Neurology Flashcards
what is the pathophysiology of parkinsons disease?
Progressive degeneration of the dopaminergic neurons in the substantia nigra
what is the classical symptoms of parkinsons disease?
triad:
tremor - pill rolling
bradykinesia - slow shuffling gait, difficulting initiating movement
rigidity - cogwheel
these symptoms are characteristically asymmetrical
what is the mean age of parkinsons disease diagnosis?
aged 65 years
is parkinsons more common in men or women?
men
what are some additional symptoms of parkinsons beyond the classic triad?
mask like face
flexed posture
depression
fatigue
postural hypotension
poor sleep
drooling of saliva
freezing of gait
constipation
how can you differentiate between parkinsons disease and drug induced parkinsonism?
drug induced - symptoms typically bilateral , more predominant motor symptoms
tremor/rigidity - less common
Management of suspected parkinsonism in general practice?
if suspected - refer urgently as appropriate diagnosis and treatment should not be delayed
If drug induced suspected - can reduce/stop the medication and assess response - but referral still needed and do not delay this whilst waiting for response
what are some common medications that can cause parkinsonism?
antipsychotics - first gen (haloperidol, zuclopenthixol, chlropromazine)
anti-emetics - prochlorperazine, metoclopramide
Other drugs more rarely - Antidepressants, such as selective serotonin reuptake inhibitors (SSRIs).
Calcium-channel blockers.
Cinnarizine.
Amiodarone.
Lithium.
Cholinesterase inhibitors, such as donepezil or memantine.
Sodium valproate.
Methyldopa.
Pethidine
what is the management of confirmed parkinsons in GP?
ensure has review every 6-12 months
refer to MDT as needed
Only alter medication on advice of specialist
what is the DVLA advice for parkinsons disease for group 1 drivers
still able to drive as long as symptoms are well controlled/not interfering with driving, license will be revoked if symptoms poorly controlled or severe
what is the DVLA advice for parkinsons disease for group 2 dirvers?
may drive as long as safe vehicle control is maintained at all times. If the individual’s condition is disabling and/or there is clinically significant variability in motor function, the licence will be refused or revoked.
what is the first line pharmacological management of parkinsons disease for patients whose motor symptoms are affecting their life?
levodopa
what is the first line pharmacological management of parkinsons disease for patients whose motor symptoms are not affecting their life?
Dopamine agonist (non-ergot derived), levodopa or monoamine oxidase B (MAO-B) inhibitor
what are some examples of oral monoamine oxidase inhibitors (MOA-B)?
selegiline
rasagiline
safinamide
how do monoamine oxidase inhibitors work in parkinsons?
monoamine oxidase is an enzyme that breaks down dopamine - monoamine oxidase inhibitors prevent the action of MOA and so increase levels of dopamine
what is the benefit of using a MOA-B?
fewer adverse effects + lower risk of hallucinations
what are some examples of dopamine agonists?
ropinorole
pramipexole
rotigotine patch
what are the benefits of using dopamine agonists?
can be administered as a patch - lower pill burden
how does levopoda work?
Levodopa (L-DOPA) is a dopamine precursor that crosses the blood-brain barrier (unlike dopamine itself).
Once in the brain, it is converted into dopamine by the enzyme DOPA decarboxylase, replenishing dopamine levels in the basal ganglia.
what are the three considerations of levodopa treatment?
1) “wearing off effect” - after prolonged use, can have treatment failure where substantia nigra no longer able to store dopamine
2) “on-off” phenomenon - sudden unpredictable fluctuations in the symptoms
3) dyskinesia - SE of prolonged use for 5-10 years, due to sensitisation of the dopamine receptors
what should always be given alongisde levodopa?
carbidopa - to stop peripheral conversion of dopamine which could lead to nausea and hypotension
what medications are given prior to levodopa to prolong its use?
MOA-B inhibitors or dopamine agonists
what are the SE of MOA-B inhibitors (selegiline, rasagiline)?
insomnia
risk of serotonin syndrome if used with SSRI’s
what are the indicators for MOA-B inhibitors?
monotherapy in mild parkinsons to delay levodopa need
adjunct to levodopa use to reduce wearing off
what are some examples of dopamine agonists?
pramipexole, ropinorole, rotigotine patch, bromocriptine
how do dopamine agonists work?
directly stimulates dopamine receptors
what are the indications for dopamine agonists?
used in early parkinsons as monotherapy to delay the need for levodopa
used as an adjunct in advanced parkinons
what are some SE of dopamine agonists?
nausea, dizziness, hallucinations, confusions
can also cause impulse control changes - gambling, hypersexuality, binge eating
how do COMT inhibitors work?
MOA - block COMT which breaks down levodopa, thus prolonging its effect
what are some examples of COMT inhibitors?
entacapone
opicapone
what is the indication for COMT inhibitors use?
used ONLY when levodopa effects are wearing off as an adjunct
what are the SE of COMT inhibitors?
orange urine
diarrhoea
liver toxicity
what is the MOA of amantadine?
increases dopamine release to reduce dyskinesia
when is amantadine used?
as an adjunct to reduce the SE of dyskinesia in levodopa use
what are some SE of amantadine?
mottled skin
ankle swelling
what is an example of anticholinergic in parkinsons?
procyclidine
when are anticholiniergics used in parkinsons?
to symptomatically improve tremor in younger patients < 65 years
what are SE of procyclidine?
memory impairement, confusion, dry mouth, urinary retention, constipation
which parkinsons medications have the highest risk of hallucinations as a SE?
dopamine agonists - ropinorole, pramipexole, rotigotine patch
what is a serious risk of suddenly stopping parkinsons medications?
acute akinesia
neuroleptic malignant syndrome
what is acute akinesia?
sudden significant worsening of parkinsons symptoms due to medication withdrawal
what are the symptoms of acute akinesia?
Profound rigidity
Fever
Increased risk of infections (e.g., pneumonia, DVT/PE due to immobility)
what is the management of acute akinesia?
restart medication immediately
if severe may need ICU support
what is neuroleptic malignant syndrome?
life threatening syndrome caused by sudden withdrawal of dopamine - same as if sudden withdrawal of antipsychotics
what are the symptoms of neuroleptic malignant syndrome?
High fever
Rigid muscles (“lead-pipe” rigidity)
Altered mental state (confusion, agitation)
Autonomic instability (sweating, tachycardia, hypertension)
Rhabdomyolysis → Acute kidney injury
management of neuroleptic malignant syndrome ??
Restart dopamine medications ASAP
Supportive care (fluids, cooling, ICU monitoring)
Dantrolene (muscle relaxant) and dopamine agonists in severe cases
who can be considered for deep brain stimulation therapy for parkinsons?
This may be considered for people with advanced Parkinson’s disease with motor complications refractory to optimal medical treatment who are fit, levodopa-responsive, and have no co-morbid mental health conditions.
which medication is appropriate to use for nausea/vomiting management in parkinsons?
domeperidone
what are the risks of domeperidone?
has been associated with sudden cardiac death due to VT/VF
what should be done before starting antidepressant medication in parkinsons?
liaise with parkinsons team - some SSRI’s can increase parkinsons symptoms
what are some common SE of levodopa?
dry mouth
anorexia
palpitations
postural hypotension
psychosis
what can cause progressive ascending weakness from lower limb upwards, and loss of reflexes?
GBS
what is the pathophysiology of guillain barre syndrome?
autoimmune demyelination of the peripheral nervous system - usually treiggerd by campylobacter jejuni gastroenteritis , or can be due to vaccination/surgery trigger
what are the features of GBS?
progressive ascending weakness
loss of reflexes
vague sensory disturbance
as ascends can lead to respiratory muscle weakness
urinary retention
diarrhoea
CN involvement
what are the investigations for GBS?
LP - normal WCC
nerve conduction studies - show demyelination
what is the management of GBS?
hospital admission needed
what causes fluctuating muscle weakness that is characterised by progressive muscle fatiguability?
myasthenia gravis
what is the pathophysiology of myasthenia gravis?
autoimmune condition characterised by production of auto antibodies against acetylcholinergic receptors
what are the causes of myasthenia gravis?
most are idiopathic
associated with thymomas + autoimmune conditions such as RA
what are the symptoms of myasthenia gravis?
muscle weakness
fatiguability - the more movement done, the weaker they feel, then improves with rest
Ocular symptoms (most common) → Ptosis, diplopia.
Bulbar symptoms → Slurred speech, difficulty swallowing.
Limb weakness → Proximal muscle weakness (arms > legs).
Respiratory involvement (severe cases) → Myasthenic crisis.
how would you distinguish GBS from myasthenia gravis?
reflexes are NORMAL in MG
reflexes are ABSENT in GBS
what are the different types of MND and their corresponding symptoms?
ALS: UMN + LMN signs
Progressive bulbar palsy: bulbar signs
Primary lateral sclerosis: UMN
Progressive muscular atrophy: LMN
what is the prognosis of MND?
2-5 year prognosis after diagnosis
may vary depending on subtype
how can you distinguish MND from other conditions?
No changes in sensation
normal cognition
how quickly do the symptoms of MND progress?
over months to years
what are is the management of MND?
no cure
riluzole can be given to slow prognosis
what is the MOA of riluzole?
prevents stimulation of glutamate receptors
used mainly in amyotrophic lateral sclerosis
prolongs life by about 3 months
what respiratory interventions can be given to help prolong life in MND?
non-invasive ventilation (usually BIPAP) is used at night
studies have shown a survival benefit of around 7 months
what are some other supportive treatments that can be given for MND?
baclofen - muscle spasticity
hyoscine - drooling
PEG feeding
what is the pathophysiology of MS?
progressive autoimmune demyelination of axons in the brain and spinal cord - leading to the formation of plaques
when is the peak age for MS?
between 20-40 years
what are the common symptoms of MS?
broad presentation
optic neuritis / vision changes
problems with speech - slurred or slow
sensory changes
motor changes
urinary incontinence
sexual dysfunction
intellectual deterioration
what are some optic symptoms of MS?
optic neuritis: common presenting feature
optic atrophy
Uhthoff’s phenomenon: worsening of vision following rise in body temperature
internuclear ophthalmoplegia
what are some sensory symptoms of MS?
pins/needles
numbness
trigeminal neuralgia
Lhermitte’s syndrome: paraesthesiae in limbs on neck flexion
what are some motor symptoms of MS?
spastic weakness: most commonly seen in the legs
what are some cerebellar symptoms of MS?
ataxia: more often seen during an acute relapse than as a presenting symptom
tremor
what are the four most common presentations of MS?
optic neuritis
transverse myelitis
cerebellar-related symptoms brainstem syndromes
what are the three types of MS?
primary progressive
relapsing remitting
secondary progressive
what is relapsing remitting MS?
The most common pattern of disease. Episodes of symptoms (relapses) are followed by recovery (remissions) and periods of stability. Typically, after several relapses residual damage to parts of the CNS remains resulting in only partial recovery during remissions
what is primary progressive MS?
in PPMS there is a steady gradual worsening of the disease from the onset, without remissions. This occurs in about 10–15% of people with MS.
what is secondary progressive MS?
occurs when there is a gradual accumulation of disability unrelated to relapses, which become less frequent or stop completely. About two thirds of people with RRMS progress to SPMS.
what is the primary care management of suspected MS?
If MS is suspected, the person should be referred promptly to a consultant neurologist — only a consultant neurologist should make the diagnosis of MS.
Blood tests should be arranged to exclude some alternative diagnoses — urgent referral should not be delayed while waiting for results. An MRI scan should not be requested by the referring doctor in advance of specialist assessment.
what is the management of a suspected MS relapse?
Infections should be ruled out, particularly urinary tract and respiratory infections.
Fluctuations in disease, disease progression, and other conditions unrelated to MS that may present with similar clinical features should be considered.
The person’s MS team should be contacted promptly to discuss appropriate management. This often includes oral methylprednisolone 0.5 g daily for 5 days which may shorten the length and severity of the relapse.
what investigations are done by neurology to confirm diagnosis of MS?
CSF - oligclonal bands
MRI - hyperintense lesions
what are the indications for DMARD therapy in MS?
relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided
OR
secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)
first line treatment for spasticity in MS?
baclofen
if unable to tolerate baclofen, consider switching to gabapentin (off label)
what is transverse myelitis?
inflammation of the spinal cord at a single level
what can cause transverse myelitis?
idiopathic
infection
vaccination
autoimmune - SLE/sjogrens, sarcoidosis
MS
malignancy
vascular
what are the symptoms of transverse myelitis?
symptoms develop rapidly over days/weeks
limb weakness
sensory disturbance
bowel and bladder disturbance
back pain
radicular pain
what is ataxia telangiectasia?
autosomal recessive disorder caused by defect in ATM gene
causes progressive cerebellar ataxis
how is ataxia telangiectasia inherited?
autosomal recessive condition
what are the features of ataxia telangiectasia?
movement disorder - cerebellar signs
telangiectasia
can present with cranial nerve signs
what is ataxia telangiectasia associated with?
immune deficiency - IgE deficiency
Increased risk of malignancies
when does ataxia telangiectasia present?
between 1-5 years old
what causes Freidreichs ataxia?
autsomal recessive condition - leading to deficiency in Frataxin
what are the symptoms of Freidreichs ataxia?
cerebellar ataxia - unsteady gait, dysarthria, poor balance - starting from childhood into adolescence
what is the typical age of onset for freidreichs ataxia?
10-15 years
what is Freidreichs ataxia associated with?
HOCM
kyphoscoliosis
DM
high arched palate
what is the inherited pattern of huntingtons?
autosomal dominant
what causes huntingtons disease?
mutation of HTT gene on chr 4
leads to the formation of a toxic form of huntingtin protein which accumulates in the nervous system causing irreversible damage
at what age does huntingtons disease present?
age 30 years and over
what are the symptoms of huntingtons?
chroea - hallmark feature
dysarthria
over time can lead to rigidity and bradykinesia - like parkinsons
poor coordination
cognitive decline - poor attention, poor memory and loss of executive function
saccadic eye movements
mood changes
what is the management of huntingtons?
management of symptoms no cure
tetrabenazine can be used for chorea
atnipsychotics
antidepressants
genetic counselling - family can have genetic testing
what is the prognosis of huntingtons?
poor - life expectancy of 15-20 years after diagnosis
what is charcot marie tooth disease?
group of progressive motor and sensory neuropathies
most common inherited neurological disorder
what are the symptoms of charcot marie tooth?
progressive muscle weakness - usually affecting distal muscles of hands and legs
foot drop
characteristic “stork leg” appearance - wasting of lower limb muscles
loss of sensation in feet and hands
foot deformities
how is charcot marie tooth inherited?
autosomal dominant
what is the prognosis of charcot marie tooth?
life expectancy near normal but symptoms can progress
management of charcot marie tooth?
mainly supportive - no cure
MDT approach
what is myotonic dystrophy?
inherited disorder leading to myopathy and multi system symptoms
how is myotonic dystrophy inherited?
autosomal dominant with genetic anticipation - meaning the symptoms worsen as it is passed through the generations
what is neurofibromatosis?
Neurofibromatosis (NF) is a group of genetic disorders affecting the nervous system, skin, and other organs, leading to tumor formation along nerves.
how are neurofibromatosis inherited?
autosomal dominant - though up to 50% are de novo mutations
what are the two different types of neurofibromatosis?
NF1 (von Recklinghausen disease) – More common (~1 in 3,000), caused by NF1 gene mutation on chromosome 17.
NF2 – Rarer (~1 in 33,000), caused by NF2 gene mutation on chromosome 22.
what are the features of NF1?
≥6 café-au-lait spots
≥2 neurofibromas
Axillary or inguinal freckling (Crowe’s sign).
Optic glioma.
≥2 Lisch nodules (iris hamartomas, asymptomatic).
Scoliosis
Phaechromocytoma
First-degree relative with NF1.
what are the features of NF2?
Bilateral vestibular schwannomas
Multiple intracranial schwannomas, mengiomas and ependymomas
what is the management of NF1?
surveillance
usually need yearly BP measurement
regular eye checks
surgical removal of neurofibromas if needed
what is the management of NF2?
yearly MRI usually to monitor for vestibular neuroma formation
cochlear implant if needed
what is prognosis of NF1 vs NF2?
Nf1 - normal
NF2 - 40-50 years, as high risk for cranial tumours
what are the different types of brain tumours?
gliomas
meningiomas
pituitary adenoma
acoustic neuroma
medulloblastomas
craniopharyngioma
what is the most common type of brain tumour in adults?
secondary mets from other primary disease - typically lung, breast, GI tract, renal
what are gliomas?
cancers of the brain arising from glial cells (astrocytes, oligodendrocytes)
what are examples of gliomas?
Glioblastoma multiforme (GBM), astrocytomas, oligodendrogliomas, ependymomas
what are meningiomas?
tumours arising from the meninges
which type of brain tumour is generally slow growing with good prognosis?
meningioma
which type of brain tumour arises from the cerebellar vessels?
cerebellar haemangioblastoma
which type of brain tumour causes bilateral hemianopia and why?
pituitary tumour
compresses the optic chiasm
what type of brain tumour causes bilateral sensorineural hearing loss?
vestibular schwannoma
what is a vestibular schwanoma?
arises from schwann cells in VIII nerve
which type of brain tumour arises from the cerebellum?
medulloblastoma
which type of brain tumor is common in children?
medulloblastoma
what is the prognosis of medulloblastoma?
highly aggressive but responsive to treatment
who does idiopathic intracranial hypertension commonly affect?
overweight young females
what medications increase the risk of IIH?
combined oral contraceptive pill
steroids
tetracyclines
retinoids (isotretinoin, tretinoin) / vitamin A
lithium
what are the symptoms of IIH?
headache
blurred vision
papilloedema (usually present)
enlarged blind spot
sixth nerve palsy may be present
pulsatile tinnitus
what is the management of IIH?
weight loss - most effective treatment if obese
acetazolamide - reduces CSF production
topiramate is an alternative to acetazolamide
regular opthalmology review
CSF shunting if severe
what are the characteristic features of tension type headache?
often described as a ‘tight band’ around the head or a pressure sensation. Symptoms tend to be bilateral, where as migraine is typically unilateral
tends to be of a lower intensity than migraine
not associated with aura, nausea/vomiting or aggravated by routine physical activity
may be related to stress
may co-exist with migraine
what is the definition of chronic tension type headache?
> 15 headaches per month
acute management of tension type headache?
simple analgesia
what is the management of chronic tension type headache?
accupuncture - is a licensed treatment for tension headaches
consider amitriptyline for prophylaxis
if no improvement - refer to headache clinic
which medications are more high risk for medication overuse headache?
frequent use of triptans + opioids
management of medication overuse headache?
simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)
opioid analgesics should be gradually withdrawn
characteristics of migraine?
a severe, unilateral, throbbing headache
associated with nausea, photophobia and phonophobia
attacks may last up to 72 hours
patients characteristically go to a darkened, quiet room during an attack
‘classic’ migraine attacks are precipitated by an aura
these occur in around one-third of migraine patients
typical aura are visual, progressive, last 5-60 minute
what are some common triggers for migraine?
tiredness, stress
alcohol
combined oral contraceptive pill
lack of food or dehydration
cheese, chocolate, red wines, citrus fruits
menstruation
bright lights
how many “migraine” attacks are required for diagnosis of migraine?
5 attacks required to fulfil criteria
how can medication overuse headache be avoided?
restricting acute medication use to 2 days a week
what is the initial management of acute migraine?
Ibuprofen (400 mg) — if ineffective, consider increasing to 600 mg or
Aspirin (900 mg) or
Paracetamol (1000 mg).
These treatments should be used for 1 dose, and should be taken as soon as migraine symptoms develop.
what is the second line management of acute migraine?
add in triptan -
sumatriptan 50-100mg first line, can take first dose at onset of aura / symptoms, and second dose if still ongoing after 2 hours
+ Consider offering an anti-emetic (such as metoclopramide 10mg or prochlorperazine 10mg) in addition to other acute medication, even in the absence of nausea and vomiting.
what are contraindications to prescribing triptans?
HTN
angina
on MOA-B
TIA
severe hepatic impairement
what are some side effects of taking triptans?
triptan sensations’ - tingling, heat, tightness (e.g. throat and chest), heaviness, pressure
who should be referred to secondary care with migraine?
A complication of migraine has developed.
Atypical symptoms (such as motor weakness or poor balance) are present.
The diagnosis of migraine is uncertain.
Optimal treatment in primary care does not adequately control the symptoms (medication overuse headache should be considered).
what are some complications of migraines?
QOL significantly impaired
progressed to chronic migraine
increased risk of stroke
depression
poor control of symptoms
when should you consider migraine prophylaxis in adults?
Migraine attacks have a significant impact on quality of life and daily function; for example, they occur frequently (more than once a week on average) or are prolonged and severe despite optimal acute treatment.
what can be used for migraine prophylaxis?
propranolol
candesartan
amitriptyline
topiramate
why should COCP be avoided in patients with migraine with aura?
increased risk of vascular events
what should be offered to women with migraines associated with menstrual cycle?
off label:
Frovatriptan (2.5 mg twice daily) on the days migraine is expected or from two days before until three days after bleeding starts.
Zolmitriptan (2.5 mg twice or three times daily) on the days migraine is expected or from two days before until three days after bleeding starts.
what are the symptoms of cluster headache?
intense sharp, stabbing pain around one eye
pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours
the patient is restless and agitated during an attack due to the severity
clusters typically last 4-12 weeks
accompanied by redness, lacrimation, lid swelling
nasal stuffiness
miosis and ptosis in a minority
how often do attacks of headaches typically happen in cluster headaches?
typically happen once a year
primary care management of cluster headache?
if suspected - refer to neuro ugrently, needs specialist management and imaging to r/o underlying lesion
offer -
subcut sumatriptan
sumatriptan nasal spray
zolmitriptan nasal spray
home oxygen can be organised with HOOF form - for short bursts ofhigh-flow 100% oxygen at a flow rate of 12–15 litres per minute via a non-rebreather face mask for 15 to 20 minutes
what are some triggers of cluster headaches?
alcohol
stress
smoking
diet
anxiety
when should a patient with bells palsy be referred to ENT urgently?
if no improvement in symptoms for 3 weeks
what is the definition of epilepsy?
At least two unprovoked seizures occurring more than 24 hours apart.
One unprovoked seizure and a probability of further seizures similar to the general recurrence risk after two unprovoked seizures, occurring over the next 10 years.
Diagnosis of an epilepsy syndrome.
what features suggest a tonic seizure?
Short-lived (less than 1 minute), abrupt, generalised muscle stiffening with rapid recovery
what features suggest a generalised tonic clonic seizure?
Generalised stiffening and subsequent rhythmic jerking of the limbs, urinary incontinence, tongue biting
what features suggest atonic seizure?
Sudden onset of loss of muscle tone
what features suggest myoclonic seziure?
Brief, ‘shock-like’ involuntary single or multiple jerks
what lifestyle advice should be given to patients whilst awaiting assessment in first fit clinic?
To stop driving while waiting to see the specialist for confirmation of the diagnosis, to avoid potentially dangerous work or leisure activities (for example working with heavy machinery or at heights, or swimming), and to be mindful of safety in the home (for example showering rather than taking baths), and at school.
About lifestyle factors that may lower the seizure threshold and make recurrence more likely, for example sleep deprivation and the use of alcohol and social drugs.
To take a witness of the seizure to the first hospital appointment, if possible.
To contact their GP if further episodes occur while they are waiting to see the specialist
how should active seizure be treated in the community whilst awaiting paramedic arrival?
place in recovery position
clear the area
watch the clock
buccal midazolam or rectal diazepam
when can you consider tapering and stopping epilepsy medication?
patient who has been seizure free for 2 years - needs to be guided by specialist input
what is the DVLA guidance re driving following first seizure?
no driving for 6 months
if no structural abnormalities on imaging or EEG changes
can be increased to 12 months if the above do find abnormalities
what is the DVLA guidance around driving with established epilepsy?
no driving for 12 months post last seizure
if seizure free for 5 years can consider until 70 years license
what is the DVLA guidance around driving whilst in the process of withdrawing epilepsy medications?
cannot drive during and until 6 months post withdrawal if no seizures present
what is the MOA of sodium valproate?
increases GABA activity
P450 inhibitor
what are some of the adverse effects of sodium valproate?
highly teratogenic
alopecia - curly hair regrowth
tremor, ataxia
liver toxicity, thrombocytopenia, pancreatitis, hyponatraemia
weight gain and increased appetite
what are the teratogenic effects of sodium valproate?
neural tube defects
global developmental delay
what is lamotrigine used for?
epilepsy
bipolar disorder
what are some adverse effects of lamotrigine?
rash - common, 10%
SJS - rare, serious
leukopenia, thrombocytopenia, anaemia
suicidal ideation
what are the indications for the use of carbamazepine?
BPD
epilepsy
trigeminal neuralgia
what are some adverse effects of carbamazapine?
dizziness and ataxia
drowsiness
headache
visual disturbances (especially diplopia)
Steven-Johnson syndrome
leucopenia and agranulocytosis
hyponatraemia secondary to syndrome of inappropriate ADH secretion
what are some initial acute SE of pnehytoin?
dizziness
nystagmus
slurred speech
ataxia - sx of being drunk!
what are some chronic SE of phenytoin?
coarse features
hirstuism
gingival hyperplasia
megaloblastic anaemia
osteomalacia
lymphadenopathy
what are the teratogenic effects of phenytoin?
cleft palate
congenital heart defects
which antiepileptic is associated with the least teratogenic effects?
lamotrigine - however least effective usually at controlling epilepsy so dose may need to be increased
can women who are taking antiepileptics breasftfeed?
yes - generally they can
what dose of folic acid should women who have epilepsy who are thinking of getting pregnant take?
5mg
can women with epilepsy take any contraceptive?
no - there are guidelines around which medications are most appropriate depending on their current antiepileptics. Across all epileptics Depo-Provera, IUD and IUS are generally considered the safest.
which of the antiepileptic medications require monitoring of blood levels during pregnancy?
phenytoin
lamotrigine
oxcarbazapine
what medication can be given for functional tremor?
Propranolol 40 mg twice daily
how long should contact sports be avoided following a mild head injury?
rest for 72 hours
avoid contact sports for 3 weeks
which medications commonly cause a tremor?
salbutamol, ciclosporin, haloperidol, lithium and sodium valproate
what dietary change can be made to improve parkinsons when taking levodopa?
protein redistribution diet - take protein in the evening - thought to improve efficacy of levodopa
what is diabetic amyotrophy?
painful motor mononeuropathy which commonly involves the femoral nerve - causes wasting and weakness of the quad muscle
what type of neuropathy does phenytoin cause?
symmetrical sensory neuropathy
what is the minimum length of time for a headache diary?
8 weeks
what are the symptoms of bells palsy?
unilateral weakness - entire face
changes in taste
ear pain / hyperacusis
lacrimation
which discs herniate most commonly in cauda equina?
L4/L5
which is the only anti-emetic to use in parkinsons?
domeperidone
what are the symptoms of third nerve palsy?
eye is deviated down and out
ptsosis
pupil may be dilated
what nerve palsy causes weakness of the foot on drosiflexion and foot eversion?
common peroneal nerve lesion
what two nerves does the sciatic nerve divide into?
tibial and common peroneal nerves
what medications should be given in parkinsons and alzheimers together?
acetylcholinesterase inhibitors (donepazil, rivastigmine)
memantine
what is a common SE of donepazil?
insomnia
