for end stage hepatic failure.

If we're talking about MRI findings pointing to those basal ganglia structures, and we're not talking about a parkinson's plus or huntingtons, it makes me think of a metal uptake problem, which they sometimes call 'adult dystonias.' Manganese, copper (similar to Wilson's) and copper, unable to be cleared by the liver, or a hemosiderosis type condition, with increased iron stores, could result in a syndrome like this. It would make sense given the compromised liver.
 
I certainly did not mean to hijack. I had a recent conversation with Sazi about interesting discussions on the psych forum, and this is definitely one of them.
 
Might not be directly relevant, but did you already post the CBC and chem 7? Magnesium?
 
Anasazi23 said:
Now you get into more complicated differentials. Elevated LFTs, as we know, are not indicitive of Hep C infection, but can be a marker for end stage hepatic failure.

If we're talking about MRI findings pointing to those basal ganglia structures, and we're not talking about a parkinson's plus or huntingtons, it makes me think of a metal uptake problem, which they sometimes call 'adult dystonias.' Manganese, copper (similar to Wilson's) and copper, unable to be cleared by the liver, or a hemosiderosis type condition, with increased iron stores, could result in a syndrome like this. It would make sense given the compromised liver.
Click to expand...

Are you saying that with Hep C, LFTs are not elevated? That's not what I heard.
 
How about a stroke, neurofibromatosis or closed head trauma? Any other hx of exposure to environmental toxins?

....I know...really out of my field....but....I love a mystery!
 
does this patient have any mood disorder symptoms? any history of mood disorder? could he be presenting with some of the lesser-known and less dramatic signs of catatonia?
 
What about peripheral blood smear? Any evidence of acanthocytosis? What about family history/pedigree?

My guess: Neuroacanthocytosis

MBK2003
 
So to sum up we have a male, late 40s with advanced Hep C, on chronic methadone. He presents with Tardive Dyskinesia.

PMHx -
--No hx of neuroleptics, including Reglan.
--Pt has been on Methadone 50 mg daily x 7 years. Is the star of the program, gets all his doses as take homes, no positive tox screens since starting tx. No illicit sources of methadone.
--No West Nile, No Lyme

In terms of the exam:
Choreoathetoid movements of the upper extremeties bilaterally. Marked adventitious orobuccolingual movements. Speech is hypophonic and nasal. All of this new in the past ~8 weeks. No new meds.


Labs –
--CBC, Chem 7, Mg/Ca/Phos all wnl.
--LFTs chronically elevated, but stable. No change in serum proteins, coags, or renal function.
--no elevation of ceruloplasm, iron studies, or heavy metal panel.
--RPR/VDRL non-reactive
--Prolactin wnl.

MRI-
--Increased uptake in the caudates and lentiform nuclei bilaterally. Read as "concerning for Creutzfeld Jacob Dz" but, of course, ""correlate with clinical exam." He does not have CJD. Other than the increased basal ganglia uptake, MRI normal.
 
Medical Student Chiming in ... (ie taking wild stabs in the dark)

How about more social history...hobbies? Employment? Smoking? Trying to Quit smoking? Drinking?

Any other problems in last 8 weeks?
Any hx of thyroid problems?
 
Has he been perhaps near any zebras😕 ?😀

Are you sure you're not making this guy up?????😳
 
I'm not sure if this was mentioned, but what is the onset of his movement disorder? Did this come on over minutes, days, weeks or months?
 
I'm not sure if this was mentioned, but what was the onset of his movement disorder? Did this come on over minutes, days, weeks or months?
 
I hate to keep coming back to this....but could this be an initial sign of methadone induced schizophrenia?

I've always heard it occurs in doses > than 60mg....but can't this one sx be a first sx occasionally?

Doesn't schizophrenia have something to do with disrupted flow (can't remember the direction actually) to or from the thalmus??? Could you see this on an MRI?
 
MRI shows increased or decreased signal intensity, with or without enhancement. I'll take your description as T2 hyperintensities in the expected areas given bilateral chorea.

In such a citizen, methanol, CO, and glue come to mind. There are numerous weird movement disorders associated with polypharm, and with doing things like chasing the dragon, and of course meth, but I don't know if they give basal ganglia changes as described. Is he ONLY on methadone?
 
OK, so first off, you guys rock. If the med students (and some of the residents) I get to deal with every day were 1/2 as enthusiastic as you guys about cases like this, my job would be much easier.

Second, I'm off to Tucson for the APM meeting tomorrow (anyone else going, BTW?), and don't want to leave you all hanging for 5 days until I get back, so here's the gist:

I, also, got hung up on the methadone as an etiology. That one article in the literature (that turned out to be about rhesus monkeys drinking methadone all day long) was something of a red herring.

Next (with the MRI in hand) I went to the heavy metals, with no joy (kinda cool though how this discussion followed my work-up).

As always, "never worry alone" so got some supervision... after digging through his files, the boss pulled out an article on Acquired Non-Wilsonian Hepatocerebral Degeneration. Essentially portosystemic shunting due to hepatic failure leads to exposure of the basal ganglia to all kinds of schmutz (manganese is thought to be a leading contributor), but serum levels of the heavy metals remain wnl. Clinically, it's a dead ringer for Wilson's disease, and has classic MRI findings IDENTICAL to the ones seen in this patient (seriously the scan in the article looked like it was lifted out of his chart). It resolves with liver transplant, which is what this pt is waiting for.

I LOVE my job.

Now, go forth and read.
 
Doc Samson said:
As always, "never worry alone" so got some supervision... after digging through his files, the boss pulled out an article on Acquired Non-Wilsonian Hepatocerebral Degeneration. Essentially portosystemic shunting due to hepatic failure leads to exposure of the basal ganglia to all kinds of schmutz (manganese is thought to be a leading contributor), but serum levels of the heavy metals remain wnl. Clinically, it's a dead ringer for Wilson's disease, and has classic MRI findings IDENTICAL to the ones seen in this patient (seriously the scan in the article looked like it was lifted out of his chart). It resolves with liver transplant, which is what this pt is waiting for.

I LOVE my job.

Now, go forth and read.
Click to expand...

One last question...did you get a fasting schmutz level?
 
You must log in or register to reply here.