Parkinson’s diseaseIntroduction
Falls assessment
Examination specific to falls assessment in primary care
Investigations for osteoporotic fracture risk
Management of osteoporotic fracture risk in patients with Parkinson's disease
Multidisciplinary support
Prognosis
Conclusion
Key points
References

 

Introduction 

Parkinson’s disease is the second most common neurodegenerative condition in the UK, affecting approximately 1% of people aged >60 years old.1 The loss of dopaminergic neurons in the substantia nigra results in the characteristic features of Parkinson’s disease: tremor, rigidity, bradykinesia and postural instability.2 Parkinson’s disease often co-exists with osteoporosis because of reduced mobility, vitamin D deficiency, hyperhomocysteinaemia and/or malnutrition.3 The cost of care after patients develop a fracture, can be more than £2 billion per annum.4

In a recent local audit of Parkinson’s disease outpatient services, it was noted that 17% (8/47) of patients with Parkinson’s disease developed fractures requiring inpatient care, compared to 0.9% of the general population over a two-year period.5 However, 57% (16/28) of patients were asked about falling by geriatricians and only 11% (5/47) of patients were on bisphosphonates.

These findings are similar to those found in the literature,6 whereby bone health is not always assessed and there is additional difficulty due to the lack of guidelines, specific to osteoporosis in Parkinson’s disease.

This article aims to discuss some of the main strategies in primary care, which can minimise the risk of osteoporotic fractures in patients with Parkinson’s disease. It will cover an approach to falls assessment to identify and address risk factors for falls. There will be an overview of the investigation of bone health in patients with Parkinson’s disease, as osteoporosis is common in this group. There will be advice on optimising bone health and clinical features of Parkinson’s disease that would warrant an earlier specialist review.

 

Falls assessment

An approach to minimising falls in patients with Parkinson’s disease is as follows:

 

Falls history

Enquire from before, during and after the fall, in addition to the recovery period. It is important to establish the frequency of falls in a year and to clarify if the patient has had previous fractures to guide bone health assessment. Enquiry into the safety of the patient’s environment is also important such as environmental hazards, mobility aids and foot wear, so that occupational therapy is introduced earlier on in the patient’s care.7

 

Assess for bone health

Enquire about dietary requirements and refer to a dietician if calorie intake is an issue. Consider the use of a Malnutrition Universal Screening Tool to gauge severity of suspected malnourishment. Ask specifically about diary product consumption and sunlight exposure. This information is to determine if calcium and vitamin D supplementation should be offered in patients with Parkinson’s disease who currently do not show a deficiency on blood tests. If these additional risk factors are present, it would be advisable to initiate replacement.

GPs should provide advice regarding reversible risk factors of osteoporosis, such as smoking cessation and to reduce alcohol consumption.8 For optimal bone health, deficiencies in vitamin D and calcium should be replaced.

A systems review is necessary to ensure that there are no additional secondary causes of osteoporosis. Table 1 offers an overview of clinical features suspicious of an endocrine cause. In addition to this, clinical examination for rheumatoid arthritis and an enquiry of symptoms related to malignancy is recommended.

Also, patients with chronic kidney disease may potentially have compromised bone health and further specialist is recommended. A review of the appropriateness of long-term steroids is vital.

 

TABLE 1: POTENTIAL ENDOCRINE CAUSES FOR SECONDARY OSTEOPOROSIS. 9

Causes of secondary osteoporosis  Suspected features 
Hypopituitarism Loss of libido, reduced body hair, weight gain, gynaecomastica, headache, visual disturbance
Hyperthyroidism Irritable, unexplained weight loss, heat intolerance, tremor, palpitations, proximal myopathy. Lid retraction, goitre
Hyperparathyroidism Symptoms of hypercalcaemia (eg. constipation, polyuria, polydipsia, depression, anorexia, fatigue, recurrent renal calculi)
Cushing’s syndrome Weight gain, round facial features, interscapular fat pad, increased abdominal obesity with striae, hirsutism

 

 

Assess for delirium

Exclusion of the multiple causes for delirium as an explanation for the patient’s fall is vital. The most common causes are sepsis and polypharmacy.10 Delirium can be detected by the Confusion Assessment Method tool, which is defined by an acute and fluctuating change in behaviour with inattention. These criteria, plus either disorganised thinking and or altered arousal, can confirm a diagnosis of delirium. Note that hypoactive delirium can manifest itself as drowsiness/reduced responsiveness and can be easily missed, so history from a relative is crucial.11 Hypoactive delirium manifests as new onset confusion with increased lethargy and an unwillingness to participate in daily activities that the patient was previously capable of. If there is participation, it is often slower and the activity is usually not completed. The patient will be less able to self care, commonly noted to develop new incontinence and the patient may have an increased tendency to be either asleep or resting in a chair.12 If delirium is suspected, this is an emergency that warrants hospital admission. If however, the confusion is more chronic, dementia is more likely and a formal assessment by a psychiatrist is desirable.

 

Examination specific to falls assessment in primary care

A Snellen chart should be used to assess for visual impairment, which could be reversible.13 A get up and go test involves asking the sitting patient to stand up and walk three metres, turn around and return to the start position.

A patient is unlikely to need social support if this can be done in less than 10 seconds, but if this is completed in more than 10 seconds, then there needs to be consideration for further social support.14 If new focal neurology is suspected on gait examination, then consideration for hospital admission is also appropriate.

A cardiac examination with postural blood pressure measurements are needed to determine if postural hypotension is contributing to a patient’s increased risk of falls. If appropriate further investigations, such as echocardiogram, 24-hour tape and/or 24-hour blood pressure monitoring can be requested, prior to a referral to geriatric medicine services. If there is loss of consciousness or concern that there is haemodynamic compromise, then an inpatient assessment is warranted.15

 

Investigations for osteoporotic fracture risk 

Osteoporosis is defined as reduced bone density with a loss of structural bone tissue, which predisposes patients to fractures. NICE guidelines recommend the use of either Qfracture or FRAX to assess the risk for osteoporotic fracture.8 The World Health Organisation defines osteoporosis for men ≥50 years old and postmenopausal women, as a bone mass density measured by DEXA scan at the femoral neck as ≤2.5 or more standard deviations below a normal young, healthy female.8 Initial blood tests for suspected osteoporosis are full blood count, liver function tests, thyroid function, urea and electrolytes, bone profile, vitamin D level, parathyroid hormone (if there is suspicion of hyperparathyroidism or if there is previous hypercalcaemia) and random cortisol (if there is suspected Cushing’s syndrome/disease).7

 

Management of osteoporotic fracture risk in patients with Parkinson’s disease

 

Address bone health

For optimal bone health, deficiencies in vitamin D and calcium should be replaced. Bisphosphonates should be considered as they have shown an approximately 64% reduction in fractures for patients with Parkinson’s disease.16 If a female patient is ≥75 years old and/or the patient has had previous fractures, an oral bisphosphate is recommended. If bisphosphonates are not appropriate (eg. due to oesophagitis, dysphagia, renal impairment, severe cognitive impairment), then parenteral bisphosphonates are recommended.8 However, the exact duration that bisphosphonates should be used for which still requires further research.

Hyperhomocysteinaemia must be prevented by treating deficiencies in vitamin B12 and folate. This is because homocysteine binds to extracellular collagen and interferes with collagen cross-linking, resulting in suboptimal bone quality. Furthermore, homocysteine reduces bone mass density by promoting osteoclast differentiation and induction of osteoblast apoptosis.3 Screening for hyperhomocysteinaemia in primary care is not advisable, as this abnormality is nonspecific. For example, hyperhomocysteinaemia is also associated with cardiovascular disease, thromboembolic events and inflammatory bowel disease.17,18 Furthermore, there is no consensus on the treatment of hyperhomocysteinaemia in Parkinson’s disease and therefore this abnormality is currently left untreated.

 

Identify complications of Parkinson’s disease 

The following is an overview of the main motor and non-motor complications of Parkinson’s disease, which could increase a patient’s risk of falls.

 

Motor complications of Parkinson’s disease

Parkinson’s disease treatment should be adjusted in the secondary care setting. Parkinson’s disease treatment can be changed in primary care so long as the clinician has a special interest in Parkinson’s disease. An alternative source of support is the Parkinson’s disease nurse, but this service is not available in all regions and the nurse may not have the experience to adjust all Parkinson’s disease drug regimes.

For the non-specialist, a safer approach is to exclude other factors that might explain the patient’s decline. If Parkinson’s medications are altered and the intercurrent illness is not addressed, this may provoke a fall, by causing confusion, hallucinations and changes in their mobility. If the decline is thought to be related to Parkinson’s disease, then one has to consider if the initial diagnosis was correct and if this could be a Parkinson’s Plus syndrome. Diagnosis is difficult and if there have been interim changes of Parkinson’s medications this might further hinder the diagnosis. In primary care it is crucial to identify levodopa induced side effects, so that an earlier review or even hospital admission is requested. Common major side effects are: motor fluctuations, dyskinesias and hallucinations. Impulse control and disinhibition are potentials side effects from dopamine agonists. If these symptoms appear after recent changes to the Parkinson’s disease medications, it is reasonable to revert back to the previous regime, whilst awaiting secondary care review.19

 

Non-motor complications of Parkinson’s disease

Autonomic disturbance resulting in postural hypotension is common.19 It is recommended that there is reduction/stopping of other potential causative medications (eg. antihypertensives, vasodilators, diuretics). Adequate salt and fluid intake with support stockings, may also help. Fludrocortisone and midodrine are options to maintain blood pressure. Dementia and hypersomnolence will impair judgement and further compound the patient’s increased risk of falls. This may improve with medication review and treatment of intercurrent illness. However, in difficult to manage dementia, a psychiatry opinion may be required. Address hypersomnolence by providing advice regarding regular sleep patterns, with avoidance of caffeinated drinks in the evening and regular daytime exercise.20

 

Multidisciplinary support

Early multidisciplinary team intervention is needed to successfully minimise a patient’s falls risk. This includes the Parkinson’s disease specialist nurse, social worker, physiotherapist, speech and language therapist and occupational therapist.21

 

Prognosis

Hip fractures in patients with Parkinson’s disease, when compared to the general population, have twice the length of inpatient stay, have a higher incidence of pressure sores and are more often wheelchair/bed dependent after 30 days.22 Whether these patients return to their baseline functioning status is variable, due to multiple factors involved in post-operative care.23 Alternatively, addressing bone protection and falls prevention can bypass this adverse outcome,12 23 so that workload and resource usage is minimised, which in turn will reduce economic burden.

 

Conclusion

Parkinson’s disease patients are of increased risk of osteoporotic fractures and should be risk stratified. Ensure the patient is aware of support from Parkinson’s disease UK, Parkinson’s disease nurse and rehabilitation services.

 

Key points

  • Parkinson’s disease patients are of increased risk of osteoporotic fractures and should be risk stratified.
  • Bisphosphonates should be considered and parenteral bisphosphonates are an option if dysphagia is an issue.
  • Refer to secondary care if there is suspicion of delirium, haemodynamic compromise, new focal neurology and/or adjustments are needed for the Parkinson’s disease medications.
  • Ensure the patient is aware of support from Parkinson’s disease UK, Parkinson’s disease nurse and rehabilitation services. 

 

Dr William Lee, Specialist registrar in Geriatric Medicine, West Yorkshire
Conflict of interest: none declared.

 

References

1. Da Lau LM, Breteler M. Epidemiology of Parkinson’s disease. Lancet Neurol 2006; 5: 525–35  

2. Galvan A, Wichmann T. Pathophysiology of parkinsonism. Clin Neurophysiol 2008; 119(7): 1459-74

3. van den Bos F, Speelman AD, Samson M, et al. Parkinson’s disease and osteoporosis. Age Ageing 2012; 42: 156–62

4. Burge R, Worley D, Johansen A, et al. The cost of osteoporotic fractures in the UK: projections for 20002020. J Med Econ 2008; 4(1-4): 51–62

5. Singer BR, McLauchlan GJ, Robinson CM, Christie J. Epidemiology of fractures in 15000 adults the influence of age and gender. Bone Joint J 1998; 80(2): 243–48

6. McNeil L, Morgan H, Stewart R, et al. Falls assessment in movement disorder clinic in the West of Scotland. Age Ageing 2014; 43(suppl 2): ii4

7. National Osteoporosis Guideline Group. Guideline for the diagnosis and management of osteoporosis in postmenopausal women and men from the age of 50 years in the UK. http://www.shef.ac.uk/NOGG/NOGG_Pocket_

Guide_for_Healthcare_Professionals.pdf (accessed 7 July 2015)

8. NICE. Osteoporosis: assessing the risk of fragility fracture [CG146]. http://www.nice.org.uk/guidance/cg146 (accessed 2 July 2015)

9. Longmore M, Wilkinson I, Baldwin A, Wallin E. Oxford handbook of clinical medicine: Oxford University Press; 2014

10. George J, Bleasdale S, Singleton SJ. Causes and prognosis of delirium in elderly patients admitted to a district general hospital. Age Ageing 1997; 26: 423–27

11. Wei LA, Fearing MA, Sternberg EJ, Inouye SK. The confusion assessment method (CAM): a systematic review of current usage. J Am Geriatr Soc 2008; 56: 823–30

12. Ondria C, Gleason MD. Delirium. Am Fam Physician 2003; 67:1027–34

13. NICE. Falls: assessment and prevention of falls in older people [CG161]. http://www.nice.org.uk/guidance/cg161 (accessed 7 July 2015) 

14. Bohannon RW. Reference values for the timed up and go test: a descriptive meta-analysis. J Geriatr Phys Ther 2006; 29: 64

15. Bowker LK, Price JD, Smith SC. Oxford handbook of geriatric medicine: Oxford University Press; 2012

16. Zhang W, Zhu C, Sun M, et al. Efficacy of bisphosphonates against hip fracture in elderly patients with stroke and Parkinson’s diseases: meta-analysis of randomised controlled trials. J Stroke Cerebrovasc Dis 2014; 10: 2714–24

17. Erzin Y, Uzun H, Celik AF, et al. Hyperhomocysteinaemia in inflammatory bowel disease patients without past intestinal resections: correlations with cobalamin, pyridoxine, folate concentrations, acute phase reactants, disease activity, and prior thromboembolic complications. J Clin Gastroenterol 2008; 42: 481–86

18. Stranger O, Herrmann W, Pietrzik K, et al. Clinical use and rational management of homocysteine, folic acid, and B vitamins in cardiovascular and thrombotic diseases. Z Kardiol 2004; 93: 439–53

19. Clarke CE. Parkinson’s disease. BMJ 2007; 335: 441

20. NICE. Parkinson’s disease: diagnosis and management in primary and secondary care [CG35]. http://guidance.nice.org.uk/CG35 (accessed 2 July 2015)

21. Walker RW, Chaplin A, Hancock RL, et al. Hip fractures in people with idiopathic Parkinson’s disease: incidence and outcomes. Mov Disord 2013; 28: 334–40

22. Critchley RJ, Khan SK, Yarnall AJ, et al. Occurence, management and outcomes of hip fractures in patients with Parkinson’s disease. Br Med Bull 2015; pii:ldv029 [Epub ahead of print]

23. Iwamoto J, Sato Y, Takeda T, Matsumoto H. Strategy for prevention of hip fractures in patients with Parkinson’s disease. World J Orthop 2012; 3(9): 137–41