Parkinsonism Practice Case - Answers PDF

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A case covering answers for a Clinical Neurology case centred around Parkinsonism....

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DUMES Neurology Revision December 2020 Case 1: Parkinsonism Learning objectives After your small group session you should be able to: •

Describe accurately the clinical features of Parkinson’s disease

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List a sensible differential diagnosis for a patient with Parkinsonism

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Elicit Parkinson’s features using an adapted neurological examination

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Form a sensible management plan

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Describe common issues faced by these patients in the long-term

You are a medical student on placement in general practice. Edward Young is a 55-year-old who attends complaining of a new tremor, “brain fog” and fatigue. He is otherwise fit and well. This is his first visit to the practice in ten years. Q1) What would you ask this patient regarding his presenting complaints? Note findings as per ppt. From Year 3, patient presentations are more complex and often involve several presenting complaints. The best way to tackle this is to take one problem at a time and find out as much pertinent information as you can. SOCRATES is a useful mnemonic for almost any problem and can be adapted to help you establish a timeline of deterioration/improvement, associated symptoms, exacerbating and relieving factors and ideas, concerns and expectations (ICE). Be thorough and allow the patient to speak, which will often tell you what the diagnosis is before you have examined them. If you’re coming up blank, it’s always worth doing a systemic enquiry. Take a head to toe approach and ask about things you think are relevant to the history: Neuro – headache, hearing, balance, vision, smell, taste Chest – pain, cough (blood?), hoarseness, wheeze, SOB Heart – (pre)syncope, pain, palpitations, ankle swelling GI – dysphagia, nausea, vomiting (blood/mucus/bile/faeculent), pain, jaundice, change in bowel habit, tenesmus, rectal bleeding GU – pain, dysuria, haematuria, frequency, flow, terminal dribble +/- gynae & STIs MSK – joint pain, swelling, stiffness Constitutional – fever, weight loss, night sweats, malaise, fatigue Psych – mood, psychosis, sleep

Q2) You suspect Parkinsonism. What are four key motor signs of this syndrome? Bradykinesia (general sensation of being slow, or slowing down) Muscle rigidity (hypertonia apparent on examination and a ‘mask-like’ facial expression) Tremor (essential to differentiate from benign essential tremor, more on this below) Postural instability (easy to push over) Q3) This patient appears to have lost his sense of smell. What is the significance of this? Anosmia and ageusia (loss of taste) are common in Parkinson’s disease and may often be the first symptoms noticed by the patient1. Q4) Can you list other non-motor symptoms which accompany Parkinsonism? Think about bodily functions which require good muscle function:      

Diplopia (double-vision caused by uncooperative extraocular muscles) Bowel and bladder incontinence (sphincters) Constipation Sleep disturbance (REM parasomnias are common; the skeletal muscle is normally atonic during sleep but this is disrupted in Parkinson’s disease2) Slurred speech (laryngeal muscles and tongue) Aspiration of food

Quite understandably, mood disorders and anxiety are common. It is important to differentiate these from psychotic symptoms such as hallucinations which may point to another diagnosis (see below). Q5) The following terms and definitions are used when describing patients with Parkinsonism. Complete the table: Term

Definition

Resting tremor

A tremor seen when the hands are still e.g in the lap. It is usually bilateral. It is the characteristic tremor of PD, though additional action tremor is found in 25% of patients3. “Pill-rolling” is a buzzword used to describe the characteristic dragging of the thumb along the palmar aspect of the hand.

Action tremor

A tremor seen when the responsible muscles fibres are contracted. Various subtypes – notably “intention”, in which the tremor is most pronounced at the end

point of a complex, deliberate movement like pointing. This is what you test for in a cerebellar examination. Parkinsonian gait

Characteristic appearance of a PD patient when standing: flexed neck and spine; short, shuffling gait and overtly rigid.

Festination

Forward movement from rest via short, shuffling steps. PD patients are unstable and therefore at high risk of falls.

Cogwheel rigidity

Term used to describe alternating “stopstart” rigidity felt when testing muscle tone. e.g passively flexing the upper limb at the elbow. It is produced by the combination of muscle rigidity and tremor.

Lead pipe rigidity

Term used to describe constant hypertonia felt when testing muscle tone. Like trying to force a door open with a crowbar.

Extrapyramidal symptoms

The motor symptoms of Parkinsonism, described above, are extrapyramidal in nature – the nerve impulses which cause them are carried by the extrapyramidal tracts.

Q6) What is the difference between Parkinsonism and idiopathic Parkinson’s disease? Can you list some other causes of Parkinsonism? Idiopathic Parkinson’s disease is caused by degeneration of dopaminergic neurons within the substantia nigra. We don’t know why this happens, though there is good evidence linking it to accumulations of protein called alpha synuclein. Parkinsonism is a clinical syndrome which describes the extrapyramidal symptoms of bradykinesia, rigidity, tremor and postural instability. Causes of Parkinsonism include idiopathic Parkinson’s disease, drug-induced Parkinson’s (most notably anti-psychotics and anti-emetics), extrapyramidal symptoms induced by trauma (e.g repeated head injury, as suspected in Muhammad Ali’s case), stroke, infection and toxin accumulation. It’s a broad umbrella term, which is why some doctors will clinically diagnose patients with Parkinsonism rather than PD - they cannot be confident it is the idiopathic degenerative disease.

Q7) This patient’s complaints of fatigue, low mood and difficulty concentrating could be suggestive of an underlying mood disorder. If he went on to say that he had been experiencing vivid hallucinations, how would your differential diagnosis change? What could you do in clinic to screen for cognitive impairment? As noted above, mood disorder is seen commonly in patients with Parkinson’s disease. You need to be aware of Parkinson-plus syndrome (PPS), which is another umbrella term describing diseases which co-exist with a diagnosis of Parkinsonism. There are a number of these, but I think the most important one is Lewy body dementia. Deposits of alpha synuclein (termed Lewy bodies) within neurons cause Parkinsonism and acute onset dementia, characteristically with psychotic symptoms like visual hallucinations. It would be important to take a thorough psychiatric history and perform a mental state examination to differentiate this from schizophrenia or drug-induced psychosis. Cognitive assessment could be carried out using an Addenbrooke’s Cognitive Assessment (ACE-III) or abbreviated AMT4. Multisystem atrophy is another Parkinson-plus syndrome in which the patient may present with Parkinsonism, postural hypotension and cerebellar signs. Q8) Using your knowledge of Parkinsonism and the neurological examinations you have learned, how do you think you could best elicit the signs of idiopathic Parkinson’s disease in this patient? The “Parkinson’s exam” is a possible OSCE station which caught me out the first time I was faced with it. You need to take elements from the neurological examinations you have learned so far (cerebellum, upper and lower limbs) and target them to detect signs of Parkinsonism based on a focused history. Some excellent resources to practice with: https://oscestop.com/Parkinsons_exam.pdf https://geekymedics.com/parkinsons-disease-examination-osce-guide/ YouTube has some good videos on this too. Make sure to practice this examination before your OSCEs and you will be really impressive on the day! Q9) PD management is complex and holistic. What is the first line pharmacological treatment? Parkinson’s disease is usually diagnosed clinically based on the UK PDS Brain Bank Criteria4 There are investigations which you should have a general awareness of (e.g SPECT, which combines computed tomography with a radioisotope scan) but these are not routinely carried out5. According to SIGN guidelines, the first line pharmacological therapy for PD is a dopamine agonist (e.g levodopa) plus a dopamine carboxylase inhibitor (e.g carbadopa). The latter reduces levodopa metabolism in the peripheral circulation to ensure more of it reaches the brain, where it’s required.

Q10) What are two important side effects of dopamine agonist therapy? The main ones to be aware of are:  

Disinhibited behaviour (i.e thrill-seeking precipitated by dopamine overload) Daytime somnolence (which may be a risk if the patient is still driving)

Both of these issues can be raised during counselling before the patient starts on medication. b) What happens to the effectiveness of dopamine agonist therapy over time? The effectiveness of dopamine agonist therapy falls over time. This can lead to worsening of symptoms. You can find out more about further management options in NICE/SIGN guidelines.

References 1. Anosmia and ageusia in PD: https://pubmed.ncbi.nlm.nih.gov/28802932/ 2. Sleep disturbance in PD: https://www.jns-journal.com/article/S0022-510X(17)300199/abstract 3. Resting vs. Action tremor in PD: https://www.ninds.nih.gov/disorders/patientcaregiver-education/fact-sheets/tremor-fact-sheet 4. UK PDS Brain Bank Criteria for diagnosing PD: https://gpnotebook.com/simplepage.cfm?ID=x20080411172747571500 5. NICE guidelines PD (2017): https://www.nice.org.uk/guidance/ng71/resources/parkinsons-disease-in-adults-pdf1837629189061 6. SIGN guidelines PD (2010): https://www.parkinsons.org.uk/sites/default/files/201810/SIGN%20guideline%20Diagnosis%20and%20pharmacological%20management %20of%20Parkinson%27s.pdf

Ross Wilson ([email protected]) DUMES ([email protected]) November 2020...