Parkinson's/Epilepsy Flashcards
How is Parkinson’s diagnosed?
Bradykinesia +1 of:
- 4-6 Hz tremor
- Mucular rigidity
- Postural instability
ASSYMETRICAL
If these symptoms are bilateral, how does this change the diagnosis?
More likely to be SECONDARY PARKINSONISM caused by drugs (e.g. neuroleptics, antiemetics), CVD, infections etc
Name some non-motor symptoms of parkinson
- REM behaviour disorder (acting out dreams) and other sleep disorders
- Reduction in olfactory function (ANOSMIA IN 90%!!!!)
- Depression/anxiety/hallucinations
- Parasthesia
- Fatigue
- Sexual dysfunction
- Bladder dysfunction
If you see a patient with rapid onset parkinsonism and dementia, what is the most likely diagnosis?
Lewy Body Dementia
What is Parkinson’s Disease?
A progressive neurodegenerative disease with two main features:
- Loss of pigmented dopaminergic neurons in the substantia nigra
- Increase in Lewy Bodies
Name some other relevant motor features of PD
Dysphagia
Dysarthria
Hypersalivation
Blurred vision
Micrographia
Dystonia
Stooped posture
Shuffling gate
Freezing
Festinant
FALLS
What does festinant mean?
Having short stride and quickened gait
What is a parkinson plus syndrome?
A group of syndromes that exhibit the same symptoms as parkinsons but with additional features:
- Multiple system atrophy
- Corticobasal degeneration
- Progressive supranuclear palsy
What are the typical pre-motor symptoms?
- Impaired olfaction
- REM behaviour disorder
- Depression
- Constipation
What imaging technique is used in parkinson diagnosis?
SPECT - measures loflupane (DaTSCAN) uptake in presynaptic dopamine transporters
What does a DaTSCAN look like in a PD patient?
More like .. than the usual “
What are the pros and cons of DaTSCANS?
PRO - high sensitivity and specificity
CON - expensive
Describe the onset and progression of PD
Insidious onset (latent period can be up to 3 decades)
Long clinical course (10-30 years)
Incurable, decreased life expectancy
Name the 7 classes of drugs used to treat PD?
- L-dopa (give with decarboxylase inhibitor)
- Dopamine agonists
- MAOB inhibitors
- COMPT inhibitors
- Amantadine
- Anticholinergics
- Oestrogen
Name two examples of L-Dopa with decarboxylase inhibitor
Madopar, Sinemet
Name two examples of MAOB inhibitors
Selegiline, Rasagiline
Name three examples of dopamine agonists
Ropinirole, Pramipexole, Rotigotine, Apomorphine
How do L-Dopa and decarboxylase inhibitors work?
L-dopa is converted to dopamine in the brain
How do COMT inhibitors work, and what is an example?
Entacapone They stop L-dopa from being converted to 3-0 methydopa (must be used alongside)
How do MAOB inhibitors work?
They stop dopamine from being converted to its inactive metabolite
Which of the drug treatments is best for symptom control?
L-dopa, however it has motor complications, unlike the others
Why is L-Dopa used in older patients and dopamine agonists used in younger ones?
L-dopa is the best for symptomatic treatment but DAs are best in delaying onset of motor complications
Also DA causes orthostatic hypotension, which could contribute to falls in the elderly
Which members of the MDT are involved in Parkinsons care?
PD nurse specialist, physiotherapy, occupational therapy, SALT, support groups
What drug is primarily used in early PD?
MAOB inhibitors (best at stopping progression of disease, but not that good at symptom control)
What medications should be stopped when prescribing for PD?
Dopamine-blocking agents:
- Neuroleptics
- Antiemetics
- Sodium valproate
- CCBs
If a PD patient starts experiencing hallucinations from their meds, what can be given to them?
Quetiapine
How does Amantadine work?
Stimulates release of dopamine
What is the pharmacology of L-Dopa?
- Absorbed from small bowel
- Motor symptoms improve 20-70%
What are the short term side effects of L-Dopa?
GI - nausea, vomiting, decreased appetite
Psychiatric - confusion, hallucinations, delusions
Cardiovascular - postural hypotension
Sleep disorders - somnolence, insomnia, vivid dream/ nightmares
What are the long term side effects of L-Dopa?
DYSKINESIAS - Abnormal involuntary movements
RESPONSE FLUCTUATIONS - end-of-dose deterioration and unpredictable on/off switching
PSYCHIATRIC - confusion, hallucinations
What is the pharmacology of Dopamine agonists?
- Act directly on D1/D2 postsynaptic receptors in the striatum
Which dopamine agonists are administered by which routes?
Ropinirole - oral
Rotigotine - transdermal
Subcutaneous - apomorphine
What are the side effects of dopamine agonists?
- Nausea, vomiting, loss of appetite
- Postural hypotension
- Confusion, hallucinations
- Somnolence
- Impulse control disorders (hypersexuality, gambling etc)
What is the pharmacology of MOAB inhibitors?
- Irreversible inhibitors
- Decrease dopamine breakdown so that there is more in the synaptic cleft
NB - in practice these are rarely used alone as they have a weak clinical effect
What are the side effects of MOAB inhibitors?
Nausea, vomiting, confusion
What is an important drug interaction to be aware of in reference to MOAB inhibitors?
Interact with anti-depressants –> SEROTONIN SYNDROME
What is the pharmacology of COMT inhibitors?
Inhibit COMT so that more levodopa is available to cross the BBB
What are the side effects of COMT inhibitors?
Nausea, vomiting, confusion
DIARRHOEA AND DISCOLOURATION OF BODY FLUIDS
Increased dyskinesias
What is the pharmacology of amantadine?
Antiviral, NMDA receptor antagonist causing increased release of dopamine
When is amantadine used?
In the later stages of disease to treat dyskinesias (however do not use in the elderly as it causes confusion)
What are the side effects of amantadine?
- Confusion
- Halluciantions, pscyhosis
- Livedo reticularis (skin condition)
- Ankle oedema
What is the pharmacology of anticholinergics?
Decrease the effects of relative ACh excess, that occurs due to dopaminergic deficiency
What are the side effects of anticholinergics?
Cognitive impairment
Dry mouth, blurred vision, constipation, urinary retention, dizziness
When are anticholinergics used?
In the young, to combat tremor
What are the future PD treatments?
- Fetal mesencephalic dopamine cell implantation
- Intraputaminal glial cell line derived neutrophilic factor
What drug is first line for generalised epilepsy?
Men: Sodium Valproate (2nd lamotrigine)
Women: Lamotrigine (less teratogenic)
What drug is first line for focal epilepsy?
Carbamazepine and Lamotrigine (better tolerated)
Which members of the MDT are involved in the care of a patient with epilepsy?
Epileptologists, neurosurgeons, nurses, EEG technicians, psychiatrists, social workers, DVLA, pharmacologists
What drug is first line for generalised absence seizures?
Ethosuximide
What are the size effects of carbamazepine, phenytoin and lamotrigine?
Tiredness, double vision, steadiness, RASH
What are the side effects of sodium valproate?
Weight gain
Tremor
Parkinsonism
Teratogenicity
What are the side effects of topiramate?
Weight loss, behavioural changes, paraesthesia, kidney stones
What are the side effects of levetiracetam?
Tiredness, dizziness, aggresion
Which AEDs are enzyme inducers of the OCP?
Carbamazepine (anything -epine) Phennytoin Topiramate
Which AEDs are metabolised by the liver and which renally?
If in doubt, CP450
Renal - Gabapentin, Levetiracetam
What are the indications for monitoring AEDs?
- As guide to dosing
- To check compliance
- Toxic symptoms
- To monitor interactions
- During pregnancy
- Learning disabilities
How is status epilepticus treated?
ABCDE
Hospital - IV lorazepam
GP - rectal diazepam
Kids - buccal midazelam
If these fail, give phenytoin, phenobarbital or transfer to ITU
At 30 min do bloods to see if there is an underlying cause
At 60 mins admit to ICU for continuous monitoring
Why do you sometimes get:
a) raised GGT
b) hyponatremia
when being treated with carbamazepine, and what is the consequence?
a) this is because carbamazepine is an enzyme induce, you can continue with treatment but monitor
b) as a consequence of SIADH - if symptomatic should discontinue treatment
Why does carbamazepine require dose adjustment as you continue treatment?
It is an AUTO-INDUCER - as treatment goes on it induces its own metabolism, so you will need to increase the dose
What are the symptoms of carbamazepine toxicity? How should it be managed?
Nystagmus Ataxia Increased seizure frequency
THESE ARE DUE TO CEREBELLAR TOXICITY
Activated charcoal and supportive care
What anti epileptic should be used in pregnancy?
Carbamazepine
(sodium valproate associated with neural tube defects)
What antiepileptic should be used in lactation?
Most of the older ones are safe!
What is delirium tremens?
Acute alcohol withdrawal with agitation, fever, confusion, hallucinations, tonic clonic seizure
Usually occurs after 8hrs with a peak at day 2 and recovery at day 5
How is delirium tremens treated?
Chlordiazepoxide oral
