Neuro Flashcards
what is a cluster headache?
severely disabling episodic headaches.
more common in men and smokers.
how do cluster headaches present?
rapid onset excruciating pain around one eye
eye becomes watery, bloodshot, lids swollen, lacrimation
facial flushing
rhinorrhoea
pain is strictly unilateral, will usually affect one side only
course - headaches last 15-60min, once or twice a day, often nocturnal
clusters last 4-12 weeks, then they might have months/years before next cluster
how do you treat cluster headaches?
acute attack - 100% oxygen for 15 mins via non-rebreathe, sumitriptan SC or nasal spray at onset (nasal spray not licensed).
preventative - verapamil (start at 40mg and build up to 960mg max, requires ECG monitoring for AV block once at high doses/whilst raising dose)
prednisolone (second line, but can be preferred as started at top dose - then quickly wean off! may relapse)
lithium - if verapamil not tolerated, requires lots of monitoring
other options:
melatonin
topiramate
sodium valproate
give some possible triggers for cluster headaches
- alcohol precipitates attacks when in a cluster, but can be drunk between clusters
- histamine and nitroglycerine
- for some patients - heat, exercise and solvents
- disruption to sleep patterns (e.g. by shift work, jet lag, etc)
list some headache red flags that should prompt further investigation
- change in pattern of headache.
- new headache at age > 50.
- onset of seizures.
- headache with systemic illness.
- personality change.
- symps suggestive of raised ICP (morning headache, headache with coughing, sneezing, straining).
- acute onset of the worst headache ever (possible intracranial aneurysm).
list some differentials to consider for an acute single episode of headache
with meningism (stiff neck etc): - meningitis - encephalitis - subarachnoid haemorrhage head injury sinusitis glaucoma (acute closed-angle) tropical illness e.g. malaria, typhus
what features of an acute single episode of headache would make you consider meningitis?
meningism - acute, severe headache felt all over with neck stiffness.
fever, photophobia, purpuric rash (although not always!)
admit urgently for CT head/LP if CT negative
what features of an acute single episode of headache would make you consider encephalitis?
neck stiffness, fever, odd behaviour, fits, reduced consciousness
admit urgently for CT head/LP if CT negative
what features of an acute single episode of headache would make you consider subarachnoid headache?
SUDDEN ONSET, ‘worst ever’ headache, often occipital (been kicked in back of head), stiff neck, focal signs, reduced consciousness
admit urgently for CT head/LP if CT negative
what features of an acute single episode of headache would make you consider head injury? what would prompt you to consider further investigations?
hx of trauma!
pain usually around site of trauma, but can be generalised.
CT head to exclude subdural/extradural haemorrhage if drowsiness ± lucid interval or focal signs.
what features of an acute single episode of headache would make you consider sinusitis? how do you treat it?
dull, constant ache over frontal or maxillary sinuses, with tenderness ± postnasal drip. pain worse on bending over. preceding coryzal symptoms. lasts 1-2 weeks. if bacterial (likely Strep pneumoniae, haemophilus influenzae, moraxella catarrhalis) treat with abx - amoxicillin - although some evidence says this doesn't achieve anything.
give some home treatment measurers you would advise for a patient with acute sinusitis
- paracetamol/ibuprofen for pain/fever.
- intranasal decongestant (oral is not recommended for sinusitis) for a max of a week.
- nasal irrigation with warm saline solution.
- warm face packs, which may provide localised pain relief.
- adequate fluids and rest.
what features of an acute single episode of headache would make you consider acute angle-closure glaucoma?
elderly, long-sighted people
constant, aching pain develops round one eye, radiating to forehead.
markedly reduced vision, visual haloes, N&V.
red congested eye, cloudy cornea, dilated non-responsive pupil (may be oval), reduced acuity.
(seek urgent expert help, if delay in treatment >1hr likely start acetazolmide 500mg IV, plus lay supine and give any topical agents not contra-indicated in the patient
topical agents inlude:
Beta-blockers - eg, timolol, cautioned in asthma.
Steroids - prednisolone 15 every 15 minutes for an hour, then hourly.
Pilocarpine 1-2% (in patients with their natural lens).
Phenylephrine 2.5% (in patients who do not have their own lens).)
what are tension headaches?
main cause of bilateral, non-pulsatile headache ± scalp muscle tenderness, with no vomiting/sensitivity to movement. often described as band round scalp, pressure, tightness.
divided into
- episodic TTH. This occurs on fewer than 15 days each month. It can evolve into the chronic variety.
- chronic TTH. This occurs on more than 15 days each month and has all the features of the episodic TTH.
chronic is more likely due to medication overuse.
how should you manage tension type headache?
reassurance, advise on stress management, hydration, risk of medicines overuse.
drug therapy - avoid codeine, ibuprofen first line (OTC), naproxen second. can try paracetamol but usually not as effective.
if nothing’s working - try amitriptyline.
what are the characteristic features of headache due to raised ICP?
worse on waking, lying, bending forward, coughing.
vomiting, papilloedema, odd behaviour, false localising signs.
must image before do LP - contraindicated otherwise!
what is a medication overuse headache?
chronic daily headache (> 15 days per month, with opiate/triptan use on >10 or paracetamol/NSAIDs on >15) due to overuse of analgesics - mixed opiates and paracetamol (Cocodamol) common culprit.
how do you manage a medication overuse headache?
reassurance/education.
withdrawal of analgesia - warn patient headache will worsen initially.
headache should resolve in 10 days or so.
what are the symptoms of trigeminal neuralgia? what are the common triggers?
paroxysms of intense stabbing pain, lasting seconds, in trigeminal nerve distribution (facial).
unilateral, typically maxillary/mandibular.
may have preceding symptoms e.g. tingling, numbness.
triggers - washing affected area, shaving, eating, talking, dental prostheses.
typical pt >50yo, woman (F:M = 2:1)
what are some red flags in a trigeminal neuralgia history that should prompt referral/further investigation?
Sensory changes, deafness or other ear problems.
Difficulty achieving pain control, poor response to carbamazepine.
History of any skin lesions or oral lesions that could lead to perineural spread.
Ophthalmic division only or bilateral as suggestive of benign or malignant lesions or multiple sclerosis.
Age of onset under 40 years.
Optic neuritis.
Family history of multiple sclerosis.
if investigation needed it’d normally be a brain MRI.
list some possible causes of secondary trigeminal neuralgia
- compression by anomalous or aneurysmal intracranial vessels or a tumour
- chronic meningeal inflammation
- MS
- varicella zoster
- skull base malformation e.g. Chiari malformation
MRI needed to exclude these causes.
how do you treat trigeminal neuralgia?
carbamazepine PO at 100mg every 12hrs, max 400mg/6hrs.
then try lamotrigine, phenytoin or gabapentin.
if drugs fail, surgery - rhizotomy, microvascular decompression, stereotactic gamma knife surgery can work.
list some differential diagnoses for facial pain
migraine trigeminal neuralgia post-herpetic neuralgia - shingles cervical disk pathology sinusitis bone neoplasia temperomandibular joint dysfunction dental problems giant cell arteritis cluster headaches MS
what is giant cell arteritis?
needs excluding in anyone >50yrs with headache lasting a few weeks.
systemic immune-mediated vasculitis affecting medium-sized and large-sized arteries, particularly the carotid artery and its extracranial branches. associated with PMR in 50%.
can cause sudden bilateral vision loss so considered an emergency.
how does giant cell arteritis present?
recent onset temporal headache, myalgia, fever. temporal artery and scalp tenderness (e.g. when combing hair), jaw claudication (pain comes on gradually when chewing), amaurosis fugax or sudden blindness.
extracranial symps - dyspnoea, morning stiffness, unequal/weak pulses.
how do you manage a patient presenting with possible giant cell arteritis?
do an ESR blood test and give high dose (40mg) prednisolone immediately - if claudication give 60mg, if visual symptoms admit for IV methylpred.
other Ix - CRP, platelets, alk phos all raised, might see anaemia. get a temporal artery biopsy within 7 days of starting treatment.
typically a 2 yr course before it resolves - reduce pred once symps controlled and ESR reduced, but don’t be afraid to bump it back up as necessary.
how do migraines present?
- visual (or other) aura for 15-30 mins before onset within 1hr of severe, throbbing, unilateral headache
- headache without aura
- aura without headache
- headache is incredible severe with N&V, photo/phonophobia
- lasts 4-72h
what are the criteria for diagnosing a headache as migraine if there’s no aura?
5+ headaches lasting 4-72hrs plus N&V or photo/phonophobia plus any 2 of the following:
- unilateral
- pulsating
- impairs usual activity
what are the possible triggers for migraine?
CHOCOLATE: Chocolate Hangovers Orgasms Cheese Oral contraceptives Lie-ins Alcohol Tumult Exercise
what kinds of aura may be experienced in migraine?
visual - chaotic distorting lines/shapes/patterns, hemianopia
somatosensory - paraesthesiae spreading from fingers to face
motor - dysarthria and ataxia (basilar migraine), ophthalmoplegia or hemiparesis
speech - dysphasia or paraphasia
how do you manage/treat migraines? (not prophylaxis)
- reassurance, education, encourage headache diary and identification of triggers, lifestyle (stress, diet and exercise, sleep)
1) soluble aspirin or ibuprofen, prochlorperazine buccal for anti-emetic if needed
2) rectal diclofenac and domperidone (anti-emetic) - not often used due to patient preference!
3) triptans or ergotamine - ‘abortive’ so must be taken immediately after onset of headache/aura
MUST stop COCP - stroke risk
list some contra-indications for triptans
People with uncontrolled hypertension.
People with coronary heart disease or cerebrovascular disease
People with risk factors for coronary heart disease or cerebrovascular disease
People with coronary vasospasm (Prinzmetal’s angina)*.
what are the options for migraine prophylaxis?
offer if 2+ per month, impacting daily activity for 3+ days each time
1) beta blockers e.g. atenolol
2) amitriptyline
3) topiramate, sodium valproate (these are started in specialist care)
4) pizotifen
5) 12 weekly botulinum toxin A injections
list some differentials for stroke (there’s bloody loads)
head injury hypo/hyperglycaemia subdural haemorrhage intracranial tumours hemiplegic migraine epilepsy (Todd's palsy) CNS lymphoma pneumocephalus Wernicke's encephalopathy hepatic encephalopathy herpes encephalitis abscesses
what are the two main types/mechanisms of stroke?
haemorrhagic vs infarction
arterial embolism (infarction) – from a distant site; e.g. carotids, vertebral or basilar arteries. embolus occludes an artery of brain resulting in infarction. may also come from heart valves in endocarditis. Haemorrhage – can be in the cerebrum itself, or also a subarachnoid haemorrhage may cause a similar effect
list some uncommon causes of stroke
Venous infarct Carotid/vertebral artery dissection (spontaneous or from neck trauma) Polycythemia Fat / air embolism – e.g. in divers MS – demyelinating plaque may act as an embolus Mass lesions (e.g. tumour) Migraine Thrombocythaemia and thrombophilia Venous sinus thrombosis Vasculitis Amyloidosis Drugs – particularly cocaine and OTC cold remedies that contain vasoconstrictors. Sepsis - sudden BP drop
list some modifiable risk factors that can reduce the risk of a stroke
mostly affect risk of infarctive stroke: HTN smoking DM heart disease - valvular, ischaemic, AF peripheral vascular disease past TIA carotid bruit COCP hypercholesterolaemia alcohol misuse clotting disorders syphilis
what is CADASIL?
rare, inherited cause of stroke and vascular dementia.
Caused by a defective NOTCH3 gene
multiple small infarcts in the brain.
Often presents as migraine and depression in teenagers, and by the 20’s and 30’s there are often TIA’s and strokes.
Dementia may follow after age 40-50
list the main causes of infarctive stroke
60% – Atherosclerosis of the carotid arteries and aortic arch
20% – valvular heart disease
20% – disease of the vessels in the brain itself
what symptoms would you expect to see for a middle cerebral artery infarction?
most common stroke presentation!
Contralateral:
Hemiparesis
Hemiplegia (initially flaccid, becomes spastic)
Limbs usually floppy, and reflexes reduced/absent
Facial weakness (not always)
Hemianopia – visual field defect in which vision is lost in half of the visual field in one/both eyes.
Aphasia – when the dominant hemisphere is affected - ask about left and right handedness!
symptoms develop rapidly, over a period of minutes, or less commonly they can develop over a few hours.
what symptoms/signs indicate a cerebral infarct rather than brainstem/lacunar?
depending on site - contralateral sensory loss contralateral hemiplegia - initially flaccid (floppy limb falls like dead weight when lifted), then spastic (UMN signs) dysphasia homonymous hemianopia visuo-spatial deficit
what symptoms/signs indicate a brainstem infarct rather than cerebral/lacunar?
wide range of effects, incl (features - location):
Hemi/tetraparesis - Corticospinal tracts
Sensory Loss - Medical lemniscus / spinothalamic tract
Diplopia - Occulomotor nuclei
Facial Numbness - 5th nerve nuclei
Facial weakness - 7th Nerve nucleus
Nystagmus and vertigo - Vestibular connections
Dysphagia / dysarthria - 9th/10th nuclei
Horner’s syndrome - Sympathetic fibres
Altered consciousness - Reticular formation
what symptoms/signs indicated lacunar infarct rather than cerebral/brainstem? where are these infarct occurring?
occurring in brainstem, internal capsule, thalamus, pons 5 main syndromes: 1) ataxic hemiparesis 2) pure motor 3) pure sensory 4) sensorimotor 5) dysarthria (clumsy hand)
may be symptomless, or present with very localised symptoms (as in pure motor/sensory) due to the very localised effect it has.
consciousness/cognition stay intact (except in thalamic stroke)
give some info on the use of thrombolysis in acute stroke
must be sure it’s non-haemorrhagic (imaging) and that you are acting within 4.5 hours of onset of symptoms (so if they woke up with it, you can’t do it!) and there’s no CIs.
IV recombinant tissue plasminogen activator (tPA) e.g. alteplase.
must do CT 24hrs post-thrombolysis to check for bleeds.
give some absolute contra-indications for thrombolysis
Previous intra-cranial haemorrhage / haemorrhagic stroke
Major surgery or trauma <2 weeks
Active internal bleed (excluding menses)
Prolonged / traumatic CPR
Pregnancy, or <18 weeks postnatal
Severe liver disease / known oesophageal varices
Hypertension >200/120
Cerebral neoplasm
Previous allergy
Head/face trauma < 3months
Previous ischaemic stroke < 3 months (except current episode)
give some relative contra-indications for thrombolysis
Hx of severe (>200/120 hypertension) Peptic Ulcer Anticoagulant therapy Infective Endocarditis Known coagulation disorder
what symptoms indicate an anterior cerebral artery infarct?
Weak leg (± shoulder), on the contralateral side
what symptoms indicate a MCA infarct?
Weak arm and face on the contralateral side.
Hemiplegia
Hemianopia
Asphasia
Visuospatial problems
what symptoms indicate a posterior cerebral artery infarct?
Eye Problems
what features of a history might indicate carotid/vertebral artery dissection as the cause of a stroke?
Accounts for 20% of strokes in those under 40
often the result of trauma - but may be spontaneous
symptoms resembling stroke, TIA, or migraine, with pain at the site of the dissection
what is locked in syndrome and what causes it?
patient is aware and awake, but virtually all motor neurons are paralysed, and thus the patient cannot move. Usually the eyes are the only structures not affected. Caused by an upper brainstem infarct.
what is pseudo-bulbar palsy and what causes it?
the result of a lower brainstem infarct. Results in bilateral impairment of the 9-12thcranial nerves. There is dysarthria and dysphagia
what is Wallenberg’s syndrome / lateral medullary syndrome / posterior inferior cerebellar artery thrombosis (PICA)? - these all mean the same!
Syndrome resulting from brainstem infarction.
presents with acute vertigo and other cerebellar signs. Due to the nature of the cerebellar pathways, there are the following signs:
Contralateral Spinothalamic sensory loss Hemiparesis (usually mild, quite rare) Ipsilateral Facial numbness (V) Diplopia (VI) Nystagmus Ataxia Horner’s syndrome 9th and 10th nerve lesions
explain the appearance of stroke on CT and MRI
Infarctions will always show up as a wedge shape on both CT and MRI.
Haemorrhage – blood appears bright white (dense) on CT – but the longer it has been present, the darker it becomes. After 1-2 weeks it may look the same as normal brain tissue.
can roughly estimate the length of time the haemorrhage has been present by density of blood on a scan.
Depending on the site of the bleed, it will have a different shape on the scan
The damage is easier to see the longer it has been present
For example, a ‘new’ stroke (e.g. <2 hours old) may not show up at all, but after 6-12 hours will be clearly visible. This has clinical consequences – because the sooner you can see the stroke, the sooner you can treat it.
how do you investigate a stroke
send for urgent CT/MRI if considering thrombolysis, or high risk for haemorrhage, otherwise aim to do within 24hrs
diffusion weighted MRI most sensitive for acute infarct, CT helps rule out primary haemorrhage.
further tests:
BP / examine for signs of HTN e.g. retinopathy.
look for cardiac source of emboli - 24h ECG (for AF), might do an echo.
check for carotid artery stenosis - carotid Doppler USS ± CT/MRI angiography - 70+ % stenosis = consider carotid endartectomy.
bloods - ESR (for vasculitis), FBC/platelets/clotting, glucose, cholesterol/lipids
how do you manage a suspected infarctive stroke if thrombolysis not an option? - also cover secondary prevention after stroke.
give everyone aspirin 300mg/day for 2 weeks
THEN
clopidogrel - long-term secondary prevention.
if not tolerated give:
aspirin 75mg day, plus dipyridamole (antiplatelet)
if AF - start on NOAC.
Carotid endartectomy – carotid stenosis of either >70% or >50% (NICE quotes two criteria??) should be referred for assessment for this within 1 week, and have procedure within 2.
explain the oxford stroke classification system
The following criteria should be assessed:
- unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
Total anterior circulation infarcts (TACI, c. 15%) -
involves middle and anterior cerebral arteries
all 3 of the above criteria are present
Partial anterior circulation infarcts (PACI, c. 25%) -
involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
2 of the above criteria are present
Lacunar infarcts (LACI, c. 25%) -
involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis
Posterior circulation infarcts (POCI, c. 25%) - involves vertebrobasilar arteries presents with 1 of the following: 1. cerebellar or brainstem syndromes 2. loss of consciousness 3. isolated homonymous hemianopia
explain the ROSIER criteria for assessing likelihood of stroke
like a grown up version of FAST.
Exclude hypoglycaemia first, then assess the following:
(assessment –> score)
Loss of consciousness or syncope –> - 1 point
Seizure activity –> - 1 point
New, acute onset of:
• asymmetric facial weakness –> + 1 point
• asymmetric arm weakness –> + 1 point
• asymmetric leg weakness –> + 1 point
• speech disturbance –> + 1 point
• visual field defect –> + 1 point
A stroke is likely if > 0
how is haemorrhagic stroke managed?
Treatment is essentially supportive. If anticoagulants and antiplatlets have been given, then the effect can be reversed with vitamin K, fresh frozen plasma (FFP) and platelet transfusions.
Hypertension should only be treated if systolic is >185
If the haemorrhage causes a mass of >3cm diameter, then surgery can be lifesaving.
what is a transient ischaemic attack (TIA)?
mini stroke! symptoms resolve completely within 24hrs
80% are due to thromboembolus.
“sudden onset of focal CNS symptoms/signs due to temporary occlusion of part of the cerebral circulation”
what symptoms/signs in a TIA indicate an anterior circulation lesion? where is the thrombus likely to be from?
Likely thrombus from carotid system
Most likely affecting cerebral function
Symptoms/signs: Aphasia/dysphasia Hemiparesis Amaurosis fugax Sensory loss (hemi) Hemianopic visual loss
what symptoms/signs in a TIA indicate a posterior circulation lesion? where is the thrombus likely to be from?
Posterior Circulation
Likely thrombus from vertebrobasilar system
Most likely affecting cerebellar/brainstem function
Symptoms/signs: Diplopia, vertigo, vomiting Chocking / dysarthria Hemianopic visual loss Sensory loss (hemi) Transient global amnesia Tetraparesis LOC (rare)
what is amaurosis fugax?
sudden loss of vision in one or both eye(s), caused by an infarct in the retinal artery(ies).
classically - curtain coming down.
how do you decide how to manage someone presenting with a possible TIA?
assess risk of stroke using ABCD2 - score of 4+ needs urgent referral to TIA clinic (within 24h - everyone with TIA should be seen within 7 days): Age 60+ --> 1 pt BP >140/90 --> 1pt Clinical features - unilateral weakness --> 2 pts - speech disturbance only --> 1 pt Duration of symptoms - 1+ hrs --> 2 pts - 10-59 mins --> 1pt Diabetes --> 1 pt
start everyone on 300mg aspirin daily (unless current bleeding disorder, already on it, or otherwise CI’ed).
then switch to clopidogrel (or aspirin + dipyridamol as per stroke secondary prevention)
investigate/treat for cause, esp carotid artery doppler/carotid endartectomy
give info on driving and stroke/TIAs
avoid for 1 month, DVLA doesn’t need informing unless multiple attacks (for TIA) or residual deficit (for stroke) after 1 month.
if HGV/passenger carrying vehicle - must inform DVLA.
explain MRC muscle weakness grading
grade 0 - no muscle contraction
grade 1 - flicker of contraction
grade 2 - some active movement when gravity removed (e.g. swinging leg sideways across bed)
grade 3 - active movement against gravity
grade 4 - active movement against resistance (can be split into 4-, 4 and 4+)
grade 5 - normal power (allowing for age)
what are upper motor neurone lesions? signs/symptoms?
damage to motor pathways (corticospinal tracts) anywhere from motor nerve cells in prefrontal gyrus of frontal cortex –> internal capsule –> brainstem –> cord –> synapse with anterior horn cells.
pyramidal weakness
loss of skilled fine finger movements to greater extent than you’d expect from weakness
spasticity in stronger muscles (arm flexors, leg extensors)
hyperreflexia - brisk reflexes
upgoing plantars (+ve babinksi sign) ± clonus ± positive Hoffman’s reflex
what is pyramidal weakness?
seen in UMN lesions
distribution of weakness, typically involving arm extensors, small muscles of hand, lower limb flexors.
weakness of extension in upper limb, and flexion in lower limb
no muscle wasting
what is spasticity?
increased tone that is velocity-dependent and non-uniform i.e. faster you move the muscle, the greater the resistance - usually seen with brisk reflexes as well.
compare to rigidity, which is constant throughout the movement
what is the Babinski reflex?
draw thumbnail from heel to toes - upgoing plantar response = positive Babinski
what is Hoffman’s sign/reflex?
flick the pulp of middle finger away from palm –> brief flexion of thumb and index finger in pincer movement
may be more pronounced if neck extended.
what is clonus?
elicited by rapid dorsiflexion of foot - 3 or less downward, rhythmic beats is normal, any more suggests UMN lesion
what are lower motor neurone lesions? signs/symptoms?
damage anywhere from anterior horn cells in cord –> nerve roots –> plexi –> peripheral nerves
weakness distribution is according to muscles supplied by the involved nerve/cord segment etc.
affected muscles show wasting ± fasciculation
hypotonia/flaccidity
reduced/absent reflexes
Babinski negative (flexor plantars)
what is fasciculation?
spontaneous involuntary twitching of a muscle, might be seen in a LMN lesion.
what is idiopathic intracranial hypertension?
occurs typically in young, obese women.
symps/signs of raised ICP but no mass lesion on CT/MRI.
thought to be due to impaired CSF absorption.
how does idiopathic intracranial hypertension present?
young, obese woman complaining of morning headache, vomiting and sometimes visual disturbance (e.g. diplopia, visual obscurations). tinnitus common.
uni/bilateral sixth nerve palsies = ‘false localising sign’ of raised ICP.
scans normal, LP confirms raised pressure but otherwise normal.
what are visual obscurations?
sudden, transient bilateral visual loss with changes in posture
how do you manage a patient with idiopathic intracranial hypertension? what are you worried about?
in some, it’ll self-resolve, or go with weight loss/a few LPs.
if progresses to more chronic - threat to vision from secondary optic atrophy.
Rx with acetazolamide, diuretics or corticosteroids, or surgery to insert lumboperiotneal shunt draining CSF.
what is Kernig’s sign?
pain and resistance to passive knee extension with hip flexed - demonstrates meningism (NB - can be negative even in presence of meningism!)
give some differentials for facial pain
trigeminal neuralgia post-herpetic neuralgia giant cell arteritis - if presenting with jaw claudication sinusitis dental/oral disease
what is post-herpetic neuralgia? how can you treat it?
patient who’ve had shingles in a branch of the optic nerve may end up with persistent facial pain after the rash.
may be very severe and intractable, lasting 2-3yrs after rash.
might respond to TCAs, carbamazepine, topical capsaicin.
outline the GCS scoring system
Motor response
- Obeys commands
- Localises to pain
- Withdraws from pain
- Abnormal flexion to pain (decorticate posture)
- Extending to pain
- None
Verbal response
- Orientated
- Confused
- Words
- Sounds
- None
Eye opening
- Spontaneous
- To speech
- To pain
- None
score = 3-15
outline motor scoring in the GCS
6 = obeys command 5 = localises to pain 4 = withdraws from pain 3 = abnormal flexion to pain 2 = extending to pain 1 = none
outline verbal response scoring in GCS
5 = orientated 4 = confused 3 = inappropriate words 2 = incomprehensible sounds 1 = none
outline eye opening scoring in GCS
4 = spontaneously 3 = to speech 2 = to pain 1 = none
list some causes of altered level of consciousness
Structural
- infratentorial (directly involving brain stem) e.g. trauma, infarction, haemorrhage, tumour, demyelination
- supratentorial (compressing brainstem) e.g. as above, esp if affect R hemisphere
Diffuse
- hypoxia
- hypoglycaemia
- renal/liver failure
- hypothermia
- vitamin deficiencies
- epilepsy
- inflammation - meningitis, encephalitis
- drugs and toxins - opiates, antidepressants, hypnotic, alcohol
explain criteria for brainstem death
Criteria for brain stem death testing:
- Deep coma of known aetiology.
- Reversible causes excluded
- No sedation
- Normal electrolytes
Testing for brain death:
- Fixed pupils which do not respond to sharp changes in the intensity of incident light
- No corneal reflex
- Absent oculo-vestibular reflexes
- No response to supraorbital pressure
- No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation
- No observed respiratory effort in response to disconnection of the ventilator
Notes:
The test should be undertaken by two appropriately experienced doctors on two separate occasions. Both should be experienced in performing brain stem death testing and have at least 5 years post graduate experience. One of them must be a consultant. Neither can be a member of the transplant team (if organ donation contemplated).
give some causes of syncope - also what is it?
syncope = LOC due to transient reduction in blood flow to brain
- cardiac arrhythmias
- prolonged standing, esp in warm surroundings
- psychogenic e.g. around needles
- excessive reflex vagal stimulation e.g. micturition syncope, cough syncope
what features in a LOC hx suggest syncope?
prodrome - lightheadedness, nausea, blurred/tunnel vision, pallor, sweating
rapid recovery - once supine, will recover in seconds to 1-2 mins.
situation e.g. standing in hot room, around needles
list some differentials for LOC
- epilepsy
- syncope
- hypoglycaemia (warnings = anxiety, tremor, unsteadiness, sweating, hunger)
- drop attacks (in middle aged and elderly woman - random falls)
what are the 4 clinical features you might see in narcolepsy?
1) daytime sleep attacks - lasting 10-20 mins, pt awake refreshed. irresistible and occur inappropriately e.g. during meals, driving, mid-convo
2) cataplexy - episodes of loss of postural control + limb weakness, with preserved consciousness - often provoked by emotional events e.g. laughter
3) sleep paralysis - inability to move while falling asleep/waking
4) hypnagogic hallucinations - frightening visual hallucinations on falling asleep
what is cataplexy?
episodes of loss of postural control and limb weakness, with preserved consciousness - often provoked by emotional events e.g. laughter
Ix - sleep studies, EEG, MRI (for SOLs)
how can you treat narcolepsy/cataplexy?
narcolepsy - amphetamines, but be sure you’ve got the diagnosis right before starting due to addictive properties! also modafinil.
cataplexy - clomipramine, other antidepressants.
what brain functions is the frontal lobe responsible for?
- higher intellectual function
- personality, mood
- social conduct, behaviour
- posterior frontal region contains motor areas
- frontal eye fields (conjugate eye movements)
- language (in dominant hemisphere)
what brain functions is the temporal lobe responsible for?
- memory
- language (in dominant hemisphere)
- visual pathway (optic radiation)
what higher brain functions is the parietal lobe responsible for?
dominant hemisphere: - language, reading, writing - calculation - praxis (learning complex motor skills) non-dominant: - visuo-spatial function both: - higher sensory function - visual pathway (optic radiation)
what higher brain functions is the occipital lobe responsible for?
- visual cortex and visual association areas
what is aphasia/dysphasia?
impairment of language function as a result of brain damage
distinguish from dysarthria - impairment of articulation due to disease of muscles/neves involved with speech production
what is dyspraxia/apraxia?
inability to perform complex motor acts despite normal muscle power, sensation and coordination, with good comprehension and cooperation.
results from parietal lobe damage
what is Broca’s aphasia?
aka expressive aphasia
due to a lesion of the inferior frontal gyrus
speech is non-fluent, laboured, and halting
comprehension is normal
what is Wernicke’s aphasia?
due to a lesion of the superior temporal gyrus
this area ‘forms’ the speech before ‘sending it’ to Broca’s area. Lesions result in sentences that make no sense, word substitution and neologisms but speech remains fluent
comprehension is impaired
what is conduction aphasia?
classically due to a stroke affecting the arcuate fasiculus - the connection between Wernicke’s and Broca’s area
speech is fluent but repetition is poor. Aware of the errors they are making
comprehension is normal
what clinical features would you expect to see in a parietal lobe lesion?
sensory inattention apraxias astereognosis (tactile agnosia) inferior homonymous quadrantanopia Gerstmann's syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation
what clinical features would you expect to see in an occipital lobe lesion?
homonymous hemianopia (with macula sparing)
cortical blindness
visual agnosia
what clinical features would you expect to see in a temporal lobe lesion?
Wernicke’s aphasia: this area ‘forms’ the speech before ‘sending it’ to Brocas area. Lesions result in word substituion, neologisms but speech remains fluent
superior homonymous quadrantanopia
auditory agnosia
prosopagnosia (difficulty recognising faces)
what clinical features would you expect to see in a frontal lobe lesion?
expressive (Broca's) aphasia: located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus. Speech is non-fluent, laboured, and halting disinhibition perseveration anosmia inability to generate a list
what clinical features would you expect to see in a cerebellar lesion?
midline lesions: gait and truncal ataxia
hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus
what’s CN I called and what does it do?
olfactory nerve –> sense of smell.
what’s CN II called and what does it do?
optic nerve –> vision:
visual acuity, visual fields, colour vision, pupillary responses.
what kind of vision loss is seen in a lesion of the optic nerve?
monocular visual loss - essentially ‘blind’ in one eye (ipsilateral to lesion)
what kind of vision loss is seen in a lesion of the optic chiasm?
bitemporal hemianopia - loss of temporal halves of vision on both sides.
due to damage to decussating fibres from the nasal halves of retinae, as light from the temporal half-field is processed by nasal part of the retina.
what kind of vision loss is seen in a lesion of the optic tract?
homonymous hemianopia e.g. left half-fields in each eye missing (lesion would then be in R optic tract i.e. contralateral).
damage is to fibres from temporal half of one retina (in this e.g. the L one) and the decussated fibres from nasal half of the other (R one).
which lobes are damaged in homonymous inferior vs superior quadrantanopias?
PITS
Parietal = inferior
Temporal = superior
contralateral!
what is a central scotoma and what might cause it?
loss of central vision, usually associated with reduction in visual acuity
diseases of optic nerve and macular region of retina
what causes enlargement of the physiological blind spot?
papilloedema - swelling of the optic disc - due to raised ICP.
usually have preserved visual acuity.
what is macular sparing and what kind of lesion could cause it?
preservation of macular (central) region in patients with homonymous hemianopia
lesion of visual cortex sparing occipital pole
what is tunnel vision and what can cause it?
loss of peripheral fields, with preservation of central region
- ophthalmological disease - chronic simple glaucoma
- retinal disease - retinitis pigmentosa
- cortical disease
what does an afferent pupillary defect look like?
when torch shines in affected eye, the light isn’t perceived so neither pupil constricts (direct or consensual).
when torch is shined in the normal eye, they both constrict.
what does an efferent pupillary defect look like?
light is perceived by affected eye but pupil can’t respond - the other pupil constricts consensually but direct reflect absent.
when light shined on unaffected eye, you get direct response but not consensual
what is a relative afferent pupillary defect? what condition is it strongly linked with?
affected eye can still respond directly to light but not as well as the other side
important sign of optic neuritis - persists after symptoms resolve.
aka the Marcus-Gunn pupil
what is a Holmes-Adie pupil?
benign cause of dilated pupil, commonly seen in women:
unilateral in 80% of cases
dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slowly reactive to accommodation but very poorly (if at all) to light
aka myotonic pupil
what is a Argyll Robertson pupil?
sometimes seen in neurosyphilis
mnemonic = Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)
Features:
small, irregular pupils
no response to light but there is a response to accommodate
Causes:
diabetes mellitus
syphilis
what are the names of CNs III, IV and VI - what do they do?
occulomotor, trochlear, abducens nerves
trochlear (IV) supplies superior oblique
abducens (VI) supplies lateral rectus
the rest are supplied by occulomotor, which also supplies levator palpebrae superioris (opens eye lid)
what is ptosis?
drooping of eyelid (partial) or unable to open eye (complete) - weakness of levator palpebrae suprioris
what is diplopia? what causes it?
double vision - neurologically, arises from malalignment of eyes distinguish binocular (occurs when both eyes open) from monocular (persists when one eye covered) - monocular = ophthalmological rather than neurological
what would you see in a third nerve palsy?
ptosis due to paralysis of levator palpebrae superioris
when examiner opens eyelid, eye is in ‘down-and-out’ position due to unopposed action of superior oblique and lateral rectus muscles
pupil may be ‘fixed’ (no reflex responses) or dilated (‘surgical’ 3rd nerve palsy) or spared (‘medical’ third nerve palsy)
list some causes of third nerve palsies
diabetes mellitus
vasculitis e.g. temporal arteritis, SLE
false localizing sign due to uncal herniation through tentorium if raised ICP
posterior communicating artery aneurysm (pupil dilated)
cavernous sinus thrombosis
Weber’s syndrome: ipsilateral third nerve palsy with contralateral hemiplegia - caused by midbrain strokes
other possible causes: amyloid, multiple sclerosis
what would you see in a fourth nerve palsy?
unilateral paralysis of superior oblique, causing vertical diplopia noticed when descending stairs or looking down at a book - may tilt head towards normal side to correct.
causes - mild head trauma
what would you seen in a sixth nerve palsy?
unable to abduct affected eye because of unopposed action of medial rectus.
diplopia on looking to affected side with horizontal separation of images.
if isolated sixth nerve palsy - vascular prob, secondary to diabetes/HTN
also can be false localising sign of raised ICP due to long, tortuous intracranial course
what is Horner’s syndrome?
Features - miosis (constricted pupil) ptosis (partial) enophthalmos (sunken eye) anhidrosis (loss of sweating on affected side of face)
lesion of sympathetic nerve supply to eye - hypothalamus –> brainstem –> cervical cord –> T1 nerve root –> cervical sympathetic chain –> eye
what is nystagmus?
involuntary rhythmic oscillatory movement of eyes, might be present on attempted sustained horizontal/vertical gaze.
what is CN V called? what does it do?
trigeminal nerve - facial sensation and masticatory muscles
divided into ophthalmic, maxillary, mandibular.
corneal reflex
lesions - loss of facial sensation and corneal reflex, problems chewing, jaw deviation - all depends which branch is affected.
what is CN VII called? what does it do?
facial nerve - muscles of facial expression, taste sensation to anterior 2/3rds of tongue, lacrimation, salivation.
lesions: flaccid paralysis of upper + lower face loss of corneal reflex (efferent) loss of taste hyperacusis
what is Bell’s palsy? features?
acute, unilateral, idiopathic, facial nerve paralysis - cause unknown, might be to do with HSV.
Features - rapid sudden onset:
lower motor neuron facial nerve palsy - forehead affected*
patients may also notice post-auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis
how do you manage Bell’s palsy?
10 day course of pred if within 72hrs of onset
advise artificial tears, eye lubricants and taping eyelid down to protect the cornea
what is CN VIII called? what does a lesion cause?
vestibulocochlear nerve - hearing and balance.
lesions cause:
Hearing loss
Vertigo, nystagmus
Acoustic neuromas are Schwann cell tumours of the cochlear nerve
explain Rinne’s and Weber’s tests
Performing both Rinne’s and Weber’s test allows differentiation of conductive and sensorineural deafness.
Rinne’s test:
512 Hz tuning fork is placed over the mastoid process until the sound is no longer heard, followed by repositioning just over external acoustic meatus
air conduction (AC) is normally better than bone conduction (BC)
if BC > AC then conductive deafness
Weber’s test:
512 Hz tuning fork is placed in the middle of the forehead equidistant from the patient’s ears
the patient is then asked which side is loudest
in unilateral sensorineural deafness, sound is localised to the unaffected side
in unilateral conductive deafness, sound is localised to the affected side
what is CN IX called? functions?
glossopharyngeal nerve
taste (posterior 1/3rd of tongue)
Salivation
Swallowing
Mediates input from carotid body & sinus
lesions - loss of gag reflex, hypersensitive carotid sinus reflex (afferent)
what is CN X called? functions?
vagus
functions:
Phonation
Swallowing
Innervates viscera
lesions: uvula deviates away from site of lesion loss of gag reflex (efferent) swallowing difficulties, dysarthria vocine cough
what is CN XI called? functions?
accessory nerve
supplies sternomastoid and trapezius muscles
sternomastoid - turning head against resistance
trapezius - shrugging shoulders
what is CN XII called? functions?
hypoglossal
tongue muscles!
lesion (if LMN) - uni/bilateral wasting and fasciculation.
if unilateral - tongue deviates to affected side on protrusion.
differentiate between bulbar and pseudobulbar palsies
bulbar palsy = LMN lesion of CN IX, X and XII.
pseudobulbar palsy = UMN of CN IX, X and XII.
list some causes of bulbar palsy
brainstem vascular disease MND syringobulbia tumour brainstem encephalitis e.g. polio Guillain-Barre syndrome skull base or meningeal infiltration myasthenia gravis some muscular dystrophies polyomyositis
what are the features of a bulbar palsy?
nasal speech absent jaw jerk palatal weakness, nasal regurg of food reduced or absent gag reflex wasted, fasciculating tongue
list some causes of pseudobulbar palsy
bihemispheric vascular disease MND MS tumour extrapyramidal disease
what are the features of pseudobulbar palsy?
slow, monotonous speech, sometimes explosive
brisk jaw jerk
dysphagia
brisk gag reflex
shrunken, immobile tongue
emotional lability - spontaneous laughing/crying
describe the gait you would see in a spastic paraparesis
spastic paraparesis = UMN lesion affecting both legs
described as scissoring, ‘wading through mud’
describe the gait you would see in a spastic hemiparesis
spastic hemiparesis = UMN lesion affecting one leg
leg is rigid and circumducts - described as semicircle rotating at hip
describe the gait you would see in a bilateral foot drop
bilateral foot drop = LMN lesion of both legs
steppage gait - legs lifted high to avoid scraping toes
describe the gait you would see in a cerebellar lesion
wide-based gait, staggering, unable to walk heel-toe
describe the gait you would see in a Parkinsons
stooping posture, rigid shuffling gait, no arm swing
describe the gait you would see in a proximal myopathy
waddling
what is epilepsy?
tendency to recurrent seizures - paroxysmal cerebral cortical neuronal discharges result in intermittent, stereotyped attacks of altered consciousness, motor or sensory function, behaviour or emotion
explain how epileptic seizures are classified
focal vs generalised
focal aware = consciousness maintained through
focal impaired awareness = consciousness impaired at any stage
generalised onset involved both sides of / whole brain, LOC occurs immediately
note focal seizures may become secondary generalised (aka bilateral tonic-clonic) - pt loses consciousness and there’s clinical evidence of more generalised involvement
give some info on generalised onset seizures and the subtypes
these engage or involve networks on both sides of the brain at the onset consciousness lost immediately. further subdivided into motor (e.g. tonic-clonic) and non-motor (e.g. absence) specific types include: → tonic-clonic (grand mal) → tonic → clonic → typical absence (petit mal) → myoclonic: brief, rapid muscle jerks → atonic
what are the features of a tonic-clonic / grand mal seizure?
prodrome/aura - dizziness, irritability
LOC ± epileptic cry and fall to the ground
then initial tonic phase - generalised muscle spasms for a few secs
then clonic phase - sharp, repetitive muscle jerks.
may see tongue biting, incontinence and salivation.
when jerks stop, patients usually unconscious for another half an hour or so, then are drowsy and confused for several hours (recovery)
may have headache (from fall) or back pain (from muscle spasms) in recovery period.
what are the features of a focal, temporal lobe epilepsy?
aura - psychic symptoms (e.g. deja/jamais vu), hallucinations (olfactory, gustatory, visual images), epigastric rising sensation
automatisms - chewing and lip smacking.
HEAD: Hallucinations Epigastric rising/emotional lability Automatisms Deja vu/dysphasia post-ictal
what are the features of a focal, frontal (motor) lobe epilepsy?
Head/leg movements , posturing, post-ictal weakness
what are the features of a focal, parietal (sensory) lobe epilepsy?
paraesthesiae
what are the features of a focal, occipital (visual) lobe epilepsy?
floaters/flashers
what are the features of a Jacksonian march seizure?
focal motor attack beginning in the corner of the mouth, the thumb and index finger, or the big toe
movements rapidly spread across face or ascend limb
associated with organic brain disease causing the epilepsy e.g. tumour in motor region
afterwards, affect limb may remain weak - Todd’s paralysis
what is Todd’s paresis/paralysis?
focal weakness after a partial seizure, usually resolves completely within 48h
describe the features of febrile convulsions
seizures associated with fever child aged 6 months - 5 years brief (< 15mins) and generalised, although some might have focal and prolonged attacks usually isolated attack doesn't require prophylactic AEDs
what is West’s syndrome (infantile spasms)?
triad of:
1) brief spasms beginning within first few months of life - shock-like flexion of arms, head and neck with drawing up of feet (salaam attack)
2) progressive learning difficulties
3) hypsarrhythmia on EEG
usually has an identifiable cause e.g. perinatal asphyxia, encephalitis, metabolic disorders, cerebral malformations
Rx - vigabatrin/steroids
what are petit mal / absence seizures?
generalised epilepsy, usually starts in childhood (peak onset 4-8yrs)
attacks occur without warning - child stares into space and stops talking, eyes may flutter/roll up under lids.
recovery within seconds, may have many attacks per day
EEG: 3Hz generalized, symmetrical
sodium valproate, ethosuximide
good prognosis: 90-95% become seizure free in adolescence
what is juvenile myoclonic epilepsy / Janz syndrome?
onset: teens; F:M = 2:1
1) Infrequent generalised seizures, often in morning
2) Daytime absences
3) Sudden, shock like myoclonic (involuntary jerking) seizure - usually in morning (patient inexplicably spills/throws breakfast across room)
usually good response to sodium valproate - carbamazepine can make it worse!!
list some causes of epilepsy in neonates
birth trauma intracranial haemorrhage hypoxia hypoglycaemia hypocalcaemia
list some causes of epilepsy in children
congenital anomalies
tuberous sclerosis
