Treating psychosis in PD and use of antipsychotics

This post will interest those dealing with hallucinations or delusions, or those using atypical antipsychotics, such as Seroquel. This contains a nice summary of why antipsychotics are used and which ones are preferred.

This was posted yesterday on the National Parkinson Foundation’s “Ask the Doctor” online forum. I believe it’s an excerpt from a larger publication on treatment of PD. I learned three things. First, “double-blinded trials of quetiapine have been disappointing.” (quetiapine = Seroquel) Second, “odansetron (a rather expensive anti-nausea medication used mainly for patients undergoing chemotherapy)” is a treatment option for psychosis in PD. I’m pretty sure that’s a typo and what is meant is ondansetron or Zofran. Third, the effects of electroconvulsive therapy (ECT) in treating psychosis are short-lived.

——————

http://forum.parkinson.org/forum/viewtopic.php?t=8846

Posted by Dr. Hubert H. Fernandez
Posted on 1/30/10

What medications can be used to treat psychosis in Parkinson’s disease?

Just like the management of cognitive decline, prior to starting any treatment, one has to search for urinary tract infections, pneumonia, metabolic derangements, sleep disturbances, brain insults (such as strokes) and social stressors, such as changes in the environment, as possible explanations for hallucinations or delusions. Medications that can alter brain mechanics because of their ability to penetrate the brain’s “iron curtain” (termed the “blood brain barrier”) that is designed to keep away unwanted substances, such as narcotics, hypnotics, antidepressants, and anxiolytics are also common culprits. If psychotic symptoms persist despite the withdrawal of other psychotropic medications, anti-Parkinson’s disease medications may be gradually reduced or, if necessary, discontinued. As mentioned in Module 4, most authorities recommend “peeling off” these medications in the following order: anticholinergic agents, amantadine, monoamine oxidase inhibitors, dopamine agonists, catechol-O-methyltransferase inhibitors, and finally, levodopa. Regular or short acting formulations of levodopa are preferred in patients prone to hallucinations over sustained-release formulations because their pharmacokinetics are more predictable and there is less potential for cumulative side-effects. If psychosis improves, the patient is then maintained on the lowest possible dose of anti- Parkinson’s disease medications. However, if the withdrawal of anti-PD drugs significantly worsens other Parkinson’s disease symptoms or does not control psychosis one must consider the addition of antipsychotic agents.

The choice of an antipsychotic agent is based largely on its ease of use and side effect profile as most antipsychotics have comparable efficacy in improving psychosis. “Atypical” antipsychotics (or newer generation antipsychotics) are generally preferred given the significant risk of motor complications and anticholinergic side effects with older, conventional antipsychotics. The use of an appropriate atypical antipsychotic agent may allow the clinician to control psychosis with fewer motor side effects and, in some cases, without the need for significantly cutting back on anti- Parkinson’s disease medications. Clinicians should be aware that the FDA issued a “black box” warning for the use of these agents in the treatment of psychosis associated with dementia due to increased cardiac mortality. However, the majority of clinicians treating these patients continue to use these medications because these medications are efficacious, the absolute risk of increased mortality is low and the risk appears to be present in the older antipsychotics as well.

The main difference in the antipsychotics lies in their propensity to worsen motor functioning in this frail and already vulnerable population. Quetiapine has been studied in Parkinson’s disease patients and appears to have less potential for worsening motor function than risperidone, aripiprazole, olanzapine and ziprasidone. While double-blinded trials of quetiapine have been disappointing, it remains the first-line agent used for drug-induced psychosis in Parkinson’s due to its tolerability and good track record in several open-label trials .

The use of clozapine is generally limited to patients who have failed other agents, despite its superior efficacy over all other antipsychotic drugs, because of its very uncommon risk of agranulocytosis (meaning, sudden drop in white blood cell count—our body’s first defense against ordinary infections). The chances of this complication developing are less than 1%. Nonetheless, in the United States, for the first six months, each patient on clozapine must undergo a weekly white blood cell count and can receive only one week’s supply of the drug at a time. After 6 months the process becomes bi-weekly.

It remains unclear how long antipsychotic medications should be continued once they are initiated. There are some data that show persistence of hallucinations in Parkinson’s disease patients with drug-induced psychosis after its initial occurrence. At the University of Florida, we prospectively followed our own patients with Parkinson’s disease on successful long-term treatment with quetiapine or clozapine to see if they could be successfully weaned off their antipsychotic drugs. The study was aborted after enrollment of only six patients due to an unacceptably high rate of psychosis recurrence (five patients, 83%).

Other treatment options include acetylcholinesterase inhibitors, odansetron (a rather expensive anti-nausea medication used mainly for patients undergoing chemotherapy) and electroconvulsive therapy (ECT). Several open-label studies have found that cholinesterase inhibitors may improve hallucinations and psychosis in Parkinson’s disease subjects. Similarly, an open-label trial with 16 Parkinson’s disease patients showed marked improvements in the areas of visual hallucinations, confusion, and functional impairment with no adverse effects on motor function. This result has yet to be reproduced by other investgators. ECT should be reserved for patients who are unresponsive to, or intolerant of, other treatments, especially if the psychosis is associated with severe depression. In general, ECT’s effects are short-lived, and repeated treatments and/or the help of other medications are required to maintain benefits.

[Robin’s note: I think the open-label trial with 16 PD patients above is a trial with ondansetron. And I think there’s a typo above in the drug’s name: an N is missing. The brand name is Zofran.]

[Brand names for some of the antipsychotic medications referred to include:
quetiapine = Seroquel
risperidone = Risperdal
aripiprazole = Abilify
olanzapine = Zyprexa
ziprasidone = Geodon
clozapine = Clozaril ]

 

Treatment of dysautonomia in PD, MSA, DLB, etc.

This medical journal article provides a good overview of autonomic dysfunction in Parkinson’s Disease, MSA, and DLB.

The non-motor symptoms addressed include:

* orthostatic hypotension:  If you are dealing with OH, I especially recommend you review Box 1, “Nonpharmacological and pharmacological treatment of orthostatic hypotension.”  I’ve copied the box below as best I can.

* supine hypertension:  This is probably the best overview I’ve seen.

* cardiovascular effects of antiparkinsonian drugs

* dysphagia (swallowing problems)

* gastric motor dysfunction (delayed gastric emptying).  Note that the medication “Domperidone speeds up the emptying of the stomach…”  This medication is not available in the US.

* constipation

* bowel dysfunction

* urinary dysfunction.  I had never seen this data before:  “More than 50% of MSA patients suffer from recurrent infections and a significant number (approximately 25%) die of subsequent complications.”

And this is a useful point as well:  “Missclassification of urogenital autonomic dysfunction as benign prostatic hyperplasia has been reported which may increase the risk of unnecessary urological surgery.”

* sexual dysfunction

* sweating abnormalities

I suggest reading only about the symptoms or disorder of interest to you.

Wonderfully, the full article is available online at no charge via the PubMed system:

www.ncbi.nlm.nih.gov/pmc/articles/PMC3002611/

Therapeutic Advances in Neurological Disorders. 2010 Jan;3(1):53-67.
Treatment of dysautonomia in extrapyramidal disorders.
Ziemssen T, Reichmann H.
ANF Laboratory, Department of Neurology, University Clinic Carl Gustav Carus, Dresden University of Technology, Dresden, Germany.

Again, Box 1 about orthostatic hypotension is copied below.

Robin


www.ncbi.nlm.nih.gov/pmc/articles/PMC3002611/table/table2-1756285609348902/

Box 1. Nonpharmacological and pharmacological treatment of orthostatic hypotension.

Nonpharmacological procedures
* Avoid sudden posture changes, particularly after long periods in supine position or during venodilating conditions (i.e. hot baths).
* Increase of daily salt (3-6 g NaCl) and water (2-3 l) intake.
* Diet low in carbohydrates; increase of meal frequency while meal size should be decreased.
* Isotonic exercise such as swimming, aerobic training, bicycling or walking at moderate level.
* Application of counter manoeuvres such as squatting or ‘derby chair’.
* Wearing of elastic stockings or an elastic suit.
* Raised upper body position during sleeping (15-30 cm).

Pharmacological procedures – Increase of blood volume
* Fludrocortisone initial dose of 0.1-0.2mg/d; up to a max of 1mg/d. Caution: cardiac insufficiency, hypocalcaemia, oedema.
* Erythropoietin 4000 IE s.c. twice a week. Caution: iron substitution; increase in haematocrit; hypertension.
* Desmopressin nasal application via pump spray, particularly indicated in nycturia. Caution: hyponatraemia, hypertension.

Pharmacological procedures – Increase of peripheral vasoconstriction
* Midodrine three times 2.5-10mg/d, up to a max 40mg/d; administration not later than 5 pm. Caution: supine hypertension, pruritus.
* Ephedrine three times 12.5-25mg/d. Caution: tachycardia, tremor, supine hypertension.
* Yohimbine two to three times 8mg/d p.o. Caution: diarrhoea, nervousness, panic attacks.
* Caffeine 250mg (=2 cups of coffee) in the morning. Caution: tachyphylaxia.

[fludrocortisone = Florinef; erythropoietin = EPO; desmopressin nasal spray = Stimate or DDAVP Nasal Spray; midodrine = Proamatine]

Improving diagnostic accuracy of PSP-P

PSP folks –

This article was written by two heroes of the PSP community — David Williams, who is now in Australia, and Andrew Lees, in the UK.

“The aim of this study was to identify particular clinical features (green flags) that may be helpful in differentiating PSP-P from…other disorders.”  PSP-P, the parkinsonism form of PSP (progressive supranuclear palsy), is easily confused with Parkinson’s Disease (PD), multiple system atrophy (MSA), and vascular parkinsonism.  The issue is that the PSP diagnostic criteria include symptoms that are specific to the dementia form of PSP.  But what if someone with PSP-P comes along?

In this study, researchers compared many Queen Square Brain Bank cases:  37 patients with PSP-P, 444 with PD, 46 with dementia with Lewy bodies (DLB), 90 with MSA, and 19 with vascular parkinsonism.

By the way, a total of 127 PSP brains from QSBB were examined.  Of those, 86 had Richardson’s Disease, or the dementia form of PSP, while 37 had PSP-P.  (Four cases must’ve had rare forms of PSP.)  The researchers describe this division as follows:

“PSP cases were further divided according to their clinical features present in the first 2 years of disease. When the clinical notes recorded falls, supranuclear gaze palsy, abnormal vertical saccadic eye movements or cognitive decline within the first 2 years patients they were classified as RD (n = 86). Patients were classified PSP-P when their history included asymmetric bradykinesia, rigidity, a positive L-dopa response or tremor, and the cardinal features of RD were not present (n = 37).”

That breakdown — 29% with PSP-P and 68% with RD — is roughly what we see in our local support group:  most have the dementia form of PSP but about a third have the parkinsonism form.

The authors state:  “The clinical differences between RD and PSP-P are most likely to be due to differences in pathological severity.”  (By the way, an effort is apparently on to rename the dementia form of PSP to “Richardson’s Disease,” or RD, rather than Richardson’s Syndrome.)

Past studies have shown that the diagnostic accuracy for RD is much higher than that for PSP-P: 86% vs. 41%.

After comparing the clinical records, researchers found no clinical features “predictive” of PSP-P.  (No wonder this form of PSP is so hard to diagnose!)

In distinguishing PD, DLB, and PSP-P, three clinical features were found to be most important:  “late drug induced dyskinesias, late autonomic dysfunction, and any visual hallucinations.”  These three symptoms are very uncommon in PSP and “may be helpful exclusion criteria.”  Note that none of these three features is an early symptom.

Researchers also found many features to distinguish MSA and PSP-P:

“Late non-specific eye symptoms and supranuclear gaze palsy were good discriminators of PSP-P. Three other clinical features, when calculated with respect to a diagnosis of MSA, appeared to be reasonable discriminators of MSA, including early autonomic dysfunction, late autonomic dysfunction, and late cerebellar signs, which occurred in more than 50% of MSA patients and less than 10% of PSP-P patients.”

These statements in the Discussion section about differentiating PSP from PD were interesting:

“The nature of bradykinesia has rarely been examined in detail in different diseases, but our impression is that rapid hypokinesia – reduced amplitude of movement, that is, fast and without decay, is more typical in patients with PSP than true bradykinesia typical of PD. Equally, fast micrographia and rapid hypophonia may also be clues to PSP pathology.”

This may be enough for most of you.  The abstract follows.

Robin

———————————–

Movement Disorders. 2010 Jan 27. [Epub ahead of print]

What features improve the accuracy of the clinical diagnosis of progressive supranuclear palsy-parkinsonism (PSP-P)?

Williams DR, Lees AJ.
Van Cleef Roet Centre for Nervous Diseases, Monash University, Melbourne, Victoria, Australia.

Progressive supranuclear palsy-parkinsonism (PSP-P) is a primary tauopathy characterised by neurofibrillary degeneration, which is frequently mistaken for Parkinson’s disease (PD), multiple system atrophy (MSA), and vascular parkinsonism (VP) at presentation. The aim of this study was to identify particular clinical features (green flags) that may be helpful in differentiating PSP-P from these other disorders.

We identified 37 patients with PSP-P from 726 patients archived at the Queen Square Brain Bank. Using a retrospective case notes review the clinical features were compared between the PSP-P group and Lewy body associated parkinsonism (PD, n = 444 and dementia with Lewy bodies (DLB), n = 46), MSA (n = 90), and VP (n = 19), using the chi(2)-test for proportions for a two-by-two contingency table.

The sensitivity, specificity, and positive predictive values (PPV) and negative predictive values (NPV) were calculated for individual clinical features. A specificity of >0.85 or a PPV of >0.85 were considered reliable discriminators.

No clinical features were predictive of PSP-P, but late drug induced dyskinesias (specificity 0.92, PPV 0.99), late autonomic dysfunction (specificity 0.94, PPV 0.99) and any visual hallucinations (specificity 0.94, PPV 0.99) were better in distinguishing PD and PSP-P than predicted using operational diagnostic criteria for PD. PSP-P shares many clinical features with PD and DLB, MSA and VP, but visual hallucinations, drug induced dyskinesias and autonomic dysfunction are very uncommon and may be helpful exclusion criteria.

PubMed ID#: 20108379   (see pubmed.gov for this abstact only – available at no charge)

Argyrophilic grain disease

This is research published several years ago from the Mayo Clinic Jacksonville Brain Bank.  I’ve been noticing some neuropathology reports that mention argyrophilic grain disease (AgD).  Usually this is in combination with progressive supranuclear palsy (PSP).  There are no diagnostic criteria for AgD for when someone is alive.  It may be associated with mild cognitive impairment but it seems we aren’t very sure!

The abstract is copied below.

Robin
———————————

Brain Pathology. 2002 Jan;12(1):45-52.

Argyrophilic grain disease: neuropathology, frequency in a dementia brain bank and lack of relationship with apolipoprotein E.

Togo T, Cookson N, Dickson DW.

Abstract
Argyrophilic grain disease (AGD) is a recently recognized disorder whose relationship to dementia as well as genetic or biochemical features remain incompletely characterized in part due to diagnostic difficulties engendered by concomitant pathologies. In the present study, we reviewed a consecutive series of over 300 brains referred for evaluation of dementia for presence of argyrophilic grains (AGs). AGs were found in the hippocampal region and amygdala, and were accompanied by coiled bodies in the underlying white matter and ballooned neurons in the limbic lobe. Ballooned neurons were also found in the limbic lobe in a number of cases of advanced Alzheimer’s disease (AD) that did not have AGs, supporting the lack of diagnostic significance of ballooned neurons confined to limbic lobe. The frequency of AGD in this series of dementia brains was 4.9% and was similar to the frequency in other autopsy series of nondemented cases, supporting the notion that there is no obligatory relationship between AGD and dementia. In the present series, ApoE epsilon4 allele frequency of AGD was dependent on concurrent AD, with AGD cases lacking AD similar to controls and cases with concurrent AD similar to AD. This suggests that AGD is an independent disease process from AD.

PubMed ID#: 11770901  (see pubmed.gov for the abstract only)

Case Rpt- “Dramatic improvement” with Ambien CR

I don’t get too excited about a report on a single case but you be the judge!
Robin

Journal of Clinical Neuroscience. 2010 Jan 11. [Epub ahead of print]

The use of zolpidem in the treatment of progressive supranuclear palsy.

Cotter C, Armytage T, Crimmins D.
Department of Neurology, Northern Sydney Central Coast Health, Gosford Hospital, Gosford, New South Wales, Australia.

Progressive supranuclear palsy (PSP) is a debilitating progressive neurodegenerative disorder for which there is no proven pharmacological treatment.

Zolpidem immediate release formulation has been reported to show short-term improvements in motor function and voluntary saccadic eye movements, but the benefits were not sustained.

A 61-year-old man with a 4-year history of PSP was observed over 6 months to have sustained improvement in motor function, pseudobulbar symptoms and ocular motility 2 months after commencing zolpidem controlled release (CR) formulation. He was admitted to hospital and a detailed neurological and functional assessment recorded on video after withdrawal of zolpidem CR, and again following re-introduction of the medication. Within 1 hour of administration of 25mg zolpidem CR the patient had a dramatic improvement in fine motor skills, dexterity, speed and fluidity of movement, facial and vocal expression, oropharyngeal coordination and function and pursuit, and voluntary saccadic eye movements. These improvements were observed for 4 hours to 5 hours post-dose and were reproducible on subsequent withdrawal and re-challenging. We found that zolpidem CR, a gamma aminobutryic acid (GABA)ergic agonist of the benzodiazepine type 1 receptor, caused sustained improvement in motor and ocular symptoms in a patient with PSP over 6 months.

Further studies are needed to determine the potential roles of GABA neurotransmission in PSP.

PubMed ID#: 20071178

[zolpidem = Ambien; zolpidem CR = Ambien CR]

Case report- PSP-P patient recvd DBS

This case report was published last year. It’s about an Italian patient diagnosed clinically with PSP-P (the parkinsonism form of PSP, not the dementia form of PSP) who received deep brain surgery, with an implant placed in an area of the brain called the nucleus tegmenti pedunculopontini (PPTg). This letter reports that the procedure was safe and the patient saw “modest benefits.”

“Gait was improved only in terms of a consistent amelioration of the primary gait ignition failure. On the other hand, the impact on postural stability and direction changes was absent. When evaluated with a specific questionnaire as the Giladi for FOG [freezing of gait] DBS-mediated effect were modest. DBS-related effect could be detected in non-motor domains (such as dysphagia and swallowing impairment). Neuropsychological tests did not reveal major cognitive changes apart from minimal improvement in verbal fluency.

The researchers considered this surgery based upon published data showing “some degree of gait impairment amelioration and cognitive benefits” to PD patients where an implant was placed in a similar part of the brain. In this PSP-P patient, the researchers saw no cognitive benefits and gait improvement only in terms of “consistent amelioration of the primary gait ignition failure.”

The researchers conclude: “Although this single case seems not to support the PPTg implantation as a critical therapeutic option for PSP-P patients, at least in advanced ones, it is possible that larger trials, centred either on PSP-P recruited at the disease onset or on PSP Richardson type, will verify further the potential of DBS-mediated stimulation to activate directly surviving fibres or even delay the disease evolution.”

I’ve copied the citation below.

Robin

Movement Disorders
Volume 24 Issue 13, Pages 2020 – 2022
Published Online: 11 Aug 2009

Letter to the Editor
Implantation of the Nucleus Tegmenti Pedunculopontini in a PSP-P Patient: Safe Procedure, Modest Benefits

Livia Brusa, MD, PhD 1, Cesare Iani, MD 1, Roberto Ceravolo, MD 2, Salvatore Galati, MD 3 4, Vincenzo Moschella, MD 2 4, Francesco Marzetti, MD 3 4, Paolo Stanzione, MD 3 4, Alessandro Stefani, MD 3 4

1 Ospedale S.Eugenio UOC Neurologia, Rome, Italy
2 Dipartimento di Neuroscienze, Clinica Neurologica, Università di Pisa, Pisa, Italy
3 Clinica Neurologica, Universita’ di Roma Tor Vergata, Rome, Italy
4 IRCCS Fondazione S. Lucia, Rome, Italy

Note: no abstract is available on PubMed. The PubMed ID# for this letter is #19672983.

FDG-PET for differentiating PD, PSP, and MSA

This article on the use of FDG-PET in differentiating PD, MSA, and PSP was published today in The Lancet Neurology. I haven’t had a chance to wade through all of the article yet but it seems to be one of the better articles we’ve seen lately on PSP and MSA. 167 patients in the NY area participated in the study. Only 9 of these patients have died and donated brain tissue thus far. So I’m not sure how “real” the diagnostic accuracy percentages are. And the diagnosis of CBD was not part of the study.

Below, I’ve copied a HealthImaging.com article on this research as well as the abstract.

Robin


The Lancet Neurology, Early Online Publication, 11 January 2010.

Differential diagnosis of parkinsonism: a metabolic imaging study using pattern analysis

Chris C Tang MD, Kathleen L Poston MD, Thomas Eckert MD, Andrew Feigin MD, Steven Frucht MD, Mark Gudesblatt MD, Vijay Dhawan PhD, Martin Lesser PhD, Jean-Paul Vonsattel MD, Stanley Fahn MD, David Eidelberg MD

Summary

Background
Idiopathic Parkinson’s disease can present with symptoms similar to those of multiple system atrophy or progressive supranuclear palsy. We aimed to assess whether metabolic brain imaging combined with spatial covariance analysis could accurately discriminate patients with parkinsonism who had different underlying disorders.

Methods
Between January, 1998, and December, 2006, patients from the New York area who had parkinsonian features but uncertain clinical diagnosis had fluorine-18-labelled-fluorodeoxyglucose-PET at The Feinstein Institute for Medical Research. We developed an automated image-based classification procedure to differentiate individual patients with idiopathic Parkinson’s disease, multiple system atrophy, and progressive supranuclear palsy. For each patient, the likelihood of having each of the three diseases was calculated by use of multiple disease-related patterns with logistic regression and leave-one-out cross-validation. Each patient was classified according to criteria defined by receiver-operating-characteristic analysis. After imaging, patients were assessed by blinded movement disorders specialists for a mean of 2·6 years before a final clinical diagnosis was made. The accuracy of the initial image-based classification was assessed by comparison with the final clinical diagnosis.

Findings
167 patients were assessed. Image-based classification for idiopathic Parkinson’s disease had 84% sensitivity, 97% specificity, 98% positive predictive value (PPV), and 82% negative predictive value (NPV). Imaging classifications were also accurate for multiple system atrophy (85% sensitivity, 96% specificity, 97% PPV, and 83% NPV) and progressive supranuclear palsy (88% sensitivity, 94% specificity, 91% PPV, and 92% NPV).

Interpretation
Automated image-based classification has high specificity in distinguishing between parkinsonian disorders and could help in selecting treatment for early-stage patients and identifying participants for clinical trials.

Funding
National Institutes of Health and General Clinical Research Center at The Feinstein Institute for Medical Research.

http://www.healthimaging.com/index.php? … e&id=20154

TOP STORIES
Lancet: FDG-PET could distinguish between Parkinsonian disorders
Written by Editorial Staff, HealthImaging.com
January 11, 2010

FDG-PET imaging-based classification has high specificity to differentiate individual patients with idiopathic Parkinson’s disease, multiple system atrophy and progressive supranuclear palsy and could help in selecting treatment for early-stage patients and identifying participants for clinical trials, according to research published online Jan. 11 in Lancet Neurology.

David Eidelberg, MD, director of the center for neurosciences at the Feinstein Institute for Medical Research in Manhasset, N.Y., and colleagues assessed whether metabolic brain imaging combined with spatial covariance analysis could accurately differentiate between patients with Parkinsonism who had different underlying disorders.

In the study, 167 patients who had Parkinsonian features but uncertain clinical diagnosis had an 18F-FDG PET scan. The researchers developed an automated image-based classification procedure to differentiate individual patients with Parkinsonian disorders and the accuracy was assessed by comparison with the final clinical diagnosis.

Eidelberg said that out of the 167 patients assessed, image-based classification for idiopathic Parkinson’s disease had 84 percent sensitivity, 97 percent specificity, 98 percent positive predictive value (PPV) and 82 percent negative predictive value (NPV).

Eidelberg and colleagues found that imaging classifications were also accurate for multiple system atrophy (85 percent sensitivity, 96 percent specificity, 97 percent PPV, and 83 percent NPV) and progressive supranuclear palsy (88 percent sensitivity, 94 percent specificity, 91 percent PPV and 92 percent NPV).

In an accompanying commentary, Angelo Antonini, MD, at IRCCS San Camillo, Venice and Parkinson Institute in Milan, Italy, wrote that the “clinical and research relevance of these findings should not be underestimated. Neuroprotective and disease-modifying drug research is intensifying and results mostly rely on accurate early diagnosis.”

“The excellent specificity and PPV of the imaging classification makes this test suitable for diagnostic use rather than as a screening tool,” Eidelberg noted.

“Although imaging might be cost effective for early diagnosis, I expect that these procedures will find their natural application in the identification of suitable candidates for drug trials or complex surgical procedures (example, deep brain stimulation, stem-cell transplantation or fetal tissue transplantation). However, additional blinded, prospective, multicenter studies will first be needed to confirm the accuracy of this pattern-based categorization procedure,” Antonini concluded.

Last updated on January 11, 2010 at 12:48 pm EST

Dementia with Lewy Bodies – “Patient page. Not all dementia is Alzheimer”

I was reading over someone’s brain autopsy report today, and it contained this sentence:

“Considering the degree of Alzheimer type pathology and the distribution of Lewy bodies, the likelihood that this patient would have had clinical features of dementia with Lewy bodies is intermediate.”

The source of the “intermediate” evaluation was the “Third report of the DLB consortium,” which was published in 2005.  That “Third report” is the key diagnostic guide for Dementia with Lewy Bodies.  You can find the criteria on the Brain Support Network website here:

www.brainsupportnetwork.org/education/lewy-body-dementia/

So…I started digging around on PubMed and discovered that you’d have to pay for the “Third report” but there’s an associated “Patient Page” that is free.  I think this “Patient Page” is designed to be given to patients and families by their neurologists.  It’s an understandable two-page description of DLB and other forms of dementia.

Here’s the citation for the “Patient Page.”

Neurology. 2005 Dec 27;65(12):E26-7.
Patient page. Not all dementia is Alzheimer: dementia with Lewy bodies.
Knopman D, Jankowiak J.
PubMed ID#: 16380603

Here are links to the “Patient Page,” available for free online:

www.neurology.org/cgi/content/full/65/12/E26 –> HTML version

www.neurology.org/cgi/reprint/65/12/E26 –> PDF version

This might be a useful document to share with your general neurologist or primary care physician.

Man with double vision and dementia; PSP upon autopsy

PSP folks –

This is an interesting case report of a 49-year-old man who was found to have the dementia form of PSP upon brain autopsy. That form of PSP is called “Richardson syndrome (RS).”

I don’t believe this man was diagnosed during life with PSP because he presented with atypical features for PSP: “young age at onset, absence of falls, and the presenting complaint of horizontal diplopia (due to vergence abnormalities). His cognitive impairment was suggestive of frontotemporal dementia. However, vertical saccades were slow at presentation.”

I note that the patient clapped exactly three times. This must refer to the “clap test,” which has now been greatly discounted as a neurological test for PSP.

The patient received extensive testing, including neuro-ophthalmological testing. The clinicians have gone back through the patient’s clinical records after death to try to solve the mystery of how they missed this patient’s PSP.
The researchers conclude “that careful examination of the speed (more than amplitude) of vertical saccades in patients with undiagnosed parkinsonian disorders remains the cornerstone for recognition of PSP and differentiation from other parkinsonian disorders.”

The citation is below.

The text refers to images of brain tissue available as a result of the brain autopsy. You can find those images at the Neurology journal’s website here:
http://neurology.org/cgi/content/full/73/24/2122/DC1 (6 images available for free)

Robin


Neurology. 2009 Dec 15;73(24):2122-4.

Evolution of oculomotor and clinical findings in autopsy-proven Richardson syndrome.

Hardwick A, Rucker JC, Cohen ML, Friedland RP, Gustaw-Rothenberg K, Riley DE, Leigh RJ.
Department of Neurology, Veterans Affairs Medical Center, Case Western Reserve University, Cleveland, OH, USA.

From the Departments of Neurology (A.H., K.G.-R., D.E.R., R.J.L.) and Neuropathology (M.L.C.), University Hospital, and Daroff-Dell’Osso Laboratory (R.J.L.), Veterans Affairs Medical Center, Case Western Reserve University, Cleveland, OH; Department of Neurology (J.C.R.), University of Louisville School of Medicine, Louisville KY; and Mount Sinai Medical Center (R.P.F.), New York, NY.

PubMed ID#: 20018641 (there’s nothing viewable at pubmed.gov on this article)

Gizmo, Care Status System, and New Caregiver Website

Here’s a recent blog post in the “New Old Age” blog in the New York Times (nytimes.com).
The article describes:

* one tech gizmo: the Wellcore fall detection and emergency response device;
* a system to stay up to date on your loved one (whom you are not living with): Connect for Healthcare care recipient status system; and
* a new website for caregivers: ecarediary.com that supplies a variety of tools for caregivers.

Here’s a link:

Old Age, New Gizmos
By Paula Span
New York Times
January 6, 2010, 9:56 am

Robin