Neurology Flashcards
What is a TIA?
- sudden onset
- brief episode of neurological deficit
Pathophysiology of TIA
- temporary, focal cerebal ischaemia
- lack of O2 and nutrients to brain
- without infarction → no irreversible cell death
Features of a TIA
- symptoms are maximal at onset
- usually lasts 5-15 mins
- classical definition = lasts <24hrs
Risk factors for TIA
- age
- HTN
- smoking
- diabetes
- a fib
- the pill
- males
- black people
Causes of a TIA
atherothromboembolism from carotid artery
cardioembolism
- in a fib
- after an MI
- valve disease/prosthetic valve
hyperviscosity
hypoperfusion
Presentation of a TIA
- amaurosis fugax
- aphasia
- hemiparesis
- hemisensory loss
- hemianopic visual loss
What symptoms do not indicate a TIA on their own?
- syncope
- dizziness
- temporary loss of consciousness
- temporary memory loss
- gradual onset
What scoring tool measures the risk of a stroke after a TIA?
ABCD2 score
- age
- BP
- clinical features
- duration of TIA
- DM
- gives 2 day risk
Investigations for TIA
- diffusion weighted MRI/CT brain
- carotid imaging → doppler US then angiography if stenosis found
- bloods
- ECG
- echo
Management of TIA
- loading dose 300mg aspirin
- control BP/cholesterol
- no driving for 1 month
- antiplatelet therapy = daily 75mg aspirin
- anticoagulation if AF
- carotid endarterectomy
What is a stroke?
- rapid onset neurological deficit
- lasting over 24hrs
- poor blood flow to brain → cell death
What are the 2 types of stroke?
ischaemic 85%
- blood clot in blood vessel to brain
haemorrhagic 15%
- bleed in small blood vessel in/around brain
urgent CT/MRI to determine type → guides treatment
Risk factors for ischaemic stroke
- age
- male
- HTN
- smoking
- diabetes
- recent/past TIA
- IHD/AF
- the pill
- black/asian
- PVD
Causes of ischaemic stroke
- small vessel occlusion by thrombus
- atherothromboembolism
- cardioembolism
- hyperviscosity
- hypoperfusion
- vasculitis
- fat emboli from long bone fracture
- venous sinus thrombosis
Presentation of cerebral infarcts
depends on site
ACA
- contralateral weakness and sensory loss of lower limb
MCA
- contralateral motor weakness/sensory loss
- speech issues
- contralateral hemiplegia
- UMN facial weakness
- dysphagia
- homonymous hemianopia
- visuo-spatial deficit
Presentation of brainstem infarcts
depends on site
- quadriplegia
- facial numbness/paralysis
- vision disturbances
- speech impairment
- vertigo → N&V
- locked-in syndrome
What are lacunar infarcts?
- small infarcts
- occlusion of a single perforating artery supplying a subcortical area
occurs in
- internal capsule
- basal ganglia
- thalamus
- pons
Presentation of lacunar infarcts
depends on site → one of:
- sensory loss
- unilateral weakness
- ataxic hemiparesis
- dysarthria
Management of ischaemic strokes
- exclude haemorrhagic stroke
- loading dose 300mg aspirin
- antiplatelet therapy → 300mg aspiring daily for 2 weeks then clopidogrel
- anticoagulation if AF
- thrombolysis → IV alteplase within 4.5hrs
- mechanical thrombectomy
acute stroke unit
- rehabilitation
- swallowing/feeding support
What are the 4 types of haemorrhagic stroke?
- intracerebral haemorrhage
- subarachnoid haemorrhage
- extradural haemorrhage
- subdural haemorrhage
What is an intracerebral haemorrhage?
- sudden bleeding into brain tissue
- rupture of blood vessel in brain
- leads to infarction (O2 deprivation)
- pooling blood increases ICP
Risk factors for intracerebral haemorrhage
- HTN
- age
- alcohol
- smoking
- diabetes
- anticoagulation
- thrombolysis
- secondary to ischaemic stroke
Pathophysiology of increased ICP
- pressure on skull/brain/blood vessels
- CSF obstruction
- midline shift
- tentorial herniation
- coning
Presentation of intracerebral haemorrhage
similar to ischaemic stroke
pointers to haemorrhage
- sudden loss of consciousness
- severe headache
- meningism
- coma
Investigations for intracerebral haemorrhage
- same as ischaemic stroke
- CT/MRI brain = essential
Management of intracerebral haemorrhage
- stop anticoagulants immediately → reverse effects with clotting factor replacement
- BP control
- reduce ICP → mechanical ventilation, IV mannitol
What is a subarachnoid haemorrhage?
spontaneous bleeding into subarachnoid space
Risk factors for SAH
- HTN
- known aneurysm
- previous aneurysmal SAH
conditions associated with berry aneurysms
- PKD
- coarctation of aorta
- connective tissues diseases
Causes of SAH
- aneurysmal rupture → Berry aneurysms
- ateriovenous malformations
- idiopathic
- traumatic injury
Pathophysiology of SAH
- tissue ischaemia
- raised ICP
- space-occupying lesion → puts pressure on brain
- blood irritates meninges → can obstruct CSF outflow
- vasospasm
Complications of SAH
- rebleeding
- hyponatraemia
Symptoms of SAH
- sudden onset excruciating headache → thunderclap, occipital
- N&V
- collapse
- loss of consciousness
- vision changes
- coma
Signs of SAH
signs of meningeal irritation
- neck stiffness
- Kernig’s sign
- Brudzinski’s sign
- retinal, subhyaloid, vitreous bleeds
- focal neurological signs
- high BP
Investigations for SAH
ASAP brain CT
- star shaped sign
lumbar puncture
- only if normal ICP
- xanthochromia → yellowish CSF
MR/CT angiography to find source of bleeding
Management of SAH
- IV fluids
- ventricular drainage if hydrocephalus
- nimodipine reduces vasospasm
- surgery if aneurysm → endovascular coiling/surgical clipping
What is a subdural haematoma?
- bleeding into subdural space
- rupture of bridging vein
- usually due to head trauma
- massive latent interval
Risk factors of subdural haematoma
- babies → traumatic injury
- brain atrophy → dementia, elderly, alcoholics
- prone to falls
- anticoagulants
Pathophysiology of subdural haematoma
- bleeding forms haematoma then stops
weeks/months later
- haematoma autolyses → increase in oncotic/osmotic pressure → water sucked in → haematoma enlarges
- rise in ICP
- midline structures shifted away from side of clot
Symptoms of subdural haematoma
- fluctuating levels of consciousness
- drowsiness
- headache
- confusion
- insidious physical/intellectual slowing
Signs of subdural haematoma
- raised ICP
- seizures
- localising neurological signs
Investigations for subdural haematoma
CT scan
- haematoma → banana shaped
- midline shift
MRI
Management of subdural haematoma
surgery
- remove haematoma → clot evacuation
- craniotomy
- burr hole washout
IV manittol
reverse clotting abnormalities
address cause
What is an extradural haematoma?
- bleeding into extradural space
- after trauma to temple → fracture → rupture of MMA
- lucid interval
Risk factors for extradural haematoma
- young people
- male
Pathophysiology of extradural haematoma
after lucid interval
- rise in ICP
- pressure on brain
- midline shift → tentorial herniation/coning
Presentation of extradural haematoma
after lucid interval
- rapidly declining GCS
- headache
- vomiting
- seizures
- coma
- deep/irregular breathing → coning
- death → respiratory arrest
Investigations for extradural haematoma
CT scan
- haematoma → lemon shaped
- midline shift
skull xray → fracture lines
Management of extradual haematoma
- stabilise
- urgent surgery → clot evacuation/ligation of bleeding vessel
- IV mannitol
- airway care
What are the red flags for headaches?
- worst headache ever
- other neurological signs
- onset >50
- severe, quick onset
- abnormal pattern of migraine
What is a migraine?
- recurrent throbbing headache
- often preceded by an aura
- associated with N&V, visual changes
most common cause of episodic headache
Risk factors for migraines
- family history
- female
- age → first in adolescence
Causes of migraines
CHOCOLATE
- chocolate
- hangovers
- orgasms
- cheese
- oral contraceptives
- lie-ins
- alcohol
- tumult
- exercise
Presentation of migraine
prodrome
- yawning
- craving
- mood/sleep changes
aura
- precedes attack, variety of symptoms
- visual disturbances
- parasthesia
Diagnosis of migraine
2+ of:
- unilateral pain
- throbbing-type pain
- moderate to severe intensity
- motion sensitivity
and 1+ of:
- N&V
- photo/phonophobia
Investigations for migraine
- bloods
- CT/MRI → look for red flags
- lumbar punture
Management of migraines
conservative = avoid triggers
mild
- NSAIDs → naproxen/ipubprofen
- antiemetic
severe = oral triptans eg sumatriptan
- not if IHD, uncontrolled HTN
- SE → arrythmias, angina
Prophylaxis of migraines
- beta blockers
- acupuncture
- amitriptyline = TCA
- topiramate = anticonvulsant
What are cluster headaches?
- episodic headaches with pain free periods
- most disabling primary headache
Risk factors for cluster headaches
- smoking
- alcohol
- male
- 20-40
- autosomal dominant gene
Presentation of cluster headaches
pain
- rapid onset excruciating
- classically around the eye
- can be temples and forehead
- unilateral, localised to one area
- rises to a crescendo over few minutes
- lasts 15-160mins, 1/2 x a day
- watery bloodshot eye
- facial flusing
- rhinorrhoea
- miosis +/- ptosis
Management of cluster headaches
- 15L 100% O2 for 15mins via non-rebreather mask
- triptans → sumatriptan
Prevention of cluster headaches
- verapamil CCB
- prednisolone
- stop smoking/drinking
What is a tension headache?
- most common chronic daily headache
- can be episodic or chronic
Triggers of tension headaches
- stress
- sleep deprivation
- bad posture
- hunger
- eyestrain
- anxiety
- noise
- clenched jaw
Presentation of tension headaches
1+ of:
- bilateral
- pressing/tight and non-pulsatile
- mild/moderate intensity
- +/- scalp tenderness
no aura, vomiting, sensitiy to movement
can have pressure behind eyes
Management of tension headaches
- avoid triggers
- symptomatic relief → aspirin, PCM, ibuprofen
- analgesia no more than 6days/month → can cause medication overuse headaches
What is epilepsy?
- recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain
- manifesting in seizures
Criteria for diagnosing epilepsy
1 of:
- at least 2 unprovoked seizures more than 24hrs apart
- one unprovoked seizure and probability of future seizures
- diagnosis of an epilieptic syndrome
What is a seizure?
- convulsions
- motor signs of abnormal electrical discharges
- epileptic seizures = convulsions due to epileptic syndromes
Causes of epilepsy
- idiopathic
- cortical scarring
- tumours/space-occupying lesions
- strokes
- alzheimer’s
- alcohol withdrawal → delirium tremens
Risk factors for epilepsy
- family hisotry
- premature babies
- abnormal cerebral blood vessels
- drugs eg cocaine
What are the components of a seizure?
- prodrome
- aura
- post-ictal
What is prodrome?
- precedes seizures by hrs/days
- weird feeling eg mood/behaviour changes
What is aura?
- part of seizure
- patient is aware, often precedes other manifestations
- eg strange feeling, deja vu, strange smells, flashing lights
- can imply partial seizure
What is post-ictal
- period after seizures
- headache, confusion, myalgia, sore tongue
- post-ictal Todd’s palsy
- dysphagia after temporal lobe seizure
What is post-ictal Todd’s palsy
temporary weakness after focal seizure in motor cortex
What are the types of seizures?
- primary generalised seizures
- partial focal seizure
- partial seizure with secondary generation
What are primary generalised seizures?
- whole cortex affected
- bilateral and symmetrical motor manifestations
- loss of consciousness/awareness
Types of primary generalised seizures
- tonic = high tone → rigid/stiff limbs
- clonic = muscle jerking
- tonic clonic = muscle jerking and rigidity
- myoclonic = isolated jerking
- atonic = loss of muscle tone
- absence = childhood, goes blank → risk of developing tonic clonic
What are the 3 types of partial focal seizures?
- single lobe features
- simple partial seizure
- complex partial seizure
Features of single lobe feature seizures
- underlying structural disease
- limited to one lobe
- progress to generalised seizures
Features of simple partial seizures
- does not affect consciousness/memory
- no post-ictal signs
- motor/sensory/autonomic/pyschic signs
Features of complex partial seizures
- memory affected
- mainly temporal lobe
- post-ictal confusion = common if temporal
Characteristics of temporal lobe seizures
- memory, understanding speech/emotion
- aura
- anxiety/out of boy experiences
- automatisms
Characteristics of frontal lobe seizures
- motor, thought processing
- jacksonian march
- post-ictal Todd’s palsy
Characteristics of parietal lobe seizures
- sensation
- sensory disturbances → tingling/numbness
Characteristics of occipital lobe seizures
- vision
- visual phenomena eg spots, lines, flashes
Diagnosis of epilepsy
- EEG → supports diagnosis
- MRI/CT head → exclude space-occupying lesions
- bloods → exclude metabolic disturbances
- genetic testing
Management of epilepsy
- sodium valproate
- if fertile female = lamotrigine
- myoclonic = levetiracetam/topiramate
- absence = ethosuximide
- partial = lamotrigine/carbamazepine
What is status epilepticus?
- continuous seizure lasting over 5mins OR
- repeated seizures with no recovery in between
- treatment = IV lorazepam then phenytoin
What are features of non-epileptic seizures?
- metabolic disturbances
- longer
- don’t occur in sleep
- no incontinence/tongue biting
- pre-ictal anxiety signs
- no muscle pain
What is meningitis?
- inflammation of the meninges
- almost always due to infection
- notifiable disease
Risk factors for meningitis
- students
- travel
- immunocompromised
- pregnancy
Causes of bacterial meningitis
- neonates = group B strep
- children <2 = strep pneumoniae
- 2-50 = n.meningitis, s.pneumoniae
50+ = s.pneumoniae, listeria meningitis
acute emergency
Causes of viral meningitis
- enterovirus
- HSV
Causes of fungal meningitis
- cryptococcus
- candida → immunocompormised HIV
Why is Neisseria meningitidis important?
- can cause meningococcoal septicaemia
- non blanching purpuric rash
- necrosis
- high mortality
Symptoms of meningitis
- triad → fever, headache, neck stiffness
- purpuric rash
- photo/phonophobia
- papilloedema
- raised ICP
- seizures
Signs of meningitis
- Kernig’s +ve
- Brudzinski’s +ve
- glass test → blanching/non-blanching rash
What is Kernig’s sign?
resistance to extension of leg while hip is flexed
What is Brudzinski’s sign?
flexion of hips and knees in response to neck flexion
Treatment of meningitis
- ABCDE and support
- empiric therapy = IV benylpenicillin
- asses GCS
- ceftriaxone/cefotaxime
- add IV benzylpenicillin for rash
- if penicillin allergy = chloramphenicol
- if immunocompromised = amoxicillin/ampicillin
Prophylaxis for meningitis
- rifampicin and ciprofloxacin
- viral = acyclovir
What is Guillain-Barre syndrome?
- acute polyneuropathy → rapid damage of peripheral nerves
- results in demyelination/axonal degeneration
- common cause = post-GI infection
What infections commonly cause GBS
- campylobacter jejuni
- EBV
- CMV
- mycoplasma
- HIV
Symptoms of GBS
- weakness
- paraesthesia
- hyporeflexia
- sudden onset toe-nose weakness
- absent reflexes
- pain in legs, back
- sensory loss in lower extremities
- urinary hesitancy
Investigations for GBS
- bloods
- lumbar puncture → protein in CSF
- spirometry
- ECG
- slow conduction velocities
Treatment for GBS
- IV Ig
- plasma exchange
- LMW heparin → DVT prophylaxis
- avoid corticosteroids
What is Parkinson’s disease?
- destruction of dopaminergic neurons
- too little dopamine
- affects ventral tier of zona compacta in substantia nigra
Causes of Parkinson’s
- drug induced → dopamine antagonists
- encephalitis
- exposire to toxins eg manganese
Presentation of Parkinson’s
- bradykinesia
- resting tremor
- rigidity
- parkinsonian gait
- sleep disorders
- depression
- monotonous voice
- difficulty with fine/repetitive movement
- cog-wheel walk
b-amyloid plaques
Diagnosis of Parkinson’s
clinical diagnosis
1. diagnosis of Parkinsonian syndrome
2. exclusion criteria
3 supportive criteria
DaTscan
Treatment of Parkinson’s
young onset, biologically fit
- Da agonist = ropinirole
- MOA-B inhibitor = rasagiline
- L-DOPA = co-careldopa
biologically frail, comorbidities
- L-DOPA
- MOA-B inhibitor
What is Huntington’s disease?
- progressive neurodegenerative disorder with 100% penetrance
- loss of main inhibitory neurotransmitter GABA
- cell loss within basal ganglia and cortex
Pathophysiology of Huntington’s
- less GABA = less regulation of dopamine to striatum
- increased dopamine → excessive thalamic stimulation → increased movement (chorea)
Inheritance of Huntington’s
- autosomal dominant
- increased in CAG repeats on chromosome 4
Presentation of Huntington’s
- hyperkinesia
- chorea
- dystonia
- incoordination
- psychiatric issues
- depression
- cognitive impairment, behavioural difficulties
- irritability, agitation, anxiety
Investigations for Huntington’s
- MRI/CT → loss of striatal volume
- genetic testing
- tests for SLE, thyroid disease, Wilson’s, dementia
Treatment for Huntington’s
- poor prognosis
- most common cause of death = pneumonia then suicide
- benzodiazepines/valproic acid for chorea
- SSRIs for depression
- haloperidol, risperidone for psychosis
What is Alzheimer’s
- most common type of dementia
- EC deposition of b-amyloid plaques
- tau-containing IC neurofibrillary tangles
- damaged synapses
- atrophy
Risk factors of Alzheimer’s
- over 65
- Down’s
- reduced cognitive activity
- depression/loneliness
- ApoE E4 allele homozygosity
Presentation of Alzheimer’s
- memory → episodic and semantic
- language → difficulty understanding/finding words
- attention/concentration issues
- psychiatric changes
- disorientation
Diagnosis of Alzheimer’s
- mini-mental state examination
- bloods
- memory clinic assessment
- MRI
Treatment of Alzheimer’s
- no cure
- supportive therapy
- medications to manage symptoms → AChEi
What is multiple sclerosis?
- cell mediated autoimmune condition
- repeated episodes of inflammation of nervous tissue in brain and SC → DC4 mediated destruction
- results in loss of myelin sheath in CNS
What are the types of MS?
relapse-remitting MS
secondary progressive MS
- follows from relapsing-remitting
- gradually worsening symptoms
- fewer remissions
primary progressive MS
- from beginning of disease
- symptoms develop and worsen over time
acute attacks followed by periods of remyelination → these periods become shorter/less frequent
Symptoms of MS
- pyramidal weakness
- spasric paraparesis
- changes in sensation
- fatigue
- chronically increasing bladder movement
- cognitive impairment
- dizziness
- depression
Signs of MS
- UMN signs
- loss of colour vision
- Lhermitte sign
- Uhthoff phenomenon
Diagnosis of MS
- symptoms disseminated in time and space
- GOLD STANDARD = MRI → GD-enhancing plaques
- lumbar puncture
- McDonald criteria
- bloods
Treatment of MS
- notify DVLA
- supportive care
relapses
- acute = methylprednisolone
- chronic = DMARDs, biologicals
What is motor neurone disease?
- group of neurodegenerative disorders
- selective loss of neurones in motor cortex, cranial nerve nuclei, anterior horn cells
- progressive, ultimately fatal
- only affects motor, not sensory
Risk factors for MND
- smoking
- exposure to heavy metals
Types of MND
- ALS → most common
- PLS
- PMA
- PBP
Signs and symptoms of MND
- mixed UMN and LMN presentation
- LMN signs predominate → weakness, atrophy, muscle fasciculations
- wrist/foot drop
- wasting in hands
- gait disorders
- excessive fatigue
Diagnosis of MND
El Escorial criteria
Treatment of MND
- supportive therapy
- riluzole slows progression
- end of life care
Features of ALS
- SOD1 gene
- loss of neurons in motor cortex and anterior horn
- UMN and LMN signs
- babinski response
- asymmetric
- corticobulbar signs = worse prognosis
Features of PBP
- CN 9-12 → UMN and LMN
- worst prognosis
- dysphagia
- flaccid tongue
- hoarse, nasal speech
Features of PMA
- anterior horn cells affected
- LMN only
- distal muscles affected then proximal
Features of PLS
- rare
- progressive tetraparesis
- UMN only
What is myasthenia gravis?
- disorder of neuromuscular transmission
- caused by binding of autoantibodies to component of NMJ → acetylcholine receptor
- can be inherited
- 30s for women, 60-70s for men
Signs and symptoms of myasthenia gravis
muscle weakness
- worse on exertion, better with rest
- marked in proximal muscles → small muscles of hand, deltoid, triceps, bulbar, chewing muscles
- ocular manifestations
- no muscle wasting
- seizures
Diagnosis of myasthenia gravis
- mostly clinical
- detect ACh receptor antibodies
- +ve tensilon test → tensilon improves muscle weakness
Treatment of myasthenia gravis
treat symptoms
- AChEis
- pryidostigmine
- methotrexate
- ciclosporin
- tacrolimus
stop exacerbating drugs
What drugs can exacerbate myasthenia gravis?
- ciprofloxacin
- azithromycin
- propanolol
- atenolol
- verapamil
- lithium
- statins
- chloroquine
- prednisolone
What is syncope
- temporary loss of consciousness
- due to disruption of blood flow to brain → fall
- syncopal episodes AKA vasovagal episodes/fainting
Causes of primary syncope
- dehydration
- missed meals
- extended standing in warm environment
- vasovagal response to stimuli → surprise, pain, blood
Causes of secondary syncope
- hypoglycaemia
- dehydration
- anaemia
- infection
- anaphylaxis
- arrhythmias
- valvular heart disease
Signs and symptoms of syncope
- hot/clammy
- sweaty
- heavy
- dizzy/light headed
- vision going blurry/dark
- headache
Investigations for syncope
- history
- ECG/24hr ECG
- echo
- bloods
Management of syncope
- primary = avoid triggers
- secondary = manage underlying pathology
What is a nerve lesion?
- damage to a nerve through compression, trauma, infection etc
- results in interruption of axonal continuity
What are the 3 categories of peripheral nerve injuries?
- stretch related
- lacerations
- compressions
Signs and symptoms of nerve lesions
depends on nerve affected
- numbness/ tingling
- muscle weakness
- dropping objects
- sharp pains
Investigations for nerve lesions
- neurological exam
- MRI
Treatment of nerve lesions
- splint/braces
- physical therapy
- exercise
- analgesia
- surgery if severe
