Day 1: Tuesday, 4 September 2018

10:15 Welcome – Review of pre-course questionnaires

Dr Peter Fletcher, Cheltenham – Academic Director, Parkinson’s Academy

At the end of this short session you will understand three how’s, two what’s and a who:

  • Who the participants that make up your Parkinson’s MasterClass are
  • What the educational needs of your group are
  • How your course is underpinned educationally
  • How the structure of your course will assist the learning process
  • How that hopefully links to your practice
  • And what exactly you have let yourself in for …enjoy!


My background is in geriatric medicine with a major interest in movement disorders and principally Parkinson’s disease. I also inhabit a parallel universe in the world of education. As Parkinson’s Academy Faculty we have been keen to use sound educational principles to underpin our MasterClasses, something that we believe makes them truly unique. How we aim to achieve this is covered in this introduction.

Not strictly specific to this session I list below one reference that as someone who practices in this field I (still!) find useful. As the only person who has read all the needs assessment questionnaires I think you may find it useful too:
Quinn N. Parkinsonism: Recognition and Differential Diagnosis. BMJ 1995; 310:447-452

Racing ahead to the work that you will be doing between modules and will be presenting in Module 2 and also perhaps pointing you towards some useful teaching tips have a look at the following which I find are worth keeping on the shelf for reference.


  1. Kevin MacKway-Jones & Mike Walker. Pocket Guide to Teaching for Medical Instructors. BMJ, london (1999)
  2. Graham Gibbs, Sue Habeshaw & Trevor Habeshaw. Fifty-three interesting things to do in your lectures. Technical and Educational Services Ltd, Bristol (1984)
  3. David Newble & Robert Cannon. Handbook for Medical Teachers. MTP Press Ltd, Lancaster (2002)
  4. There is also a neat and concise publication on keeping a personal professional journal, essentially written reflection – which is of relevance to the between module mentoring:
    Mary Louise Holly, Keeping a Personal-Professional Journal Deacon University Press, Victoria (Australia) (1992)
  5. If you are interested in learning the bare bones of research method and in particular how this relates to the qualitative techniques used in social sciences and psychology (and therefore education) try:
    Colin Robson, Real World Research, Blackwell Oxford (1993)
  6. Please, please, please; if nothing else understand what is research and what is audit. In the current NHS climate conducting the former and calling it the latter guarantees an early call from the GMC – not nice at all.
  7. As one starts to get a bit “serious” about medical education, one drifts away from the medical bit towards the literature on adult learning generically. An easy but sound introduction is provided by:
    George Brown and Madeleine Atkins, Effective Teaching in Higher Education Routledge, London (1993).
  8. For the real “anoraks” in adult education, one of the best texts is:
    Leslie Curzon, Teaching in Further Education – An Outline of Principles and Practice, Cassell Educational Ltd, London (1990)
  9. … and there are loads of texts on curriculum evaluation, student assessment etc etc.
  10. The two journals that deal with medical education in the UK are:
    Medical Education, published by the Association for the Study of Medical Education
    Medical Teacher, published by the Association for Medical Education in Europe

With the huge changes going on in medical education at the moment, the only thing that is certain is that no part of the NHS will be left untouched. If interested feel free to buttonhole me over coffee for a chat.


10:45 Scene setting & basic science: Epidemiology, genetics, anatomy, pathology

Dr Lara Teare, Coventry

At the end of the session participants will have an overview of Parkinson’s including risk factors, epidemiology and basic pathophysiology of Parkinson’s disease, including the role of genetic factors, and will have an understanding of the midbrain motor circuits relevant to PD.


Parkinson’s disease is the second commonest neurodegenerative disorder after Alzheimer’s disease, affecting up to 120,000 people in the UK. There is a slight male preponderance, with most studies reporting 1.2–1.5 times as many men as women affected. The risk of developing Parkinson’s increases with age, but most are diagnosed in their 60s and 70s reflecting the demographics of the population.
Risk factors for Parkinson’s include older age, non-smoking, low caffeine intake and possibly pesticide and herbicide exposure, though this remains controversial. A “premotor” syndrome of hyposmia, anxiety or depression, REM-sleep behaviour disorder and constipation may precede the onset of the motor symptoms, and has reinforced the notion that that the pathology of Parkinson’s begins well in advance of the motor syndrome.

The definition of Parkinson’s disease is to some degree a matter of perspective. To some it is still defined by its cardinal clinical motor features, to others as a complex neurological and neuropsychiatric syndrome. The pathological hallmark of Parkinson’s is loss of neurons in the substantia nigra and the presence of Lewy bodies in those remaining. As pathological confirmation will usually only take place post-mortem, consensus clinical diagnostic criteria are used in practice.

Depletion of dopamine is the most important neurochemical abnormality in PD. Other neurotransmitters affected include acetylcholine, serotonin and noradrenaline but the role of these substances in the clinical syndrome is uncertain. 80% of dopamine in the brain is found in the striatonigral complex (putamen, caudate and substantia nigra), the main source of dopamine in the complex being the substantia nigra.

Disruption of normal dopaminergic output from the substantia nigra interferes with the basal ganglia motor circuit. The basal ganglia allow complex learnt motor tasks to be done while attention is directed elsewhere. The connections within the motor circuit are complex and not fully understood. The main output from the basal ganglia to the cortex is from the thalamus. Direct and indirect dopaminergic pathways have been described. In Parkinson’s disease there is increased inhibitory output from the globus pallidum interna.
Autosomal recessive forms of parkinsonism have been described which do not exhibit Lewy body pathology but Lewy bodies are present in the more common sporadic form of PD as well as some other autosomal dominant forms. They are intra-cytoplasmic inclusion bodies consisting of an amorphous core surrounded by a less dense ‘halo’. They contain a number of elements including ubiquitin, a-synuclein and proteases. Their biological function is thought to involve the disposal of abnormal or damaged proteins through the ubiquitin-protease system.

The pathological changes in PD are widespread. Areas involved include thalamus, hypothalamus, limbic cortex, neocortex, locus cereleus, raphe nucleus, nucleus basalis of Meynart and autonomic nervous system. The most important area affected is the substantia nigra pars compacta. It is damage here that is responsible for most of the clinical motor syndrome with cell loss in excess of 50% required for symptoms to develop.

The clinical correlates of pathology in other areas are poorly understood, but cholinergic deficit in the nucleus basalis of Meynert is increasingly implicated in impairments of memory and cognitive function. Recent pathological studies have demonstrated that the pathology of PD begins in the brain stem and progresses in an ascending course, towards the cortex (Braak stages 1–5).

Most PD patients do not have a family history of the disease but this can be found in 20–30% of cases. In case control studies the relative risk for a first-degree relative of an affected patient of developing PD is about 3.5. Twin studies vary in their conclusions as to the amount of genetic contribution to sporadic PD. It is possible that heritability is higher for nigrostriatal dysfunction but that the subsequent development of symptomatic PD depends on an environmental insult. A number of genes for Parkinson’s disease have now been reported. Where known, the protein products of these genes have been showed variously to be associated with abnormal protein accumulation and degradation, oxidative stress and mitochondrial dysfunction.

The cause of PD is unknown but research has implicated the roles of oxidative stress, mitochondrial dysfunction, inflammation and excitotoxicity as potentially important mechanisms in pathophysiology. The effects of these problems may result in cell loss through apoptosis.

A number of strands of evidence point to a possible role for gut bacteria in the development of PD: Lewy bodies have been found in bowel biopsies from patients who subsequently developed clinical features of PD; people who have undergone total vagotomy appear less likely to develop PD; there is an increased incidence of PD following H. pylori (eradication); in a genetically modified mouse model of PD, mice with sterilised guts did not develop PD but those with normal mouse gut flora did – also stool from patients with PD transplanted into these mice resulted in more Lewy body pathology than transplanted stool from normal humans.


11:30 Differential diagnosis including clinical imaging: Challenge tests, structural imaging, functional imaging

Dr Sarah Marrinan, Edinburgh

By the end of the session participants will:

  • Recognise the interaction of ageing with PD
  • Increase their knowledge of the diagnosis of Parkinson’s disease in older patients
  • Understand the impact of age on signs and symptoms
  • Understand motor and non-motor symptoms
  • Understand differential diagnosis in older patients
  • Recognise the place of challenge tests in the diagnosis of PD
  • Understand the role of structural and functional imaging in the diagnosis


Parkinson’s disease (PD) is a chronic neurodegenerative condition. The incidence and prevalence rise dramatically with age, and 6:7 cases are older than 60 years at diagnosis. Ageing is associated with neuro-degeneration and parkinsonism is common among older people. Thus the prevalence of PD rises from 0.6 % of the population aged 65–69 years to 3.5% of those aged 85–89 years, when the prevalence of parkinsonism is estimated to be as high as 52%. Increasing age is the main known risk factor for PD and also the most important determinant of the rate of clinical progression of PD.

PD has an insidious onset over several years and early symptoms and signs may be ascribed to increasing age, low mood or arthritis. After diagnosis patients and their family may recall a gradual impairment of dexterity, changes in writing, fatigue or constipation for some years. The diagnosis of PD is clinical and is made using the UKPDS Brain Bank Criteria, which are based on motor symptoms and require unequivocal bradykinesia with at least one of resting tremor, muscular rigidity or postural instability.

A trial of medication, increasing the dose gradually to that recommended, will lead to a response in idiopathic PD. Failure to respond raises the possibility of a different diagnosis and imaging may be indicated. Acute challenge testing with levodopa is no longer recommended because of the possibility of increasing the risk of future dyskinesia. Functional imaging may demonstrate striatal dopamine terminal function (PET or SPECT scans) as an aid to clinical diagnosis, but is not required routinely to make a firm diagnosis. The scan is normal in essential tremor and drug-induced parkinsonism. It will not differentiate idiopathic PD from the Parkinson’s plus syndromes or Lewy body dementia as all will have abnormal scans. In vascular parkinsonism the cerebrovascular disease can give a false positive scan and an MRI may be required to quantify this.

A trial of medication is often indicated as patients may still respond to dopamine replacement. Magnetic resonance imaging shows normal nigral structure in PD but can exclude structural causes of parkinsonism, e.g. normal pressure hydrocephalus, and can identify the extent of cerebrovascular disease in the basal ganglia. Diffusion weighted MRI may have a role in discrimination of PD from PSP or MSA. In accordance with the NICE guidelines in England and the SIGN guidelines in Scotland patients with suspected PD should be referred untreated to a specialist, defined as someone who regularly manages people with this condition. Evidence suggests that when specialists diagnose PD using the Brain Bank criteria there is a 90% concordance with the presence of nigral Lewy bodies at autopsy, while the diagnostic error of parkinsonian syndromes diagnosed by non-specialists may be up to 50%.


13:15 Clinical skills

Drs Sarah Marrinan & Lara Teare

At the end of this session, delegates will:

  • Describe the purpose of the neurological examination
  • Understand the principles underlying the conduct of a basic neurological examination
  • Be able to perform a simple neurological examination with particular emphasis on extrapyramidal function


The first step in management of neurological conditions is to make a diagnosis, and this requires a careful history and thorough examination. In daily practice, neurological diagnosis often depends on ‘pattern recognition’, the ability to elicit relevant historical information from the patient, make accurate clinical observations and rapidly translate the information gathered into a clinical diagnosis, often without the need for expensive and time consuming tests, which are then used simply to confirm clinical suspicions. There is no substitute for experience – if you have seen 10 cases personally, you are usually better able to make the diagnosis than if you have only seen a case presentation at a conference, although “every little helps”!

If you cannot make a quick ‘spot diagnosis’ as is often the way, it’s back to first principles. There are three components to the neurological diagnosis: anatomy (where is the lesion?), pathology (what is the lesion?) and aetiology (how and why did it arise?). All three of these components must be determined in order to make a complete diagnosis. The neurological history, in particular the tempo of symptom onset, helps the clinician to try to determine the pathology (strokes usually come on suddenly and rapidly, PD comes on slowly) and aetiology (risk factors or known causes of stroke or PD).

The neurological examination continues to be shrouded in mystery and being asked to perform this under observation strikes fear into the heart of many an undergraduate medical student. ‘Hands off’ accurate observation of the patient in different settings and positions to determine exact phenomenology is an important component of the diagnosis of movement disorders, (e.g. type and frequency of tremor or other involuntary movements, the presence and severity of bradykinesia).

However, traditionally the examination is primarily concerned with accurate ‘lesion
localisation’, answering two key related questions:

  1. Can the patient’s symptoms and signs be explained by a single anatomical lesion, or do we need more than one lesion (e.g. in MS) to explain the presentation?
  2. What is the highest level in the nervous system e.g. muscle, neuromuscular junction, nerve, plexus, nerve root, spinal cord, brainstem, cerebrum etc) for which there is evidence of neurological dysfunction or damage?

The exact bedside tests performed will be informed by the history; plainly, attention will focus on the anatomical areas where the patient complains of symptoms, but a ‘wide angle lens’ approach must be taken to avoid missing signs that may not be predicted from the history.


14:30 Early treatment options: When to start, what with and why

Dr James Fisher, Northumbria

At the end of the session participants will:

  • Understand the rationale for starting initial drug treatment in Parkinson’s disease (PD)
  • Understand how the decision is made to use a specific class of drugs in early Parkinson’s
  • Review published guidelines about the use of drugs in early PD


In early Parkinson’s Disease (PD) the decision about when to start treatment, and with what medication, is a difficult one. In this talk we’ll review some of the evidence that underpins this decision-making process – key research studies will be signposted and summarised, and we’ll also try to highlight some of the gaps in our understanding. We’ll consider the recently published NICE guidelines and suggestions will be offered as to how these might be operationalised in the messy reality of day-to-day practice. We’ll discuss the risks, benefits and potential pitfalls of pharmacological intervention in early PD, and we’ll reflect on how to get the most out of the meds. We’ll also share a series of other strategies and top tips for early PD management, including both the pharmacological and the non-pharmacological.


15:45 Palliative Care

Prof Richard Walker, Northumbria

Areas covered in this session will be:

  • Outline the case for palliative care in PD, looking at the qualitative and quantitative evidence, as this often seems to be quite contentious.
  • Outline potential red flags for unmet palliative care need.
  • Discuss methods of palliative care provision, the relative roles for a general palliative approach vs specialist palliative care provision.
  • Briefly discuss the models of service delivery, with reference to the integrated PD palliative care services which are starting to spring up.


16:45 Getting your consultants job (session specific)

Dr Peter Fletcher, Cheltenham – Academic Director, Parkinson’s Academy

This is very different in the public sector and the NHS in particular compared with the private sector [generically, not health] – at least up until consultant level. Much of what is valued in the private sector is valued at [Advisory] Appointments Committees (AACs) for what will be senior and expensive consultant appointments. As what will be left of the NHS in April 2013 becomes part of a ‘competitive dialogue’ the employers’ expectation of all employees is that they will bring value to the organisation and this is already being rehearsed at consultant AACs.

So by the end of this session:

  • You should know where the points of transition are in a doctor’s training as seen by the GMC post PMETB
  • You should understand the process of becoming a consultant
    Why you should start it at ST3
    Why you should have a rolling CV
    Why there should be no surprises when you make that application
  • You should understand what will happen at an AAC
    Who will be there and why
    Who has the power
    And what those with the power want


Day 2: Wednesday, 5 September 2018

08:30 Welcome

Dr Peter Fletcher, Cheltenham – Academic Director, Parkinson’s Academy

08:45 Do non-motor symptoms impact on quality of life and does it really matter?

Dr Chandrasekhara Padmakumar, Australia

To include:

  • Sleep problems
  • Autonomic problems
  • Gastrointestinal problems
  • Sensory problems

This session aims to:

  • Briefly review non-motor features throughout the stages of PD
  • Review methods and importance of detection
  • Review the management of sleep, autonomic, sensory and pain non-motor symptoms (NMS) in PD with interactive cases


Parkinson’s disease (PD) is traditionally viewed as a motor disorder with a characteristic triad of tremor, rigidity and bradykinesia. There is now increasing awareness that PD is a complex systemic disorder with many non-motor symptoms (NMS) which include autonomic dysfunction, sleep disorders, sensory and neuropsychiatric features. NMS are commoner in elderly persons with PD and increase in severity and frequency with advancing disease when they dominate the clinical picture. NMS are strongly correlated with quality of life for patients and their families as well as institutional care placement. NMS may be caused by PD therapy side effects as well as common comorbidities of advancing age.

Despite their importance, NMS are poorly recognised by clinicians and often undeclared by patients. Use of a validated screening tool such as NMS QUEST followed by specific symptom assessment instruments strengthens the recognition and holistic management of NMS in PD. Some NMS such as mood disturbance, anxiety, pain and insomnia may be improved by optimisation of dopaminergic therapy. Conversely, psychosis, excess daytime somnolence (EDS) or impulse control disorder (ICD) may be triggered by dopaminergic drugs.
Other NMS such as autonomic dysfunction, cognitive impairment, fatigue, EDS and pain may be unresponsive to dopaminergic treatment and may reflect perturbations in cholinergic, serotonergic or noradrenergic neurotransmitter function. This presentation will review the importance of screening for NMS in older PD patients and will briefly consider the management of autonomic dysfunction, sleep disorders and pain (neuropsychiatric issues are a separate lecture). The urgent need for novel therapies and more controlled trials with current therapeutic strategies is highlighted.


  1. Chaudhuri KR, Healy DG, Schapira A. (2006) Non-motor symptoms of Parkinson’s disease: Diagnosis and management. Lancet Neurol 5:235-245
  2. Grosset DG, Macphee GJA, Nairn M. (2010) Diagnosis and pharmacological management of Parkinson’s disease: Summary of SIGN Guidelines. BMJ 340: b5614.
  3. Wishart S, Macphee GJA. (2011) Evaluation and management of the non-motor features of Parkinson’s disease. Therapeutic Advances in Chronic Disease vol. 2 no. 2 69-85
  4. Zeseiwicz TA, Sullivan I, Arnulf KR et al (2010) Practice Parameter: Treatment of nonmotor symptoms of Parkinson disease: report of the Quality standards subcommittee of the American Academy of Neurology. Neurology 74: 924-931.


10:00 Inpatients with Parkinson’s

Drs Richard Genever, Chesterfield & Sandy Thomson, Salford

From this session delegates will:

  1. Appreciate the risks associated with Parkinson’s patients being unable to access or absorb their medications, and be able to identify solutions to address drug delivery problems.
  2. Be able to adopt a general approach to the assessment of a person suspected to have Parkinsonism, when they are a hospital inpatient.
  3. Understand the causes of confusion and hallucinations in inpatients with Parkinson’s disease, and be able to assess and manage such cases.


11:30 Managing late-stage disease: Drugs, invasive options, surgery

Dr Christopher Kobylecki, Manchester

At the end of the session participants will:

  • Understand what happens in late stage PD
  • Understand the treatment options for late stage PD
  • Recognise the limitations of these therapies, and have an understanding of which symptoms can and cannot be improved with such approaches
  • Understand when, and for whom such interventions might be appropriate, and for whom they are not (and why)


Despite the controversies, the management of early PD is usually straightforward; the problems start as patients begin to fluctuate (wearing off, dyskinesias, on/off fluctuations), and non-motor symptoms (NMS) evolve. NMS are the subject of another session, but their importance in terms of quality of life, and dictation of who may or may not be suitable the complex interventions below, are crucial, and thus warrant mention here.

Broadly, one has three options when faced with PD motor fluctuations:

  • Conservative
  • Tinker with oral/transdermal medication
  • Consider complex therapies (apomorphine, intestinal l-dopa, deep brain stimulation surgery)

I shall review the complex therapies, but more importantly provide a guide on who you should consider for which therapies, and when, using case presentations to highlight the (difficult) decision making process. Even more importantly, I shall highlight the kind of patients for whom such therapies are positively a bad idea.


  1. Worth PF. When the going gets tough: how to select patients with Parkinson’s disease for advanced therapies Pract Neurol 2013;13:140–152.
    Excellent, up to date comprehensive review of the area, read this if nothing else.
  2. Vlaar A, Hovestadt A, Van Laar T, et al. The treatment of early Parkinson’s disease: levodopa rehabilitated. Pract Neurol 2011;11:145–52.
    Reminds you why LD remains the best medical treatment for PD, as imperfect as it is, and not the root of all evil.
  3. Clarke CE, Worth P, Grosset D, et al. Systematic review of apomorphine infusion, levodopa infusion and deep brain stimulation in advanced Parkinson’s disease. Parkinsonism Relat Disord 2009;15:728–41.
    The “evidence” part 1
  4. Bronstein et al. Deep brain stimulation for Parkinson disease. An expert consensus and review of key issues. Arch Neurol. 2011;68:165-171.
    The “evidence” part 2


13:30 Neuropsychiatric complications in PD including cases

Dr Ross Dunne, Manchester

The aim of the session is to give SpRs an overview of how to manage a patient with mental health complications of PD. Participants will learn about assessing diagnosing and treating common neuropsychiatric complications of PD, be aware of potential complications of its treatment and hear strategies to prevent and treat such disorders.

Neuropsychiatric complications of Parkinson’s disease are extremely common. They can be found at all stages of the condition and are a source of distress for patients and carers alike. In this session we describe a number of the complications. These include:

  • Depression
  • Anxiety
  • Cognitive impairment and dementia
  • Psychosis
  • Impulse control disorders
  • Apathy

We will look at how to identify these conditions in the context of Parkinson’s disease and consider the strategies that can be implemented (including potential pitfalls). Screening and assessment tools can be a great aid to the diagnosis and monitoring of some of these complications and we will describe their use.



→ Back to Foundation MasterClass 35F