PSP, CBD, and MSA Conference – Extensive Notes (Nov 2009, Australia)

This post provides the notes Brain Support Network volunteer Robin Riddle took from the recordings on this conference:

“The Challenge of Movement Disorders: Exploring diagnosis, management and best practice interventions in relation to PSP, MSA, and CBD”

Topic: “Coping with Diagnosis: An Intro and Overview of the conditions (CBD, MSA and PSP), including diagnosis, current treatment options and recommendations”

Attendees: allied health professionals (MDs, RNs, PTs, OTs, STs, social workers, etc)

Date: November 25, 2009

Organizer: Parkinson’s Victoria ( and PSP Australia (

Speaker: Dr. David Williams, The Alfred and Cabrini Hospital, Melbourne


The notes are provided by part or segment as follows:

Part 1 (8 minutes) – On all atypical parkinsonism disorders (PSP, MSA, CBD)

Part 2 (10 minutes) – On PSP (mostly on Richardson’s syndrome with an intro to PSP-P and PAGF at the end)

Part 3 (10 minutes) – On PSP (specifically on PSP-Parkinsonism and pure akinesia with gait freezing)

Part 4 – (10 minutes) – On PSP

Part 5 (9 minutes) – On PSP (first half) and MSA (second half)

Part 6 (8 minutes) – On MSA (first third) and CBD

Part 7 (5 minutes) – On CBD (first half) and all atypical parkinsonism disorders (PSP, MSA, CBD)


Part 1 (8 minutes) – On all atypical parkinsonism disorders (PSP, MSA, CBD)

If it’s not Parkinson’s disease (PD), what is it? Many disorders can look a little like PD including: PSP, MSA, CBD, vascular parkinsonism (caused by strokes), Huntington’s disease (inherited), Wilson’s disease, Neuronal intranuclear inclusion disease, neurofilament inclusion body disease, spinocerebellar ataxia 6 (3, 7; rare). Today, we are talking about the first three. You might see patients described as having “parkinsonism” as we aren’t sure which of these disorders it is. Only Wilson’s disease has curative treatments.

Diagnosis is important for patients: disease label and identity. I prefer to err on the side of riskiness and make an early diagnosis. Having a diagnosis helps for planning. Diagnosis is important for research and quality assurance.

PD is 25 times more common than any other bradykinetic rigid syndrome. (I see 20 patients with PD and only one or two with PSP or MSA.) Medication can improve many of the symptoms. Survival is usually 15 to 25 years after onset. Symptoms: loss of sense of smell; REM behavior disorder (during sleep; act out dreams); visual hallucinations (usually developed later in the disease); good or excellent response to levodopa. These four symptoms don’t happen in the other three conditions we are talking about today — PSP, MSA, and CBD.


Part 2 (10 minutes) – On PSP

Here are the notes I took from this segment, which focuses on the classic form of PSP, called Richardson’s syndrome though, near the end, there’s an intro to other PSP forms, including PSP-Parkinsonism and pure akinesia with gait freezing:

Richardson, Steele, and Olszewski described PSP in late 50s and early 60s. John Steele is still alive and lives on Guam. Dr. Steele argues that the disease should really be known as Richardson’s disease or Richardson’s syndrome.

It’s really wrong to say that patients with PSP look like those with Parkinson’s because they really don’t get much in the way of bradykinesia (slowed movement) until five or more years after onset.

Mild dementia is often developed in PSP. It may happen early on.

Restriction of full lateral gaze. The eyes often become completely fixed.

Rather than the hunched posture of PD, PSP patients are often upright, with the neck usually extended backwards.

The postural reflexes are much more impaired.

The necks are stiff. The eyes tend to close over.

How do we identify patients with PSP? Diagnostic criteria are: gradually progressive disorder; onset later than 40 years; postural instability and falls in first year of disease AND vertical (up or down) supranuclear palsy. By definition, someone 39 or younger doesn’t have PSP.

Supranuclear = coming from the brain rather than the brain stem.

Supportive criteria of PSP: symmetric akinesia or rigidity (often in the neck; usually less in the arms than in PD); abnormal neck posture (severe axial dystonia in the neck, which is typical); frontalis overactivity (patients often look surprised or startled); poor or absent response to levodopa; early dysphagia (swallowing problems) or dysarthria (speech disturbance); early onset of cognitive impairment (executive dysfunction; decreased verbal fluency; not frank dementia; not loss of memory); normal sense of smell; no visual hallucinations; no REM behavior disorder. The last three are in contrast to PD patients.

Clinical features of PSP: 65 years is mean age of onset; 7 years is mean disease duration with Richardson’s syndrome (so 50% die before 7 years and 50% of people die after 7 years); most common modes of death are respiratory dysfunction or as a result of a fall (causing a brain hemorrhage, for example).

PSP is caused by abnormal protein accumulation, predominantly in the basal ganglia, which is where movement comes from. Spontaneous movement is slow. Static movement like neck posture is exaggerated. And eye movements are reduced.

Not everyone with PSP has these diagnostic features. This is what my PhD was about. What if a patient comes into the clinic with normal eye movements and a bit of tremor? Unfortunately most people don’t go by the textbook and there is a range of different presentations of PSP pathology. Most don’t respond well to medications, and there is usually the same mode of death at the end. But in some cases we can say to the patient that “you’ve got the good form of PSP; you are going to live 12 to 14 years” if they ask that question.

What if there is no supranuclear gaze palsy (SNGP)? Usually SNGP develops within the first two years. But in about 30% of patients, it doesn’t. They might have a different type of PSP. Other clinical syndromes specific for PSP-tau pathology including: PSP-Parkinsonism (patient looks like they have Parkinson’s for the first two to eight years and then develop more classic signs of Richardson’s syndrome), pure akinesia with gait freezing; corticobasal syndrome.


Part 3 (10 minutes) – On PSP

[This segment focuses on two less common forms of PSP — PSP-Parkinsonism and pure akinesia with gait freezing.]

I’m emphasizing the importance of research. Prior to our publishing this paper in 2005 [Williams et al, Brain 2005], the only way to diagnose PSP in the clinic was adhering to the diagnostic criteria I showed you before. But 32% of cases studied for our 2005 paper (with pathologically-confirmed PSP) lacked classic Richardson’s syndrome features. These people were told they had “atypical parkinsonism” because they didn’t fit under the PSP banner. This subgroup is called PSP-Parkinsonism: asymmetric onset of symptoms (just one side or one arm or one leg); tremor; moderately good response to levodopa. So, they have no early falls, no eye movement abnormality, and no early cognitive dysfunction in contrast to those with Richardson’s syndrome. They look much more like they have Parkinson’s disease for the first few years.

Video of woman with PSP-Parkinsonism. She had unilateral rest tremor that was treated with levodopa. Her posture is more upright than what you’d expect with PD. Very subtle eye movement changes several years into the disease. She’s 13 years into the disease.

Video of man with PSP-Parkinsonism. He lived 11 years. Never developed eye movement abnormalities. Rest tremor in leg. Small handwriting. Unusual stride pattern. He had only PSP upon brain analysis. The people looking after him thought he had PD for the whole duration. We don’t know if he had visual hallucinations, loss of sense of smell, or REM behavior disorder but the lack of these symptoms might have alerted his clinicians to something other than a PD diagnosis. He had no sign of Parkinson’s pathology upon brain tissue analysis.

PSP-P can be differentiated from PD by: normal sense of smell; no visual hallucinations; no REM behavior disorder; normal cardiac autonomic function (as seen through a cardiac MIBG).

What about the other condition of pure akinesia with gait freezing? I was always told in medical school that this was always due to vascular parkinsonism, so parkinsonism caused by small strokes in the frontal lobe or the basal ganglia. But most of the patients that have this type of clinical picture have PSP-tau pathology.

The diagnostic criteria we put together for pure akinesia with gait freezing are: marked by gradual onset, which implies neurodegeneration (in contrast to sudden onset, which would imply stroke) and early freezing of gait or speech (in the first one or two years). Absent are: sustained response to levodopa; tremor; rigidity in arms and legs (sometimes there’s a little in the neck); imaging changes suggestive of vascular disease or Binswanger’s. Absent in first five years are: limb rigidity; dementia; opthalmoplegia; vascular disease.

Video of man with PAGF. Good arm swing. His only problem in gait freezing. Blepharospasm. Has developed some slowing of vertical eye movements, ten to twelve years into the disease. Rapid but small amplitude movements; this is a lot different than what we see in PD. He has rapid hypophonia: speaks quickly but softly. (In PD, patients speak softly and slowly.) These are clues that it’s PSP-tau pathology, rather than PD. The biggest clue is probably that they don’t get better at all with medication. And, gait freezing, if it happens early in PD, always gets better with medication.

Video of man with PAGF. Costs $1500/day to see a specialist at Mayo Clinic. This patient was told the same thing by Mayo that the specialists in London had told him. For about the first eight years, his only problem was occasional gait freezing. This leads to falls at home. He’s been given the visual cue (paper on the ground), and he steps over it.

What’s the difference in these conditions? Very importantly, we can talk about prognosis. This is important for a lot of patients. Some patients don’t want to hear anything about what’s going on but others do want to know and plan things out.

Prognosis rate varies by disease subtype: Richardson’s syndrome, PSP-P. This is important for therapeutic interventions and counseling as well. If you are older at onset, your survival is a bit less. You can’t pick on any one person and say exactly what their survival is going to be but you can imagine that the accumulation of disabilities is going to increase at a faster rate if you are older.


Part 4 – (10 minutes) – On PSP

[This segment focuses on pure akinesia with gait freezing (first third) and is then about PSP overall.]

How do we separate PAGF from PD and from VP (vascular parkinsonism)?

PAGF: rapid hypophonia (talk fast but softly; fast micrographia (write in small letters but quickly)

PD: rigidity; tremor; response to levodopa; visual hallucinations

VP: leg rigidity; tremor; early cognitive dysfunction; pyramidal signs; history of stroke on scans

PAGF is differentiated from PD by: normal sense of smell; no visual hallucinations; no REM behavior disorder; normal cardiac autonomic function (cardiac MIBG)

Microtubule associated protein tau is ubiquitous in the adult brain. Its normal function is assembly and stabilization of microtubules (neuronal cell structural elements). Normally tau protein binds to microtubules in axons.

In tauopathies, like PAGF, tau is redistributed to the cell body and accumulates to form insoluble, fibrillary deposits, or tau protein clumps. We don’t know if tau causes the disease or if it’s the result of the disease. We do know it characterizes the disease. It happens in PSP, not in PD.

There is a genetic basis. This doesn’t mean it’s inherited. About 70% of us have a certain type of genetics for this tau protein. The 30% who don’t are less likely to get PSP. This is a genetic modifier, not a risk factor or a cause.

If on brain autopsy a patient’s brain has mainly the basal ganglia being involved with the tau pathology, that patient is more like to have had PSP-Parkinsonism or pure akinesia with gait freezing. Compared to if a lot of the cortex is involved, these patients will only have Richardson’s Syndrome. So knowing what brain regions are involved and what symptoms this causes should give us insight into whether a patient has PSP-Parkinsonism or Richardson’s Syndrome. My view is that there are other genetic modifiers that make the outlook better for those with PSP-Parkinsonism and worse for those with Richardson’s Syndrome. We will find this out over the coming years.

Are there any diagnostic tests for PSP? No.

Cardiac MIBG looks at nerves around the heart. The MSA patient has a normal scan. In PD, the heart doesn’t take up the tracer due to loss of nerves around the heart. It doesn’t usually cause heart problems. Patients with PSP would be expected to have a normal scan. This type of scan would be somewhat useful in differentiating between PSP and PD but they aren’t accurate in everyone.

Smell Sense (UPSIT) includes 40 items for a scratch and sniff test. Patients with PD score in the 10th percentile for smell discrimination. PSPers score in the 18th percentile — well into the normal range. As a group we can separate the two conditions quite well but on an individual level there may be great variability. So it’s not good at separating the two conditions.

What about other biomarkers? There’s a lumbar puncture test that’s being shown in Italy to separate out PSP. Tau fragments in CSF are a biomarker. Problem is that the pathology is very similar between PSP and CBD so those patients should be similar. That’s a criticism of the technology in the paper. But what it means is that it’s very difficult to develop in vivo (during life) tests that discriminate between PSP and Parkinson’s and other conditions.

What are the treatment options for PSP?

* levodopa: if parkinsonism present, I always try this. I always try levodopa if patients have rigidity and bradykinesia; usually there’s not a response. Sometimes when you stop the medication, people feel worse so you’ll see a lot of people with PSP on a small dose of Parkinson’s medications just because they felt a bit worse off it it but you can’t really tell much difference.

* amantadine: developed in the 1950s by the US Army to reduce the risk of flu. It was found to improve PD symptoms a little bit in the 1960s. Occasionally we’ll find that gait freezing in PSP can improve a little bit if we use this medication but the result usually is unfortunately disappointing.

* amitritypline: tricyclic antidepressant. Probably the most prescribed medication in all of neurology (used for pain, migraines, depression, hyper-salivation, urinary problems). One in five patients with PSP find that they have louder speech and improvement in swallowing. It’s certainly worth trying if those are issues.

* botulinum toxin: used for blepharospasm (tendency for eyes to close over; injection around the eyes) and in the neck (if the extension rigidity is very uncomfortable; axial dystonia).

* zolpidem CR: helpful in the odd patient. There are a few case reports of someone getting out of their chair when they are on the right dose of zolpidem. I’ve never had that experience but I’ve seen the videos so I do believe it happens. Might be helpful for gait freezing.

* DBS: not a worthwhile option in PSP. This has been shown several times.

PSP Australia, in conjunction with Parkinson’s Australia, has developed a 100-page carer’s manual with important info about the management of PSP, prognosis, welfare issues, and end of life decisions. It provides expert advice.

There are a few emerging drug trials for PSP. We are starting to try to adjust some things about how that tau protein accumulates in the cells and is associated with nerve cell death.

Lithium is one of the oldest and one of the simplest drugs around. It’s been used in bipolar disorder and depression for 50 years. It’s a GSK inhibitor that reduces phosphorylation of tau. Lithium stops the enzyme that makes the tau bunch together. CurePSP-sponsored study in the UK and US is now going on: lithium vs. placebo. 30 planned in each group. Lumbar puncture is mandated, which is probably why the recruitment for this study has been slow. And they’ve had lithium toxicity problems. No results expected for several years. I don’t believe lithium is the answer. I’ve had one patient on lithium for 15 years and still developed PSP. And another patient who was started on lithium because of the rumor of this study emerging a couple of years ago, and he died due to lithium toxicity during the heatwave in London. [Robin’s note: This Australian conference was before the NIH-funded lithium study was ended due to tolerability issues.]


Part 5 (9 minutes) – On PSP (first half) and MSA (second half)

Co-enzyme Q10 is supposed to change the progression of the disease, not improve symptoms. Quite expensive so a lot of people try to get it on the internet from North America. In a study published in the Movement Disorders journal in 2008, there was a miraculous recovery of patients with PSP patients who took CoQ10 (500mg of CoQ10 for six weeks). So miraculous that it’s unbelievable. We should look carefully at these studies. The patients taking the placebo were on average seven years older than those taking CoQ10. I’d also argue that a two-point improvement on a 100-point scale has no clinical significance. If you repeat the test a further six months down the line, you’d find the improvement goes the other way. A bit naughty publishing there. If I was reviewing it, I would’ve rejected it.

NP-12 is another GSK3-inhibitor. It doesn’t have the toxicity of lithium, another GSK inhibitor. It is a molecule originating from a rational design program with inhibitory activity of GSK-3. (The molecule was specifically designed for this task.) There is a multicenter, placebo-controlled trial in PSP, with up to 300 patients. It has started in Europe. It will probably go for three or four years. It’s called the “Noscira trial.” Noscira is a Spanish company. Tools used to measure outcomes: Golbe rating scale and PSP QoL scale.

Allon – davunetide intranasal is a neuroprotective agent. This is an NIH/CurePSP-sponsored trial. This is an exciting trial. Preclinical experiments indicate that davunetide has neuroprotective (look after brain cells so they aren’t dying), neurotropic and cognitive protective properties. Supposedly stabilizes sick and dying nerve cells. Vasoactive intestinal peptide-like properties. Phase II clinical trial (safety and efficacy). Placebo-controlled trial. Patients will have to have lumbar puncture, MRI, and clinical assessments (PSP Rating Scale) five times over a 12-month period. Australian site – Melbourne. Looking to start April 2010. The medication is delivered via nasal spray, which is always good for patients who can’t swallow very well.

Unfortunately many of the neuroprotective studies looking particularly at stroke models haven’t been very useful. There is a fair degree of skepticism about a neuroprotective study. But it hasn’t been tried in a tauopathy, particularly one that progresses like PSP.


(Starts at 4:07) Multiple system atrophy is about as common as PSP. It looks completely different under the microscope in post-mortem examination, where there isn’t any tau accumulation but rather other proteins.

How do we make an MSA diagnosis and how do we differentiate it from PD? Well, these guys surely have parkinsonism (slow movements, muscle stiffness, they often have a little bit of tremor as well). But the defining feature is that other systems are involved as well. And the autonomic system is absolutely a part of that diagnostic paradigm. If there’s no autonomic dysfunction, then you can’t diagnose MSA.

It’s not “multi system atrophy,” and it’s not “multiple systems atrophy.”

MSA = autonomic dysfunction + parkinsonism + cerebellar dysfunction. There’s MSA-Parkinsonism and MSA-Cerebellar.

Yes, there are autonomic symptoms in PD but, in MSA, autonomic failure almost always precedes parkinsonism. Autonomic failure includes: (measurable) postural hypotension (simply because they don’t have the autonomic response to lower blood pressure that gravity gives us when we stand); impotence (reported by men; early signs are some ED rather than complete impotence; sexual dysfunction in women, though this is hard to get at); constipation (bowel changes over the last three or four years, which have been getting worse); urinary difficulties (ubiquitous; I consider these essential for diagnosis of MSA; hard to determine in multiparous women and in men with prostate problems but usually we look for a pattern of urinary problems that has emerged over the last couple of years; includes urinary urgency, frequency, and nocturia).

Between 25% and 50% of MSA patients have cerebellar dysfunction as well. The cerebellum is involved with coordination and balance. Sometimes cerebellar dysfunction can be the primary problem. In MSA-C, there is often little parkinsonism. Idiopathic late onset cerebellar dysfunction with autonomic failure.

In MSA, tremor is quite rare.

In MSA, response to medication is variable. It’s disappointing compared to PD. But I must say that I usually find that I’m using dopaminergic medication to improve muscle stiffness and slowness of movement. (The slide says: “the response with dyskinesias can be excellent.”)

Diagnostic criteria of MSA:

* Autonomic: BP drops > 20/10 after 3 minutes of standing; urinary urgency, nocturia, or frequency; erectile dysfunction in men; abnormal sweating

* Parkinsonism: often symmetrical at onset (in PD, it’s usually one side)

* Cerebellar: eye movements are normal

* Pyramidal: extensor plantar responses

Mean age of onset in MSA is 55 years — about 10 years earlier than PSP. Mean disease duration is 7 years. But this is a skewed view of things. In maybe a third of people, it’s rapidly progressive such that death occurs in 2 or 3 years. On the other side of that 50% percentile, equally, there are plenty of people who make it out past 15 years and out towards 20 years with MSA. An idea about prognosis (3 years vs. 15 years) can usually be guessed at during the first consultation after you’ve reviewed the progression. Most common modes of death in patients who die after 2 or 3 years are: respiratory dysfunction; sudden death due to muscle spasm around the neck (nocturnal apnea/asphyxia/central); falls.


Part 6 (8 minutes) – On MSA (first third) and CBD

Video of man with MSA. Dysmetria. Nystagmus. Extrapyramidal rigidity. Not much in the way of bradykinesia; a little bit on the left side. He noticed symptoms on the left side. The voice has become soft.

MSA can be differentiated from PD to some extent by: normal sense of smell (sense of smell usually better than in PD, though there can be abnormalities); no visual hallucinations; can have REM behavior disorder; normal cardiac autonomic function (cardiac MIBG isn’t so reliable, particularly if you are younger than 60 years of age).

Prognosis in MSA: patients with severe autonomic dysfunction at the outset have worse survival; rapid fall-off and then a long survival; the older you are, the faster the disease progresses. Comparing survival in those over 65 and under the age of 55.

Massive MSA research effort in Europe going on now. It’s still in the phase of understanding what the research is telling us. Hopefully we’ll start getting involved in the clinical trials once they start internationalizing them.


(starts at 3:09) Corticobasal degeneration is a pathological diagnosis, and none of us is a pathologist. Which means that none of us can make this diagnosis. During life, we call this “corticobasal syndrome.” Diagnostic accuracy is less than 50%. There is no validated diagnostic criteria for CBD. We should talk about “corticobasal syndrome” as a constellation of clinical features. I encourage you to use that terminology. We are demanding this in the research literature as well.

The pathology is caused by the tau protein. It causes:

* Asymmetric parkinsonism: dystonia (abnormal muscle tone, usually down one side; often in just one limb); cortical sensory loss (demonstrated by drawing the number in someone’s affected hand); myoclonus (brief, shock-like jerks); alien limb (arm feels like it’s not part of the body and it doesn’t it’s own thing; German in the wheelchair in “Dr. Strangelove” exhibits alien limb phenomenon)

* Frontotemporal dementia is often present. It may be a speech disturbance (eg, progressive non-fluent aphasia) or a behavioral disturbance (eg, frontal behavior syndrome).

If you see someone with the syndrome, you can’t say that they definitely have the pathology. What else can cause corticobasal syndrome? CBS can be caused by: CBD, PSP, TDP-43 frontotemporal dementia (FTD-U), vascular disease, Alzheimer’s disease.

If you say someone has “CBS caused by CBD pathology,” it’s just as likely as you’ll be wrong.

I don’t have any videos of people with pathologically-confirmed CBD.

Video of man with CBS (can’t guess at underlying pathology): stiff, useless right arm that is held in a dystonic posture. If it had been a stroke, you’d expect right facial problems and right limb problems. He has partial alien limb. Has a few myoclonic jerks. Can’t conceptualize because of basal ganglia and cortical pathology. Asymmetry. Often the other side will get involved 5 or 6 years down the trail.

Video of woman with CBS. Again, this could be confused as a stroke but the history isn’t that of a stroke. Useless hand. Subsequently developed blepharospasm and eye movement abnormalities. So you will agree with me that she probably has underlying PSP-tau pathology as the cause of this syndrome.

CBD = pathology. CBS = clinical syndrome.


Part 7 (5 minutes) – On CBD (first half) and all atypical parkinsonism disorders (PSP, MSA, CBD)

CBD patients often have ideomotor and limb kinetic apraxia, which is uncommon in PSP, PD, and DLB.

Myoclonus is a good feature to separate them except it’s only present in about 50% of the patients.

Eye movements can be abnormal. Usually there are some subtle differences which we try and pick up clinically. The slide says: “poor correlation in the literature with pathology.”

To try an illustrate the difficulties of diagnosing this condition… This is a paper we’ve just submitted of 1440 brains that came to the Queens Square Brain Bank over a 20 year period. 21 cases clinically diagnosed with CBD (using the old terminology). Of those 21 cases, 16 cases did NOT have CBD. This is a useless diagnostic paradigm! Of the 21 cases, 5 had pathologically confirmed CBD. Of the 1440 brains, 19 cases were pathologically diagnosed with CBD. Of the 19 cases, 5 cases had the clinical diagnosis of CBD (and were diagnosed during life) and 14 cases had other clinical diagnoses.

Of the patients that actually had that tau pathology of CBD, the diagnoses were:

* Initial clinical diagnosis: 8 PD, 2 PSP, 2 spastic paraparesis, 1 akinetic rigid syndrome, 1 AD, 1 CBD, 1 depression, 1 FTD, 1 MSA, 1 Tourette’s dynrome.

* Final clinical diagnosis: 8 PSP, 5 CBD, 2 PD, 1 FTD, 1 PNFA, 1 focal cortical atrophy with myoclonus; 1 Tourette’s syndrome

I’m not sure I could’ve gotten the diagnosis right either!

(At 2:31) If it’s not PD, what is it? Prognosis is worse; burden of care is worse; medications less likely to help; injuries more likely to occur.

Retrospective study from a couple of years ago looking at the time from symptom onset to falls. Patients with PD tend not to fall in the first 10 years. Patients with PSP tend to fall in the first 2 years. In MSA, they tend to fall in the first 3 or 4 years. In vascular parkinsonism, in the first 6 or 7 years. In dementia with Lewy bodies, in the first 4 or 5 years. Just from simply looking at falls, and the ramifications of that, the burden of care is more severe in the non-PD conditions.

What can we do about it? The PSP Information Kit is vitally important for every patient, family, and nurse to have. [Robin’s note: this kit is available online at]

It’s the role of all of us to provide: education; optimize home and community environment; maximize function (this may be through inpatient or outpatient rehab; this may be through medication trials; this may be through equipment optimization at home); carer support (carers have a big impact on quality of life and disease duration); encourage research.

One very rich man in Canada lived with what he thought was PD for 30 years. Turned out it was PSP. This family pumped in heaps of money for a fulltime physiotherapist and a couple of fulltime carers. Even a couple of years before he died, he was still being walked with 2 physiotherapists. Now he had an atypical form of PSP but this story goes to show that if you are maximizing the support for the carers and the physiotherapy, you are really going to get the best out of the patient and improve the quality of life.