Transcript Tremor assessment - Swindon General Practice Education

Tremor assessment, basic PD management,
trigeminal neuralgia, new treatments of MS,
basic assessment of peripheral neuropathies,
single seizures and epilepsy from GP
perspective, general rules for pain management
Wojciech Pietkiewicz
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Essential tremor
Parkinsonian Tremor
Dystonic Tremor
Cerebellar Tremor
Holmes Tremor
Orthostatic tremor
Task-Specific Tremor
Neuropathic Tremor
Toxic tremor
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The most common neurological disorder
The most benign neurological disorder
Only 5% of patietns need treatment
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Fine in frequency
Increasing with intentional movement, with
anxiety or when concentrating on it, tiredness
Often positive family history
Very slowly progressing
Mostly involving hands and head
Patient typically is afraid of having PD and
complaines of embarassment
Decreases radically on little amount of
alcohol
Propranolol
– Start 80 mg CR OM and increase according to the
response
– Can be used PRN
Prymidon
Start with 62.5 mg and increase according to the
response to maximum 250 mg tds
Combine if necessery
Gabapentin
Maximum 1200 tds (poor evidence)
Deep brain stimulation
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Coarse
Can be stopped at will! Mostly not very
worrying for the patient
Appearing mostly at rest when patient’s
attetnion is somewhere else
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Increased tone
Bradykinesia
Impaired postural reflexes
(apart from typical resting tremor)
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make the patient aware that what they cannot
expect:
– Imbalance/falls
– Difficulty speaking (dysarthria)
– Freezing
– Urinary frequency, urgency and leakage
Will not respond to antiparkinsonian medications
There is no proof that starting medication early
has any effect on the progression of PD
Thus patient needs to take part in decision making.
Often wait and watch approach is enough
• In general younger patients are traditionally put
on dopamine agonists (not evidence based)
• Anyone can be started on levodopa especially
when prompt response is needed
• Other medications are of very limited value
unless in the beginning of the disease
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Drugs for PD may take time to reach their
optimal effectiveness (especially agonists)
Early side effects often improve
Levodopa is the most effective
There is no reason to delay the use of
levodopa or keep the dose low
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Write the medications down with their timing
The most typical symptoms is early wearing
off the dose.
◦ Either devide the tablets and spread over the day or
add additional dose in between. Experiment and
encourage the patientt to help you with it.
◦ Replace the preparation with the one containing
Entecapon (Stalevo)
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Stiffeness in the morning
– Add a small dose of levodopa an hour before
planned leaving bed
– Addd CR preparation in the evening
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Early wearing off the dose
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Discomfort at night
– Divide the doses and add small ones in between.
Use rapid release preparations to tweak.
– Possibly change preparations to those with added
Entacapone (Stalevo). Use the same dose of
Levodopa
– Use CR preparations (Madopar 250)
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3 year history of PD, tremor predominant.
Now difficulty turning in bed at night, trouble
going to the toilet. Stiff in the morning.
Slower at 3pm and 7pm. Gets out of bed at
8am.
Current drug regime:
– Co-Careldopa 125:
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8am
12am
4pm
8pm
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3 year history of PD, tremor predominant. Now
difficulty turning in bed at night, trouble going to
the toilet. Stiff in the morning. Slower at 3pm and
7pm. Gets out from bed at 8am.
Change in drug regime:
– Co-Careldopa 125:
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8am
12am
4pm
8pm
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7am
10am
1pm
4pm
+7pm
+CR 250 9pm
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Orthostatic hypotension
– Management
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Discontinuing/decreasing BP medications
Proper hydration
Arising slowly, especially after a meal
Sleeping with the head 30° up
Sitting down if light headed
Increase salt intake
ƒFludrocortisone?
Glass of warm water on waking
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Nausea (mild and transient, usually in the
beginning of treatment)
– Domperidone 10–20 mg 3–4 times daily
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ƒ eg swelling
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ƒConfusion. Decrease the dose if necessery.
ƒHallucinations and delusions (usually mild- no
treatment necessery). Decrease the dose if
necessery.
ƒDaytime sleepiness. No specific treatment.
Sudden onset of sleepiness on dopamine
agonists
Obsession and compulsion disorders on
dopamine agonists
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Refer for Apomorphine injections
Rapid onset of action (10-15 min)
Aimed at OFF time
Needs hospital admission to start
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Sudden suicidal pain, electric like sensation,
brief but repetitive, triggered by movement or
touch in the distribution of the trigeminal
nerve. Bouts during the day with fluctuations
and spontaineous remissions
Physically: typically nothing of note. Often
decrease in light touch/pain sensation and
decreased corneal/conjunctival reflexes
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Refer to Neurology
MR scan? Controversial
Start treatment:
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Carbamazepine is the only drug of proven value!
Gabapentin- second choice
Amitryptyline-less useful
Baclofen?
Occipital nerve block
Treatment of MS:
• Treamtent of a relapse
• Disease modyfying treatment
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Use in relapses only
Dose: Methylprednisolone from 0.5g OM for 3 days to 2g
om for 5 days (NICE)
Absorbtion of oral MP is 100%. There is no statistical
difference in oral or IV use. Oral administration is simplier,
cheaper and more comfortable for the patient.
No more than 3 sessions per year (NICE)
Check for signs of infection prior administration. Urine
dipstick test
Steroids only make relapses shorter. They do not have any
effect on the disease course. Many patients are
psychologically dependent on steroids. Improved mood as
much as depression is a common side effect
There is no need to prescribe Omeprazole
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Most commonly used :
– Copaxone (NICE)
– Interferons (NICE)
Expensive, only decrease 30% of relapses. Do not
have any influence on progression to progressive
phase. Need self-injecting. Range from once a day to
once a week (Avonex-im). On avarage they decrease
number of relapses by one over 6-9 years!
Currently prescribed to patients having 2 or more
relapses per 2 years
Curretnly there is no therapy available for
progressive forms.
Progressive MS is more neurodegenerative
disease than inflammatory.
There is a suspicion that Fingolimod may have a
role but the clinical trials are ongoing.
Natazulimab (Tysabri), monthly 300mg iv
Available for patients with agressive forms or
when other treatmetns are not tolerated.
Decreases relapse frequencey 60%.
Significant risk of PML (1:1000) but after 2
years of continuation much higher
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Fingolimod (the only oral medication. 1.25
mg ot 0.5 mg OD). In UK-only clinical trials.
Approved by FDA
Significant risk of bradycardia on initiation.
Efficacy comparable with Tysabri
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Mitoxantrone
◦ rapid onset of action and infrequent administration
schedule (3-monthly infusion)
◦ Acute leukemia is of primary concern incidence
after the therapy is 0.21% and may be
underestimated
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Alemtuzumab (Campath)- under evaluation
Vitamin D- under evaluation
Low dose Naltrexone- of unproven value
Jugular vain angioplasty- of unproven value
Stem cell transplantation- of unproven value
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MS is a clinical diagnosis. Patient needs two clear
neurological symptoms separated by time and
space. Do not mention MS unless there is a good
clinical suspicion of it! (NICE)
Demyelination/ischaemic changes on MR are
found in 30-60% of population. Do not raise the
suspicion of MS because of abnormal lab tests
Do not push the diagnosis. Currently there is no
reason to diagnose MS very early and it will
increase patient’s anxiety. First answer yourselff
a question: What am I to offer my patient if the
diagnosis is confirmed.
Clinically the most common situations are:
• Sensory gloves and stockings neuropathy,
pain and numbness in distal hands and more
commonly legs
• Mixed motor and sensory neuropathies may
show as wekaness in distal muscles
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CTS- typical pain and p&n in the first three
fingers, typically more at night with
characteristic chaking of the hands. Weakness
usually on turning keys and whilst grasping
haevi objects.
May be complication of other neuropathies
– NCS
– Surgery or overnight splinting
– Referal to independent treatment centre
Ulnar neuropathy. Difficult to miss. Surgical
treatment is rarely useful.
–Typically: wait and watch. Advise not to
bend hands during sleep. Recovery time
from 3 to 12 months
Radial Neuropathy wrist drop and sensory
symptoms in the distribution ot radial
nerve. Tratmemt as for ulnar neuropathy.
Peroneal neuropathy. Advice not to cross
legs. Conservative.
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Check light touch sensation. The symptoms
are typically in stockings or gloves and
stockings distribution. What you check are
small calibre fibres. These are often
responsible for p&n and pain with paradoxal
numbness. They also carry autonomic
signals.
Check proprioception (vibration sense and
position of the joints). These are large calibre
fibres. Only they are seen on NCS!
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NCS
– typically show axonal type damage the
management is symptomatic. Treat pain but there
is no help for numbness.
– Use chronic pain killers like Gabapentin,
Amitryptyline rather than Paracetmol or
nonsteroids.
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There are only 3 blood tests for PN as
evidence based! According to our audit only
5% of GPs perform the tests appropriately.
– Glucose (possibly tolerance tests)
– Vitamin B12 (possibly with Folate)
– Serum electrophoresis
SE is nearly never done with initial assessment of
neuropathies.
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Careful history. Assess whether this is first
seizure or not
– Faint:
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Prodrome symptoms
Only when standing or standing up
Not confused afterwards
Motor activity is frequently seen!
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Purple on the face
Bitten tongue
Confused afterwards
(incontinent)
(injured)
– Seizure markers:
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Neuro assessment
MR scan
Do not request or ask for EEG
Do not start treatment
Refer to Neurology, ask to bring a witness.
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Reassure (10% of population can experience
one seizure)
Probability of another one (epilepsy) is
around 30%. But after a second one
probability is around 60%
DVLA advice. 6 months of driving after the
first seizure, 12 after any next one within 7
years.
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Advice according to DVLA regulations!
Do not advise that a neurologist should
decide about driving. Unexplained loss of
consciousness is by definition 6 months off
driving. It is unlikely this will be explained
taking the same history.
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Seizures and epilepsy are diagnosed
clinically!
EEG is very poor support. It is usually
negative even in patients with epilepsy.
It is only useful if positive or in assessment of
pseudoseizures if negative
It is better to diagnose a pseudoseizure and
to make a mistake than the other way round.
9 in ten seizures in front of a doctor or in the
waiting area are pseudoseizures
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Typically treatment resistant
Many admissions to ICU
Rare injuries
No incontinence or tongue biting
Lasting a long time
Inconsistent presentation
• Acute and acute on chronic pain:
 Use acute pain killers
• Chronic pain:
 Use chronic pain killers
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Have limited value in management of chronic
pain especially neuropayhic pain.
Can be responsible for headaches.
Start immidiatiely after commenced
Narcotic based should not be used for
headaches
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Used for pain lasting in general longer than 3
months
Either antiepileptics (Gabapentin, Pregabalin,
Topiramate, Valproate)
Or antidepressants (Amitryptyline,
Nortryptyline, Dosulepine, Duloxetine)
Onset of action after a few weeks.
Act centrally
Need very high doses.
Firstly give only side effects
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The most common reason for noncompliance:
◦ Not being told that the drug is antiepileptic or
antidepressant
◦ Not being told that it kicks in slowly over weeks
◦ Not being told to persevere minor side effects
◦ Using microscopic doses
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Choose accoding to desired undesired effects
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Problems with sleep? Use Amitryptyline
Problems with sedation? Use Nortryptyline
Loosing weight? Use Valproate
Waight gain? Use Topiramate
Having depression, mood swings, anxiety,
headaches? Use Valproate
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Pizotifen, Gabapentin, Pregabaline, SSRIs for
headaches
Narcotic drugs for headaches and especially
for migraines
Triptans in hemiplegic migraines
Acute antimigraine drugs (simple analgesia or
triptans or caffeine) in frequency of more
than two sessions per week
Paracetamol
• Caffeine
In Headaches during pregnancy.
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