Neurology Flashcards
What is parkinsons disease
progressive reduction in dopamine in the basal ganglia
- describe the typical patient that gets parkinsons
- what is the typical onset of parkinsons like
old man
gradual onset of symptoms
Is parkinsons symmetrical or asymmetrical?
asymmetrical
What is the triad of parkinsons
resting pill-rolling tremor (tremor worse at rest) 3-5Hz
cogwheel rigidity (resistance against passive movement in the form of jerky resistance)
bradykinesia (slow movement)
BRAT (bradykinesia, rigidity and tremor)
What are the other characteristics of parkinsons outside of the triad 5
shuffling gait
stooped posture
reduced arm swing on one side
smell (loss of)
facial masking (not using facial muscles as much to express themselves)
5 Ss
Does parkinsons tremor change with alcohol and what condition is the opposite of this
no change
benign essential tremor improves with alcohol
what are the three main parkinsons plus syndromes and what does this term mean?
- multiple system atrophy
- dementia with Lewy bodies
- parkinsonian dementia
-> disorders with the triad of Parkinson’s disease but with additional features
What is the difference between lewy body dementia and parkinsonian dementia
When dementia is experienced within a year of the parkinsonian symptoms, a diagnosis of Lewy body is made
If longer than a period of a year, then it is Parkinsons dementia
what is multiple system atrophy as a parkinsons plus syndrome 4 and what is its pathophysiology 1
parkinsons symptoms eg bradykinesia and tremor PLUS autonomic dysfunction eg urinary incontinence and postural hypotension PLUS cerebellar dysfunction eg poor balance and gait PLUS reduced speech ability due to weakness
Damage of the nerves- no known causes
how is parkinsons diagnosed and how is this diagnosis regulated
clinical diagnosis with bradykinesia plus one of the following:
rigidity
resting tremor
posturla instability
6/12 month regular reviews of diagnosis
How can an essential tremor be clinically differentiated from parkinsonian if it is not clear from clinical hx/ examination
single photon emission computed tomography
will show reduced dopamine activity in parkinsons
what is the first line treatment for parkinsons where motor symptoms are affecting their life?
levodopa combined with benserazide or carbidopa
co- beneldopa /co-caroldopa
what is the first line treatment for parkinsons where motor symptoms are NOT affecting their life? 3
dopamine agonist/ levodopa/ MAO B inhibitors
What is the treatment for parkinsons where levodopa therapy has not worked and parkinsons has progressed
add dopamine agonist/ MOA B inhibitor/ COMT inhibitor
How does levodopa work?
it is a synthetic dopamine
What are 2 common combination drugs for Parkinsons and what is their mode of action and why is it combined?
co-beneldopa (levodopa and benserazide)
co-careldopa (levodopa and carbidopa)
carbidopa and benserazide are both peripheral decarboxylase inhibitors (which stop the metabolism of levodopa in the body before it reaches the brain)
What is the main side effect of levodopa?
dyskinesia (abnormal excess movements) eg dystonia (sustained muscle contration= noticeable abnormal postures) and chorea (discrete jerky movements)
What can mitigate the main side effect of levedopa and its mode of action?
amantadine
glutamate antagonist
which manages dyskinesia associated with levodopa
How do COMT inhibitors work for parkisons and give an example
inhibit catechol-o-methytransferase which metabolises levodopa in the body
eg entacapone
how do dopamine agonists work for parkinsons and give examples. How is it used in medicine and its main SE
mimic dopamine action by stimulating dopamine receptors
eg ropinirole (non-ergoline)
used with levodopa to reduce its dose required
SE: ergoline dopamine agonists eg bromocriptine/ cabergoline can cause pulmonary fibrosis with long term use
How does MAOB inhibitors work for parkinsons and give examples.
blocks monoamine oxidase B enzymes and whose regular function is to breakdown dopamine= increase circulating dopamine
eg rasagiline or selegiline
What treatment should be given for parkinsons if symptoms are not controlled by medical therapy (NOT FIRST LINE)
deep brain stimulation via a electrical current
Complications of having parkinsons 2
recurrent falls due to motor issues
cognitive impairment
if cognitive impairement is identified early in parkinsons, what can help
Acetyl cholinesterase inhibitors eg rivastigmine or donepezil
What are the visible pathological changes for Alzheimer’s disease on an MRI 3
macroscopic: widespread cerebral atrophy
microscopic: deposition of beta amyloid protein plaques and increase of neurofibrillary tangles
What is the protein called that makes up the neurofibrillary tangles and what happens in Alzheimer’s
tau
excess phosphorylation of tau, impairing the normal function of tubulin in cetromeres
What are the 3 main clinical features of Alzheimer’s and explain characteristics of each
cognitive impairment: memory loss of more recent events, finds it hard to make decisions, nominal dysphasia (unable to identify objects/ people) but normal speech otherwise
dementia symptoms: agitation, apathy, depression
difficulties with ADLs: progresses from difficulty tasks to simple tasks like getting dressed
What is the non pharmacological treatment of Alzheimer’s 2
-> offer cognitive stimulation therapy
-> offer activities that the person prefers
What is the pharmacological treatment of Alzheimer’s disease?
- acetylcholinesterase inhibitors eg donepezil and rivastigmine for mild to moderate
- second line/ severe Alzheimer’s= add on NMDA receptor antagonist memantine
Should antidepressants and antipsychotics be given to Alzheimer patients according to NICE
antidepressants only for severe depression
antipsychotics only for patients at risk of harming themselves/ others or when hallucinations/ delusions cause severe distress because it can cause DEATH
SE and CI of donepezil for Alzheimer’s 1,1
SE= insomnia
CI= bradycardia
What is essential tremor and what demographic does it affect
a common neurological condition that can affect all ages and causes involuntary rhythmic shaking
What is the cause/risk factors of an essential tremor
genetic link, can pass from parents to child autosomal dominant
prevalence and severity increases with age (it is a progressive chronic condition)
what is the pathophysiology of essential tremor
increased activity of cerebello-thalamo-cortical pathway= rhythmic stimulation of neurones= rhythmic muscle contractions
What is the most common cause of intention tremor in adults?
essential tremor
Clinical features of essential tremor 3
-> intention tremor: exacerbated on intentional movements
-> bilateral but affects dominant side more
-> affects hands and arms first then progresses to head
What does the diagnostic criteria for essential tremor state
must be an absence of other neurological signs
greater than 3 years duration
What are soft neurological signs in essential tremor and give examples 2. If a patient has this how is their diagnosis changed?
other manifestations of disease
eg gait issues and cognitive impairment
essential tremor plus
Tests done for essential tremor 3
U&E- hypocalcaemia can cause tremor
TFT- exclude hypothyroidism as cause of tremor
NO brain imaging recommended unless other neurological findings suggesting other differentials to essential tremor (brain imaging is normal in essential tremor)
Treatment for essential tremor 4
1st line: propranolol or primidone
2nd line: gabapentin
surgical: deep brain stimultion into thalamus or botox injections into tremoring limbs
Typical prognosis and progression of essential tremor
the typicaly patient only experiences mild symptoms that don’t impact quality of life
however, tremor gets worse and can spread to other parts of body which impacts quality of life
What two things that are not medications that improve essential tremors
alcohol and rest
What are the 3 types of vascular dementia and explain each one
stroke related VD (single/ multi-infarct dementia)
subcortical VD (due to small vessel disease)
mixed dementia (VD plus alzhiemers)
What is vascular dementia?
Dementia caused by reduced blood flow to brain which causes major cognitive impairment
Typical progression of vascular dementia
sudden or stepwise deterioration of cognitive function over months or years
What symptoms can be included in vascular dementia 4
attention difficulties
problem-solving difficulties
gait issues
trouble with new information
How is vascular dementia diagnosed? 4
- presence of cognitive decline that affects ADL from clinical examination
- brain imaging/ neurological signs that show cerebrovascular disease
- stepwise or sudden decline
- dementia onset 3 months after a stroke
Management of vascular dementia 3
- address CV risk factors
- Non- Pharmacological: cognitive/ sensory stimulation or music/ animal assisted therapy
- Pharmacological: no specific treatment, only use Acetylcholinesterase inhibitors eg donepezil if comorbid with Alzheimers/ Lewy body/ Parkinsons
What is motor neuron disease?
neurological condition that presents with BOTH upper and lower motor neurone signs- it only involves motor symptoms so sensation will always be intact
What are the 4 types of motor neuron disease?
amytrophic lateral sclerosis
primary lateral sclerosis
progressive muscular atrophy
progressive bulbar palsy
How does amytrophic lateral sclerosis present
LMN signs in arms
UMN signs in legs
How does primary lateral sclerosis present
UMN signs only
How does progressive muscular atrophy present
LMN only
affects distal muscles then proximal
How does progressive bulbar palsy present and why
palsy of tongue, facial muscles and muscles of chewing/ swallowing
loss of function of brainstem motor nuclei
What symptoms suggest motor neurone disease?
fasciculations
mixtures of lower and upper motor neurone signs
wasting small hand muscles
abdominal reflexes intact and eye muscles preserved
Diagnosis/ investigations of motor neurone disease 3
clinical
nerve conduction studies will show normal motor conduction
electromyography shows reduced action potentials with increased amplitude
Management of motor neuron disease
- riluzole prolongs life for 3 months by preventing stimulation of glutamate receptors, usually for ALS
- non invasive ventilation BIPAP at night
- PEG for nutritional support
What is the most common presentation of ALS
asymmetric limb weakness
What are UMN signs 4
weakness/ paralysis
increased tone
increased reflexes and Babinski
NO muscle wasting
What are LMN signs 4
weakness/ paralysis
decreased tone
decreased reflexes and Babinski
rapid muscle wasting
LMN forehead sparring
What is multiple sclerosis and the official criteria for diagnosis
when immune system attacks myelin in CNS
McDonalds criteria: 2 episodes of autonomic neurological dysfunction separated in space and time
What are some risk factors of MS 3
female
smokers
family history
What is the histopathological character of MS 3
loss of oligodendrocytes
widespread demyelination
loss of axons in white matter
Symptoms of MS 12
demyelination
D-Diploplia
E-Eyes: painful movement and vision loss/ colour blindness
M-Motor: general weakness and high tone spasticity
Y-nYstagmus
E-Emotion: depression and anxiety mood disorders
L-Lhermitte’s phenomenon (neck flexion= shock radiating down spine)
I- Impotence (erectile dysfuction/ loss of libido)
N-Neuropathic pain
A-Ataxia
T-Talking slurred due to weak bulbar muscles and difficulty swallowing
I-Intention tremor of upper limb
O-Overactive bladder
N-Numbness
Types of MS 3
- relapsing remitting: acute attacks for 1/2 months followed by periods of remission, after each attack they’re never back to the same baseline
- secondary progressive: relapsing remitting patients develop into progressive primary patients with progressive deterioration and no relapses
- primary progressive: progressive deterioration from onset, less common, seen in older people, no remissions
Investigations for MS 5
1st line: bloods (NICE recommends FBC, inflammatory markers, LFTs, U&E, calcium, glucose, TFTs, B12, HIV serology)
when normal bloods and likely clinical picture of MS then:
1. refer to consultant neurologist
2. MRI brain
3. MRI spine to confirm MRI brain
CSF exam required when still not enough evidence, atypical MS demographic or atypical investigations: will show oligoclonal bands and increased igG synthesis
How is MS diagnosed for relapsing remitting
relapsing remitting:
-> MRI shows lesions disseminated in time and space AND hypotense T2 lesions
How is MS diagnosed for primary progressive
primary progressive:
1+ years of progression of disability AND two of the following:
1+ T2 hypertense lesions in brain
2+ T2 hyertense lesions in spinal cord
Presence of CSF-specific oligoclonal bands
how is MS acute relapse managed 1 and why 1. What does this drug not do 1
acute relapse: high dose IV/ oral meythlpred given for 5 days to shorten the duration of the relapse
change whether the px returns to baseline function
What drug reduces the risk of relapse in MS patients with relapsing remitting
IV natalizumab
how is fatigue in MS specifically treated 2
- amantadine
- CBT
how is spasticity in MS specifically treated 3
1st line: baclofen and gabapentin
physiotherapy is also very important alongside
how is bladder dysfunction in MS specifically treated 3
- US of bladder emptying
- if no significant residual volume, anticholinergics can improve urinary frequency eg oxybutynin
- if significant residual volume, intermittent self-catheterisation
complications of MS 3
recurrent UTIs
cognitive impairment
motor limitations
What is muscular dystrophy?
genetic disease that causes progressive weakness and degeneration of skeletal muscles
What are the three types of muscular dystrophy
Beckers, Duchennes and myotonic
What is the genetics for beckers and duchennes muscular dystrophy
x-linked recessive disorder (affects mostly males)
mutation of gene coding for dystrophin on chromosome 21
duchenne= framshift mutation= severe form
becker= non frameshift insertion= milder form
What is the symptoms of duchenne/ beckers muscular dystrophy 4
- proximal muscle weakness
- gait abnormalities
- motor milestones delayed
- Gower’s sign: child uses arms to stand up from a squatted position
What age does duchennes and beckers muscular dystrophy occur
3-5 years= Duchennes
10-15 years= Beckers
Ix for duchennes and beckers muscular dystrophy 2
CK (usually raised)
genetic testing to confirm diagnosis
Mx of duchennes and beckers muscular dystrophy 1
- oral pred to improve muscle function
Prognosis for duchennes and beckers muscular dystrophy 1
Many patients now live into their 30s.
What is the genetics of huntingtons inheritence and what mutation is this and what chromosome
autosomal dom
trinucleotide repeat of CAG, chromosome 4
What is the pathophysiology of Huntingtons
mutation causes degeneration of cholinergic and GABAnergic neurones in the striatum of basal ganglia
What are the symptoms of huntingtons 5
chorea (involuntary jerking movements)
personality changes (irritability and apathy)
intellectual impairment
dystonia (uncontrollable painful muscle spasms)
saccadic eye movements
What is the prognosis 1 of huntingtons
familial- anticipation where disease presents at earlier age going thorugh generations and with increasing severity
What is the mx of huntington patients
MDT
tetrabenazine for chorea
SSRI for depression
How is huntingtons diagnosed 3
combination of:
genetic testing (for CAG repeats 36+ is definately Huntingtons)-> definitive diagnosis
family history
can do neuro MRI to see if there is striatial atrophy but this is not specific to huntingtons only)
What is a brain abscess
pus filled pocket in the brain
What are the casues of brain abscesses 3
sepsis
neurosurgery
trauma
What are the clinical features of brain abscesses 4
headache (dull and progressively worsening, localised to site of abscess)
focal neurological deficits
fever
symptoms of raised ICP: nausea, seizures, papilloedema
Why is it hard to identify a brain abscess based on its symptoms 2
Non specific symptoms
Symptoms can mimic other neurological conditions
How are brain abscesses diagnosed 1
MRI with contrast
What is contraindicated for a brain abscess and why
LP- due to risk of brain herniation
What is the management for a brain abscess
- craniotomy + abscess drained
- IV antibiotics: ceftrioxone + metronidazole 9metronidazole convers for anaerobic species)
- intracranial pressure management: e.g. dexamethasone
What is the risk of craniotomy for draining brain abscesses
the abscess may reform because the head is closed following abscess drainage.
What are the complications of brain abscesses 4
seizures
meningitis
hydrocephalus
herniation
What is Guillain Barre syndrome
immune mediated demyelination of peripheral nervous system after an infection- usually campylobacter jejuni
what is the pathophysiology of Guillain Barre
antibodies to current infection react with the gangliosides in the peripheral nervous system
Type 4 reaction
anti-GM1 antibodies found in 25% patients
Symptoms of guillain barre
-progressive weakness of all four limbs, affecting the legs first and in a proximal to distal pattern
-mild sensory symptoms eg distal paraesthesia
-can be autonomic involvement eg urinary retention, respiratory muscle weakness and cranial nerve involvement eg oropharyngeal weakness
What is important to ask the patient in guillain barre 1
history of gastroenteritis/ diarrhoeal illness a few weeks before onset of symptoms
Investigations for guillain barre syndrome 2
- lumbar puncture (CSF has normal WCC and high protein found in 2/3 of cases)
- Nerve conduction studies show decreased motor nerve conduction velocity due to demyelination
guillain
What is the management for guillain barre 3 What is not useful for management
- plasma exchange or IV immunoglobulins
- FVC spiromtery to monitor respiratory function
- ventilatory support if needed
steroids have not proven to be beneficial in the managment of guillain barre
steroids for MG, patients with guillain barre get better (GB) without steroids
What are the risk factors for poor prognosis of guillain barre syndrome 3
over 40 years
Hx of a diarrhoeal disease
need for ventilatory support
What is meningitis and what is encephalitis
meningitis= inflammation of the meninges (3 membranes around the brain and spinal corod)
encephalitis= inflammation of the brain
What are the symptoms of meningitis (including triad 3) 2
triad:
neck stiffness
photophobia
severe headache
general symptoms: fever, rash
What is important to remember about acute meningitis and encephalitis
must be reported to Public Health England
Who is at risk of each cause of bacterial meningitis
- listeria monocytogenes: pregnant, neonates, elderly
- staph aureus: all ages
- strep pneumonia/ nissesria meningitidis: children, adults, elderly
- group B strep agalactaie: neonates from mother’s genital tract
- cyrtococcus neoformans: immunocompromised
What are the causes of meningitis 2, 6
viral:
enterovirus eg Coxsackie virus
herpes virus
bacterial:
listeria monocytogenes, staph aureus, S pneumoniae, N meningitidis, group B strep, cyrococcus neoformans
Who is most at risk of chronic meningitis 1 and what does this appear as on imaging 1
immunocompromised eg TB
brain covered with green grey exudate
compare symptoms of viral and bacterial meningitis
bacterial: suddent onset, papilloedema, reduced GCS, vomiting
viral: self limiting 1 week and headache for months after
investigations for meningitis 3
- blood cultures
- black and green throat swabs
- lumbar puncture within an hour in order to give abx within an hour timeframe (IF no signs of raised ICP)
What does a non blanching purpuric rash indicate for meningitis
meningococcal septicaemia caused by N meningitis/septicaemia
What is the treatment for meningitis 5
-community: IM/IV benxylpenicillin then bring into hospital ASAP
-hospital: IV cefotaxime (+ vancomycin in travellers, + amoxicillin in neonates and elderly)
-then IV dexamethasone to prevent neurological complications
-anyone in contact with in past 7 days should be given single dose oral ciprofloxacin prophylaxis
-if penecillin allergy, give chloramphenicol
Compare the LP results for bacterial, viral and fungal/TB microorganisms
bacterial: cloudy, low glucose, high protein, neutrophils, high opening pressure
viral: clear, normal/ raised protein, high glucose lymphocytes
fungal/TB: clear, low glucose, high protein, lymphocytes
What are the normal values for CSF
appearance: clear
opening pressure 90-180
WBC <8
protein 15-45
glucose 50-80
What are the symptoms of encephalitis 4 and what is its onset like 1
compare to meningitis sx
fever, headache, altered mental status/ personality change, neurologial focal features eg aphasia in HS1 (HS1 usually affects temporal lobes)
gradual onset
vs meningitis: no photophobia, more likely to have AMS, onset is more gradual, commonly associated with seizures
Investigations for encephalitis 3
PCR of CSF for HSV 1
CT/ MRI: medial temporal and inferior frontal changes (petechial haemorrhages )
CSF: high lymphocytes, high protein
EEG: lateralised periodic discharges at 2 Hz
main cause is HSV1, so testing mainly for this, otherwise VZV is another cause
treatment for encephalitis 1
IV acyclovir in suspected encephalitis
What is the main cause of encephalitis 1
Herpes simplex virus 1
What is chickenpox caused by and what type of infection is this
primary infection with varicellar zoster
How can chickenpox be spread and who from
respiratory droplets
from both people with chickenpox and shingles
When is someone with chickon pox infective
infective 4 days before rash appears to 5 days after rashes first appeared
What is the incubation period of varicella zoster in chickenpox
21 days
what are the symptoms of chickenpox 3
fever
itchy rash on head/ trunk then spreading
rash: macular-> papular-> vesicular-> crusting over
Management for chickenpox 4
- conservatively at home (kids shouldn’t go to school until lesions crusted over!!)
- calamine lotion and chlorphenamine for itching
- aciclovir if severe
- varicella zoster immune globulin vaccine for prophylaxis of close contacts who are immunocompromised (if they get chickenpox then start acyclovir)
Management for chickenpox in immunocompromised 2
varicella zoster immunoglobulin vaccine for prophylaxis of close contacts who are immunocompromised (if they get chickenpox then start acyclovir)
Complications of chickenpox
in paeds: secondary bacterial infection of lesions, causing cellulitis or group A strep invasion causing necrotizing fasciitis
in adults: viral pnuemonia
What is shingles and its presentation
rash caused by reactivation of the Varicella Zoster Virus
characteristic single dermatome distribution
Compare age epidemiology for chickenpox and shingles
shingles: 70+
chickenpox: 6-15
where does varicella zoster lay dormant until reactivation into shingles 2
dorsal root or cranial nerve ganglia
What type of virus is varicella zoster
double stranded DNA herpes virus
Explain the symptoms of shingles throughout its difference stages
PRODROME:
2-3 days long
acute neuralgia (nerve pain=tingling/ burning/ itching)
INFECTIOUS STAGE:
10-12 days
rash: across single dermatome, unilateral, macular-> papular-> vesicular-> pustular-> crusting
pain: around rash area
RESOLUTION:
crusted lesions take 1 months to disappear
Management of shingles 3
- analgesia: paracetamol/ ibuprofen first line and go up pain ladder (step up and use amitryptyline or gabapentin/ pregabalin instead)
- calamine lotion
- oral aciclovir antiviral within 72 hours rash onset (can be considered up to a week) alongside corticosteroids- only taken for 2 weeks (only if bad pain, immunocompromised, over 50 years old or affects limbs/ face)
What are the complications of shingles 4
- post-herpetic neuralgia: persistant pain where rash was despite resolution
- herpes zoster opthalmicus: CN5 involvement involves CN5- opthalmic branch palsy and causes a rash on eye and potentially vision loss
- Ramsey Hunt syndrome: CN7 involvement causes lesions in ear and facial paralysis
- encephalitis
Tell me about the shingles vaccine 3
offered above 70-79 years old
live attenuated so CI for immmunosuppressed
What are the most commonly affected dermatomes in shingles
T1 to L2 (torso and front groin area)
What causes malaria and how is this spread
Palsmodium protozoa
female Anopheles mosquito
What are the four species of plasmodium, which is the most common and which is the most severe
Plasmodium falciparum
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
common: vivax
severe: falciparum
What are the protective factors for malaria 2
sickle cell
G6PD deficiency
What is the pathophysiology of malaria plasmodium 6
- mosquito bite injects sporozoites into the bloodstream
- sporozoites go to liver where they asexually reproduce and mature in schizonts
- schizonts rupture from liver cells and release merozoites
- merozoites infect RBC, multiply and burst out of them
- both male and female gametocytes are produced
- mosquito picks gametocytes when taking a blood meal and these sexually reproduce in the mosquito
(sexual reproduction via male and female gametocytes which releases sporozoites- only occurs in mosquito)
Which two species of plasmodium remain dormant and how
vivax and ovale
lay hyponozoites in liver which remain dormant for many years
What are the symptoms for malaria 6
- fever patterns accompanied by chills
- GI symptoms: nausea, vomiting, diarrhoea, abdo pain
- neuro: altered mental state
- GI organs: splenomegaly and AKI
- jaundice
- non specific symptoms: headache and fatigue
Malaria Fights GNASTY
mental state altered
fever plus chills
gi sx
non specific: headache
aki
splenomegaly
tiredness
yellowing (jaundice)
Investigations for malaria 3
GS: blood film
-> thick for sensitivity to malaria
-> thin to determine species
bloods: normocytic anaemia, thrombocythaemia (high platelets)
What are the types of malaria categorisation and explain each 6,4
complicated:
- severe malaria that can cause organ failure
- usually associated with P falciparum
-Parasitaemia >2%
- schizonts in blood smear
-complications
-patient not walking
uncomplicated:
-no fever
-no complications
-walking patient -Parasitaemia <2%
What is the treatment for uncomplicated malaria 1
6 doses artemether + lumefantrine
Why are there many complications in complicated malaria and give examples 3
due to adherence of schizonts and sequestration of erythrocytes to the vascular endothelium
= DIC, AKI, severe anaemia
What is the treatment for complicated malaria 1
IV artesunate
then once stable: artemether + lumefantrine
What are the 2 drugs for malaria prophylaxis and how are they taken, any contraindications, SE
atovaquone +proguanil (malarone) start 2 days before travel and end 7 days after travel
taken OD
avoid in pregnancy
SE: GI upset
doxycycline
start 2 days before adn end 4 weeks after
taken OD
avoid in under 12
SE: oesophagitis
What can be used to repel mosquitos and has shown to repel up to 100% mosquitos if used correctly 1
what is the advantage of this 1
DEET containing spray
can be used for children over 2 months old
What are migraines and features 2,3,2
Unilateral Recurrent, severe headaches
Prodrome: Aura (zigzag lines/ flashing lights), mood swings
ictal: severe unilateral headache +/- photophobia, N+V
post ictal: drowsy and fatigue
What are the triggers of migraine 9
MIGRAINED:
menstruation, insufficient sleep, glare (bright lights), red wine, anxiety and stress, irregular/ skipping meals, nitrates, chEEse and chocolatE, dehydration
What is the management for migraines
acute: sumitiptan combined with either NSAID or paracetomol
prophylaxis: propranolol or topiramate if asthmatic (topiramate avoided in pregnant women so pregnant asthmatic women give amitryptylline)
What are tension headaches
recurrent, bilateral headaches like a tight band
What is the management for tension headaches
acute: aspirin/ paracetomol/ NSAID
prophylaxis: amitriptyline
What are cluster headaches
Each attack is around 15 min to 3 hours
Intense pain around one eye + lacrimation, lid swelling
What is the treatment for cluster headaches
Acute: high flow O2 + subcut triptan
Prophylaxis: Verapamil (Cluster=CCB)
Temporal/ Giant cell Artritis features 4 and what is it
- Unilateral headache
- Jaw claudication (pain caused by chewing/ speaking, goes down when not using jaw)
- Tender scalp + palpable temporal artery
- in an elderly pt
medium and large vessel vasculitis
What are the ix and mx for temporal artritis
ix: raised ESR, GS= temporal artery biopsy
mx: URGENT glucocorticosteroids (prednisolone) + ophthalmology review (because they can quickly loose all of their sight)
What is trigeminal neuralgia
Unilateral electric shock pains
Evoked by light touch
What is the mx for trigeminal neuralgia
Carbamazepine
Define seizure
Seizure: sudden, uncontrolled and disorganised electrical activity in the brain that can cause temporary changes in behavior, muscle tone, and awareness
Define epilepsy
Epilepsy: a neurological disorder that causes a person to experience recurring seizures
What is the first line management for a patient who presents with an unprovoked seizure and normal bloods/ CT 2
arrange EEG
neurology referral
What is status epilepticus 2 and management 5
- Single seizure lasting more than 5 minutes
- 2 or more seizures within a 5 minute period
MX:
1. A to E
2. Pre-hospital: PR diazepam/buccal midazolam or if in hospital: IV lorazepam
3. if not resolving, give another dose of BZD after 5-10 min
4: 2nd line agent if ongoing status IV phenytoin or levetiracetam, sodium valproate
5. If reached refractory status (no response 45 mins after onset), induce general anaesthesia to achieve control of seizure activity
What seizure characteristics correspond with different lobes of the brain
Frontal lobe: Jacksonian march, head/leg movements
Parietal lobe: Paraesthesia
Occipital lobe: Floaters/Flashers
Temporal lobe: Automatisms, aura
What are the seizure characteristics with different seizure types 5
Tonic : Tensing, clenching
Atonic: Complete loss of tone, collapse
Clonic: rhythmic jerking
Myoclonic: brief muscle twitching
Tonic + clonic: rigidity then jerking (grand mal)
Absence seizure: zoning/spacing out + post-ictal confusion (petit mal)
What are the treatments for different types of epilepsy (M/F)
Focal
M Levetiracetam
F Levetiracetam
Generalised tonic-clonic
M Sodium Valproate
F Levetiracetam
Myoclonic
M Sodium Valproate
F Levetiracetam
Tonic/Atonic
M Sodium Valproate
F lamotrigine
Absence
M Ethosuximide
F Ethosuximide
generalised= encompasses Tonic, clonic, myoclonic, absence
males: sodium valproate
females: levetiracetam
except ethosuximide for absence and lamotrogine for tonic/ atonic in females
focal= seizure starts in one part of brain so lobe based symptoms, unilateral, complete/ partial awareness during seizure
levetiracetam
What is a stroke and two types
a sudden interruption in the vascular supply of the brain
ischaemic: vessel blockage
haemorrhagic: vessel bursting and bleeding
define a TIA
a transient episode of neurologic dysfunction caused by focal (brain, spinal cord, or retinal) ischaemia, without acute infarction
compare stroke and tia
TIA= sx for less than 24 hours
stroke= more than 24 hours
What are the features of a stroke/ TIA 5
- facial drooping
- UNILATERAL weakness/ sensory loss
- Slurred speech
- Swallowing problems
- Visual field defects: homonymous hemianopia/ amaurosis fugax
FUSSY (Y being a V)
Explain stroke localisation for ACA and what it supplies
Frontal + parietal lobes
Contralateral weakness and sensory loss in lower limbs
(remember this by drawing a stickman with A as its legs)
Explain stroke localisation for MCA and what it supplies and where this clot comes from
Temporal + parietal
Contralateral weakness (hemiparesis) and sensory loss in upper limbs
Aphasia if it affects wernickes area in temporal lobe
from internal carotid artery (as this directly conencts to middle cererbal artery and the clot will go down the path of least resistance with the blood flow)= this means it is the most common type of stroke
(remember this by drawing a stickman with M as its arms and yelling out YMCA- to remember this causes aphasia)
Explain stroke localisation for PCA and what it supplies
Occipital + thalamus (thalamus processes visual information)
Contralateral homonymous hemianopia with macular sparing
Visual agnosia (seeing a picture of a cat, recognising its a cat but unable to say that it’s a cat)
(drawing two Ps as sunglasses on a stickman)
Explain stroke localisation for Webers syndrome, what it supplies and who is affected
PCA branches supply the mid brain, sepcifically the Cerebral peduncle
Ipsilateral CN III palsy AND
Contralateral weakness in arm and leg
Explain stroke localisation for Posterior Inferior Cerebellar Artery and what it supplies
Brainstem + cerebellum
Ataxia, nystagmus (any cerebellar signs)
Pain and temperature loss: ipsilateral for face, contralateral for limbs (spinothalamic tract)
ipsilateral horners
Explain stroke localisation for Anterior Inferior Cerebellar Artery and what it supplies
Brainstem + cerebellum + **dura of internal acoustic meatus **
Ataxia, nystagmus
Pain and temperature loss: ipsilateral for face, contralateral for limbs (spinothalamic tract)
Deafness +
Facial paralysis (branches can compress the facial nerve)
Explain stroke localisation for ophthalmic artery, where does the artery come from and what it supplies
branch of hte internal cortid artery
supplies Optic nerve
blockage= Amaurosis fugax (darking of vision in one eye)
Explain stroke localisation for Basilar artery and what it supplies
Ventral pons of the brainstem (neuronal pathways between your cerebrum, spinal cord and cerebellum)
Locked-in syndrome- paralysis of all muscles except for eyes
What is a lacunar stroke and features
occurs when an artery that supplies blood to the deeper portions of the brain ie subcortex (thalamus, basal ganglia)
sensory loss/ weakness BUT intact awareness and speech
the sensory loss/ weakness will be one of the following
pure motor stroke (C/L weakness but no sensory defecit)
pure sensory stroke (C/L sensory loss but no motor weakness- involves thalamus as this processes sensory information, thalamus= THenTHory information)
sensorimotor stroke= C/L sensory loss and weakness of arms and legs
What is the Oxford Bamford classification
System that classifies strokes based on the initial systems
LOOK SPEAK MOVE:
Homonymous hemianopia
Dysphasia (or other higher cognitive dysfunction)
Weakness/sensory loss
All 3 = total anterior infarct (anterior + middle cerebral arteries)
⅔ = partial anterior infarct
ONLY weakness/ONLY sensory loss = lacunar infarct
ONLY homonymous hemianopia = posterior circulation infarct
What are the first ix for stroke in the ER
- Rosier’s tool for stroke (in ER) (U/L face, arm, leg, speech issues and vision issues all +1 point and LOC and seizure activity -1 each) a score of greater than 0 indicates stroke
- non contrast CT head 1st line
How is a TIA managed?
*Step 1: exclude hypoglycaemia and haemorrhage with MRI imaging *
Step 2: When did the suspected TIA occur?
Within 7 days→
*300mg aspirin * + specialist assessment within 24h
-> This involves carotid artery doppler imaging within 24 hours- if intervention needed then carotid endarterectomy done within 7 days
More than 7 days ago → specialist assessment within 7 days
Step 3: Secondary prevention
Initial 21 days: dual antiplatelet therapy with aspirin 75 + clopidogrel 75 (PLUS PPI!)
Long-term prevention: clopidogrel
If AF: DOAC
+ high-dose statin 80mg
Driving:
Single TIA: don’t drive for 1 month, no need to inform DVLA
Multiple TIAs: don’t drive for 3 months, notify DVLA
Stroke: don’t drive for 1 month, no need to inform DVLA
How is a stroke managed
Step 1: Rule out haemorrhage with CT (hyperdense collection meaning lighter on CT)
Step 2: aspirin 300mg IF AFTER 24 hours
Step 3: Is patient presenting within 4.5h of stroke?
If YES → thrombolysis IV alteplase
If NO → no thrombolysis unless CT shows potential to salvage brain tissue, in which case, thrombolysis allowed within 9 hours of sx onset
Step 4: Is patient presenting within 6h of stroke?
Perform CT/MR angiography: if proximal anterior circulation occlusion confirmed → mechanical thrombectomy
Step 5: Is patient presenting within 24h of stroke?
Perform CT/MR angiography: if proximal circulation occlusion confirmed AND potential to salvage brain tissue → mechanical thrombectomy
Step 6: Is stenosis in carotid artery >50% ?
** consider carotid endarterectomy**
Step 7: secondary prevention
Clopidogrel 75mg OD (this is postponed to 24 hours after any alteplase/ mechanical thromebctomy is done to reduce the risk of bleeding)
simvaastatin high dose 80mg
If AF → DOAC
T2DM control, HTN control
What is mononeuritis multiplex and appropriate mx
stand alone episodes of neuropathy involving both sensory and motor function (including being isolated to nerve palsies) in different areas with no pattern and gradual recovery taking a few weeks
mx= tends to be in diabetics so tighter glucose control to reduce the risk of future episodes happening and otherwise physiotherapy of affected limbs
What shape are extradural haemorrhages, location, artery affected, way of presentation, management
half lemon= lentiform (lemonform)
location: between dura and skull but cannot cross suture lines
meningeal artery (usually middle meningeal artery)
LOC (often a contact injury) then short lucid interval (improvement in condition) then LOC- in younger
Craniotomy + evacuation of haematoma
What shape are subdural haemorrhages, location, artery affected, way of presentation, management
crescent shaped
location: between dura and arachnoid- can cross suture lines
Bridging veins (veins)
hx head trauma then lucid interval (can be acute or chronic) then decreasing consciousness- in older
Conservative/surgical decompression with burr hole evacuation
What shape are subarachnoid haemorrhages, location, artery affected, way of presentation, management 3
outline of edge of entire skull shape- acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.
location: between arachnoid and pia mater
Berry aneurysms in cerebral artery (MC MCA)
Thunderclap occipital headache, meningisms (n/v, neck stiffness)
Oral nimodipine to prevent vasospasm + coil, VTW prophylaxis
what is the investigation for subarachnoid management 3
- non-contrast CT
- if CT head done after 6 hours of sx onset and is normal= do LP at least 12 hours after sx to allow the development of xanthochromia (breakdown of RBC) CSF findings= xanthochromia, normal/ raised opening pressure, raised bilirubin
- 3.if CT shows SAH evidence, urgent referral to neurosurgery and CT intracranial angiogram to identify the lesion
A 52 year old man comes in complaining of a sudden severe headache that started 12 hours ago. There is no significant past medical history. He is unsure of his family history.
On examination he is in significant pain and distress. He is not confused and neurological assessment is unremarkable. An urgent CT head is requested. It came back normal and a lumbar puncture was requested.
Given the most likely diagnosis, what are you likely to see in the LP results?
Bilirubin
Light chain and raised protein
Oligoclonal bands and Bence-Jones proteins
Oligoclonal bands and low glucose
Normal LP
Bilirubin
most likely diagnosis is subarachnoid haemorrhage= bleed in brain
blood will get broken down= bilirubin
What is a glioblastoma and what is it and effect and mx
aggressive cancer of CNS/ brainstem
solid tumours with central necrosis and a rim that enhances with contrast
Disrupts the blood-brain barrier and therefore are associated with vasogenic oedema- treated with dexamethasone
What is vestibular schwannoma and Sx 2
cancer of vestibulocochlear nerve CN8
Sx: ipsilateral hearing loss + facial nerve palsy CN 7
What is the most common cancer in children and sx 5
astrocytoma
Sx: increased ICP sx n/v, weakness/ gait/ visual disturbance (similar to stroke symptoms in a kid)
(Increase ICP cushings triad- bradycardia, irregular bradypnoea and hyPERtension)
do MRI as LP is CI here- 48 hour referral
What is Meniere’s disease and its features
fluid build up in inner ear
- recurrent episodes of vertigo, tinnitus and hearing loss from minutes to hours
- starts off unilateral sx then after years becomes bilateral
What is the Mx for Meniere’s disease 4
- ENT assessment for diagnosis
- patient to inform DVLA and do not drive during episodes
- for acute attacks give buccal/ IM prochlorperazine (pro chlorine pair of (swimming trunks) zine= like seine river)
- for prevention betahistine and vestibular rehabilitation
(Bad Ears Don’t Process Voices)
What is narcolepsy and what are its associations 2
early onset of REM
HLA DR2 (also causes MS and hayfever)
low levels of orexin (protein that is responsible for controlling sleep patterns)
What are the features of narcolepsy
- hypersomnolence (excessive daytime sleepiness)
- cataplexy (sudden loss of muscle tone often triggered by emotion)
- sleep paralysis
- vivid hallucinations on going to sleep or waking up
medical student tired in lectures goes to sleep (excessive daytime sleepiness)
gets hallucination of monster chasing her (vivid hallucinations on going to sleep/ waking up)
cannot run away (sleep paralysis)
when she wakes up, lecturer tells her off but she gets angry because narcolepsy is not her fault and collapses (cataplexy)
bel
What is the ix and mx for narcolepsy
ix: multiple sleep latency test (EEG that monitors brain activity whilst taking naps)
mx: daytime modafinil to keep you awake and at night sodium oxybate
What is neurofibromatosis, how is it inherited and what is the mutation in both types
genetic condition that causes benign tumours to grow along nerves
chromosome 17 mutation in type 1
chromosome 22 mutation in type 2
autosomal dominant
What are the features of neurofibromatosis 1/2
type 1: cafe au lait spots, axillary/ groin freckles, phaechromocytoma, iris hamartomas (ocular hamartomas)
C: café-au-lait spots (greater than six seen during one year)
A: axillary or inguinal freckling
F: fibromas (neurofibroma (two or more) or plexiform neurofibroma (one))
E: eye hamartomas (Lisch nodules)
S: skeletal abnormalities, e.g. sphenoid wing dysplasia, leg bowing
P: positive family history
OT: optic tumour (optic nerve glioma)
type 2: bilateral vestibular schwanommas
What is normal pressure hydrocephalus and who presents with this
hydrocephalus due to reduced CSF absorption at the arachnoid villi
elderly patients with dementia (reversible cause of dementia)
What are the features of normal pressure hydrocephalus 4
wet (urinary incontinence)
wacky (dementia)
wobbly (wide gait- can be similar to Parkinsons)
symptoms develop over several months
What is the ix 1 and mx 1 for normal pressure hydrocephalus
ix: CT: shows enlarged fourth ventricle and not proportionate sulcal enlargement
mx: ventriculoperitoneal shunting
What is the peripheral neuropathy caused by diabetes and management 3
glove and stocking distribution of lower leg sensory loss, which may also be painful
mx:
first line is amitriptyline, duloxetine, gabapentin or pregabalin
if first line dose not work then try one of the other 3
neuropathic pain exacerbation= tramadol short term
What are the causes of cauda equina 3
- central disc prolapse occurs at L4/5 L5/S1
- tumours
- trauma
these all can compress ther nerves at cauda equina
What are the features of cauda equina 3
- lower back pain
- bilateral sciatica (tingling/ numbness + pain in buttocks
- urinary dysfunction (incontinence, loss of urge to void)
leaning down to get something= ow (lower back pain)
feels tingling and numbness + pain in buttocks= oh
wets themself= (oh) no
What are the Ix and mx for cauda equina
ix: urgent MRI spine
mx: surgical decompression
What are the mc for spinal cord compression
mc cause is extradural compression from vertebral body metastases (cancers)
features of spinal cord compression and how to located site of lesion
- back pain worse on lying down and coughing
- lower limb weakness
- sensory loss
- neurological signs
-> lesion above L1= UMN signs in legs and sensation
-> lesion below L1= LMN signs in legs and perianal numbness
-> tendon reflexes increased below level of lesion and absent at level of lesion
imagine princess and pea (pea symbolises spinal cord compression)
-> princess realises back pain is worse when lying down/ coughing
-> she tries to get up but her legs won’t move (weakness LL)
-> she picks up one leg to swing it over to the side but realises she can’t feel it (sensory loss)
(((((neuro signs: tries to get up before 1am- LMN signs in legs + perianal numbeness so she decides to rest and try again. tries to get up after 1am, UMN signs in legs and can feel sensation)))))
What are the ix and mx for spinal cord compression
Ix: urgent MRI spine
Mx: high dose oral dexamethasone and urgent oncological assessment for consideration of radiotherapy/ surgery
What level is cauda equina
L1
What are the two ascending tracts, what information do they carry
ascending tracts carry sensory info from body to brain
dorsal column: fine touch, vibration, proprioception
spinothalamic tract: pain and temp
What is the most important descending tract
corticospinal tract (main motor pathway for voluntary movement)
What level of spinal cord lesions do the following symptoms indicate:
respiratory difficulties
autonomic dysfunction
all four limbs
legs only
- C3-C6
- T1- L2
- cervical C1-7
- thoracic T1 and below
What are the causes of anterior/ posterior cord syndrome
- external metastatic mass
- anterior or posterior spinal artery blockage
What is anterior cord syndrome and features
- bilateral loss of pain and temp (spinothalamic)
- bilateral paralysis and UMN (corticospinal)
- all symptoms occur below the level of the lesion
What is spinal stenosis and features and what is the most common part of spine to be affected and ix 2 and ddx
spinal canal narrowing which compresses the spinal cord
presents with glute/ leg pain on walking/ standing and is relieved by forward flexion or sitting
lumbar spine
MRI, ABPI to rule out intermittent claudication
ddx: peripheral arterial disease
only spinal compression presentation that gets better with position
What is posterior cord syndrome and features and causes
- bilateral loss of fine touch, proprioception and vibration below side of lesion (dorsal column)
- poor co-ordination/ unsteady walking (due to lack of proprioception)
- all symptoms occur below the level of the lesion
What is syringiomyelia? How can you differentiate between this and other spinal cord conditions?
fluid filled cyst forms in the spinal cord which can press on nerve fibres in and spinal cord
syringiomyelia: affects upper limbs first and dorsal root column not affected, unlike other spinal cord conditions
syringio= like syringe to draw up injections and injections go into the arm= upper limb affected first + inject DNA= dorsal
What is Brown sequard syndrome presentation
- Ipsilateral paralysis below the level of the lesion
- Ipsilateral loss of fine touch, proprioception and vibration sense (dorsal)
- Contralateral loss of pain and temperature sensation (spinothalamic)- contralateral as the spinothalamic tract is the only tract who’s fibres decussate as they enter the spinal cord and ascend contralaterally
What is the presentation of long thoracic nerve injury?
medial winging of scapula
What is the presentation of radial nerve injury? What nerve endings? Cause?
wrist drop
C5-T1
midshaft humerous fracture
What is the presentation of common peroneal nerve injury? Nerve ending? Cause?
foot drop and weak eversion with absent ankle jerk
L4-5
fibular head fracture
What is the presentation of posterior tibial nerve injury?
pain and numbness in the plantar foot and heel
What is the presentation of ulnar nerve injury? What nerve endings? Cause?
claw hand (flexion of last two digits and extension of others)
C8-T1
Medial Epicondyle fracture
What is the presentation of median nerve injury, nerve endings, sx, dx, mx, causes
carpal tunnel: tingling in palm with thenar muscle wasting, pts often wake up at night due to symptoms and shake their hand around (wake and shake)
C6-T1
dx tinel (tap) and phalen (prayer sign in reverse) test positive, nerve conduction studies in hand show decreased conductivity
mx splints, last resort is surgery
causes: acromegaly, repetitive overuse, RA, pregnancy
What is the presentation of horners syndrome
anhydrosis (loss of sweating on affected side)
myosis (on affected side of face)
ptosis (on affected side of face)
ipsilateral
What is the pathophys of myasthenia gravis and what type of hypersensitivity is it
autoimmune condition with insufficiency functioning acetylcholine receptors of skeletal muscle
T2
astrocyt
What are the features of myasthenia gravis
muscle weakness worse with activity and improve with rest
- muscle weakness starting from head to lower body
- weak eye muscles= diplopia + ptosis
- face: myasthenic snarl (difficulty smilling), speech fatiguability (=slurred speech), jaw fatiguability (tired after chewing)
HEAD-> EYE-> MOUTH/JAW
What are the causes of myasthenia gravis
- thyomas (thymus gland tumour)
- thymic hyperplasia
- autoimmune conditions: pernicious anaemia, autoimmune thyroid disorders, RA, SLE
What are the ix for myasthenia gravis 3
- single fibre electromyography= repetitive stimulation= redeuced muscle actiona potentials
- Abx testing: Anti Ach-R (1st line) and Anti- MuSK (2nd line)
- CT thorax of thymus to look for thymoma
myasthenia
What is the management for myasthenia gravis 3
- acetylcholinesterase inhibitors eg pyridostigmine first line
- immunosuppression eg pred
- thymectomy/ thymic hyperplasia if thyomas is the cause, generally can cause long term benefits even in pts without thyoma
What is the sx and management for a myasthenic crisis 2
sx: acute worsening of sx + respiratory failure
tx: plasma exchange, IVIG
What does C5+6 innervate
skin: lateral forearm + thumb + index
muscle: elbow flexion, shoulder abduction and flexion (like a guy flexing his biceps in the mirror)
reflex: bicep jerk, C6 supinator
What does C7 innervate
skin: middle finger
muscle: wrist flexion, finger and elbow extension (like showing an engagement ring to someone)
reflex: tricep
What does C8 +T1 innervate
skin: medial forearm + lateral 2 fingers
muscle: C8 finger flexion, T1 finger add and abd
What does L5 innervate
skin: big toe and dorsum
muscle: dorsiflexion of foot
What does S1 innervate
skin: heel and sole
muscle: plantarflexion of foot
reflex: ankle
What innervates the knee jerk
L4
Ix for DVT
if wells 2+ then proximal leg vein US
if wells 1- then do d-dimer
whenever proximal leg vein US cannot be done within 4 hours, give LMWH
treatment for DVT
DOAC apixiban (LMWH if renally impaired) for 3 months if provoked (and event that provoked is no longer a rfx) or 6 months if unprovoked
investigations for PE (4)
if wells >4 then CTPA (diagnostic)
if wells <4 then D-dimer
ECG: sinus tachycardia, new RBBB, S1Q3T3 (large S wave in lead 1, Q wave in lead 3, inverted T wave in lead 3)
What is the wells criteria
Active cancer/ tx within 6 months
Bedridden recently >3 days or major surgery within 12 weeks
Calf swelling >3 cm compared to the other leg (Measured 10 cm below tibial tuberosity)
Collateral (non varicose) superficial veins present
Entire leg swollen
Localized tenderness along the deep venous system
Pitting edema, confined to symptomatic leg
Paralysis, paresis, or recent plaster immobilization of the lower extremity
Previously documented DVT
Alternative diagnosis to DVT as likely or more likely
(each is +1 point, except last one is -2)
how do you identify the cause of a bitemporal hemianopia?
bitemporal hemianopia with mostly lower quadrants affected= craniopharyngioma, causing superior optic chiasm obstruction
bitemporal hemianopia with mostly upper quadrants affected= pituitary tumour,
causing inferior optic chiasm obstruction
(second one= UP= upper quadrants affected, pituitary tumour)
