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PD/Movement Disorders

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Belinda Kessel Geriatrician and Movement Disorder Specialist Princess Royal University Hospital Orpington, Kent Kings College Hospital Trust BGS February 2016 Trainees Weekend

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What to do with the ill Parkinson patient…

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… so they can be fighting fit again!

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Objectives

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• Acute management of PD emergencies • Drugs to use and those to avoid • Prevent making sick PD patients a whole lot worse

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Case 1

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• 75 year old gentleman who had PD diagnosed 10 years ago • Deteriorated in the last year so now poorly mobile • Presented with fever and shortness of breath

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• Sinemet 125mg tds • Ropinorole XL 8mg od

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• Usual medication is

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Diagnosis and Management plan…

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Sick patients with PD

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Higher risk of aspiration Higher risk of poor mobilisation and falls Higher risk of delerium Longer time to recover

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• • • •

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• Treat appropriately for the acute illness but beware;

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Beware Nil By Mouth

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Don’t leave a SPACE Sugar Parkinson Meds Antibiotics Corticosteroids Epilepsy

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3 golden rules 1. Recognise the importance of PD drugs

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Golden Rules for NBM

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2. Challenge every NBM decision 3. Give treatment as close to normal as possible

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• If ‘Nil by mouth’ ensure alternate route

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Beware Nil By Mouth

• NG tube and crush sinemet or dispersible madopar

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• Consider Rotigotine patch (Neupro©)

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• Apomorphine

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• Can be given by injection (apo-go pen) • Can be given by subcutaneous infusion

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• With Apo pump

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• With normal Graseby pump

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• Also give domperidone (po/NG/pr)

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What doses of PD Medicines to give?

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pdmedcalc.co.uk

Your Results: Name

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Based on the entry of the following medications:

Frequency

Sinemet (co-careldopa) 125mg (100mg/25mg)

3 per day

Ropinirole (Requip XL) 8mg

1 per day

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the total levodopa equivalent dose for this patient is 460 mg per day.

The equivalent dose of levodopa for this patient can be provided in 3 different ways; below is a brief explanation of each option and the accompanying prescription.

(co-beneldopa)

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Option 1: Conversion of all usual medications for administration via naso-gastric tube using dispersible madopar

NB - this should be the default option for use, assuming a naso-gastric tube is tolerated and is appropriate.

1200

2 x Madopar Dispersible

1 x Madopar Dispersible

125mg (100mg/25mg)

125mg (100mg/25mg)

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1 x Madopar Dispersible

1 x Madopar Dispersible

125mg (100mg/25mg)

125mg (100mg/25mg)

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Option 2: Conversion of usual levodopa containing medications for administration via naso-gastric tube using dispersible madopar (co-beneldopa)

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Conversion of usual dopamine agonist medications for administration via rotigotine trans-dermal patch

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NB - this option may be preferred by some Parkinson's Disease specialist doctors and nurses

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1200

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1 x Madopar Dispersible

1 x Madopar Dispersible

1 x Madopar Dispersible

1 x Madopar Dispersible

125mg (100mg/25mg)

125mg (100mg/25mg)

62.5mg (50mg/12.5mg)

62.5mg (50mg/12.5mg)

1 x Rotigotine Patch 4mg

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(Replace every 24 hours)

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Option 3: Conversion of all usual medications for administration via rotigotine trans-dermal patch NB - this option may be considered if a NG tube is contraindicated or if the patient is for palliation (caution for precipitation of confusion and/or delirium with high doses of rotigotine)

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1 x Rotigotine Patch 4mg (Replace every 24 hours)

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OPTIMAL calculator: A guideline for inpatient management

Sample drug conversion using OPTIMAL Calcula

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• Pramipexole: Rotigotine patch= 1:5 • Ropinorole: Rotigotine Patch=1:1

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• Sinemet doses same as Madopar • Dopamine Agonists;

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Some Rough Rules:

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• Don’t worry too much about MAOB or COMT inhibitors • Remember the dose can be adjusted with regular review

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Why cant you leave PD patients ‘Nil By Mouth’?

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Neuroleptic malignant like syndrome

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NMS can be caused not only by neuroleptics but also by abrupt withdrawal or decrease of antiParkinsonian treatment

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Neuroleptic Malignant SyndromeLevenson’s criteria

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Minor Criteria: • Tachycardia • Abnormal BP • Tachypnoea • Altered Mental status • Diaphoresis • Leukocytosis

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Major Criteria: • Rigidity • Fever • Elevated CK

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Diagnosis requires three major or two major and four minor criteria

(Pandya Mayur, Lepoldo Pozuelo: A Malignant Neuroleptic spectrum: review of Diagnostic Criteria and treatment implications in three case reports: International Journal of Psychiatry in Medicine; Jan 2004; 34;3 ).

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Management

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• i.v. fluids • Cooling down • Consider HDU/ITU

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• Supportive care

• Restart Parkinson medication • Other options

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Apomorphine (or Rotigotine patch) Lorazepam ECT } Methyl prednisolone } Experimental

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• L-dopa through NG tube

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Aspiration Pneumonia Rhabdomyolysis leading to acute renal failure Thrombo-embolism Disseminated Intravascular Coagulopathy Death in 4-30% and long term sequelae in one third

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Complications of NMLS

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Remember

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Bladder Bowels Swallow Analgesia

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   

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Watch

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Don’t leave ‘nil by mouth’

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Avoid certain drugs

Anti-dopaminergics • Anti-emetics

• Anti-psychotics

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• Prochlorperazine (stemetil ) • Metoclopramide (maxalon) But can use Domperidone

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Drugs to avoid

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• Haloperidol • Chlorpromazine • Atypical anti-psychotics If necessary use Quetiapine orally or iv benzodiazepines

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Analgesia

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• Fentanyl can cause muscle rigidity in normal and PD patients • Morphine can also exacerbate akinesia at high dose • Beware the increased risk of acute confusion in PD patients if giving opioids

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Case 2

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• occurring at rest and action • affecting her writing • worse when stressed

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74 year old lady presented 1 year ago with a tremor of right hand for up to 2 years before

Given sinemet by neurologist for PD

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• Family felt she had got worse since then mentally

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Admitted Jan 08

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• Hallucinations of snakes all over body • Feels dirty and wants to bathe in bleach • Anxiety ++ and panic attacks • Not eating and drinking O/E • Paranoia • MTS 5/10 • No other abnormalities found by junior doctor

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History of OA, Hypothyroidism, IHD

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PMH

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Admitted elsewhere 2 weeks earlier with paranoia and weight loss

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• MMSE 27/30 • CT scan organised of abdomen for wt loss - normal

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FBC, U&E, LFT, B12, folate Normal TSH 8.8 on thyroxine (?compliance) Refused ECG and CXR Originally refused CT head but done eventually- NAD

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• • • •

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Investigations

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Further history from son

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Started sinemet in January 2007 for ?Parkinson’s disease Unclear when drug stopped but was restarted in September 2007 Since then has become paranoid with hallucinations Sinemet stopped at Christmas but paranoia worsened Family convinced that Sinemet is the cause of her illness

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right sided hand tremor for at least a year associated with drooling of saliva possibly more slow and shuffly anxiety and hallucinations started after sinemet

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• • • •

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Patient gave history of

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Review 28/1/8

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Avoids eye contact and very wary Intermittent resting tremor of right hand No increased tone Bradykinesia R>L Gait not typically Parkinsonian

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• • • • •

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On examination

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Clock drawing test

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?Lewy Body Disease ? Other psychiatric diagnoses

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Diagnosis

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Management

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• Avoid further dopamine drugs • Also avoid dopamine antagonists • Consider certain atypical antipsychotics; Quetiapine or Clozapine • Consider anticholinesterase inhibitor; Rivastigmine • Consider DAT scan if tolerates

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Progress

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• Possibly better on Rivastigmine patch • Still refusing to eat and drink with significant weight loss • Still paranoid “blood tests will erase her memory” • Family problematic, seeking second opinions • Neurologist saw and agreed with present management but advised Psychiatric opinion • Psychiatric review – taken to Psychiatric hospital under Mental Health Act 83 for further assessment

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Lewy Body Dementia

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Lewy bodies were first described by the scientist Friedrich H Lewy in the early 1900’s whilst he was researching into Parkinson’s disease and he discovered abnormal protein deposits that disrupt the brains functioning. In Parkinson’s disease they are found mainly in the brain stem where they deplete the neurotransmitter dopamine.

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WHAT IS A LEWY BODY?

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Lewy bodies are eosinophilic structures located within the cytoplasm of neurons. Characteristically, although not consistently, they are circular and have a dense protein core surrounded by a peripheral halo.

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Pathology of DLB

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• DLB defined by lewy body formations

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• cerebral cortex • brainstem nuclei (substantia nigra and locus coeruleus) • basal forebrain

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• Extensive depletion of acetylcholine neurotransmission in neocortical areas which leads to disruption of perception, thinking and behaviour.

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Presenting features of DLB

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• Dementia is usually but not always the presenting feature • A minority present with parkinsonism alone • Some present with psychiatric disorders in the absence of dementia • It can present as orthostatic hypotension, falls or transient loss of consciousness

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Epidemiology

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Age at onset ranges from 50-83 Mean survival is similar to Alzheimers but occasionally some patients have rapid decline with death 1-2 years from onset

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Core Features

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• Fluctuation in cognitive performance and levels of consciousness day to day even over a few hours • Visual hallucinations two thirds usually animals and people • Parkinsonism in 70% • Falls and syncope in up to a third

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Clinical diagnosis of DLB

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• Obligatory features:

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• Presence of progressive disorder of cognitive functions NB. Memory impairments not obligatory in initial stages • Frontal-subcortical component to the cognitive abnormalities (impairments in attention, visuospatial functions, thought)

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Clinical diagnosis of DLB (2)

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• 2 of the following signs for “probable” DLB and 1 for “possible” DLB:

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• Fluctuations of cognition • Visual hallucinations • Parkinsonism (not associated with previously used neuroleptics)

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Recurrent falls Sensitivity to neuroleptics Syncope Transient loss of consciousness Systemised delusions Hallucinations of other modalities REM behaviour sleep disorder Depression

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• • • • • • • •

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Other supportive features

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1. Other dementia syndromes

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Differentials of DLB

e.g. AD, vascular dementia

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2. Other causes of delirium e.g. Infections

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3. Other neurological syndromes

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e.g. PD, PSP, MSA, CJD

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4. Other psychiatric problems

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e.g. Late-onset delusional disorder, depressive psychosis, mania

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Management of DLB

L-Dopa↑

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Mobility

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• Psychosis – avoid typical neuroleptics • Cholinesterase inhibitors – improves symptoms of hallucinations and delirium (Samuel et al 2000) • SSRIs – drugs of choice for depression • Levodopa – cautious trial for motor disability

AChEI’s↓

Cognition L-Dopa↓

AChEI’s↑

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Differentiation DLB from AD

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DLB vs AD

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• Can be difficult, especially where initial presentation of DLB is impaired cognition • Accurate diagnosis is required in order to direct appropriate management • DLB and AD share many clinical symptoms, although some occur more frequently in DLB than AD

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DLB vs AD (McKeith, 2002)

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Types of dementia with Age

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Imaging

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• Brain imaging in DLB shows generalised atrophy , although 40% show preservation of the temporal lobe structures compared to AD (typically medial temporal lobe atrophy)

Brain Imaging

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N

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AD

AD

N

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Hippocampus

AD

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Imaging

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• SPECT studies (DAT scans) show significant reduction in striatal uptake of a ligand for the presynaptic dopamine transporter site in DLB

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SPECT Scan

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SPECT Scan

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Differentiation of DLB from PDD

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Differing Views

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• Differentiate by which comes first; dementia or Parkinsonism • Consensus Opinion 2005 and research use the 1 year rule (Dementia within 1 year of Parkinsonism)

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Reality is that it is likely to be a spectrum of the disease entity and sometimes better to use the term Lewy Body disease. Unfortunately imaging not helpful

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Case 3

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History of Presenting Complaint

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• Mr C is a 76 year old gentleman who was admitted on 19/3/14 • Found by his son-in-law on the floor, presumed to have fallen 1/7 ago. • Slightly confused on admission, doesn’t remember the fall although is able to recall medication details and medical history. • He complained of back pain but denies any other symptoms • He normally stays with his wife but she is now in convalescence with his son after a recent hospital admission.

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Parkinson’s disease – diagnosed 6 years ago CABG – 22 years ago Permanent pacemaker – 22 years ago T2DM AF

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• • • • •

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Past Medical History

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Drug History

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• Stalevo (Carbidopa 150mg/Levodopa 37.5mg/Entacapone 200mg) 6X/day • Ropinirole MR 4mg OD – recently stopped • Metformin 1g BD • Sitagliptin 100mg OD • Ramipril 2.5mg OD • Atorvastatin 10mg ON • Verapamil MR 120mg OD • Digoxin 125mcg OD • Warfarin

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Social History

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• Lives at home with wife • No carers • Needs assistance with shopping and cleaning but otherwise independent • Mobilizes without aids • Non-smoker • No history of alcohol use

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Clinical Examination

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• HR 90 (irregular), BP 148/79mmHg (no postural drop), apyrexial, RR 16, SpO2 100% (RA) • Well perfused, appears dry • Chest clear • Abdomen SNT, Bowel sounds present • Increased tone in all four limbs, GCS 15 • No focal neurology

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Bloods – significant findings  WBC 12.8; CRP 2; CK 1550 Urine dip – NAD CXR – NAD, pacemaker in situ ECG – rate controlled AF

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Investigations

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Diagnosis and Management

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• Impression: i. Exacerbation of Parkinsonism secondary to him missing his medications due to the fall or vice versa ii. Rhabdomyolysis

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• Management: IV fluids, regular PD medication

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Detailed Parkinson’s history

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• Diagnosed 6 years ago aged 70 although possibly symptomatic 23 years before • Initially started on Sinemet (carbidopa, levodopa), then changed to combination of Ropinorole (dopamine agonist) and Stalevo (carbidopa, levodopa, entacapone) • Features of excessive DIY, frequent use of stepladder and balancing a plank between two chairs to carry out tasks • Lack of insight as even though his wife has expressed concerns he still does it ‘out of boredom’ • Expects wife to pick him up when he falls

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• Becomes agitated at night, sleeping very poorly, cries out for assistance to go to toilet • Does not feel that his PD is being well managed, complains of ‘freezing’ in between stalevo doses • No evidence of tablet hoarding or excessive use • Denies gambling, sex, eating problems or other compulsions • Most recently seen at Queen’s Square (Mar 2014) where Ropinorole was stopped in hopes of improving his impulse control disorder • It was noted in his most recent clinic appointment that although Mr. C claimed to be feeling in an ‘off’ state, he was actually able to move freely and was seen running down the corridor

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• During admission, the dose of levodopa was slowly titrated up as he did exhibit true ‘off’ periods, possibly secondary to ropinorole being stopped recently • Increased in small increments and in alternate doses • On-off charts do not reveal any obvious pattern in off periods but can happen 5X/day • Patient can be found running up and down ward one moment and then appearing stiff and unable to mobilise in bed soon after • Frequent and wide fluctuations in symptoms • Often very anxious and complains that nurses are not giving him correct doses • Complains of feeling ‘off’ and not getting enough medication even when examined he is not rigid or bradykinetic

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Example of On-Off chart Tuesday

Wednesday

Thursday

Friday

Saturday

0800-1000

Off

Off

Off

Off

Off

Off

1200-1400

Off

On

On

Off

On

Off

1400-1600

On

On + dys

On

On

On + dys

On

1600-1800

On

On + dys

On

Off

On

On

1800-2000

On + dys

On

On

On

Off

On

2000-2200

Off

On

On

On + dys

On

On

2200-0000

On

On

Off

On

On

On

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Monday

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Management

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• Eventually, Stalevo was titrated up to alternating doses of 200mg/175mg with reasonable symptom control • Rasagiline (MAO-A inhibitor) was added as an adjunct • Low dose mirtazepine was started to alleviate symptoms of anxiety and insomnia • Mr. C was discharged for 1/52 respite care as agreed between him and his family with a view of eventually arranging TDS POC and private carers overnight as his wife has been increasingly unable to cope with his demands • Referred to neuro-psychiatrist for further input as significant behavioural component

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Conclusion

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• Mr. C has complex PD with frequent and unpredictable fluctuations in symptoms • May be complicated by impulse control disorder in the form of hobbyism secondary to long term dopamine replacement therapy and use of dopamine agonists • Generally, PD medication reduction is attempted • Levodopa is necessary for treatment but dose needs to be titrated incrementally • Prone to dopamine dysregulation syndrome so fast acting dopamine replacement therapy (e.g. Madopar dispersible, apomorphine injections) and dopamine agonists (e.g. Ropinorole, Apomorphine, Rotigotine, Pramipexole) were avoided

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Case 4 20 16

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• PMH:

• PD, diagnosed 1991 •

Under care Sevenoaks team

• Previous Breast Ca • Scoliosis

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• 56 year old woman • Admitted to the PRUH on 19/11/13 following an overdose 20x15/500 of co-codamol • Took it with intention of ending her life • Impulsive act • Regretted it afterwards • Had abdo pain, nausea and vomiting • 2/52 hx of worsening PD and audio-visual hallucinations • State voices said they were going to rape her and carers would leave her • Carers finding behaviour increasingly difficult to manage

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History

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Co-beneldopa 125mg 9x/day Quetiapine 12.5mg BD and 12.5mg PRN Diazepam 2mg TDS Apomorphine s/c infusion 1.46mls/hour over 24 hours Omeprazole 20mg od

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• DHx:

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• SHx

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• Independently mobile • Lives at home with 24 hour carer • Non-smoker, Non-drinker

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• General:

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On examination

• Thin, agitated, multiple bruising on legs

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• Cardio:

• Normal Heart sounds • Chest clear

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• Abdo:

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• Resp:

• Neuro:

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• Soft. Non-tender. Bowel sounds present

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• PD voice • Very Dyskinetic

Imaging

FBC: WCC 4.6, Hb 127, Plt 238, INR 1.0

CXR: NAD

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Bloods

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U+E: Na 142, K 4.2, Ur 9.8, Cr 56, CRP 6

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LFTs: Bil 19, Alb 40, ALP 99, ALT 13, GGT 12

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Investigations

Microbiology Urine Dip: No growth

• Initial impression:

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• PD psychosis leading to overdose

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Management

• R/V by Dr Kessel on 20/11/2013. Advised following plan

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Increase quetiapine to 25mg BD Add Mirtazepine Continue to monitor LFTs/INR post OD Psychiatric R/V If remains dyskinetic to decrease apomorphine pump

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Management

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• Collateral hx obtained form PD CNS at Sevenoakes

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• Had previously tried to reduce dose of apomorphine pump due to dyskinesia • However, patient had been resistant to this and had been increasing her own dose of apomorphine • Concerned about worsening ‘off’ periods

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Impression Dopamine dysregulation syndrome

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Progress

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• Psychiatric R/V on 23/11/13

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Apomorphine dose gradually reduced overnight Hallucinations settled No further thoughts suicide/self harm Was eventually discharged back home with 24 hour care and CMHT f/u

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• • • •

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• Still experiencing auditory/visual hallucinations • Advised increasing quetiapine to 25mg TDS

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Management of DDS and ICD

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Overlap of the different syndromes has led to a proposal for an umbrella concept of ‘disinhibitory psychopathologies’

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Impulse Control Disorders

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Defined as a failure to resist an impulse, drive or temptation to perform an act that is harmful to the person or others-may lead to distress and impaired social and occupational functioning;

‘Parkinson’s pill made me bet’ The Sun, Feb 2008

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Hypersexuality Pathological gambling/shopping Hobbyism Euphoria Altered appetite Heightened aggression Craving Psychosis Punding

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• • • • • • • • •

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Behavioral Phenomena

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Punding

Characterised by stereotyped, repetitive, aimless behaviours;

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• Simple such as shuffling papers/buttons • Complex as seen in hobbyism eg playing computer games • Going walkabout-walking great distances without destination or purpose and unaware of time

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Parkinson's drugs ‘made me gambler, thief and gay sex fiend’

Dec 2007

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Dopamine Dysregulation Syndrome

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Dopamine Dysregulation Syndrome

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• Occurs in patients with PD who have had long term exposure to dopamine replacement therapy • Characterised by self control problems such as addiction to medication, gambling, hypersexuality and punding • Most common symptom is craving of dopaminergic medications, often in the absence of symptoms • Patients often dyskinetic • Psychosis is common

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Diagnostic Criteria for Dopamine Dysregulation due to DRT Misuse

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• Need for increasing doses of dopamine replacement therapy (DRT) in excess of usual requirements • Pattern of pathological use • Impairment in social or occupational functioning • PD with L-dopa responsiveness • Development of hypomanic, manic or cyclothymic affective syndrome in relation to DRT • Development of a withdrawal state • Duration of disturbance >6/12

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Lawrence AD et al. Lancet Neurol. 2003;2:595-604; Giovannoni G et al. J Neurol Neurosurg Psychiatry. 2000;68:423-428.

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Impulse Control Disorders and Dopamine Dysregulation Syndrome • 4.0% Giovannoni 2000 • 3.4% Pezzzella 2005

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• Prevalence of Dopamine Dysregulation Syndrome (formerly Hedonistic Homeostatic Dysregulation)

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• Prevalence of pathological gambling

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0.3% to 1.5%; Similar to pathological gambling in the general population

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Risk factors

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• Sex; M>F • Early onset PD • Familial or previous personal psychiatric history • Impaired cognition • D3 receptor stimulation • Past drug/alcohol abuse Red Flags • Early dyskinesias • Punding

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Mechanism of DDS

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• Model of addiction suggests that drug taken not only for pleasure but also to avoid unpleasant withdrawal symptoms • DRT overuse gives similar psychomotor side effects as amphetamines and cocaine e.g. restlessness, insomnia, aggression, hypomania, hypersexuality, impulsivity and vivid dreams

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The Reward system

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Treatment Options and Management:

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• Reduction of total dopaminergic stimulation • Avoiding short-acting and rescue agents • Apomorphine “bolus” • Madopar dispersible

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• Atypical antipsychotics for manic episodes • Clozapine/quetiapine • Watch for depression/suicidal ideation • Psychiatric/psychotherapy input • ?Deep Brain Stimulation • ?change D3 to D2 agonist

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Best management is avoidance

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• Screening Questionnaire for HHD/ICD • Drug hoarding present? • Mood disturbances present? • Is violent behaviour, aggression or social isolation present? • Any compulsive behaviour; shopping, gambling, eating? • Any hypersexuality/sexual inadequacy • Heighten awareness of patient and partner

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Information sheet of Dopamine Agonists

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The following drugs are commonly used in patients with Parkinson’s disease and are classed as Dopamine Agonists. They are Ropinirole (Requip ®), Cabergoline (Cabaser ®), Pramipexole (Mirapexin ®). There is also a transdermal patch called Rotigotine (Neupro ®). These drugs can be useful to help the tremor and the slowness seen in Parkinson’s patients. Occasionally side effects occur, the most common one being nausea on first starting the drug, so often you will be given an anti-nausea drug called Domperidone (Motilium ®) to prevent this.

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Other side-effects sometimes seen are swelling of the ankles, dizziness on standing due to blood pressure dropping and also occasionally some confusion or hallucinations. Sleepiness can occur and it is advisable when first starting this drug and during the period of increasing the dose (titration period) that if you drive a car you should always be with another person, in case the sleepiness comes on whilst driving. A very rare side-effect with Cabergoline is fibrosis of the lungs and narrowing or leaking of the heart valves. This would give increasing shortness of breath over a period of time. If you get shortness of breath whilst taking the drug let your GP or Specialist know but don’t stop the drug immediately as it is much more likely that the breathing problem is due to other causes not related to the Parkinson treatment. We now monitor by yearly chest X-rays and heart scans (echocardiograms).

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The Rotigotine patch can occasionally cause a local skin reaction (1 in 20).

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Very rarely with Parkinson drugs people taking them do normal things more excessively than usual, for example; eating, gambling, shopping, hoarding objects or having sex. Do let the doctor/nurse know if you or your partner thinks this is happening to you.

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Most of the side-effects are mild and it is not necessary to stop the drug. However, if you feel the side-effects are outweighing the benefit of the drug, then we would consider stopping the drug. It is best to try and contact either Anne Martin or the doctor who prescribed the drug to discuss this, as it is usually not advisable to stop the drug suddenly, unless you have just started it. Often the symptoms go away if the dose of the drug is decreased, rather than completely stopping the drug. You may not notice any difference in your movements/tremor on starting the new drug but this may be because the dose to start with is small and is gradually built up. Therefore please continue taking it. If you need further information, please do not hesitate to get in touch with Anne Martin, the Parkinson Nurse, or your Consultant through their secretary, whose numbers are available via the hospital switchboard (01689 863000). If you do not understand the above information or have concerns then do not start the new drug until you have further discussed them with either Anne Martin or your Specialist.

• At this stage had

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• Prolonged freezes • Dyskinesias • Weight loss

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• Stalevo 50 qds • Cabergoline 2mg od • Quetiapine12.5 bd

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• Diagnosed at age 65 with PD • 23 years later in 2006 was on;

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Case 5 Mrs SR

Constipation and urinary urgency Depression Decreasing mobility with falls Cognitive impairment and hallucinations

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• Her symptoms continued to deteriorate

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SR

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• She required 24hr live in care

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Weighed in at 4 stone Worsening dyskinesias Developing pain and lethargy Gastric absorption problems and peak dose dyskinesias

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• Further deterioration

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• Decision was for palliative care intervention and medication review

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• Stalevo was reduced to sinemet 62.5 initially but this induced more extensive freezes and increasing pain • Peak dose dyskinesias persisted • Eventually patient agreed to apomorphine to help control her motor symptoms. Previously she had resisted this

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• Apomorphine was started up at home on low dosage at 2mg/hr and bolus 0.3mg. • Sinemet was stopped as was all her oral medications except 12.5mg quetiapine od. • Decision was made for SR to end her life at home however “panic” kicked in and SR was admitted to hospital.

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• Both the freezes and dyskinesias stopped when Apomorphine started as did the hallucinations • SR passed away 3 days later while in hospital pain free on Apomorphine only

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Palliative Care and PD

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Palliative care is the active total management and care of patients whose disease is not responsive to curative treatment

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Focus on quality of life Holistic approach Care of the dying and their carers Autonomy and choice Open and sensitive communication

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Key Principles

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Bowels Bladder Nutrition and hydration Pain Neuropsychiatric Sleep Pressure sores and contractures

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• Usual principles of palliative care apply • Don’t forget their non-motor symptoms

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In practise

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• Medication

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• Beware contra-indicated palliative drugs eg haloperidol, stemetil, maxalon, hyoscine • Continue/with hold PD drugs?? Consider down-titrating • Review all drugs and remove unnecessary eg statins, warfarin • Alternative routes cf. oral

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• NG tube/PEG-unlikely to be appropriate • Transdermal patch; Rotigotine • S/c infusion apomorphine

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• Legal and ethical issues

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• Living wills • Withholding/withdrawing treatment

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Aim for ‘good’ death rather than prolonging life at all costs

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Learning Points

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• Beware the ‘Nil by Mouth’ • For DLB and behavioural problems atypical anti-psychotics and ACE-I can be useful • In cases of ICD/DDS avoidance is better than cure – heighten awareness • The usual principles of palliative care apply in PD patients. Non-motor symptoms may be more important than motor symptoms

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Any Questions?

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Thank you