13 replies to this topic

[NG_F]

I have major problems with dopamine efficiency in the frontal cortex due to probable cell and efferent loss of dopamine from the left Caudate nucleus to the different areas of the frontal cortex.

Based on what Futurist 1000 has wrote,I have experienced these difficulties in the last 2 years........

Orbital syndrome :Emotional lability,Poor judgement and Insight,Distractability
Frontal convexity syndrome: Apathy,Psychomotor retardation,poor word list generation,Segmented visual-spatial analysis

Medial frontal syndrom(akinetic): Sparse verbal output,Lower extremity weakness,Gait abnormalities(frontal-cerebellum)ataxia>minor and bladder(urgency and frequency.


It appears that I have an ovoid lesion(8mmx3mm)from the blooming effect in the anterior portion of the left Head of the caudate nucleus,with a more mild susseptabilty of the globus pallidi(iron or mild calcification).

The origin remains a mystery.I have with the advice DDX of the original neuroradiologists ruled out Parkinson's,Huntington's,Wilsons disease,MS, Hallovordadn Shpatz variant,Hemachromatosis and Fahr's disease.

I dont have a history of hypertension and my MRA and CTA(CT angiogram) were negative for any large vessel disease or malformations.Although it's ability to view the anterior lenticulostriate arteries are limited.An MR with 7 tesla strength with a black blood aquasition sequence would be needed and is not available in North America yet for clinical purposes to my knowledge.However it is being used in Notingham England,where the MR first originated.

My MRI in Jan/07 shows this lesion to be very subtle compared to Mar/08 which the radiologists say has increased significantly based on T2 weighted and DWI sequences,howver no T2*Gradient echo was done in 2007.It has for the last 5 MRI's since Mar/08

I have had 2minor and 1 moderate concussions.1990,91 and 99 respectively, and my neurologist was insisting that this lesion was from the concussions.This from my knowledge was not possible as the forces were not severe enough to cause a shear injury.She sent me to a very intelligent Neurometabolic doctor who specializes in these non specific findings.
The junior Dr-assistant told me he thought it was a small stroke.The main doctor viewed my scans and felt that it was not a garden variety stroke and wanted to run a gambit of tests for Mitochondria disease.Blood tests MRI/MRS(Spectroscopy) and muscle biopsy.He is one of the best and deals with MIto diseases like Melas,MERFF,KKS which are genetic but can be brought on by certain neurotoxins.He also has expertise in CFS/ME and Fibromyalgia. If a Mito condition exists it can explain the propensity for a stroke-like lesion.

In 2007 I started noticing subtle cognitive problems but never gave much thought to it,but in Jan/08 I made a mistake and went to a rapid detox centre in USA for a CT withdrawal from a 14 year xanax addiction.I started on 0.5mgs and over the years it escalated to 4mgs,fighting all the time not to increase my dose.It was basically a cold turkey detox with bandaids-Neurontin,phenobarb and clonodine for Withdrawals! as needed?! Nothing first line for blood pressure which the records now show was 158/91 on discharge! I had some real bad palpitations the first 2 weeks and was not instructed to monitor my BP and the psych doctor in my province(Ontario) who agreed to monitor me post detox was ignorant and never inquired or instructed.
The few times I checked in Jan,Feb and March 04 they were within normal,but what happened for 2 weeks before BP was taken in Jan or after discontinuation of clonodine which they did NOT tell me to taper gradualy! I may have suffered from clonodine rebound hypertension.After my MRI on Mar.17/08 revealed this lesion which the first radiologist missed I was devestated and thought for sure I was damaged.

I wouldn't make it cold turkey anyway.

Sorry for all the details but I felt it was needed to give you an idea as to the complexity of the situation so you would be better suited to give me some possible advice.

Since 2008 I have symptoms of fatigue,abulia,Anxiety,processing and concentration problems.Retrieval difficulties and short/long term memory problems that were not there before.As well as some vocal tics.
I haven't been to the gym or sociable since this occured.

I was using pharm grade piracetam from a compounder(2400mgs/day) cobined with AOR citicholine and loved it.This was from 2005 to the end of 2007.I am more sensitive to all supplements now and am not sure that my symptom emergence and "lesion increase" are not from a failed withdrawal syndrome that might have caused a huge glutamate influx.
I am determined to try again slowly if I get approval from this Neurometabolic doctor.
I was considering Neuroreplete which was developed by Dr.Marty Hinz and has been shown to be clinically efective on neurotransmitter balance and repair instead of depletion from long term AD and stimulant medication.I was also going to restart my Pir/CDP choline combo.I have some Nootropil but it is expensive.What brand of bulk powder do you recommend?

I'd really appreciate any and all advice as to your thoughts of how to balance and increase dopamine afferent to the wounded caudate so that I can increase my efferent projections to the prefrontal cortex and mitigate my symptoms. I dont know how much can be improved but feel free to suggest any supps or meds that you would recomend and please look into Neuroreplete and tell me what you think.

Just an update> the neurometabolic doctors have found a slightly mild IgG cardiolipin level last week : 17 and it should be <15 although negative for antibodies is <6.

The hematologist did an IgM cardiolipin and a Lupus coagulant antibody to rule out phospholipd antibody syndrome.He doubts I have it,however even a mild positive result in IgG means that the antibodies are attacking my vessel walls and making me sensitive to clots(thrombosis) especially in the small feeding arteries and arterioles in subcortical structures.


BTW once 7Tesla MRI's are available in a clinical setting you will be able to visualize neuochemical activity instead of just structure because they will measure and track sodium changes and spin dynamics unlike regular MRI's which can only track proton molecules. I just had a SPECT on thursday.It probably wont add much but we'll see if there is any perfusion problems.

Left Head of Caudate via T2 Fast-Spin Echo Axial sequence


Left Head of Caudate on Coronal Gradient Echo


Left Head of Caudate via T2*Gradient Echo Axial sequence

This is less evident then the coronal gradient echo because of slice thickness 5mm vs.2mm

Left Head of caudate via Susceptability Weighted Image Axial sequence


Lesion is more evident and pronounced due to the susceptability of 3-D GRE and the BOLD component which is highly sensitive to signal loss from Iron or Hemosiderin

Other than Nootropics and medications to help with the prefrontal loss of dopamine input,I have to remain hopeful for the successful use of stem cell therapy to help me one day,as they have been used for Basal Ganglia strokes or other conditions like cerebral microbleeds and hopefully degenerative diseases like Huntingtons and Parkinsons.

Here is a link to a 60yr old lady who suffered Dysarthia from a Right-sided Caudate microbleed with a history of Hypertension.She presented in the acute phase with dysarthia and her lesion appears Hyperintense(bright white) on T1 and T2 Images because MRI is based on the deoxyhemoglobin in immediate scanning.Itis not until >14 days that the lesion will break down to hemosiderin that it can be seen as a low intensity T2 shortening(black)lesion on the gradient echo sequences accompanied by other smaller pettechial hemorhagic lesions on subsequent slices.

Caudate Microbleed

Thank you in advance to all advice,information and suggestions

Attached Files

•  Caudate_coronal_GRE.jpg   7.55KB   4 downloads

Edited by NG_F, 12 September 2009 - 11:01 PM.

[Blue]

There are various prescription dopamine agonists available. Have you discussed them with your neurologist?
http://en.wikipedia....opamine_agonist

Edited by Blue, 12 September 2009 - 11:33 PM.

[Rational Madman]

There are various prescription dopamine agonists available. Have you discussed them with your neurologist?
http://en.wikipedia....opamine_agonist

Since there is no sign of a serious cognitive deficit, and because you've offered no evidence to suggest that you've experienced the most suggestive symptoms of a small stroke:

-Sudden weakness, numbness or paralysis in your face, arm or leg, typically on one side of your body
-Slurred or garbled speech or difficulty understanding others
-Sudden blindness in one or both eyes or double vision
-Dizziness, loss of balance or coordination

I'm inclined to believe that the lesion has a different, and perhaps less threatening origin. At the same time, though, the empirical evidence that you've presented suggests that there you face a heightened risk of suffering a stroke. So, perhaps it might be appropriate to address these concerns in some way. But, since my understanding of neurology is relatively limited, I could be terribly wrong. Therefore, because no one in this community possesses the requisite expertise to render a diagnosis with high confidence, and because of the implications of this diagnosis, I would seek a second opinion.

Due to the seriousness of your situation, I think a prescription for Razadyne or Aricept might be warranted. Because both agents are acetylcholinesterase inhibitors, and increase dopamine levels in the prefrontal cortex, they are likely to be immensely helpful with your cognitive complaints. Eventually, you should probably add a dopaminergic agent, and possibly, an atypical antipsychotic for normalizing dopamine concentrations in the limbic system and the prefrontal cortex. But before this happens, you need to find a physician amenable to this approach.

Edited by Rol82, 13 September 2009 - 10:00 AM.

[NG_F]

There are various prescription dopamine agonists available. Have you discussed them with your neurologist?
http://en.wikipedia....opamine_agonist

Since there is no sign of a serious cognitive deficit, and because you've offered no evidence to suggest that you've experienced the most obvious symptoms of a transient ischemic attack:

-Sudden weakness, numbness or paralysis in your face, arm or leg, typically on one side of your body-
-Slurred or garbled speech or difficulty understanding others
-Sudden blindness in one or both eyes or double vision
-Dizziness, loss of balance or coordination

I'm inclined to believe that the lesion has a different origin. At the same time, though, the empirical evidence that you've presented suggests that there you face a heightened risk of suffering a stroke. So, perhaps it might be appropriate to address these concerns in some way. But, since my understanding of neurology is relatively limited to the understanding of your physician, I could be terribly wrong. Therefore, because no one in this community possesses the requisite expertise to render a diagnosis with high confidence, and because of the implications of this diagnosis, I would get a second opinion.

Due to the seriousness of your situation, I think a prescription for Razadyne or Aricept might be warranted. Because both agents are acetylcholinesterase inhibitors, and increase dopamine levels in the prefrontal cortex, they are likely to be immensely helpful with your cognitive complaints. Eventually, you should probably add a dopaminergic agent, and possibly, an atypical antipsychotic for normalizing dopamine concentrations in the limbic system and the prefrontal cortex. But before this happens, you need to find a physician amenable to this approach.

Thank you Blue and Rol82 for your advice and recommendations.I will address these suggestions as well as my own to my neurologist,who I will be seeing this week coming up.
She will also be receiving a letter from the neuro-metabolic clinic outlining their findings as well as their strong opinion that this lesion is not due to trauma or toxins as they explained to me in clinic.

I'm aware of all the dopamine agonists,but did not know which one would be efficacious for my condition,unless it's a trial and error as many others have to go through.I was not aware that galantamine increases dopamine in the pre-frontal cortex so thanks for that piece of information as well as needing to modulate between limbic and frontal cortex.What about the addition of racetams-CDP choline or DMAE to the galantamine?

Rol82 what is your outlook for something like Neuroreplete to bolster neurotransmitters in the brain added with the medications?

Also is stem cell therapy a viable approach in the near future?I dont know if the cells were able to be implanted and proliferate if they would make more nigrostriatal connections to the pre-frontal cortex or not.

I am having such a hard time in this last year.I have been stripped of most of my strongest physical,mental and sexual abilities.You should read about the cognitive and MS like fatigue and weakness associated with Phospholipid antibody syndrome apart from the stroke damage that can occur,as it is an attack somewhat on the Mitochondria's and this antibody is elevated in many conditions including MS,CFS,ME, alzheimers and parkinson's and a lot of conditions that present with debilitating fatigue.

I am religious and don't believe in suicide,however it get's unbearable and I cannot see myself living like this for another 5 years.Especially since I get a lot of negative intrusive thoughts that just circle over and over in my mind all day and night,and it's hard to distract myself physically as I get exhausted very easily.I was an honour student in school.I had a decent job a few years ago,a girlfriend and was very sociable with an ability to make others laugh and feel positive energy.I had a strong confident mind,personality and body.
I guess suicide isn't an option as no one knows about a possible afterlife,as another member from here already mentioned.

Rol82 I was curious as to what you thought could be another possible origin for this lesion?

I dont think that this was a TIA but possibly a small stroke(thrombotic) in the small feeding medial lenticulostriate arteries or arterioles and I'm not sure as to whether one would experience temporary physical or sensory loss or not? Although the 60 year old lady did experience dysarthia upon presentation so you would think so.

Thanks again for everyone's suggestions and input!

Edited by NG_F, 13 September 2009 - 03:42 AM.

[Blue]

I would be careful regarding claims for Neuroplete:
http://www.fda.gov/I...5/ucm075646.htm

I would not try many new substances at the same time. Add one, like the ones mentioned by Rol82, and see the effects before changing anything else (while also being aware that there are placebo effects).

If you are strongly depressed and not merely having a lack of energy then an antidepressant may be appropriate.

You could try starting a thread on Neurotalk, maybe their "General Health Conditions & Rare Disorders" forum. There may be more people with clinical neurological knowledge there.
http://neurotalk.psychcentral.com/

[Rational Madman]

There are various prescription dopamine agonists available. Have you discussed them with your neurologist?
http://en.wikipedia....opamine_agonist

Since there is no sign of a serious cognitive deficit, and because you've offered no evidence to suggest that you've experienced the most obvious symptoms of a transient ischemic attack:

-Sudden weakness, numbness or paralysis in your face, arm or leg, typically on one side of your body-
-Slurred or garbled speech or difficulty understanding others
-Sudden blindness in one or both eyes or double vision
-Dizziness, loss of balance or coordination

I'm inclined to believe that the lesion has a different origin. At the same time, though, the empirical evidence that you've presented suggests that there you face a heightened risk of suffering a stroke. So, perhaps it might be appropriate to address these concerns in some way. But, since my understanding of neurology is relatively limited to the understanding of your physician, I could be terribly wrong. Therefore, because no one in this community possesses the requisite expertise to render a diagnosis with high confidence, and because of the implications of this diagnosis, I would get a second opinion.

Due to the seriousness of your situation, I think a prescription for Razadyne or Aricept might be warranted. Because both agents are acetylcholinesterase inhibitors, and increase dopamine levels in the prefrontal cortex, they are likely to be immensely helpful with your cognitive complaints. Eventually, you should probably add a dopaminergic agent, and possibly, an atypical antipsychotic for normalizing dopamine concentrations in the limbic system and the prefrontal cortex. But before this happens, you need to find a physician amenable to this approach.

Thank you Blue and Rol82 for your advice and recommendations.I will address these suggestions as well as my own to my neurologist,who I will be seeing this week coming up.
She will also be receiving a letter from the neuro-metabolic clinic outlining their findings as well as their strong opinion that this lesion is not due to trauma or toxins as they explained to me in clinic.

I'm aware of all the dopamine agonists,but did not know which one would be efficacious for my condition,unless it's a trial and error as many others have to go through.I was not aware that galantamine increases dopamine in the pre-frontal cortex so thanks for that piece of information as well as needing to modulate between limbic and frontal cortex.What about the addition of racetams-CDP choline or DMAE to the galantamine?

Rol82 what is your outlook for something like Neuroreplete to bolster neurotransmitters in the brain added with the medications?

Also is stem cell therapy a viable approach in the near future?I dont know if the cells were able to be implanted and proliferate if they would make more nigrostriatal connections to the pre-frontal cortex or not.

I am having such a hard time in this last year.I have been stripped of most of my strongest physical,mental and sexual abilities.You should read about the cognitive and MS like fatigue and weakness associated with Phospholipid antibody syndrome apart from the stroke damage that can occur,as it is an attack somewhat on the Mitochondria's and this antibody is elevated in many conditions including MS,CFS,ME, alzheimers and parkinson's and a lot of conditions that present with debilitating fatigue.

I am religious and don't believe in suicide,however it get's unbearable and I cannot see myself living like this for another 5 years.Especially since I get a lot of negative intrusive thoughts that just circle over and over in my mind all day and night,and it's hard to distract myself physically as I get exhausted very easily.I was an honour student in school.I had a decent job a few years ago,a girlfriend and was very sociable with an ability to make others laugh and feel positive energy.I had a strong confident mind,personality and body.
I guess suicide isn't an option as no one knows about a possible afterlife,as another member from here already mentioned.

Rol82 I was curious as to what you thought could be another possible origin for this lesion?

I dont think that this was a TIA but possibly a small stroke(thrombotic) in the small feeding medial lenticulostriate arteries or arterioles and I'm not sure as to whether one would experience temporary physical or sensory loss or not? Although the 60 year old lady did experience dysarthia upon presentation so you would think so.

Thanks again for everyone's suggestions and input!

While worrisome, and of an unsure origin, the lesion might be relatively harmless. If that ends up being the case, it's possible that your previous bout with Xanax is one of several possible independent variables--because of its pharmacological profile and the relatively high incidence of cognitive impairment associated with use. The duration and level of impairment, of course, is a function of the dose.

Edited by Rol82, 13 September 2009 - 11:10 AM.

[NG_F]

I would be careful regarding claims for Neuroplete:
http://www.fda.gov/I...5/ucm075646.htm

I would not try many new substances at the same time. Add one, like the ones mentioned by Rol82, and see the effects before changing anything else (while also being aware that there are placebo effects).

If you are strongly depressed and not merely having a lack of energy then an antidepressant may be appropriate.

You could try starting a thread on Neurotalk, maybe their "General Health Conditions & Rare Disorders" forum. There may be more people with clinical neurological knowledge there.
http://neurotalk.psychcentral.com/

Blue of course Marty Hinz would be addressed with a letter from the FDA. Think about the profits that Big Pharma stand to lose if a majority or people could treat depression,ocd, ADD and weight gain by balancing out but more importantly giving the brain the raw materials to manufacture neurotransmitters.

I agree they should not claim that it will help cure any diseased state,but you cannot refute the science behind it-repleting instead of transporting to different sites and preventing re-uptake but with long term depletion.This is why so may people tank on certain psych meds and when they try to withdrawal they have a difficult time.
It has been used succesfully as an ajunct or to help withdrawals off of various meds when their reserves are nullified.My viewpoint is it cannot hurt being 100% pharm grade unless the patient is in need of something more immediate and stronger.

What I like to do with anything is type in the name of something I'm interested in and then add reviews at the end to get various unbiased opinions and results from a large variety of affected individuals.

Which antidepressant would you recommend? I would only try zoloft from the ssri's or a MAO inhibitor like parnate to avoid any further cognitive decline.

Thank you for your recommendation for posting at Neurotalk.I haven't been there in a while but have been a member for over a year

[NG_F]

There are various prescription dopamine agonists available. Have you discussed them with your neurologist?
http://en.wikipedia....opamine_agonist

Since there is no sign of a serious cognitive deficit, and because you've offered no evidence to suggest that you've experienced the most obvious symptoms of a transient ischemic attack:

-Sudden weakness, numbness or paralysis in your face, arm or leg, typically on one side of your body-
-Slurred or garbled speech or difficulty understanding others
-Sudden blindness in one or both eyes or double vision
-Dizziness, loss of balance or coordination

I'm inclined to believe that the lesion has a different origin. At the same time, though, the empirical evidence that you've presented suggests that there you face a heightened risk of suffering a stroke. So, perhaps it might be appropriate to address these concerns in some way. But, since my understanding of neurology is relatively limited to the understanding of your physician, I could be terribly wrong. Therefore, because no one in this community possesses the requisite expertise to render a diagnosis with high confidence, and because of the implications of this diagnosis, I would get a second opinion.

Due to the seriousness of your situation, I think a prescription for Razadyne or Aricept might be warranted. Because both agents are acetylcholinesterase inhibitors, and increase dopamine levels in the prefrontal cortex, they are likely to be immensely helpful with your cognitive complaints. Eventually, you should probably add a dopaminergic agent, and possibly, an atypical antipsychotic for normalizing dopamine concentrations in the limbic system and the prefrontal cortex. But before this happens, you need to find a physician amenable to this approach.

Thank you Blue and Rol82 for your advice and recommendations.I will address these suggestions as well as my own to my neurologist,who I will be seeing this week coming up.
She will also be receiving a letter from the neuro-metabolic clinic outlining their findings as well as their strong opinion that this lesion is not due to trauma or toxins as they explained to me in clinic.

I'm aware of all the dopamine agonists,but did not know which one would be efficacious for my condition,unless it's a trial and error as many others have to go through.I was not aware that galantamine increases dopamine in the pre-frontal cortex so thanks for that piece of information as well as needing to modulate between limbic and frontal cortex.What about the addition of racetams-CDP choline or DMAE to the galantamine?

Rol82 what is your outlook for something like Neuroreplete to bolster neurotransmitters in the brain added with the medications?

Also is stem cell therapy a viable approach in the near future?I dont know if the cells were able to be implanted and proliferate if they would make more nigrostriatal connections to the pre-frontal cortex or not.

I am having such a hard time in this last year.I have been stripped of most of my strongest physical,mental and sexual abilities.You should read about the cognitive and MS like fatigue and weakness associated with Phospholipid antibody syndrome apart from the stroke damage that can occur,as it is an attack somewhat on the Mitochondria's and this antibody is elevated in many conditions including MS,CFS,ME, alzheimers and parkinson's and a lot of conditions that present with debilitating fatigue.

I am religious and don't believe in suicide,however it get's unbearable and I cannot see myself living like this for another 5 years.Especially since I get a lot of negative intrusive thoughts that just circle over and over in my mind all day and night,and it's hard to distract myself physically as I get exhausted very easily.I was an honour student in school.I had a decent job a few years ago,a girlfriend and was very sociable with an ability to make others laugh and feel positive energy.I had a strong confident mind,personality and body.
I guess suicide isn't an option as no one knows about a possible afterlife,as another member from here already mentioned.

Rol82 I was curious as to what you thought could be another possible origin for this lesion?

I dont think that this was a TIA but possibly a small stroke(thrombotic) in the small feeding medial lenticulostriate arteries or arterioles and I'm not sure as to whether one would experience temporary physical or sensory loss or not? Although the 60 year old lady did experience dysarthia upon presentation so you would think so.

Thanks again for everyone's suggestions and input!

While worrisome, and of an unsure origin, the lesion might be relatively harmless. If that ends up being the case, it's possible that your previous bout with Xanax is one of several possible independent variables--because of its pharmacological profile and the relatively high incidence of cognitive impairment associated with use. The duration and level of impairment, of course, is a function of the dose.

Rol82 I pray your right! I've thought about a failed detox and my body still being in withdrawal state.I have noticed a slight problem with memory in 2007,this is when the lesion was very subtle and I could still remember most things and muti-task and had no fatigue,abulia or vocal tics.
With thrombotic strokes from Phospholipid antibody syndrome when strokes reoccur they usually do so in the same vascular beds.Hard to believe that i could have such bad luck as to have 3 concussions,a small subtle asymtomatic stroke in 2007 and then an MRI in Mar/2008 with the radiologists stating that there has been a significant increase from Jan.15/07 to Mar17/08 with many debilitating symptoms.

Howver I have done SPECT on Friday,I will do MRI spectroscopy to determine glutamate and gaba levels as well as Lactate,choline/creatine and N-acetyl asparate levels. N-A-A can be used to see how much cell loss has occurred roughly and then compare it to the contra-lateral non-lesioned caudate to get an estimate.
I will also do MRI perfusion weighted imaging to see quantative arterial perfusion as well as DWI tensor imaging.

Rol82 would you recommend galantamine over donzepil combined with DMAE?

Mirapex or Amantadine? I found fenoldopam as weak D1 partial agonist and I
will suggest to Strange Aeons as I know he was looking for a specific D1 agonist.

For atypical anti-psychotic: Serequel,Risperidone or amilsulpride?

I dont want to add too many neurochemicals/noots to the mix as one can be asking for trouble and not knowing what med/supp is doing what.This was also recommended by Blue but was just wondering about racetams-Pir or Ani?

Thanks again for your help

[NG_F]

I got my SPECT scan back yesterday and to no surprise it was totally normal.
No perfusion problems.It's to be expected other than in cases of severe dementia and major-large strokes or tumors.

QEEG and some more quantitative MR sequences would be a good step from here.

[NG_F]

Here is a great article on Caudate vascular lesions...Caudate Stroke

Notice Images #11 and # 25.There is obvious simillarities in lesion size,area and appearance to the one that I have sustained.You can compare to the other larger more involved strokes or hemorhages that involve maybe several small arteries or the recurrent artery of Heubner.
Template of Vascular lesions

[Galantamine]

There are various prescription dopamine agonists available. Have you discussed them with your neurologist?
http://en.wikipedia....opamine_agonist

Since there is no sign of a serious cognitive deficit, and because you've offered no evidence to suggest that you've experienced the most suggestive symptoms of a small stroke:

-Sudden weakness, numbness or paralysis in your face, arm or leg, typically on one side of your body
-Slurred or garbled speech or difficulty understanding others
-Sudden blindness in one or both eyes or double vision
-Dizziness, loss of balance or coordination

Although it does look like an infarct, the symptoms you listed above are not likely to be experienced based on where the lesion is located. The first symptoms would have to be a lesion to the internal capsule (posterior limb for the limbs, and genu for the face), brainstem, exc. The second symptoms would be indicated for a lesion to a number of different places including the neocortex (production - brocas, comprehension - wernicke's - comprehension), thalamus, or their tracts, and the last symptom would be indicated for a dorsal column (proprioception) or cerebellar lesion.

The location of the lesion above would likely produce motor deficits; speficically hyperkinetic deficits (hemiballismus).

Edited by Irish MD, 06 November 2009 - 04:12 PM.

[NG_F]

The location of the lesion above would likely produce motor deficits; speficically hyperkinetic deficits (hemiballismus).

That's not true.That would be more specific for the body of the caudate.The head is responsible for multimodal functioning,processing,executive functioning,shot/long term memory(aquasition,retention and retreival) and for motivation and task completion as it is involved heavily in the dopamine reward system.

The left head of caudate is strongly intervated with dopamine and gabaergic neurons and serves as a dense subcotical grey structure in the basal ganglia.It receives strong afferents from the substantia Nigra pars compacta and from the Ventral Tagmental area which is then further delivered from caudate efferent pathways/circuits to the PFC.

Lesions to the caudate are very similar to lesions/damage in the frontal cortex.Since it's density and size are very small a small lesion can cause devastational effects.

Left damage is more severe then right as far as cognition goes because the left brain is more responsible for thinking,logic,memory,problem solving and executive functioning where the right side is more for creative,art and abstract.

It also serves as being inhibitory from over stimulation of efferent projections from the frontal,temporal and parietal lobes where dysfunction to the thalamic loop can cause agitation,anxiety,ocd and schizoaffective type behaviours

therefore damge to the left head of the caudate nucleus can cause fluctuations with abulia,apathy,depression,slowness and a corresponding agitation,anxiety and hyperstimulation.

Please read the Caudate link in post # 10 and tell me what you think.Thank you

[Galantamine]

Please read the Caudate link in post # 10 and tell me what you think.Thank you

I read the link. The individuals that experience these symptoms would have infarct including and outside of the caudate (watershed phenomenon) - which is what is described in the link I believe.

That's not true.That would be more specific for the body of the caudate.The head is responsible for multimodal functioning,processing,executive functioning,shot/long term memory(aquasition,retention and retreival) and for motivation and task completion as it is involved heavily in the dopamine reward system.

I'm not sure where you are getting your information, but this is unlikely (or highly theoretical at best).

The left head of caudate is strongly intervated with dopamine and gabaergic neurons and serves as a dense subcotical grey structure in the basal ganglia.It receives strong afferents from the substantia Nigra pars compacta and from the Ventral Tagmental area which is then further delivered from caudate efferent pathways/circuits to the PFC.

I believe you are trying to describe the tract deficits producing the hyperkinetic symptoms (if present) i.e. basal ganglia tracts.

[NG_F]

I read the link. The individuals that experience these symptoms would have infarct including and outside of the caudate (watershed phenomenon) - which is what is described in the link I believe.

Image #11,23L, 25 R, and 29 are not watershed.The only problem is to find out which slices are CT and which are MRI? As a small old infarct in # 29R is on CT and would be much larger on MRI because of the susceptability effect.

I tried emailing Emre Kumral who is in the Stroke and Neuropsychology Unit and contributed to the article but the email is old and dead.I also tried calling the Department of Neurology in Ege University but they all speak Turkish and I need to find a translator here or there.

Another possibility is a caudate microbleed,but those are rarely solitary and are almost always round(punctate) and are roughly 2-5mm in diameter.My lesion is ovoid and is 8mm longx 3mm in the tranverse dimension,

Caudate Microbleed

I'm not sure where you are getting your information, but this is unlikely (or highly theoretical at best).

Caudate Head

I think this is where an AP like amilsulpride may have some potential?

I believe you are trying to describe the tract deficits producing the hyperkinetic symptoms (if present) i.e. basal ganglia tracts.

Long term Impairment with Caudate lesions