This has helped me to better understand my husband's recent diagnosis Major Neurocognitive Disease, stage 4. He sees a gerontologist. Three years ago he scored 27 on the FAST test, Recently, he scored a 24, so he is declining. We needed a letter with a diagnosis for our lawyer, financial advisor and credit union. Thank you.
Thank you so much! I have a hard time in my Diagnosis class and this lecture helped me to understand clearly what is written in the DSM-5. I shared with my classmates as well 😁 Thank you!
Dementia with Lewy bodies (DLB) is a subtype of PD, these two terms are not used interchangeably. "Parkinson's disease with dementia (PDD) and dementia with Lewy bodies (DLB), which are two different presentations of a single underlying disease process leading to the deposition of alpha-synuclein. Clinically, PDD is distinguished from DLB alone by the different temporal manifestations of extrapyramidal motor symptoms." (www.ncbi.nlm.nih.gov/pubmed/18787881)
Exactly. There is dementia with Lewy Bodies and there is Parkinson's dementia. Both are referred to as Lewy Body but they differ is the order in which symptoms appear.
Dr...thks 4 your help....in min 44.00 Wilson disease, you mention It is because a ceruloplasmin deficit, when it should be mention as a ATP7a receptor déficit that impedes copper transport to Golgi and cytoplasmic accumulation with rising free copper levels in bloodstream. Cheers
With thiamine deficiency section, did you mean to say that giving folic acid before B12 can cause subacute combined degeneration? I don't see information for thiamine causing it?
Both deficiencies have similar presentations. However, if you treat with folic acid without making sure the Vit B 12 is corrected, that may continue to affect the patient, even though the patient may feel somewhat better, since both work together for DNA synthesis. Folic acid supplementation in the face of Vitamin B12 deficiency may actually worsen the neurologic deficit as it goes on untreated.
I think he mistakenly connected thiamine deficiency to subacute combined degeneration as that is related to vitamin B12 (which the patient might be deficient in as well due to chronic alcoholism and malnutrition). I think the main issue here is that thiamine is an important co factor for the Pyruvate Dehydrogenase enzyme that converts Pyruvate into Acetyl-CoA so it can enter the krebs cycle. By giving a patient deficient in thiamine dextrose, all the sugar will be unable to enter krebs cycle and undergo anaerobic metabolism and lactate production eventually leading to lactic acidosis (which can be fatal).
This has helped me to better understand my husband's recent diagnosis Major Neurocognitive Disease, stage 4. He sees a gerontologist. Three years ago he scored 27 on the FAST test, Recently, he scored a 24, so he is declining. We needed a letter with a diagnosis for our lawyer, financial advisor and credit union. Thank you.
Great review even in 2021! Good to listen on 1.5x or 1.75x speed.
Thank you so much! I have a hard time in my Diagnosis class and this lecture helped me to understand clearly what is written in the DSM-5. I shared with my classmates as well 😁 Thank you!
Dementia with Lewy bodies (DLB) is a subtype of PD, these two terms are not used interchangeably.
"Parkinson's disease with dementia (PDD) and dementia with Lewy bodies (DLB), which are two different presentations of a single underlying disease process leading to the deposition of alpha-synuclein. Clinically, PDD is distinguished from DLB alone by the different temporal manifestations of extrapyramidal motor symptoms." (www.ncbi.nlm.nih.gov/pubmed/18787881)
exactly. I got confused when he said its the same thing
Exactly. There is dementia with Lewy Bodies and there is Parkinson's dementia. Both are referred to as Lewy Body but they differ is the order in which symptoms appear.
Thank you for posting this video. We are covering neurocognitive disorders in my graduade psychology program and this has helped immensely!
loving it bro 7 years on.
Thank you. No studying medicine but your lecture has me wondering why I have not thought to study medicine.
Never too late!
thanks for Dr paul Bolin
Dr...thks 4 your help....in min 44.00 Wilson disease, you mention It is because a ceruloplasmin deficit, when it should be mention as a ATP7a receptor déficit that impedes copper transport to Golgi and cytoplasmic accumulation with rising free copper levels in bloodstream. Cheers
for CJD it worth to mention the 14-3-3 protein on CSF sampling
thank you for the video
Excuse me, what do you mean by "14-3-3"?
Thanks for sharing such wonderful review
Thanks
Thank you so much for sharing your wisdom with us. Great videos.
In the pie chart, why is Lewy body a segment different from Parkinson's disease dementia?
Thank you so much for your hard work--
thank you
Benztropine is an antagonist of cholinergic receptors it is not a dopamine analogue
It does both but more strongly anticholinergic according to Stahl prescriber's guide
Dr, can you update this video with the DSM 5TR please!!
Thank u so much sir that was very helpful ❤❤
Thank you Doc 👍
Thank you very much!
Happy New Year Dr Paul Bolin and thank you :)
Outstanding
thank
@25.08 , it’s Dysphasia Not Dysphagia , respected Sir
Benzatropine is a centrally acting anticholinergic/antihistamine agent. Did you mean bromocriptine, which is a dopamin agonist?
With thiamine deficiency section, did you mean to say that giving folic acid before B12 can cause subacute combined degeneration? I don't see information for thiamine causing it?
Both deficiencies have similar presentations. However, if you treat with folic acid without making sure the Vit B 12 is corrected, that may continue to affect the patient, even though the patient may feel somewhat better, since both work together for DNA synthesis. Folic acid supplementation in the face of Vitamin B12 deficiency may actually worsen the neurologic deficit as it goes on untreated.
I think he mistakenly connected thiamine deficiency to subacute combined degeneration as that is related to vitamin B12 (which the patient might be deficient in as well due to chronic alcoholism and malnutrition).
I think the main issue here is that thiamine is an important co factor for the Pyruvate Dehydrogenase enzyme that converts Pyruvate into Acetyl-CoA so it can enter the krebs cycle. By giving a patient deficient in thiamine dextrose, all the sugar will be unable to enter krebs cycle and undergo anaerobic metabolism and lactate production eventually leading to lactic acidosis (which can be fatal).
Thiamine is vitamin b1!!!!!!!
The
the what?
Hey, you're pretty cute! I'll look you up when I'm in the Boston area :P