36 replies to this topic

[BioFreak]

I could need some help in terms of supplementation tips for my grandmother.

beginning march 2013 she was in the hospital, for a few days she didn't get her supplements, which at that time were:

A multivitamin / fish oil supp for her dry macular degeneration
longvida curcumin 1000mg
gingko 240mg
and a new addition, ppq. PPQ might be the reason she needed to go into the hospital in the first place - she had much more energy and overdid it in the result.

Anyways, shortly after she was in the hospital she had strong disorientation(space/time), was unable to move her arms to the point where she could not eat / drink alone anymore, had strong hallucinations.
Prior to this, she was living alone, walking around, doing her stuff by her own with 100 years of age. The only things I had to do for her was to sort her supplements, go shopping for her, change the bed, and wash her stuff.

I went home and got her supplements, and within 1-2 hours, she was almost back to her old self.
Her condition was stable for the rest of the days in the hospital. I made sure she got her supps every day.

Turns out, she did not fully recover to this day.

Unfortunately 2 weeks later on the way home from the hospital a medic broke her leg, so she had to be in bed until today, which further puts stress on the mind, and on her, because she has to adjust to this situation. Today, she is so weak that she can not stand alone, but we started to train with her to get her going again.

Her mind got worse again since she left the hospital, she developed hallucinations again, spacial and time orientation is still bad and her short term memory is often nonexistent. I tell her something, she says ok, and after 10sec, she asks me again. In addition she has a lot of anxiety, and in her extremes tried to attack me verbally and physically. This is not who she is, in the 34 years I know her, she never, ever, did that.

So she got dementia. The problem is, while it was progressing very slowly, it now progresses so fast that I can not even adjust to the situation. All of this was just in 1,5 months!!!!! So basically it should not be alzheimers, it could be vascular dementia. Or curcumin and gingko masked the symptoms for years / protected her brain despite more amyloid buildup. After the supps were gone, the amyloid attacked the brain cells, causing irreparable damage in short time. That are my 2 theories.

What I tried:
Of course she still takes curcumin and gingko.
I've added noopept. (10mg twice a day)
cdp-cholin should come soon.
I removed one of her pain medications (novalgin) but she still needs tilidin (an time released opiate with antagonist which she seems to tolerate better, the side effects say nothing about hallucinations or other problems we have).
I've added NAC, 600mg twice a day. basically, because she had problems with breathing, and it helped.
I have added valeriana and humulus to calm her down, as well as lavendula. Her anxiety and panic seems to decrease since then.
We tried melperon but that stuff just made her unable to move at all, while doing nothing to calm her. damn chemicals.


I thought novalgin was the problem, but it turns out that the symptoms didn't change with stopping it.
Tilidin may be a problem too, since its an opiate. I can not get her off her pain meds though, in addition to her foot she also has rips that break very easily, which a caretaker unfortunately demonstrated some 3-4 weeks ago. :(

Her state right now:
Hallucinations (People standing in the room, insects overall, or rats, etc...)
Extreme anxiety
Not aware of time and space
Severe short term memory problems
(still) sleeping problems.
It's better in the morning.

Its obvious she needs melatonin, but in germany there are only 2mg capsules availiable, and they work exactly for 2 hours then she's awake again. Retard laws prevent us from getting better stuff.

Sleeping pills, basically anything not-that-strong on gaba receptors do work for like 1-2 days, then they stop working. And the strong stuff, has a too long half life to give it to her daily. And, honestly, I'd like to find a better way... So basically, we need to find better a melatonin supplement, and she gets nothing to sleep better right now.

Her MD is an idiot. Looking at her one time, for 5 minutes, she says that my grandma has no dementia symptoms. Often I wonder how they were able to get their MD degree...

Another thing that comes to mind is huperzine a. We might try another doctor first, or get this instead. The problem is, acetylcholinerase inhibitors are only for early stages dementia, and she progresses so fast... the question is if this helps.

I promised her that I will keep her brain healthy until she dies, but it does not look good right now.


So folks, what else ideas do you have?

Edited by BioFreak, 24 April 2013 - 03:52 PM.

[zorba990]

Sounds like she had a TIA. Get a good mri with contrast of the head and possibly ct as well. Something still going on there and needs better doctor detective work. Push hard for more testing. Cover the infection angle wirh high dose liposomal vitamin c and glutathione and check teeth and appendix and extremeties for hidden infections.

[BioFreak]

TIA?

[nowayout]

ALCAR may be a good addition, as long as it doesn't increase her anxiety.

[Godot]

Such rapid change in mental status suggests either a reaction to medication, infection, or a vascular event -- but the hallucinations are not consistent with vascular dementia.

So, was she given any new meds while hospitalized? Is she taking any now?

Otherwise, infection seems likely. Is she running a fever? Blood tests for this would be a good idea.

[Godot]

I missed the part about the meds -- it is not uncommon for opioids to induce delirium in older adults. They're a likely culprit. See if the doc can substitute something else for short-term pain control. Maybe benzos, although they can also give paradoxical reactions in the elderly sometimes.

[BioFreak]

She already got a benzo, bromazepam, at 1,5mg/day, the result was that after 3 days so much built up in her system that she was sleeping day and night. So we discontinued it. Maybe we'll get a lower dose version.

She also gets enoxaparine because she can't get out of bed, 40mg/day.

Are you sure that hallucinations are not a part of vascular dementia? Google told me otherwise but thats all I got.

While in hospital, where she first hat hallucinations, she also got pantozol, and valoron which is another name for tilidine the opiate...
mhhh. So this might be the culprit after all, at least for her hallus, after I've eliminated novalgin from the suspicion list.

The question now is - after about 4 weeks of continuous usage, can we simply stop it?

[Godot]

There's an off off chance that vascular dementia could cause hallucinations, but they likely wouldn't be part of this type of syndrome of agitation. Also, vascular dementia tends to show sudden onset, with some improvement over the first few months. Since your grandma is getting worse over time, I'm thinking she has delirium, rather than dementia.

I'd seek a second opinion from another doctor, but yeah the opioids may very well be the problem. Depending on her physical state, it may be tricky getting her off them. I wouldn't stop them all at once.

[zorba990]

TIA?

http://en.m.wikipedi...ischemic_attack

Edited by zorba990, 24 April 2013 - 05:15 PM.

[nowayout]

Those are strong psychoactive drugs to be on. Basically, I doubt you will ever know if she has organic dementia unless/until the drugs are withdrawn.

Edited by viveutvivas, 24 April 2013 - 05:35 PM.

[BioFreak]

which ones do you mean exactly?

[nowayout]

The benzos and opioids.

[BioFreak]

you were talking in plural, that made me confused. She is only taking the opiate, mixed with an opiateantagonist.
I will check with her doctor and then if possible quit the opiate, and see what happens.

[zorba990]

Also check for b12 deficiency.

[killshot]

No sleep could be causing the hallucinations also

[BioFreak]

She's already taking 1mg b12 as cyanocobalamine a day. Unfortunately her doc does not want to check "they are all deficient anyways at that age"...

still working on the no sleep thing, but she still gets plenty of sleep throughout the day, its more like her day-night cycle is broken.

As of today we will switch from the opiate back to novalgin for pain management. Let's see how it goes.

[BioFreak]

It seems like the worst withdrawal symptoms are over, after one day in agony. BP and pulse (and were) are stable, she's awake and happy, just a bit tired.
I am worried that she might have progressed in dementia further, like one study shows (post mortem brain examination of healthy young adults and same age opiate addicts). There seems to be at least one theory showing that opiate use is strongly correlated with oxygen deficiency in the brain - basically through not breathing enough, and I know my grandma was stopping to breath regularly on the opiate.
So I predict the hallucinations to be gone, and her reasoning to come back (already on the way). I am not so sure about her short term memory. I keep telling her things, and 10sec later she asks the same again ... again... and again... and again... and again... and again... and ... *sigh*

Anyone knows how long it takes after opiates for the short term memory to return?

Noopept may play its role with this too. I'm still waiting for my cdp-choline order to arrive.

Next step would be the uridine stack to help her brain to recover. Also, I need to get a prescription for a stronger, time released melatonin supp, so her sleep will be of a regenerating sort. Any other suggestions?

Thanks Goodot for pointing out the opiate thing, and all others for their posts so far.

[zorba990]

Hydergine?

[BioFreak]

Hydergine?

Thanks for suggesting this, sounds promising. I will research it a bit more thoroughly soon.

So it's day 3 since we stopped the opiate. Withdrawal symptoms are getting less quite fast, but it's too soon to tell how it is today since it seems always better in the mornings. Her hallucinations are almost nonexistent now, and her short term memory *seems* to get better.

She is now off all the hard stuff modern medicine has to offer.

Anyone knows how long it takes for short term memory to return after withdrawal from an opiate?

Bad Short term memory seems to be a possible side effect from noopept too, but starting yesterday, we have added cdp-choline to the mix. I hope this cancels out the possible negative effects from noopept(did it for me).

So basically, to get her better, the basic plan would be:

• For her to have all necessary building blocks and cofactors in her diet for neurogenesis and synaptogenesis,
• to activate her memory, and exercise as much as possible with her condition,
• to increase neurotropic growth factors,
• while trying to reduce the buildup or even reverse the existing amyloid deposits, and
• to protect her brain from the negative effects of already existing amyloid

[Godot]

I'm glad to hear your grandma seems to be getting better. It sounds like the delirium is passing now that she's off opioids.

I think introducing the uridine stack is smart, but would be extremely hesitant to try her on noopept. It's not very well studied and its potential side effects in an elderly person are totally unknown. Could bring about kidney failure or something.

[pleb]

there is an article on the web, try looking for coconut oil, an MD in the states has almost cured her husband after she couldn't get him in a trail for a new drug he was pretty bad and according to reports is 90 percent toward being cured,he had already been on two earlier trials but they didnt work

Edited by pleb, 27 April 2013 - 02:04 PM.

[renfr]

++ for the coconut oil.
the opioid is definetely the culprit for hallucinations and short term memory impairment.
you should try out huperzine A, she sounds lile she has a huge lack of cholinergic activity.

[pleb]

i use it for all my fried stuff now, not as good taste wise as beef dripping for chips or fried bread but better than vegetable oil

[BioFreak]

I'm glad to hear your grandma seems to be getting better. It sounds like the delirium is passing now that she's off opioids.

I think introducing the uridine stack is smart, but would be extremely hesitant to try her on noopept. It's not very well studied and its potential side effects in an elderly person are totally unknown. Could bring about kidney failure or something.

The only studies I've seen have been done withpatients, and there were no adverse effects so far?
I.e.: http://www.ncbi.nlm....pubmed/19234797
I got the study, maximum age 60, 53 patients, 20mg daily split into two doses. In short, 20mg were comparable to 1200mg piracetam, with 1,8fold less undesirable effects compared to piracetam. They conclude that noopept is superior to piracetam in dosage, effects, and side effects. And that was without
a choline source.

http://www.ncbi.nlm....pubmed/22500312
Noopept is a neuroprotector and nootropics. Literature data revealed the treatment effect of noopept on mild cognitive impairment in patients with discirculatory encephalopathy. The present open prospective study included 60 patients with stroke treated with noopept during 12 months. Cognitive functions were assessed before and after treatment using neuropsychological tests. An analysis of MMSE scores and lateral and categorical associations revealed the significant improvement of cognitive functions after 2 months in patients of the main group compared to the controls. The global assessment of efficacy revealed the mild improvement in the main group while no changes were found in the control group. The results have demonstrated that noopept, used in dose 20 mg daily during 2 months, improves cognitive functions in stroke patients and has a high level of safety.

http://www.ncbi.nlm....pubmed/19008801
An effect of a new nootropic drug noopept on the dynamics of main EEG rhythms and narrow-band spectral EEG characteristics in patients with cerebral asthenic and cognitive disturbances caused by traumas or vascular brain diseases has been studied. Noopept caused the EEG changes characteristic of the action of nootropics: the increase of alpha- and beta-rhythms power and reduction of delta-rhythms power. The reaction of alpha-rhythm was provided mostly by the dynamics of its low and medium frequencies (6,7-10,2 Hz), the changes of beta-rhythm were augmented in frontal and attenuated in occipital areas. The analysis of frequency and spatial structure of EEG changes reveals that noopept exerts a nonspecific activation and anxyolytic effect. The differences in EEG changes depending on the brain pathology were found. The EEG indices of nootropic effect of the drug were most obvious in cerebral vascular diseases. The EEG changes in posttraumatic brain lesion were less typical.

http://www.ncbi.nlm....pubmed/18318195
The meteoadaptogenic properties of a series of drugs with peptide (cortexin, noopept, dilept) and nonpeptide (vinpotropil) structure were investigated in a climate thermobarocomplex (Tabay, Japan) on a group of healthy volunteers aged 20-24. All the studied drugs produced a meteoadaptogenic action, the extent of which depended on the environmental test conditions (overcooling, overheating, hypobaric hypoxia). Vinpotropil, optimizing a physiological component of the functional state, can be recommended as a meteoadaptogen for both cold and hot climate as well as for hypobaric hypoxia, where it improved the psychological component of the functional state. Cortexin is qualified as an adaptogen and actoprotector only for hypobaric hypoxia conditions (uplands). Noopept, affecting positively a psychological component of the functional state, can be used for rapid adaptation to both cold and hot climate. In the hot climate, noopept also enhanced the physical work capacity. Dilept mostly elevated the psychological component of the functional state and can be considered as a psychomotor enhancer and adaptogen. Therefore, all the drugs studied (vinpotropil, cortexin, noopept and dilept) can be recommended as the agents producing activation, support and recovery of the physical and psychological efficiency under rapidly changing environment conditions.

Good for my granny surviving the coming summer. (And the other substances sound generally interesting as well)

http://www.ncbi.nlm....pubmed/19253467 no abstract. :(

http://www.ncbi.nlm....pubmed/12962045
Although the modern concept of neuroprotection has been formulated quite recently, the basis of this approach was laid about four decades ago when Zakusov initiated the study of mechanisms involved in the neuroprotector action of GABA shunt metabolites (in particular, alpha-hydroxybutyric acid and succinic semialdehyde) during hypoxia. It was suggested to consider these agents as a system of endogenous neuroprotectors. The interest of Zakusov in endogenous regulators (including oligopeptides) had stimulated research in this direction and gave impact to the investigations of A. P. Skoldinov and T. A. Gudasheva initiated in the early 1980s. Proceeding from the original concept of the possibility of imitation of the action of neurotropic agents by their structural-conformational oligopeptide analogs, a number of biologically active stable dipeptides were obtained, based on pyroglutamate and proline, and high specific bioaccessibility of these dipeptides for the brain was established. Our investigations showed that these compounds not only possess nootropic activity (in a dose 1000 times lower than that of piracetam), but produce a pronounced neuroprotector action as well. Most thoroughly studied in this respect were substituted acyl-prolyl dipeptides, in particular, the drug noopept exhibiting a combined neuroprotector effect both in vitro and in vivo. Noopept decreases the extent of necrotic damage caused by photoinduced thrombosis of cortical blood vessels. It was established that the neuroprotector effect of noopept is related to its action upon the well-known "triad", whereby the drug reduces neurotoxic effects of excess extracellular calcium, glutamate, and free radicals. Two additional components of the neuroprotector action of noopept are related to the antiinflammatory and antithrombotic activity. The prospects of using direct and indirect action upon neurotrophin system for neuroprotection purposes are considered. Taking into account common secondary mechanisms of the neuronal damage, it is possible to provide for pleotrophic brain protection with dipeptides in a broad spectrum of pathological states, including strokes, cerebral traumas, neurodegenerative processes, epilepsy, and schizophrenia.

http://www.ncbi.nlm....pubmed/12962042
The paper considers a new strategy in the field of neuropsychotropic dipeptide drug design, the main points being as follows: (i) determination of the structural elements of dipeptides, such as fragments of amino acid side radicals and peptide bonds, in nonpeptide drugs; (ii) design of peptide analogs topologically close to the drug; (iii) synthesis and activity testing of these analogs; (iv) determination of the corresponding endogenous neuropeptide among the known neuropeptides or identification of the new neuropeptides in the brain of experimental animals. Using this approach, new pyroglutamyl- and prolyl-containing dipeptides were obtained based on the structure of the well-known classical nootropic drug piracetam. The new drugs exhibit nootropic activity in doses 100-10,000 times lower than those of piracetam. The structure of most active pyroglutamyl dipeptide pGlu-Asn-NH2 coincides with that of the N-end fragment of the endogenous memory peptide AVP(4-9). Noopept (N-phenylacetylprolylglycine ethyl ester), patented in Russia and USA as a new nootropic drug, is currently under stage 2 of successful clinical trials. The main metabolite of noopept, cyclo-Pro-Gly, is identical to the endogenous dipeptide designed in this work and is most close analog of piracetam with respect to pharmacological activity. The universal character of the proposed strategy is demonstrated by the design of active dipeptide analogs of an atypical neuroleptic drug sulpiride. As a result, a potential dipeptide neuroleptic dilept was obtained, which has been patented in Russia and now passes broad preclinical trials.

Stage 2 of successful clinical trials, that was 2003, makes me wonder how they ended...

http://www.ncbi.nlm....pubmed/12711349
The neuroprotective activity of a novel N-acylprolyl-containing dipeptide analog of the nootropic 2-oxo-1-pyrrolidine acetamide (Piracetam) designated as GVS-111 (DVD-111/Noopept) was tested in two in vitro models of neuronal degeneration mediated by oxidative stress: normal human cortical neurons treated with H(2)O(2), and Down's syndrome (DS) cortical neurons. Incubation of normal cortical neurons with 50 microM H(2)O(2) for 1h resulted in morphological and structural changes consistent with neuronal apoptosis and in the degeneration of more than 60% of the neurons present in the culture. GVS-111 significantly increased neuronal survival after H(2)O(2)-treatment displaying a dose-dependent neuroprotective activity from 10nM to 100 microM, and an IC(50) value of 1.21+/-0.07 microM. GVS-111 inhibited the accumulation of intracellular free radicals and lipid peroxidation damage in neurons treated with H(2)O(2) or FeSO(4), suggesting an antioxidant mechanism of action. GVS-111 exhibited significantly higher neuroprotection compared to the standard cognition enhancer Piracetam, or to the antioxidants Vitamin E, propyl gallate and N-tert-butyl-2-sulpho-phenylnitrone (s-PBN). In DS cortical cultures, chronic treatment with GVS-111 significantly reduced the appearance of degenerative changes and enhanced neuronal survival. The results suggest that the neuroprotective effect of GVS-111 against oxidative damage and its potential nootropic activity may present a valuable therapeutic combination for the treatment of mental retardation and chronic neurodegenerative disorders.

Neuroprotection, exactly what she needs with possible amyloid deposits.

And there are more studies, although I only searched for noopept NOT mice NOT rat so those are either human or cell studies. I also did not search for GVS-111 or DVD-111.

So the body of evidence could be bigger, yes, but it sounds pretty good so far.

Any obvious organ damaging effects should be known by now, and there are none. Maybe there are adverse long term effects, but if long term means 14 years for example, her chances to find out are extremely slim. In addition, we are a bit desperate, and in the light of those studies the risk seems very low. But you are right, it is a relatively new compound. And you are also right that there are no studies on people older then 60 years (that I know of), but they should display at least signs of organ problems if it should be worse for older patients. Or do you know of substances that are completely harmless to young and middleaged people up to 60 years, but dangerous for older people? I am curious, as this is my reasoning and I'd love to hear if it is wrong.

In any case, thanks for looking out for me and my granny.

there is an article on the web, try looking for coconut oil, an MD in the states has almost cured her husband after she couldn't get him in a trail for a new drug he was pretty bad and according to reports is 90 percent toward being cured,he had already been on two earlier trials but they didnt work

Thanks for the tip! I'll check it out.

Edited by BioFreak, 27 April 2013 - 04:32 PM.

[Godot]

Wow, that's a very interesting lit review! Thanks for posting it.

[pleb]

i found the links i hope they help, its the mary newport article i found interesting

Coconut Oil For Alzheimer's Disease
By Michael Mooney June, 2012
Recently a good friend asked me if what she'd heard about coconut oil helping reverse symptoms of Alzheimer's Disease was true.
It sounded interesting so I did a search and found http://www.anh-usa.org/coconut-oil-and-alzheimer%E2%80%99s-disease/
This notion has been looked at and it does have merit.
An article at http://www.naturalnews.com/032727_coconut_oil_Alzheimers.html by Dr. Carolyn Dean points at a book by Dr. Bruce Fife, called Stop Alzheimer's Now! that provides more details.
Another book, Alzheimer's Disease: What If There Was a Cure? by Dr. Mary Newport focuses only on the use of coconut oil, detailing the biochemical reasons it addresses Alzheimer's, presenting a YOUTUBE video about it, along with case studies.
Also see the CBN TV report: http://www.cbn.com/media/player/index.aspx?s=/mp4/LJO190v1_WS
DOSING
So what dose of coconut oil might help? Doses suggested have ranged from two to five tablespoons a day to address Alzheimer's.
This is interesting enough that I've decided to take 2 daily teaspoons of extra virgin coconut oil as a preventive. Insightful naturopath, David Getoff recommends Tropical Traditions brand Virgin Coconut Oil as a good product to use and I have used it. I just bought some Trader Joe's Organic Virgin Coconut Oil because it was more convenient than driving across town to buy the Tropical Traditions product.
The most important consideration when buying oils is that they are virgin or, better yet, extra virgin and organic is even better.

Coconut oil has a multiplicity of other health benefits, including anti-infective properties, cardioprotective effects, skin and hair health support and as an efficient energy source because of the high medium chain triglyceride content, which means it will mostly be burned for energy rather than stored as fat.
Michael Mooney

Edited by pleb, 27 April 2013 - 04:43 PM.

[BioFreak]

Do I understand it right, the primary course of action for coconut oil in dementia is through providing an alternative energy source (ketones)?

Even if it is the primary course of action, it might be very interesting. Because it could have a neuroprotective and even neuroregenerative effect(on neurons in the process of dying because of starvation) outside the brain such as the nerves, the eyes (think macular degeneration!), affecting neuropathy positively etc...

Update:
So it's been 6 days since she stopped the opiate.

Withdrawal:
Withdrawal seems to be over (lasted only 2-3days). Yay!


Short term memory:
Her short term memory is getting better, but she is also getting cdp-choline now, I think its the combined action of stopping the opiate and starting cdp to counteract possible(most likely reversible - why? Because all studies done on humans with noopept suggested a much lower side effect profile then piracetam, and that was without a highly available choline source, yet choline seems to reduce sides further - anecdotal evidence) side effects from noopept. So we have not run into extreme situations where she asks me something, I answer, and 10sec later she asks me again... and again... maybe 1-3 times, but thats it: I call that a significant improvement. Better to tell her something 3 times then to tell it 20+ times before giving up, leaving her in agony because nothing can be done..

Hallucinations:
She does not have hallucinations while someone like me is present. Significant improvement.

However, she still has a colorful fantasy about what is happening when I am not present. I.e. "The police came and looked through the window (1st floor), or people were in the apartment, etc.
Also, she still can not distinguish perfectly between what a dream was, and what she experienced in reality.

Reasoning:
I can reason with her, use logic to tell her what is real and what not - while this was not possible when the hallucinations were too strong.

So the last two points are a big improvement, but still, I am disappointed. I hoped that the hallus would end with opiate use, they are better, but still there. Does it only take time to resolve?

"Problematic handling"/anxiety:
Her anxiety seems to decrease further, not sure to tell where this effect comes from, it could be any of the natural supps, noopept, or the now missing opiate. She can be alone longer before going nuts which is very important so I can do some stuff myself...

Her spacial and temporal abilities are better, but not perfect. However, this can also be due her advanced macular degeneration - she can not read the clock, or see exactly where she is (and her sleeping room has changed).

What else to check? I don't know.

At this point I wish I had some sort of questionnaire to rate the improvements better, its highly subjective.

Upcoming changes:
This week we will probably start with coconut oil.
Her herbal supps need 14day+ to start working fully, so there is still minimum a week to go(mostly anxiolytic, calming effects)
She started physiotherapy a week ago, so this will affect her brain positively as well
Hopefully she will recover further from the opiate (basically no hallus, and better understanding of the difference between dream and reality)

In the pipeline(so far):
Uridine stack
Hydergine research
More coconut oil research

[tunt01]

It's probably the benzo withdrawal. That will make a person delirious. I would say consider a sustained release beta blocker. It helps w/ the anxiety/panic attacks.

[BioFreak]

It's probably the benzo withdrawal. That will make a person delirious. I would say consider a sustained release beta blocker. It helps w/ the anxiety/panic attacks.

What are you referring to exactly? The anxiety/panic(I guess those)? The still occurring hallus, or the inability to differentiate between dream and reality?

[tunt01]

What are you referring to exactly? The anxiety/panic(I guess those)? The still occurring hallus, or the inability to differentiate between dream and reality?

The fact that it took place over such a rapid period of time -- 1.5 mo, makes me think it is withdrawal, unless there was a legitimate TIA event. I've seen it first hand with one of my family members.

If you search around for beta blocker or metoprolol and the term benzos, you will find some people use beta blockers to help with benzo withdrawal. Beta blockers have a very good safety profile, extend life in some studies and they quiet the flight/fight response. It's not a cure-all, but I think it's a good idea to deal with the constant anxieties.

It would be at the top of my list for a benzo-withdrawal patient.