Category Archives: PSP

“Diagnostic criteria of dementia” (Canadian journal article)

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I’ve been looking lately into the definition of dementia. When caregivers of those with progressive supranuclear palsy (PSP) call me for the first time, I often ask “does your loved one have dementia,” knowing that at least half of those with PSP have dementia as a primary symptom. Often the caregivers will say “no,” and then go on to tell me how their loved one can no longer balance a checkbook, make investment decisions, or make any sort of decisions. Perhaps these caregivers are embarrassed to say that their loved ones are demented. Or perhaps the only kind of dementia they are aware of is Alzheimer’s Disease, and they know their loved ones don’t have that. Or perhaps we are using different definitions or criteria.

The only standard definition of dementia I’m aware of is the DSM IV criteria. (DSM = Diagnostic and Statistical Manual for Mental Disorders, Fourth Edition, published by the American Psychiatric Association, Washington, DC.) According to a University of Alberta website:

“Dementia is a clinical state characterized by loss of function in multiple cognitive domains. The most commonly used criteria for diagnoses of dementia is the DSM-IV. Diagnostic features include: memory impairment and at least one of the following: aphasia, apraxia, agnosia, disturbances in executive functioning. In addition, the cognitive impairments must be severe enough to cause impairment in social and occupational functioning. Importantly, the decline must represent a decline from a previously higher level of functioning. Finally, the diagnosis of dementia should NOT be made if the cognitive deficits occur exclusively during the course of a delirium.”

(Wikipedia definitions: aphasia = loss of the ability to produce and/or comprehend language; apraxia = loss of the ability to execute or carry out learned purposeful movements, despite having the desire and the physical ability to perform the movements; agnosia = loss of knowledge or loss of the ability to recognize objects, persons, sounds, shapes, or smells)

The problem is that there are many different types of dementia (70 or 80 types) and their characterizations are all so different. And, as the abstract below indicates, not all types of dementia have memory impairment.

Robin

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The Canadian Journal of Neurological Sciences. 2007 Mar;34 Suppl 1:S11-8.

Bouchard RW.
Clinique de mémoire et unité de recherche Alzheimer, CHA Hôpital de I’Enfant-Jésus, Québec, QC, Canada.

In the past two decades there has been a tremendous effort among clinicians and searchers to improve the diagnostic criteria of the dementias on the basis of the differential neurological and neuropsychological profiles. This was an obligatory requirement for clinical trials and the development of treatments. Over the years it became rapidly evident that the cohorts of patients in studies had some degree of heterogeneity, making it difficult to interpret the results of some studies, particularly in the vascular dementias and the mild cognitive impairment (MCI) group. For example, many sub-types of the vascular group were included in clinical trials, such as the cortical strokes, the lacunar states and the diffuse white matter disease cases, and some of the patients might have had also mixed pathology. In addition, the standard DSM IV criteria for dementia no longer represent our present knowledge of the clinical profile of some of the dementias such as vascular dementia (VaD) and fronto-temporal dementia where the memory impairment is not necessarily the first requirement. To improve the validity of clinical trials and eventually help developing more appropriate treatments, we revised the present diagnostic criteria and made recommendations for some changes in the context of the 2nd Canadian Conference on the Development of Antidementia Therapies, held in 2004 and reviewed in the light of the recent literature as of early 2006. It is expected that in the near future, these dementia criteria for clinical trials will have to be revised again in order to include specific subtypes of the dementias as well as biomarkers, structural and functional imaging.

PubMed ID#: 17469675 (see pubmed.gov for the abstract only)

Riluzole study – MSA+PSP

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This news article was sent to me by a local support group member whose mother with MSA died a few months ago. She regularly reads Medscape and saw a news article on the results of a study of the drug riluzole in MSA and PSP. Rather than being disappointed by the results (that showed that riluzole had no effect on survival), she finds it cheering to know that researchers are actually studying these diseases. Also, she says: “The interesting point is the study design, which included a lot of people fairly early in their diseases and may be a good model for future drug studies.”

The study was done through the European group NNIPPS (Neuroprotection and Natural History in Parkinson Plus Syndromes). The lead author was P. Nigel Leigh, MD, PhD, from King’s College, London. I don’t know of an equivalent group in the US that is looking into all the atypical parkinsonism disorders.

Here’s a link to the news article, and a copy of the full text. To gain access to anything on Medscape, you must log in, which requires (free) registration.

http://www.medscape.com/viewarticle/557908

NNIPPS: No Benefit of Riluzole on Survival in MSA and PSP

Susan Jeffrey
Medscape Medical News 2007.

June 7, 2007 (Istanbul) — A randomized trial of the neuroprotectant drug riluzole (Rilutek, Sanofi-Aventis) in patients with the “Parkinson plus syndromes” of multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) shows no effect on survival, either in the population as a whole or within the PSP or MSA strata, with treatment vs placebo.

However, the study supports the idea that large trials in neurodegenerative disorders can use survival as an end point and that it is feasible to include patients with these conditions quite early in their disease using the Parkinson-plus-syndrome concept.

The concept, for which this group has developed and validated diagnostic scales based on these data, “may be worthwhile when we have drugs that are promising,” lead author P. Nigel Leigh, MD, PhD, from King’s College, London, United Kingdom, who presented the results on behalf of the Neuroprotection and Natural History in Parkinson Plus Syndromes (NNIPPS) Consortium, told attendees here.

“It has simple, pragmatic diagnostic criteria, which I suggest have some merit,” he added, as well as high sensitivity and specificity for these difficult-to-diagnose conditions. The results were presented here at the 11th International Congress of Parkinson’s Disease and Movement Disorders.

No Survival Benefit

PSP and MSA often present as Parkinson plus syndromes — that is, having some of the classical features of Parkinson’s disease but with some additional features. Early in the disease course, it can be very difficult to distinguish these conditions from each other, but for any intervention to be useful, it is important to enroll patients before diagnosis of PSP vs MSA is definitive.

PSP and MSA each have roughly the same frequency as amyotrophic lateral sclerosis (ALS), Dr. Leigh told Medscape, and “so are not insignificant adversaries.” The idea of NNIPPS was to design a trial that would give a definitive answer, he said. “The whole field is deviled by small trials that never, ever, could have gotten a result. If we’re going to choose a drug that’s not ideal, like riluzole — no one was really expecting it to be a cure — let’s at least be 80% or 90% sure that we’re going to know in the end that it doesn’t work or it does work.”

They decided to use survival as an end point for this trial. “Everybody said, you can’t do it, it takes too long, but I think we’ve shown you can do it. It’s tough, and it takes a long time, but maybe that will be worth it when we do have really good drugs,” he noted.

Still, they had started out with the hope that riluzole might be effective. The natural history of MSA and PSP is poorly understood, they note in their abstract, but excitotoxicity may contribute to the neuronal damage. Riluzole, already approved for use in ALS, is a glutamate-release inhibitor and has been shown to prolong survival by about 2 months in clinical ALS trials and possibly between 6 and 19 months in retrospective data.

The NNIPPS trial, then, was a European multicenter, randomized, and stratified trial of riluzole in a dose of 50 to 200 mg per day vs placebo in patients with PSP and MSA. At the same time, investigators meant to investigate the natural history of these conditions presenting as Parkinson plus syndromes, acquiring prospective data on diagnostic criteria, MRI changes, and pathology.

The primary outcome was survival at 36 months; secondary outcome measures included functional status, cognition, quality of life, healthcare costs, and MRI abnormalities.

Power calculations were based on published estimates of survival in these conditions. In total, they enrolled 766 subjects from participating centers in the United Kingdom, France, and Germany. Six were later excluded because they either were found not to have proper informed consent or did not actually receive the drug, leaving 362 patients diagnosed clinically as PSP and 398 as MSA.

They used their own NNIPPS diagnostic criteria rather than the retrospectively validated existing criteria, he pointed out, because “we decided they were operationally extremely difficult in the setting of a clinical trial; they’re too complicated, too complex,” he said. In addition, “they’re very good on specificity but they’re weak on sensitivity, and we wanted sensitivity as well.”

Median survival from onset was 7.8 years for PSP and 8.7 for MSA, with 171 deaths occurring in the PSP group and 171 in the MSA group.

Blinded Data

In his presentation of the primary results here, Dr. Leigh noted that they have not yet unblinded the riluzole/placebo comparison because they hope still to do the other secondary analyses in a blinded fashion. Instead, he simply presented the survival results as “treatment A” vs “treatment B.” Looking at the survival curves, however, he pointed out, “It doesn’t take much to show you that there was no significant difference, with the log rank clearly not significant. There was no difference, despite having adequate power.”

Analysis of the intent-to-treat population showed no evidence of a significant treatment effect of riluzole either in the population as a whole or in the PSP or MSA strata.

“So the very least we can say is that riluzole does not work in this condition, but maybe this is a model for looking at other drugs, which we hope indeed it will be,” he said.

Pathological diagnosis was confirmed in 112 cases where brain tissue has been donated and analyzed; another 20 brains have been donated but not yet analyzed, he noted. Overall, pathology-confirmed diagnosis showed that clinical diagnosis using the NNIPPS diagnostic criteria had an overall positive predictive value of 90% for PSP and 93% for MSA, “so we were encouraged by that,” Dr. Leigh noted.

In an interview, Dr. Leigh pointed out that an earlier session here on the genetics of movement disorders underlines the “scary” genetic diversity of these diseases, making finding specific treatments for each subgroup with a different molecular mechanism a daunting task. “If you’re going to find disease-modifying therapy in neurodegenerative diseases, the real challenge is to try to break across the boundaries of individual diseases and find common mechanisms.”

They were disappointed with these results not only because they had hoped to help patients, but because if it had been positive that would have pointed to a common mechanism and provided some insight into how riluzole may be working in ALS as well, since this has not been well described.

“Still, I think, after recovering from the bad weekend when we got the news, that there’s still a huge resource there,” Dr. Leigh said.

Rich Resource

Despite the fact that the trial was ultimately negative, NNIPPS provides a rich data set for understanding motor, cognitive, neuroimaging, and genetic factors in MSA and PSP.

For example, they devised and validated 2 diagnostic scales, the Parkinson Plus Scale and the Short Motor Scale, specifically designed for early use before a diagnosis of PSP or MSA is certain. They also have quality-of-life data and health costs that can be used in healthcare planning, he noted.

In addition, they have 633 baseline MRIs in these patients, with follow-up scans done at the end of the study in 187 patients; 521 DNA samples; and brains now from 131 patients, prospectively collected and being analyzed. Dr. Leigh invited any researchers interested in accessing these data to contact him about it.

The study was supported by the European Community. Study drug was provided by Sanofi-Aventis. Dr. Leigh disclosed has worked as a consultant for ONOPharma, Teva, Trophos, and GlaxoSmithKline.

11th International Congress of Parkinson’s Disease and Movement Disorders: Oral Platform Presentations 4602: Abstract 10. June 3-7, 2007.

Gastrointestinal and Urinary Dysfunction

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This post is of interest to those dealing with gastrointestinal problems, urinary dysfunction, problems with saliva, dysphagia, etc.

This article on gastrointestinal and urinary dysfunction in PD was published today in PDF News.  PDF = Parkinson’s Disease Foundation.  The author is Dr. Ron Pfeiffer, the same neurologist who spoke on non-motor symptoms at last year’s PD Symposium in the Bay Area.

Here’s a  link to the article online:

www.pdf.org/en/spring07_gastrointestinal_and_urinary_dysfunction_in_pd

Gastrointestinal and Urinary Dysfunction in PD
By Dr. Ronald Pfeiffer
PDF News, Spring 2007

I’ve copied a few excerpts below on dysphagia and stomach problems.

Robin

——————————–

Excerpts from:

Gastrointestinal and Urinary Dysfunction in PD
By Dr. Ronald Pfeiffer
PDF News, Spring 2007

Dysphagia
Difficulty swallowing, or dysphagia, is a very common problem in Parkinson’s.  At least 50 percent (some studies even suggest over 80 percent) of people with PD experience difficulty in swallowing, and an even greater percentage show abnormalities on x-ray tests of swallowing.

Difficulty swallowing is usually due to the lack of coordination among the many muscles in the mouth and throat that must work together in perfect precision to produce normal swallowing.  When food gets stuck in the mouth, the person may have to try several times to complete a swallow.  The muscles in the back of the throat — and in the esophagus — may also lose coordination, and individuals who have difficulty swallowing are at increased risk for food or liquid to get into the windpipe.  From there, it can get into the lungs (called aspiration), which can result in pneumonia.

Although treatment of dysphagia can be difficult, speech/swallowing therapists can instruct patients on swallowing techniques and on designing changes in food consistency that reduce the risk of aspiration.  Some improvement in coordination of the muscles used in swallowing may be achieved through adjustments in PD medications.  Only very rarely is it necessary to place a feeding tube.

Stomach problems
Impaired ability to empty the contents of the stomach, called gastroparesis, is another potential gastrointestinal complication of PD.  This may produce a bloated sensation and cause people to feel full even though they have eaten very little.  Sometimes nausea may develop.

Failure of the stomach to empty in a timely fashion may also impair or delay the effectiveness of PD medications, especially levodopa, since levodopa is absorbed from the small intestine and cannot get to its destination if it is trapped in the stomach.
Treatment of gastroparesis in Parkinson’s has not been extensively studied.  Domperidone is an effective medication, but unfortunately it is not available in the US.

Treatment routes that bypass the stomach, such as transdermal drug delivery by skin patch, may become available in the near future.  Another potential treatment under investigation involves a form of levodopa designed to be delivered directly into the small intestine via a feeding tube.

Progression of dysarthria + dysphagia in DLB, CBD, MSA, and PSP

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This will be of interest to anyone dealing with dysarthria (speech problems) and dysphagia (swallowing problems), which, according to the article should be everyone within one year of disease onset.  (I thought dysarthria meant slurred speech.  But, according to this article, it can also mean hypophonic speech or monotonic speech.)

This article is about dysarthria and dysphagia in autopsy-confirmed cases of DLB, CBD, MSA and PSP, all APDs (Atypical Parkinsonian Disorders).  PD cases are part of the study as well.

Here’s the citation and abstract:

Archives of Neurology. 2001 Feb;58(2):259-64.  

Progression of dysarthria and dysphagia in postmortem-confirmed parkinsonian disorders.

Muller J, Wenning GK, Verny M, McKee A, Chaudhuri KR, Jellinger K, Poewe W, Litvan I.

BACKGROUND: Dysarthria and dysphagia are known to occur in parkinsonian syndromes such as Parkinson disease (PD), dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Differences in the evolution of these symptoms have not been studied systematically in postmortem-confirmed cases.

OBJECTIVE: To study differences in the evolution of dysarthria and dysphagia in postmortem-confirmed parkinsonian disorders.

PATIENTS AND METHODS: Eighty-three pathologically confirmed cases (PD, n = 17; MSA, n = 15; DLB, n = 14; PSP, n = 24; and CBD, n = 13) formed the basis for a multicenter clinicopathological study organized by the National Institute of Neurological Disorders and Stroke, Bethesda, Md. Cases with enough clinicopathological documentation for the purpose of the study were selected from research and neuropathological files of 7 medical centers in 4 countries (Austria, France, England, and the United States).

RESULTS: Median dysarthria latencies were short in PSP and MSA (24 months each), intermediate in CBD and DLB (40 and 42 months), and long in PD (84 months). Median dysphagia latencies were intermediate in PSP (42 months), DLB (43 months), CBD (64 months), and MSA (67 months), and long in PD (130 months). Dysarthria or dysphagia within 1 year of disease onset was a distinguishing feature for atypical parkinsonian disorders (APDs) (specificity, 100%) but failed to further distinguish among the APDs. Survival time after onset of a complaint of dysphagia was similar in PD, MSA, and PSP (15 to 24 months, P =.7) and latency to a complaint of dysphagia was highly correlated with total survival time (rho = 0.88; P<.001) in all disorders.

CONCLUSIONS: Latency to onset of dysarthria and dysphagia clearly differentiated PD from the APDs, but did not help distinguish different APDs. Survival after onset of dysphagia was similarly poor among all parkinsonian disorders. Evaluation and adequate treatment of patients with PD who complain of dysphagia might prevent or delay complications such as aspiration pneumonia, which in turn may improve quality of life and increase survival time.

PubMed ID#: 11176964  (see pubmed.gov for this abstract)

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These results were the most interesting (and depressing):

“Dysarthria or dysphagia within 1 year of disease onset was a distinguishing feature for atypical parkinsonian disorders (APDs).”

“Median dysarthria latencies were short in PSP and MSA (24 months each), intermediate in CBD and DLB (40 and 42 months), and long in PD (84 months).”

“Median dysphagia latencies were intermediate in PSP (42 months), DLB (43 months), CBD (64 months), and MSA (67 months), and long in PD (130 months).”

“Survival time after onset of a complaint of dysphagia was similar in PD, MSA, and PSP (15 to 24 months).”

On this last point, here’s the actual chart on this from the article:

Survival Time After Onset of Dysphagia, months
PD        24 (2-61)
CBD     49 (25-89…..including a single patient with dysphagia but without dysarthria)
DLB     10 (3-17)
MSA     15 (6-68)
PSP       18 (6-96)

Based on this, I don’t understand why DLB’s short survival time isn’t highlighted.

Here are some excerpts from the article’s Comment section:

“(Early) dysarthria and perceived swallowing dysfunction are not features of PD.”

“[Dysarthria] as a presenting symptom has been described in clinical series of CBD, MSA, and PSP.  In PD and DLB, hypphonic/monotonous speech represented the most frequent type of dysarthria, whereas imprecise or slurred articulation predominated in CBD, MSA, and PSP.”

“In a clinical study of CBD, Rinne et al described dysarthria as one of the initial symptoms in 11% of the patients, which is close to our findings.  At follow-up, on average 5.2 years, dysarthria was diagnosed in 70% of the patients…  According to our findings, dysarthria occurred in almost every patient with CBD.”

“In agreement with our results, Quinn described the speech of patients with MSA as more severely affected than that of patients with PD, with slurring dysarthria, as well as the low volume and monotone of parkinsonism.”

“In both PSP and MSA, progressive dysarthria is believed to represent a manifestation of brainstem and cerebellar involvement.  In fact, PET studies revealed marked hypometabolism in the cerebellum and brainstem of patients with MSA, which correlated with dysarthria.”

“In our study, dysphagia was associated with concomitant dysarthria in all parkinsonian patients except one.  This sequence of dysphagia following dysarthria has also been reported in clinical studies of PD, MSA, and PSP.”

“…Golbe et al reported dysphagia after a median of 1 year after the onset of dysarthria in PSP.”

In all these disorders, “bronchopneumonia has been reported as a leading cause of death, which may be subsequent to silent aspiration resulting from dysphagia.”

“Most of our patients with MSA and PSP complained of a swallowing dysfunction, in contrast to patients with PD, CBD, and DLB…  Impaired lingual proprioception is hypothesized to contribute to the unawareness of swallowing difficulties in PD and might in part explain significantly longer latencies to dysphagia in our PD cases.  In contrast, patients with PSP were reported to be keenly aware of swallowing problems, including those with cognitive impairment.”

“(The) similarly short remaining survival time in PD and PSP after the onset of perceived dysphagia suggests that this symptom represents a reliable marker for the onset of functionally relevant swallowing abnormalities in both disorders.”

“Our findings of increased latency to dysarthria and dysphagia and similar time interval from onset of dysphagia to death in patients with PD compared with patients with APDs suggest that extrastriatal and nondopaminergic lesions represent an important factor for the development of dysarthria and dysphagia.  Indeed, Bonnet et al reported that dysarthria, gait, and postural stability had a decreased levodopa response in patients with long-standing PD who still benefited from the levodopa effects on tremor, rigidity, and akinesia.  Whereas the APDs are characterized by multiple system neuronal degenerations, in PD disease progression is determined by a progressive dopaminergic deficit arising from the selective neuronal degeneration of the substantia nigra pars compacta.”

Robin

eMedicine on feeding tubes + some personal info

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This will only be of interest to those dealing with dysphagia (swallowing problems) and who are open to the idea of a feeding tube.

Personally, I never understood what the big deal was about getting a feeding tube during the time period when quality of life is still good.  When my Dad (with progressive supranuclear palsy) stopped eating and drinking over a week ago (he reported that it was too fatiguing to chew and swallow, the swallow was delayed by 5-15 minutes, and quite a bit of chewed food was spat out because he couldn’t perform the swallow), I started mentioning to a few people that I was looking into the ins-and-outs of a feeding tube.  Many of the people not involved in healthcare took it to mean that he was at the end of life.  I guess that’s why they got so upset talking to me and wanting to know if I was OK and if we were ready for hospice.  So I’m not quite sure how to bring up the topic anymore.  Basically, I view the feeding tube in the same way I view the walker or wheelchair — it makes life a little safer.  He said he wanted it.  And if I were he I would want it as he still has pretty good quality of life.

Anyway, I can report to you today that my Dad had surgery this morning (with Versed, a sedative, and fentenyl, an analgesic, both given via IV).  (They initially said they’d be using the intravenous anesthetic propofol.  I said “what about the 1/23/07 issue of Biochemistry which indicated that propofol leads to amyloidbeta peptide aggregation in the brain?”  The MD said “amyloid-beta aggregation is not an issue in PSP.”)  A G-J tube was placed.  Endoscopy (a procedure using a probe with a camera on the end) was not used.  Because most people getting a feeding tube have an NG (nasal gastric) feeding tube in place — it goes through one of the nostrils down to the stomach — and they were unsuccessful in placing such a tube in Dad on Monday, the prep time for the surgery was longer than normal.  In total it was supposed to take 2 hours; it took 3.  The procedure was done by an interventional radiologist.  Normally, the NG tube is used to insert a dye so that the colon is highlighted so it won’t get hit.  They, instead, inserted a tube into Dad’s rectum and injected the dye that way.  Then they inserted a tube down his esophagus in order to blow air into the stomach so that they could “see” the stomach from outside the body.  They had lots of trouble inserting that tube.  So much so that the MD asked me later why we were worried about acid reflux and aspiration.  She was thinking that if it’s so hard to get things down the esophagus, it must be hard for things to come back up.  I mentioned that Dad was at risk for aspiration, based on the modified barium swallow study.  After telling her that, she agreed that the G-J tube was better than the G-tube for Dad.  (It would’ve been better to have had that conversation beforehand but no harm done.)  There is one small tube going into Dad’s body.  Inside, the tube splits — one part goes off to the G (which stands for “gastric” and refers to the stomach) and one part goes off to the J (which stands for “jejunum” and refers to the intestine).  This small tube comes out of Dad’s body for about 7 inches.  (It’s long!)  At the end of it is a rather large and firm set of three tubes or ports; there’s a G port, J port, and a Bal port (don’t know what that one’s for yet).  All of the feeding, hydration, and medication will occur via the J port.  I’m not really sure why there’s a G port.  Perhaps as a back-up or something.  Right now, stomach bile is draining out of the G port.  This is supposed to end at some point (days? weeks?).  The idea is that if you can get the liquid further down into the gastrointestinal system, there’s less chance it will back up into the esophagus and therefore less risk of aspiration.  The MD said that if there were no risk of aspiration a G tube would be better as the stomach is the best place for the body to receive nutrition and digest it.  The MD gave me one tip, which I thought I’d pass on:  if the G-J tube gets loose, insert a Foley catheter into the tube, inflate the balloon, and get to an ER soon.  The catheter will keep the hole open; if there’s not something there keeping the hole open, it will start to close up.  (Note to self: buy an extra Foley catheter and syringe to inflate balloon.)

I’m still learning about the feeding process so I don’t want to say too much about that.  Our plan is to feed him over a 12-hour period while he’s in bed at night.  (One bummer is that he’ll have to sleep with the head of the bed at a 30-45 degree angle to avoid reflux.)  We are very lucky that one of Dad’s feeders has a daughter who has been fed via NG tubes and PEG tubes, so she’s way ahead of us in terms of knowing how to handle all of this.  I have some concerns about finding a feeder who can come start the 12-hour feed around 8pm.  And I want to try to find a belt or cover so that I can protect the tube and ports as everyone says they can be accidently ripped out.  When I learn more, I’ll pass it on.

I haven’t had much access to the internet over the last few days, so I’ve relied on the rather poor info that’s been given to me about PEGs and G tubes by the hospital (in Salt Lake City).  Tonight, after the fact, I’ve gone to emedicine.com, which is one of my favorite sources.  They do cover the topic of feeding tubes, and the G-J tube (picture 8 looks a little short and small to me).  I thought I’d pass on the link to that:

www.emedicine.com/radio/topic798.htm

Percutaneous Gastrostomy and Jejunostomy
Last Updated: March 26, 2003
eMedicine.com