Dr G nther Edgar Wihl MD Consultant Neurologist

1. Dr Günther Edgar Wihl MDConsultant Neurologist Harrogate District Hospital BMI Harrogate

2. cv Medical school in Dusseldorf and London (National Hospital, Queen’s Square) Training at University Hospital Dusseldorf and Grenoble MD in 1998 3 years research in PD (DBS) and AD Involved in building 1. stroke unit in Dusseldorf Consultant Neurologist in 2004 (hospital and community based) neuro rehabilitation and acute neurology Moved to UK in 2006

3. Associate Specialist in Halifax: MS, PD, Epilepsy clinics Consultant Neurologist in Harrogate since June 2007 Built PD and stroke services PD and Stroke nurse specialists employed in 2008 Weekly specialist TIA and specialist Mov Dis clinic Commenced office hours thrombolysis in July 2009 PD, stroke prevention, headache, epilepsy MSc in stroke medicine to complete 2011

4. Transient Ischaemic AttackParkinson’s disease

5. Transient Ischaemic Attack Sudden onset focal neurological deficit lasting <24 hours Proposed definition Rapidly resolving neurological symptoms, typically lasting <1 hour, with no evidence of infarction on MRI, DWI Albers et al. NEJM 2002; 347: 1713-1716 Transient ischaemic attack is defined as a focal neurological deficit, most often weakness, slurred speech or sensory disturbance, that comes on suddenly and persists for less than 24 hours. More recently, there has been a proposal to alter the definition of a TIA to the same clinical presentation, but lasting for less than an hour, and classifying anything that lasts for longer as a stroke. Another useful tool in differentiating TIA from stroke is the absence of infarctive lesions on DWI MRI. The longer the clinical features persist, the more likely it is that a lesion will be seen. Transient ischaemic attack is defined as a focal neurological deficit, most often weakness, slurred speech or sensory disturbance, that comes on suddenly and persists for less than 24 hours. More recently, there has been a proposal to alter the definition of a TIA to the same clinical presentation, but lasting for less than an hour, and classifying anything that lasts for longer as a stroke. Another useful tool in differentiating TIA from stroke is the absence of infarctive lesions on DWI MRI. The longer the clinical features persist, the more likely it is that a lesion will be seen.

6. NICE Guidelines Stroke Guideline issued July 2008 Diagnosis and initial management of acute stroke and TIA Recommends use of ABCD2 score for risk stratification of TIA patients

7. ABCD-2 Score This score is used to predict the risk of stroke after TIA. It should be calcualted in the acute setting. It is based on the age, blood pressure, clinical features, duration and DM status of the patient at the time of the TIA. It is most valid for prediction of stroke in the 7 days following the TIA event, but also correlates with risk at 2, 7, 30 and 90 days after. The score was also found to be useful in diagnosis of TIA, when trying to differentiate e.g. from focal migraine. Risk: Score < 5 = 0.4% risk; Score of 5 = 16% risk; Score of 6 = 35% risk Rothwell et al. Lancet; 2005; 366: 29-36This score is used to predict the risk of stroke after TIA. It should be calcualted in the acute setting. It is based on the age, blood pressure, clinical features, duration and DM status of the patient at the time of the TIA. It is most valid for prediction of stroke in the 7 days following the TIA event, but also correlates with risk at 2, 7, 30 and 90 days after. The score was also found to be useful in diagnosis of TIA, when trying to differentiate e.g. from focal migraine. Risk: Score < 5 = 0.4% risk; Score of 5 = 16% risk; Score of 6 = 35% risk Rothwell et al. Lancet; 2005; 366: 29-36

8. There is currently a lot of coverage in the media about stroke and spotting the early signs of stroke or TIA. The emphasis is on quick action to limit the damage caused by infarction of brain tissue. Some centres are offering thrombolysis for stroke, where time is clearly of the essence, but even in centres without this facility, prompt assessment is important as it allows diferentiation of infarction from haemorrhage, and implementation of the correct treatment.There is currently a lot of coverage in the media about stroke and spotting the early signs of stroke or TIA. The emphasis is on quick action to limit the damage caused by infarction of brain tissue. Some centres are offering thrombolysis for stroke, where time is clearly of the essence, but even in centres without this facility, prompt assessment is important as it allows diferentiation of infarction from haemorrhage, and implementation of the correct treatment.

9. Transient Ischaemic Attack TIA increases the risk of stroke and other vascular events Stroke risk 5% at 7 days and 10-15% at 90 days 50% occur within 48 hours of TIA 15-20% stroke patients have a preceding TIA Risk can be estimated in the acute phase. Note: stroke risk after crescendo TIA can be reduced by 80 % Transient ischaemic attack occurs more frequently than was previously thought. Standardised incidence is 1.08 per 1000 of population, is not declining and may be expected to grow further with the ageing population. The importance of TIA lies in the early risk of stroke and other vascular events. It is recognised that major stroke is often preceded by TIA, although the symptoms may neither have alarmed the patient nor been reported. Prospective prognostic studies have shown that the early risk of stroke after TIA is approximately 5% at 7 days and 10-15% at 90 days depending on clinical settings and study methodology. Predicting the risk of stroke following TIA can be estimated by the use of predication tools based on clinical features, aetiology and investigations.Transient ischaemic attack occurs more frequently than was previously thought. Standardised incidence is 1.08 per 1000 of population, is not declining and may be expected to grow further with the ageing population. The importance of TIA lies in the early risk of stroke and other vascular events. It is recognised that major stroke is often preceded by TIA, although the symptoms may neither have alarmed the patient nor been reported. Prospective prognostic studies have shown that the early risk of stroke after TIA is approximately 5% at 7 days and 10-15% at 90 days depending on clinical settings and study methodology. Predicting the risk of stroke following TIA can be estimated by the use of predication tools based on clinical features, aetiology and investigations.

10. Preventing stroke after TIA Well established evidence for stroke prevention after TIA Urgent initiation of interventions can substantially reduce the subsequent risk of stroke Because not all patients are at same risk, tools are used to stratify patients into high and low risk groups, ABCD2 score The evidence base for stroke prevention in the long term after TIA is well established for antiplatelet agents, statins, antihypertensive medication, anticoagulation and carotid endarterectomy, and recent studies have shown that the combination of these initiated urgentyl after TIA can substantially reduce the subsequent risk of stroke. Prediction of individual risk can guide the use and urgency of these interventions.The evidence base for stroke prevention in the long term after TIA is well established for antiplatelet agents, statins, antihypertensive medication, anticoagulation and carotid endarterectomy, and recent studies have shown that the combination of these initiated urgentyl after TIA can substantially reduce the subsequent risk of stroke. Prediction of individual risk can guide the use and urgency of these interventions.

11. Start daily aspirin (300mg) immediately Introduce measures for secondary prevention as soon as the diagnosis is confirmed, including discussion of risk factors Use diffusion weighted MRI for brain imaging excpet where contraindicated, where CT scanning should be used. Crescendo TIA is 2 or more TIAs in a week. Late presentation is presenting more than 1 week after symptoms have resolved. Specialist assessment includes exclusion of stroke mimics, identification of vascualr treatment, identification of likely causes and appropriate investigation and treatment.Use diffusion weighted MRI for brain imaging excpet where contraindicated, where CT scanning should be used. Crescendo TIA is 2 or more TIAs in a week. Late presentation is presenting more than 1 week after symptoms have resolved. Specialist assessment includes exclusion of stroke mimics, identification of vascualr treatment, identification of likely causes and appropriate investigation and treatment.

12. TIA Clinic Set up in July 2007 Aims to see patients referred by GPs, A+E and other specialties waiting time is limiting factor Investigate patients and advise on management Same day Doppler, ECG, MRI brain scan if indicated People with stable neurological symptoms from acute non-disabling stroke or TIA who have symptomatic carotid stenosis of 50–99% according to the NASCET (North American Symptomatic Carotid Endarterectomy Trial) criteria, or 70–99% according to the ECST (European Carotid Surgery Trialists’ Collaborative Group) criteria, should: be assessed and referred for carotid endarterectomy within 1 week of onset of stroke or TIA symptoms undergo surgery within a maximum of 2 weeks of onset of stroke or TIA symptoms • receive best medical treatment (control of blood pressure, antiplatelet agents, cholesterol lowering through diet and drugs, lifestyle advice). 1.2.4.2 People with stable neurological symptoms from acute non-disabling stroke or TIA who have symptomatic carotid stenosis of less than 50% according to the NASCET criteria, or less than 70% according to the ECST criteria, should: not undergo surgery receive best medical treatment (control of blood pressure, antiplatelet agents, cholesterol lowering through diet and drugs, lifestyle advice). People with stable neurological symptoms from acute non-disabling stroke or TIA who have symptomatic carotid stenosis of 50–99% according to the NASCET (North American Symptomatic Carotid Endarterectomy Trial) criteria, or 70–99% according to the ECST (European Carotid Surgery Trialists’ Collaborative Group) criteria, should: be assessed and referred for carotid endarterectomy within 1 week of onset of stroke or TIA symptoms undergo surgery within a maximum of 2 weeks of onset of stroke or TIA symptoms • receive best medical treatment (control of blood pressure, antiplatelet agents, cholesterol lowering through diet and drugs, lifestyle advice). 1.2.4.2 People with stable neurological symptoms from acute non-disabling stroke or TIA who have symptomatic carotid stenosis of less than 50% according to the NASCET criteria, or less than 70% according to the ECST criteria, should: not undergo surgery receive best medical treatment (control of blood pressure, antiplatelet agents, cholesterol lowering through diet and drugs, lifestyle advice).

13. Recommendations ABCD2 should be calculated as soon as possible and acted upon Refer to stroke physician asap Scanning requirements determined by stroke physician and radiologist, Doppler and MRI is method of choice Commence Aspirin 300mg immediately

14. Summary TIA is a treatable condition. If treated appropriately strokes can be prevented ! Stroke risk can be determined using a simple scoring system TIA clinic useful way of assessing risk and ensuring appropriate investigation and management

15. Parkinson’s disease  PD is a progressive neurodegenerative condition resulting from the death of the dopamine-containing cells of the substantia nigra. There is no consistently reliable test to distinguish PD from other conditions with similar symptoms. Diagnosis is primarily clinical, based on history and examination.PD is a progressive neurodegenerative condition resulting from the death of the dopamine-containing cells of the substantia nigra. There is no consistently reliable test to distinguish PD from other conditions with similar symptoms. Diagnosis is primarily clinical, based on history and examination.

16. How is PD diagnosed ? Diagnosis remains clinical in most cases, but diagnostic error rate -in a community sample: 47% -Standard neurological and geriatric practice: 26% -Expert movement disorder clinics: 4% DD: essential tremor, PSP, MSA, drug induced Parkinsonism, Wilson’s disease As diagnosed by UK brain bank series

17. James Parkinson MRCS 1817 “An Essay on the Shaking Palsy” “involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported; with a propensity to bend the trunk forward…the senses and intellects being uninjured” Cardinal symptoms described: shaking, stiffness, slowness and poverty of movements, 6 cases

18. Incidence and prevalence PD is estimated to affect 100–180 in 100,000 people (1.000.000 patients in Europe) UK 30-40 newly diagnosed patients each day annual incidence of 4–20 per 100,000 rising prevalence with age (4% in population over 80 years, 2% in population over 60 years), dramatic increase of prevalence anticipated Depression affects around 40% of PD patients PD is a common, chronic, progressive neurological condition, estimated to affect 100–180 per 100,000 of the population (between 6 and 11 people per 6000 of the general population in the UK). It has an annual incidence of 4–20 per 100,000, and there is a rising prevalence with age and a higher prevalence and incidence in males. Depression affects around 40–50% of people with PD. There are difficulties in diagnosing mild depression in people with PD as the clinical features of depression overlap with the motor features of PD. PD is a common, chronic, progressive neurological condition, estimated to affect 100–180 per 100,000 of the population (between 6 and 11 people per 6000 of the general population in the UK). It has an annual incidence of 4–20 per 100,000, and there is a rising prevalence with age and a higher prevalence and incidence in males. Depression affects around 40–50% of people with PD. There are difficulties in diagnosing mild depression in people with PD as the clinical features of depression overlap with the motor features of PD.

19. Motor Symptoms Classic motor features slowness of movements (bradykinesia) stiff muscles (rigidity) rest tremor of low frequency postural instability In addition micrographia, masked face, freezing etc People with PD classically present with the symptoms and signs associated with parkinsonism, namely bradykinesia, rigid or stiff muscles, and tremor in a part of the body when it is not being used. Parkinson’s disease mainly affects movement, but other symptoms can include: psychiatric problems such as depression and dementia autonomic disturbances and pain. PD can progress to cause significant disability and handicap with impaired quality of life for the individual, and for their family and carers People with PD classically present with the symptoms and signs associated with parkinsonism, namely bradykinesia, rigid or stiff muscles, and tremor in a part of the body when it is not being used. Parkinson’s disease mainly affects movement, but other symptoms can include: psychiatric problems such as depression and dementia autonomic disturbances and pain. PD can progress to cause significant disability and handicap with impaired quality of life for the individual, and for their family and carers

20. Non Motor symptoms Recognised non motor (non dopaminergic symptoms) -neuropsychiatric (cognitive impairment, dementia, hallucinations, mood disorders) -pain -sleep disorders (nightmares, parasomnias, RLS, day time sleepiness) -autonomic dysfunction (constipation, orthostatic hypotension, urinary problems) -falls

21. How is PD treated ? Pharmacologic treatment (? Neuro protection, L-dopa, Dopa agonists, COMT inhibitors, MAO B inhibitors, infusion therapies) Surgical treatment (ablative procedures, DBS, TMS, cell based therapies) Management of non dopaminergic and non motor features (neuropsychiatric symptoms, sleep disorder, falls) Non pharmacologic (PT, OT, SALT etc.)

22. Conclusion I PD is second most common neurodegenerative disorder: it affects the whole brain and presents with motor and non motor features Ideal management of motor features is CDS with Dopa agonists such as Requip XL, Neupro patch, Pramipexole PR or Apomorphine L-Dopa remains the gold standard of motor symptom control at the expense of dyskinesia (pulsatile stimulation as opposed to CDS)

23. Conclusion II Management of non dopaminergic and non motor features remains challenging No neuro protective agent for PD has been identified to date PT, OT, SALT and counselling are potent non pharmacologic treatment options Tailor therapy to patient’s individual needs!

24. My aim To offer neurological skills to the York area TIA/ stroke services/ PD/ Headache/Epilepsy Work closely with GPs Intensify links with York colleagues