Stroke Flashcards
What is the role of the pre-frontal cortex?
Decision and planning
How does one calculate CPP?
CPP = Mean blood pressure – ICP
What is a lentiform bleed?
Extradural haematomas - ARTERIAL BLEED
- Lense shaped depression on scan
- Usually due to middle meningeal artery bleed
What is the Monroe-Kellie doctrine?
The relationship between ICP, CSF, CPP, blood and brain tissue
What % of stroke patients have diabetes?
20% - 2-4x risk of stroke with diabetes
What % of stroke is associated with AF?
16%
What patients are at the highest risk of stroke?
Patients that have already had one
15% of patients with untreated AF will have another stroke within a year
What is a carotid endarterectomy?
Surgical procedure to remove build up of fatty deposits in carotid arteries
What is clopidogrel?
Prevents platelet function, blocks P2Y12ADP receptor thus preventing cross linking of fibrin
What % of strokes are bleeds?
20%
What are the roles of the frontal cortex?
- Contralateral movements
- Broca’s area (dominant hemisphere, which is the left in 96% of people)
- cortical inhibition of bladder and bowels
- prefrontal – personality, initiative, sequencing
What are the roles of the parietal lobes?
- Post central gyrus – sensory cortex
- Wernicke’s area – receptive, comprehension
- Handling numbers (dominant hemisphere)
- non dominant – concepts of body image
- visual pathways in Meyer’s loop
What are the roles of the temporal cortex?
- Auditory cortex
- Learning and memory
- Olfaction
- Emotional behaviour
- Visual pathways
What % of ischemic stroke is due to atheroembolism?
50%
What is a lacunar infarction?
Most common type of ischemic stroke, due to occlusion of small penetrating arteries that provide blood to deep structures
What would be the consequences of a stroke in the posterior circulation?
- Vertigo
- Ataxia: cerebellar syndrome
- Isolated hemianopia
What is a TACI?
Total anterior circulation infarct
(top half of circle of Willis)
*Diagnosed when all three are present:
- hemi motor and sensory deficit: has to be at least 2/3 of face, arms/ legs
- hemianopia
- cortical (higher) dysfunction
What is a PACI?
Partial anterior circulation infarct
- same as a TACI but when 2/3 are present
What is a LACI?
Lacunar infarct
- pure motor hemiplegia
- pure sensory loss
- Motor and sensory loss
What is dysarthria?
Problem with the muscles, make speaking difficult or impossible – disorder in the motor aspect of speech
What is dysphasia?
Inability to generate or comprehend speech
What is Broca’s aphasia?
Inability to form words correctly – expressive aphasia
What is Wernicke’s aphasia?
Receptive aphasia, cant understand speech but can say words without trouble
*due to receptive loss, words said don’t make sense as a sentence
What are the roles of the frontal lobe?
- Intellectual function
- Paraxis - Giving instructions in an ordered sequence
- Bladder continence
- Saccadic eye movement - Voluntary horizontal eye movements
- Motor function
- Expression of language - In dominant lobe (normally left)
What are the roles of the temporal lobes?
- Memory
- Smell
- Hearing
- Vestibular function
- Emotion (limbic system)
What is the role of the parietal cortex?
- Sensory integration - Information on sight/smell etc comes from the other lobes, the parietal lobe interprets this information andintegrates it together
- Receptive language-Making sense of language
What is the most common type of stroke?
Lacunar infarct
Often as a result of hypertension, small vessels become thickened and occlude and are prone to blockages
What are the consequences of an anterior cerebral artery stroke?
LEGS Loss of sentation and motor function on the contralateral side
Consequences of a middle cerebral artery stroke
ARMS AND FACE - loss of sensory and motor function on the contralateral side
BROCA’S APHASIA
Consequences of a posterior cerebral artery stroke
Occipital lobe - homonymous hemianopia - loss of the same visual field in both eyes
Consequences of a basilar artery stroke
Locked in syndrome - corticospinal tracts on both sides affected
Vertical eye movements and awareness maintained
Which type of stroke is associated with cranial nerve 7 paralysis?
Anterior inferior cerebellar
Posterior cerebral artery stroke consequences
- Visual problems
- Prosopagnosia (facial recognition)
- Alexia (inability to read)
- Aphasia (can’t comprehend spoken words)
Middle cerebral artery stroke
- Contralateral face and arm weakness and sensory loss
- Mild/ no leg weakness
- Head and eyes deviated to side of stroke
- If left-sided (most people are left-dominant) aphasia
Anterior cerebral artery stroke
- Contralateral leg weakness and sensory loss
- Mild/ no upper extremity involvement
- Balance problems
- Aphasia if left-sided
Lacunar infarct
- Pure motor stroke without sensory symptoms
- Pure sensory stroke without motor symptoms
- Ataxia (loss of coordination)
- Absence of higher cortical functions e.g. language, vision, facial recognition
- Clumsy hand syndrome
Vertebrobasilar stroke
- Vertigo
- Dizziness
- Vision problems
- Facial weakness
- Dysphagia
- Dysarthria
- Loss of pain and temperature sensation
- Ipsilateral Horner’s syndrome
Which sequence of MRI pick up oedema due to ischaemia?
DWI - diffusion weighted imaging
Looks for cytotoxic edema which occurs becayse a lack of ATP causes ion channels to stop working and cells swell
Define a stroke
Sudden onset focal neurological deficit of presumed vascular aetiology lasting >24hrs
Stroke epidemiology
3rd commonest killer in UK
£2.8 billion direct care costs
300,000 disabled survivors
Rsik factors for stroke
Non-modifiable
- Age
- Gender
- Race
- FHx
Modiafiable
- Smoking
- BP (most important by far for cerebral haemorrhage)
- AF
- Hyperlipidaemia
- Obesity
What can mimic a stroke?
Metabolic: hypoglycaemia
CNS causes: epilepsy, Todd’s paresis, migraine, mass lesion, MS, encephalitis
Functional disorders
Things that look like something else but is stroke
- Acute confusional state
- Abnormal movements/ seizures
- PNS symptoms
- Acute vestibular syndrome
Causes of stroke
Atheromatous disease: 50%
Heart: AF, valve, endocarditis, myxoma: 25%
Small end arteries: 25%
Others: air, fat etc (rare)
TACS
Total anterior circulation stroke
All three of:
- Unilateral weakness of arm, leg or face ± sensory deficit
- Homonymous hemianopia
- Higher cerebral dysfunction e.g. dysphasia, visuospatial disorder
PACS
Partial anterior circulation stroke
Two of the following:
- Unilateral weakness of arm, leg or face ± sensory deficit
- Homonymous hemianopia
- Higher cerebral dysfunction e.g. dysphasia, visuospatial disorder
LACS
Lacunar stroke syndrome - most common ischaemic stroke syndrome
One of:
- Pure motor stroke
- Pure sensory stroke
- Sensori-motor stroke
- Ataxic hemiparesis
POCS
Posterior stroke syndrome
One of:
- Cranial nerve palsy + contralateral motor/ sensory deficit
- Bilateral motor/ sensory deficit
- Conjugate eye movement disorder e.g. gaze palsy
- Isolated homonymous hemianopia or cortical blindness
Commonest complications of stroke
- Urinary incontinence (30-65%)
- Acute confusion
- Pain
- Malnutrition (8-35%)
- Chest infections
- VTE
- Epilepsy
- Pressure sores
- Aspiration
Secondary prevention of stroke
- Clopidogrel 75mg
- Atorvastatin 40mg
- Antihypertensives
- Lifestyle advice
Where would we listen for a carotid bruit?
Angle of the jaw
Arterial supply to the brain
Sources of intracerebral haemorrhage
- Aneurysm rupture
- AVM
- Cavernoma (blood blister/ raspberry cluster of blood vessels, abnormality bleeds into itself)
- Bleed into infarct
- Trauma
- Amyloid angiopathy (amyloid deposits in vessels, vessels are frail and can bleed)
What is amyloid angiopathy?
Accumulation of amyloid protein in blood vessels - increases risk that the vessel will rupture because the proteins cause vessel walls to become more frail
Commonest site for subarachnoid haemorrhage?
Junction of anterior cerebral and anterior communicating arteries
Clinical presentation of a subarachnoid haemorrhage
- Thunderclap headache
- Sudden collapse/ coma
- Seizures
- 1/3 die within 1st 2hrs
- Vasospasm can occur leading to ischaemic stroke (for this nimodipine is used, it is a Ca2+ channel blocker than opens vessels and prevents spasms)
Risk factors for thrombo-embolic stroke
- HTN
- Smoking
- DM
- Lipid abnormalities
- Hormones
- Age
- Vaculitis
- AF
- Endocarditis
- Valvular heart disease
What is Weber syndrome?
Midbrain stroke syndrome: causes ipsilateral 3rd nerve palsy and contralateral motor dysfunction
Which type of stroke is most common?
Ischaemic - 80%
Haemorrhagic - 20%
What are the three factors that precipitate thrombosis?
- Blood stasis
- Vessel wall changes
- Changes in blood consituency
= VIRCHOW’S TRIAD
What is the cause of most ischaemic strokes?
- Atherosclerosis: either within the vessels in the brain itself or within systemic vessels that embolise
- AF: causes cardioembolism
Conditions which increase the likelihood of ischaemic stroke
- Inflammatory vascular disease/ vasculitis
- Collagen vascular disease e.g. Marfan’s
- Infection
- Arterial dissection
- Coagulopathy e.g. polycythemia
Consequences of haemorrhagic stroke
- Disruption of BBB
- Cerebral oedema
- Neuronal damage
- Increased ICP
- Hydrocephalus if haemorrhage occurs into ventricles
What is the biggest cause of intracerebral haemorrhage?
HTN: small cerebral vessels are weakenes by high pressures
What is the Oxford classification of stroke?
AKA Bamford classification
- Divides stroke into 4 categories
1. Anterior circulation syndromes: either total or partial (MCA and ACA)
2. Posterior circulation syndrome
3. Lacunar syndrome
Discuss hemispheric dominance
Cerebral dominance = term used to describe the lateralisation f brain functions
- The activity associated with some functions is located in one hemisphere only e.g. speech
Dominant hemisphere = language, mathematical processing, writing
Non-dominant hemisphere = emotion, tone of language, spatial recognition, musical interpretation
Most people = left-sided dominance
**The clinical pattern of higher cortical dysfunction indicates whether the stroke has occurred in the dominant or non-dominant hemisphere
Patient has difficulty reading, writing and calculating but they have insight - dominant or non-dominant hemisphere affected by stroke?
Dominant - the dominant hemisphere does all the essential, non-arty stuff
How to tell if a stroke is ischaemic or haemorrhagic clinically
You can’t - typically headache is worse in haemorrhagic stroke but the only way to distinguish is imaging
What would the clinical features of a posterior communicating artery aneurysm be?
Aneurysm compresses 3rd nerve:
- Ptosis
- Restriction of eye movements
- Pain in eye
- Dilated pupil (this occurs 1st as parasympathetic fibres encase the motor fibres of the 3rd nerve)
Discuss the clinical features of a posterior circulation stroke
Involves damage to the area of the brain supplied by the posterior circulation (e.g. brainstem and cerebellum)
One of the following need to be present for a diagnosis of POCS
- Cranial nerve palsy and contralateral motor/ sensory deficit
- Bilateral motor/ sensory deficit
- Conjugate eye movement disorder (inability to move both eyes in the same direction
- Cerebellar dysfunction e.g. vertigo, nystagmus
- Isolated homonymous hemianopia
Are higher cortical functions lost following a lacunar stroke?
No - these are sub-cortical strokes that occur due to small vessels disease
No loss of higher cerebral functions
One of the following needs to be present
- Pure sensory stroke
- Pure motor stroke
- Sensori-motor stroke
- Ataxic hemiparesis (ataxia = group of disorders that affect coordination, balance and speech
Differentials for stroke
Graciaa Charlotte So Sassy Haaris Didn’t like
Glucose derrangement
Complicated migraine
Sepsis
Seizures
Hepatic encephalopathy
Drugs
Lesions
What is the first investigation done when stroke is suspected?
Urgent CT - used to differentiate ischaemic and haemorrhagic stroke or to identify other pathology
Does infarction show on CT immediately?
No - it takes a few hrs
Early signs are subtle:
- Cortical sulci lose definition due to oedema
- Loss of differentiation between grey and white matter due to oedema
- Occluded MCA appears hyperdense on CT
Imagine in haemorrhagic stroke
CT - rapidly localises haemorrhage and visualises associated complications e.g. if ventricles are involved
CT angio/ MRI if aneurysm or AVM is suspected
Repeat MRI 6-8 weeks after haemorrhage as tumours/ space occupying lesions can hide under the bleed
Why is it important to re-image a brain 6-8 weeks after a haemorrhagic stroke?
Space occupying lesions can hide underneath the bleed
What are the goals of CT in an acute stroke setting?
- Exclude haemorrhage
- Look for early features of ischaemia
- Rule out other intracranial pathologies that may mimic a stroke
What is the mainstay imaging technique in acute stroke?
Non-contrast CT
Other than head CT/ MRI what investigations are important following stroke?
ECG: look for arrhythmias that can cause stroke mimic e.g. heart block OR rhythms that precipitate embolism formation e.g. AF
Bloods: Hypoglycaemia, hyperlipidaemia, electrolytes, thrombophilia screen, vasculitis screen
Diagnostic approach for acute stroke
- Assess presentation
- Acute stabilisation if needed A-E
- Localise lesion: hx and examination
- Identify timing of symptom onset: collateral hx?
- Identify cause and risk factors
- Imaging: urgent CT to exclude haemorrhage
- Assess suitability for thrombolysis
Other than thrombolysis and thrombectomy, discuss management of acute stroke patients
BP: treat if there are HTN related complications e.g. aortic dissection, hypertensive encephalopathy - important not to over manage as decent BP required for function of colateral vessel formation. IV labetalol = 1st line
Glucose control: hyperglycaemia associated with poor outcomes aim for 4-11mmol/L
Nutrition and hydration: hypovolemia can worsen ischaemia and increase delirium, DVT and infection risk
DVT prophylaxis
Seizure prevention: 2% have seizures after stroke
PT: prevent pressure sores, contractures, restore function
Neuropsychiatric
Communication is key
What is the overall aim in sichaemic stroke?
Salvage to ischaemic penumbra
This is the area of ischaemia around the infarction that is at risk of progressing to infarction but is salvageable if reperfused
Discuss thrombolysis in acute stroke
Must be given within 4.5hrs of symptom onset
- ALTEPLASE
**Only used once haemorrhagic stroke has been excluded
How do thrombolytic drugs work?
E.g. alteplase, streptokinase
- Convert plasminogen into plasmin which breaks down fibrin
Discuss thrombectomy in acute stroke
Offere ASAP and within 6hrs symptom onset
How is warfarin anticoagulation reversed following haemorrhagic stroke?
Give prothrombin complex concentrate and IV Vitamin K
Discuss BP control in patients with acute intracerebral haemorrhage
Aims for systolic BP 130-140mmHg within 1hr and maintain for at least 7 days
Discuss involvement of SaLT following stroke
- Ensure that patients have swallowing screened by SALT before any oral fluid, medication or food given
- If admission screen indicates problems ensure patient has specialist assessment within 24hrs and not more than 72hrs afterwards
- Patients unable to take nutrition, fluid and medication orally should have NG tube inserted and be fed within 24hrs admission unless they’ve had thrombolysis and have oral medication reviewed to amend route of administration
Acute ischaemic stroke management
- Give 300mg aspirin as soon as bleed ruled out
- Thrombolysis: only give if <4.5hrs since symptoms began
- Thrombectomy: within 6hrs of symptom onset OR within 24hrs if patient known to be well previously and have confrimed total occlusion of proximal posterior circulation
Contraindications to thrombolysis
- Previous intracranial haemorrhage
- Seizure at stroke onset
- Intracranial neoplasm
- Suspected subarachnoid haemorrhage
- Stroke or brain injury in past 3 months
- Lumbar puncture in last few days
- GI haemorrhage in past 3 weeks
- Current bleeding
- Pregnancy
- Varices
- Uncontrolled HTN >200/120
Secondary prevention of stroke
Continue aspirin until 2 weeks after symptom onset
After 2 weeks start long-term antithrombotic treatment e.g. clopidogrel
Carotid endarterectomy for stroke patients
Recommended if patient has had a TIA in the carotid territory and they are not severly disabled
Considered if carotid stenosis >70%
Acute haemorrhagic stroke management
No specific medial treatment for most causes or haemorrhagic stroke
- Stop all antiplatelet and anticoagulant drugs
- Correct coagulation deficits
- Monitor BP
- Discuss with neurosurgeons: if intraventricular bleed CSF diversion may be needed, ruptured aneurysms may need clipping
What is a TIA
Transient ischaemic attack, acute symptoms and signs of neurological dysfunction resolve completely within 24hrs
Suggests presence of atherosclerotic disease and high risk of stroke
Stroke risk following TIA
15% strokes are preceded by a TIA
8-12% 7 days troke risk following TIA
18% 30 day stroke risk following TIA
Secondary prevention, if started within 72hrs, can reduce 90-day stroke risk to 2%
Most common cause of TIA
Atherosclerosis causing embolism or cardioembolism
What is amaurosis fugax?
Common TIA syndrome caused by embolism occluding retinal artery, causes painless, rapid loss of vision in on eye ‘like a curtain coming down’
What is the ABCD2 cirteria?
Used to predict stroke risk following TIA but it is actually poor at discriminating low and high risk and is therefore not used anymore (since 2020)
Investigation for TIA
Imaging of brain, blood vessels, heart investigations, bloods
Same as acute stroke
Management of TIA
Overall aim is to reduce risk of stroke
Control risk factors: stop smoking, HTN control, DM control, hyperlipidaemia control
Antiplatelets: aspirin 300mg for 2 weeks then clopidogrel 75mg for life
Warfarin indicated if TIA caused by cardioembolism and patient has risk factors for cardioembolism e.g. prosthetic mechanical valve
What is the HASBLED score?
Used to estimate the risk of major bleeding for patients on anticoagulation who have AF
Scored from 0-9 with a score closer to 9 meaning bleeding risk is more likely
What is the CHADS2 VASC score?
Helps calculate the risk of stroke in patients with AF
- Congestive heart failure
- HTN = 1
- Age >75 = +2
- DM = 1
- Stroke or TIA in past = +2
- Vascular disease = 1
- Age 65-74 = 1
- Sex female = 1
Score 1 = consider anticoagulant
Score 2 = recommend anticoagulant
Primary prevention of stroke and TIA
- HTN, smoking, DM and hyperlipidaemia: all precipitate atherosclerosis
- Measure: lifestyle changes, medical treatment of HTN, DM and hyperlipidaemia
- Use CHADS2VASC score to calculate stroke risk in patients with AF and then give anticuagulant appropriately - this used to be warfarin but recently NICE have recommended the use of DOACs e.g. apixaban, dabigatran, rivaroxaban
Imaging for TIA
Do not offer CT to patients with suspected TIA
After patient has been seen in TIA clinic, consider MRI to detect the terrioty of ischaemia
Carotid imaging for all who have had a TIA and considered a candidate for carotid endaterectomy
What is the ROSIER tool?
Recognition of stroke in emergency room
Used to differentiate stroke and stroke mimics - recommended by NICE
Scores range from -2 to 5
Score <0 - unlikely to be a stroke
Important to exclude when assessing a suspected stroke patient?
Hypoglycaemia
What is Todd’s paresis?
- Focal weakness in a part/ all of body following a seizure
- Usally affects one side and can mimic a stroke
- Usually lasts <48hrs
- Can affect speech, gaze and vision
Presentation of Todd’s paresis
Transient (<48hrs) weakness of a hand, arm or leg following a focal seizure
Weakness can range from mild to complete paralysis
- Weakness usually occurs when seizure has affected motor cortex
Aetiology of Todd’s paresis
Idea is that the affected cortex is exhausted/ neurones are exhausted following seizure
Management of Todd’s paresis
None - rest until paralysis disappears
Used of thrombolytic agents is contraindicated if a seizure has occurred following a stroke
What are the functions of the facial nerve?
Taste to anterior 2/3 tongue
Supplies stapedius muscle
Muscles of facial expression
Difference bwteen UMN and LMN facial nerve palsy
UMN: forehead is spared
LMN: whole side of face affected
Presentation of a facial nerve palsy
Weakness in muscles of facial expression and eye closure: can lead to damage of conjunctiva and cornea
Face sags on affected side
UMN lesion: forehead spared
LMN lesion: whole face affected
Causes of UMN facial nerve palsy
Stroke, tumours, MS, syphilis, HIV, vasculitis
Causes of LMN facial nerve palsy
Bell’s
Pregnancy
DM
Local anaesthetic following dental work
Infective: otitis media, HIV, EBV
Trauma: forceps delivery
Neurological: GBS, mononeuropathy e.g. due to DM
What is Bell’s palsy?
Most common cause of acute LMN palsy
Lifetime risk 1 in 60
Probably due to sichaemic compression f facial nerve within facial canal due to inflammation - this is most commonly due to viral infections (latent herpes simplex type 1)
7% have a recurrence
Higher incidence in those with DM
A lesion in which cranial nerve can cause hyperacusis?
Facial - innervates stapedius muscle
How is Bell’s palsy managed?
Steroids: if presenting within 72hrs
Advice re eye care and explain that recovery can take several months
85% recover spontaneously
Consider referral if concern regarding aberrant re–nervation e.g. jaw twitching
Surgery: facial nerve decompression
What is Ramsay Hunt syndrome?
Facial nerve paralysis + rash affecting ear or mouth
Occurs when herpes zoster becomes reactivated in the geniculate ganglion of the 7th cranial nerve
LMN facial palsy
Pain is a prominent feature
Vesicles seen in the ar, on the hard palate and anterior 2/3 tongue
Deafness, tinnitus and vertigo can also occur
Management of Ramsay Hunt syndrome
Treat within 72hrs symptom onset with specific antiviral and steroids
Eye pad to protect eye + lubricants
When to refer a patient with a facial nerve palsy
Worsening neurological features
Features suggesting an UMN cause
Features suggestive of cancer: >6months, head/ neck lesion, hx of cancer, hearing loss on affected side
Explain the patterm of motor and sensory function loss in UMN and LMN facial nerve lesions
Forehead is supplied by bilateral fibres e.g. thr right forehead is supplied by fibres on the right and left
Lower half of face only supplied by contralateral fibres
What are the functions of the oculomotor nerve?
CNIII
Motor functions: majority of extraocular muscles
Parasympathetic: causes pupillary sphincter muscles to contract > this constricts the pupil and causes the lense to become more round/ thicker for near vision
(contraction of the ciliary muscle weirdly causes it to move inward towards centre of eye and this relaxes suspensory ligaments which makes lense more round and thick)
Most common causes of CNIII palsy
- Raised ICP causes compression of nerve against temporal bone
- Posterior communicating artery aneurysm
- Cavernous sinus infection/ trauma / thrombosis
Which cranial nerve is most commonly affected by cavernous sinus thrombosis?
Abducens
Clinical features of CNIII palsy
- Down and out eye
- Ptosis
- Dilated pupil
Outline abducens nerve palsy
Caused by anything that causes downward pressure on the brainstem e.g. space occupyin lesion
Clinical features: diplopia, eye resting in adduction because it doesn’t have the lateral rectus to oppose the action of the occulomotor nerve which controls the medial rectus
What is bulbar palsy?
Bulbar palsy refers to a set of signs and symptoms linked to the impaired function of the lower cranial nerves, typically caused by damage to their lower motor neurons or to the lower cranial nerve itself. The impacted cranial nerves are a set of nerves that arise straight from the brainstem and include cranial nerves IX (9), X (10), XI (11), and XII (12).
Demographic of patients commonly affected by bulbar and pseudobulbar palsy?
Men aged 75+
Discuss bulbar palsy
LMN problem - think B for bulbar and B for below then think lower
Result of diseases affecting the lower cranial nerves (9-12)
Causes: brainstem stroke, muscle disorders e.g. MND, disease of peripheral nerves supplying the muscles, Guillain Barre
Classified as progressive or non-progressive
Symptoms: think LMN lesion in face and neck
- Lip tremor
- Weak and wasted tongue
- Drooling
- Absent palatal movement
- Dysphonia **NOT DYSPHASIA**
- Speech is slurred, patient can’t pronounce ‘r’ for example
Management of bulbar palsy
No known treatment - supportive only
Medication to prevent drooling: anticholinergics
Feeding tube if difficulty swallowing
SaLT for help with chewing, swallowing, speaking
Prognosis of bulbar palsy
Can be fatal in progressive cases, often occurs from 1-3yrs after symptom onset due to aspiration pneumonia
Extensive damage can affect respiratory centre in brainstem leading to inability to breathe
What is pseudobulbar palsy?
UMN problem: damage along the corticobulbar tract
Presentation of pseudobulbar palsy
Tongue: unable to move but no wasting
- Dribbling
- Dysphonia
- Dysphagia
- Absent facial expressions
- Emotional liability
- Exaggerate jaw jerk (tap on chin, causes brisk closure of jaw)
Cause of pseudobulbar palsy
Stroke in internal capsule: corticobulbar tract runs through here - note, has to be bilateral to produce clinical signs
MND
High brainstem tumours
Head injury
Management of pseudobulbar palsy
*No known treatment for irreversible causes
Supportive: anticholinergics, baclofen for spasticity, PEG tube for dysphagia, SSRIs for emotional liability, SaLT
Bulbar vs pseudobulbar palsy
Symptoms of brainstem stroke
- Cessation of breathing
- Difficulty chewing, swallowing and speaking
- Weakness/ paralysis in arms/ legs/ face
- Difficulty with balance
- Visual problems
- Vertigo
- Locked-in syndrome
- Coma
