1. Debra Vincent Scott Clinical nurse specialist in Parkinson's disease MOBILE
This presentation has been produced by GlaxoSmithKline

2. Aims Prevalence Diagnosing Non Motor symptoms Stages of PD Treatment
Patients experience

3. Prevalance 1 in 500 UK resident have PD 1 in 100 > 60 yrs have PD
Pt have formal PD diagnosis (GPRD database)
1 in 20 Pt; Develop symptoms under 40 yrs of age
By 2020: PD no will rise
28% rise in PD cases
Economic burden of PD is ~ £2 billion annually (Imperial College) (1, 2)

4. Diagnosing PD
A set of characteristic symptoms that affect motor control:
resting tremor,
bradykinesia, and
hypertonia.
Resting tremor is an oscillating movement (4—6 Hrzd) that occurs when the patient is trying to be still; disappears on action
Essential Tremor: Persists on movement
Cerebellar Tremor: Intentional tremor

5. Bradykinesia means slowness of movement.
Usually experienced as ‘weakness’ or ‘stiffness’ of limb
Hypertonia means excessive muscle tone.
Manifest itself as rigidity or stiffness.
Other typical features: are
a Stooped posture/ Slow, shuffling festinant gait/ Reduced arm swing/ Facial appearance (Masked like ‘hypomimia’)/ Low volume speech/ Excessive drooling of saliva

6. The ‘Braak hypothesis’
Stage 5 and 6: Changes spread to the cortex
Stage 3 and 4: Pathology spreads to the midbrain and basal ganglia
Stage 1 and 2: Pathology confined to certain structures in the brain stem, not yet the substantia nigra
Neurodegeneration happens elsewhere in the brain in Parkinson's, and may precede damage to the substantia nigra.
The neuropathologist Braak has suggested that pathological changes which occur in Parkinson's can be divided into six stages – The ‘Braak hypothesis’ 13
Braak has suggested that the condition may begin in the olfactory bundle and lower brainstem, and studies are underway to detect Parkinson’s disease at a premotor phase.16
As illustrated in the slide
This may explain the onset of sleep disturbance and loss of sense of smell prior to the onset of motor symptoms, as well as other ‘non-motor’ symptoms of Parkinson's.13
Image adapted from The Professionals Guide to Parkinson’s Disease, Parkinson'sS 6

7. Non-motor symptoms of PD 3
Neuropsychiatric
Autonomic
Sleep disturbance
Sensory symptoms
Dementia
Depression
Apathy
Anxiety
Loss of libido
REM sleep disorder
RLS
Vivid dreams
Daytime somnolence
Dystonia
Constipation
Urinary incontinence
Erectile dysfunction
Excessive sweating
Postural hypotension
Excessive salivation
Pain
Paraesthesia
Non-motor symptoms are a common source of disability in PD. Many patients do not spontaneously volunteer information about these symptoms, specific questions about them should be part of routine assessment. The Non motor symptom questionnaire is used for patients to self report.26
Dementia:
When dementia develops more than one year after the onset of the motor features of PD, it is defined as ‘Parkinson’s Disease with Dementia’ (PDD). When it develops within a year it is defined as ‘Dementia with Lewy Body’ (DLB).27 They present with decline in visuospatial abilities, category learning, verbal fluency, set switching and executive function, rather than the memory loss seen in Alzheimer's. There is evidence of spontaneous hallucinations and psychosis, which maybe worsened by dopaminergic drugs or systemic illness such as infection. 28
Depression:
Depression is a major clinical problem in patients with PD. It affects around 40% of patients with PD and leads to significant reduction in quality of life. Clinicians and nurses should have a low index of suspicion for depression in PD.
Constipation:
Constipation is extremely common, if not universal, in PD. It can even occur before the onset of the motor disorder. It is probably caused by direct involvement of the myenteric plexus in the pathology of the condition as lewy bodies are found in the gut wall.
Sleep disorders:
Sleep disturbance occurs in nearly all patients with PD. Patients should be asked about sleep problems regularly and, if present, a thorough sleep history should be taken.27
Of the 13,000 respondents from the PDS members survey 34% reported that they were getting a good nights sleep and 80% regarded it as very important.24
Up to 98% of patients with PD report sleep disturbances.25
Dystonia:
Dystonia often occurs in the early hours of the morning and is a common reason for disturbed sleep in patients with PD.30

8. Parkinson's Disease Criteria for entry into staging categories
Diagnosis / early
Knowledge of disease
Ideas and perceptions
Employment issues
Neuro rehab
Levodopa or Dopamine agonists
Rasagiline. selegiline
Maintenance
Promote normal function
Regular reviews-red flags
Support
MDT input
Entacapone
Stalevo
Complex
Motor complications.
Neuropsychiatric complications
Reduction of drugs.
Carer support/respite/hospice
Amantadine.
Apomorphine
Duodopa
DBS
Managing PD is a complex process due to the range of symptoms, rate of progression and range of treatment options
This 'Pathways Paradigm' was developed by MacMahon and Thomas (1998), ‘to improve the prognosis and reduce the impact of this [Parkinson's] disease on patients and their caregivers (1)
It is now the most accepted paradigm for PD and comprises four stages: diagnosis, maintenance, complex and palliative
Each stage, although by necessity relatively flexible, represents a specific area for clinical management for the disease duration
Palliative
Symptoms versus side effects
Advanced care needs
4 .MacMahon D.G Thomas.S Practical Approach to Parkinson’s Disease. Journal of Neurology (1998) 245 (SUPP1)S19.S22

9. Patient education.MDT input
TREATMENT
Begins with
Diagnosis
Patient education.MDT input
Discussion of when and which drug Treatments. Bradykinesia dominated disease may need earlier treatment than tremor dominated disease
People with suspected Parkinson’s should be referred quickly and untreated to a specialist (NICE 2006)

10. Drug classes in Parkinson’s
Levodopa
DAs Dopamine agonists
MAO-B inhibitors Monoamine oxidase B inhibitors
COMTs Catechol-O-methyltransferase inhibitors
Anticholinergics

11. Drugs to avoid Generic name Brand name Usually prescribed for
prochlorperazine
metoclopramide
Stemetil
Maxalon
Dizziness, nausea and vomiting
fluphenazine
perphenazine
flupentixol
Motival
Triptafen
Fluanxol
Depixol
Depression
chlorpromazine
haloperidol
Largactil
Moditen
Serenace
Haldol
Fentazin
Confusion, hallucinations, disorientation, or disturbed thinking
All of these drugs, block dopamine receptors in the brain.
The only anti emetic that can safely be taken is domperidone as it does not cross the blood brain barrier.
New atypical neuroleptic’s decrease the risk of aggravating Parkinson’s symptoms.35

12. Drug management
As responses to drugs are variable, treatment regimes differ from person to person
The timing of drugs is important in order to achieve continuous dopaminergic stimulation
Nurses have a key role in helping the patients manage complex drug regimes
Sudden discontinuation of treatment should be avoided as it can result in Neuroleptic Malignant Syndrome.
Get it on time campaign. NH homes to send in medication with patient
To achieve the right balance between benefit and any side effects, the individual will need to understand and be involved in which drugs are being used and why drug timing is so important.
Neuroleptic malignant syndrome is a rare, life-threatening reaction in people exposed to neuroleptic medication. It can also occur in Parkinson’s patients after sudden withdrawal of anti-Parkinson's drugs. It is characterised by hyperthermia, muscle rigidity, altered levels of consciousness, autonomic instability and elevated serum creatine kinease (CK) level.
Therefore anti-Parkinson’s medication should not be withdrawn abruptly or allowed to fail suddenly due to poor absorption (e.g. gastroenteritis, abdominal surgery)35

13. End note Start ‘slow and low’
Watch for side effects; low BP, Orthostatic hypotension, ICD
NMS are more common in older pts
NMS are often confusing & poorly recognised
Insomnia: likely due to Akathisia (inner restlessness), stiffness (rigidity), difficulty turning in bed, as well as tremor
Anxiety: likely due to Akathisia
Cramps: could be ‘dystonias’: inspect feet for inversion, great toe
Pain/ Paresthesia/ depression: may be levodopa responsive
Avoid hospitalisation
The patient is the expert

14. References
findley LJ The economic impact of Parkinson's disease. Parkinsonism Relat Disord Sep;13 Suppl:S8-S12. Epub 2007 Aug 16.
Oliver H.H. Gerlach, MD,* Ania Winogrodzka, MD, PhD, and Wim E.J. Weber, MD, PhD; Clinical Problems in the Hospitalized Parkinson’s Disease Patient: Systematic Review Movement Disorders, Vol. 26, No. 2, 2011
Huse DM, Schulman K, Orsini L, Castelli-Haley J, Kennedy S, Lenhart G. Burden of illness in Parkinson’s disease. Mov Disord 2005;20:1449–1454
Parkinson’s-UK. ‘‘Get It on Time.’’
Shulman LM, Taback RL, Rabinstein AA, Weiner WJ. Non-recognition of depression and other non-motor symptoms in Parkinson’s disease. Parkinsonism Relat Disord. 2002;8(3): 193–197.
Miyasaki JM, Shannon K, Voon V, et al. Quality Standards Subcommittee of the American Academy of Neurology. Practice Parameter: evaluation and treatment of depression, psychosis, and dementia in Parkinson disease (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006;66(7):996–1002.
Poewe WH, Lees AJ, Stern GM. Low-dose L-dopa therapy in Parkinson’s disease: a 6-year follow-up study. Neurology1986;36:
Kumar N, Van Gerpen JA, Bower JH, Ahlskog JE. Levodopa-dyskinesia incidence by age of Parkinson’s disease onset. Mov Disord 2005; 20:
Holloway RG, Shoulson I, Fahn S, Kieburtz K, Lang A, Marek K, et al. Pramipexole vs levodopa as initial treatment for Parkinson disease: a 4-year randomized controlled trial. Arch Neurol 2004;61:
Dodd, Klos KJ, Bower JH, Geda YE, Josephs KA, Ahlskog JE. Pathological gambling caused by drugs used to treat Parkinson disease. Arch Neurol 2005;62:
Nirenberg MJ, Waters C. Compulsive eating and weight gain related to dopamine agonist use. Mov Disord 2006;21:
Voon V, Hassan K, Zurowski M, de Souza M, Thomsen T, Fox S, et al. Prevalence of repetitive and reward-seeking behaviors in Parkinson disease. Neurology 2006;67:

15. Parkinson’s-UK. ‘‘Get It on Time.’’ www.parkinsons.org.uk.
Shulman LM, Taback RL, Rabinstein AA, Weiner WJ. Non-recognition of depression and other non-motor symptoms in Parkinson’s disease. Parkinsonism Relat Disord. 2002;8(3): 193–197.
Miyasaki JM, Shannon K, Voon V, et al. Quality Standards Subcommittee of the American Academy of Neurology. Practice Parameter: evaluation and treatment of depression, psychosis, and dementia in Parkinson disease (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006;66(7):996–1002.
Poewe WH, Lees AJ, Stern GM. Low-dose L-dopa therapy in Parkinson’s disease: a 6-year follow-up study. Neurology1986;36:
Kumar N, Van Gerpen JA, Bower JH, Ahlskog JE. Levodopa-dyskinesia incidence by age of Parkinson’s disease onset. Mov Disord 2005; 20:
Holloway RG, Shoulson I, Fahn S, Kieburtz K, Lang A, Marek K, et al. Pramipexole vs levodopa as initial treatment for Parkinson disease: a 4-year randomized controlled trial. Arch Neurol 2004;61:
Dodd ML, Klos KJ, Bower JH, Geda YE, Josephs KA, Ahlskog JE. Pathological gambling caused by drugs used to treat Parkinson disease. Arch Neurol 2005;62:
Nirenberg MJ, Waters C. Compulsive eating and weight gain related to dopamine agonist use. Mov Disord 2006;21:
MacMahon D.G Thomas.S Practical Approach to Parkinson’s Disease. Journal of Neurology (1998) 245 (SUPP1)S19.S22
Voon V, Hassan K, Zurowski M, de Souza M, Thomsen T, Fox S, et al. Prevalence of repetitive and reward-seeking behaviors in Parkinson disease. Neurology 2006;67: