Neuro Flashcards
What are the 2 main causes of strokes
Inadequate blood supply (ischaemia/infarction)
Intracranial haemorrhage
What is a transient ischaemic attack
Transient neurological dysfunction due to ischaemia/infarction
Often come before full strokes
What is a crescendo TIA
2 TIAs in 1 week
High risk of developing stroke
How might a stroke present
Sudden onset neurological symptoms
Usually asymmetrical
Weakness of limbs
Facial weakness
Dysphasia (slurred speech)
Vision loss
Sensory loss
What are the risk factors for stroke
Cardiovascular disease
Previous stroke/TIA
Atrial fibrillation
Carotid artery disease
Hypertension
Diabetes
Smoking
Vasculitis
Thrombophilia
COCP use
How are strokes recognised in the community
FAST
Face
Arms
Speech
Time to call 999
How are strokes recognised in A&E
ROSIER
Based on clinical features and duration
Stroke likely if score > 0
What specialist imaging is needed in the recognition of strokes
Diffusion-weighted MRI: gold standard
Carotid ultrasound: looks for carotid stenosis (if found, consider endarterectomy/stenting)
Used to establish vascular territories affected
What is the initial management for strokes
Admit to specialised stroke centre
Exclude hypoglycaemia
Immediate CT brain (exclude haemorrhage)
Aspirin 300mg stat (after CT, continue for 2 weeks)
What are the definitive managements for stroke
Alteplase:
- Tissue plasminogen activator (breaks down clots)
- After CT has excluded haemorrhage
- Monitor for haemorrhage (may need repeat CTs)
Thrombectomy
- Depending on location/duration of clot (not used >24 hrs after onset)
How are TIAs managed
Aspirin 300mg daily
Secondary prevention for cardiovascular disease
Seen by stroke specialist within 24 hours
What is the secondary prevention for strokes
Clopidogrel 75mg OD
Atorvastatin 80mg
Consider carotid endarterectomy/stenting
Treat modifiable risk factors
What percentage of strokes are caused by intracranial bleeds
10-20%
What are the risk factors for intracranial bleeds
Head injury
Hypertension
Aneurysms
Ischaemic stroke (can progress to haemorrhage)
Brain tumours
Anticoagulants
How might intracranial bleeds present
Sudden onset
Headaches
Seizures
Weakness
Vomiting
Reduced consciousness
Sudden onset neurological symptoms
What is the Glasgow coma scale
Used to assess levels of consciousness
Involves eyes, verbal response, and motor response
<8, consider need to secure airway
What is involved in the eyes section of the GCS
4 - spontaneous
3 - speech
2 - pain
1 - none
What is involved in the verbal response section of the GCS
5 - orientated
4 - confused conversation
3 - inappropriate words
2 - incomprehensible sounds
1 - none
What is involved in the motor response section of the GCS
6 - obeys commands
5 - localised pain
4 - normal flexion
3 - abnormal flexion
2 - extends
1 - none
What is a subdural haemorrhage
Rupture of bridging veins
Between dura mater and arachnoid mater
Crescent shape on CT (not limited by cranial sutures)
Mostly in elderly and alcoholics (due to brain atrophy)
What is an extradural haemorrhage
Rupture of middle meningeal artery
In temporo-parietal region
Associated with temporal bone fractures
Between skull and dura mater
Bi-concave shape on CT (limited by cranial sutures)
Usually young patients with traumatic head injury
Get ongoing headaches
Get improved neurological symptoms, then rapid decline
What is an intracerebral haemorrhage
Bleeding into brain tissue
Similar presentation to ischaemic stroke
Can be anywhere in brain tissue
Due to: spontaneous event, bleeding into ischaemic infarct/tumour, ruptured aneurysm
What is a subarachnoid haemorrhage
Bleeding into subarachnoid space
Between pia mater and arachnoid membrane
Usually due to rupture of cerebral aneurysms
Very high morbidity and mortality
Typical history: sudden onset occipital headache, during strenuous activity, ‘thunderclap headache’
Associated with cocaine use and sickle cell anaemia
What is the management for intracranial bleeds
Immediate CT head
Check FBC and clotting
Admit to specialised stroke unit
Consider surgical treatment
Consider intubation/ventilation/ITU admission if have reduced consciousness
Correct clotting abnormalities
Correct severe hypertension (but avoid hypotension)
How might a subarachnoid haemorrhage present
Thunderclap headache
Neck stiffness
Photophobia
Visual changes
Neurological symptoms (speech changes, weakness, seizures, loss of consciousness)
What are the risk factors for subarachnoid haemorrhage
Hypertension
Smoking
Alcohol
Family history
Black ethnicity
F>M
45-70
Cocaine use
Sickle cell anaemia
Connective tissue disorders
Autosomal dominant polycystic kidney disease
What investigations are needed for a subarachnoid haemorrhage
CT head (first line)
Lumbar puncture (if CT head negative): red cell count raised, xanthochromia
Angiography (CT/MRI): locate source of bleeding
What is the management for a subarachnoid haemorrhage
Manage in specialised neurosurgical unit
MDT support
Surgery: repair vessel to prevent re-bleeding, coiling/clipping
Nimodipine: CCB, prevents vasospasms (can cause brain ischaemia)
Lumbar puncture/stent: to treat hydrocephalus
Antiepileptics: if having seizures
What is multiple sclerosis
Chronic progressive condition
Disseminated in time and space
Demyelination of neurones in CNS
Immune cells attack myelin
Mostly in young adults
F>M
Re-myelination possible in early disease
Linked to: specific genes (MHC-HLA), EBV, low vitamin D, smoking, obesity
How might multiple sclerosis present
Optic neuritis
Eye movement abnormalities
Focal weakness
Focal sensory symptoms
Ataxia
Describe the optic neuritis of multiple sclerosis
Most common presentation
Demyelination of optic disc
Loss of vision in one eye
Central scotoma (enlarged blind spot)
Pain on eye movements
Impaired colour vision
Relative afferent pupillary defect
Need urgent ophthalmology review
Treat with steroids for 2-6 weeks
Describe the eye movement disorders of multiple sclerosis
Double vision (6th nerve lesion)
Internuclear ophthalmoplegia (unilateral lesions)
Conjugate lateral gaze disorder (when looking laterally towards side of lesion, no movement of affected eye)
Describe the focal weakness of multiple sclerosis
Bell’s palsy
Horner’s syndrome
Limb paralysis
Incontinence
Describe the focal sensory symptoms of multiple sclerosis
Trigeminal neuralgia
Numbness
Paraesthesia
Lhermitte’s sign (electric shock down spine and into limbs when flexing neck)
Describe the ataxia of multiple sclerosis
Problems with coordinating movements
Sensory: loss of proprioception, positive Romberg’s test
Cerebellar
What are the disease patterns of multiple sclerosis
Clinically isolated syndrome
Relapsing-remitting
Primary progressive
Secondary progressive
Explain what is meant by clinically isolated syndrome of multiple sclerosis
First episode of demyelination and neurological abnormalities
Not enough to diagnose MS (symptoms need to be disseminated in time and space)
More likely to progress to MS if lesions seen on MRI
Explain what is meant by relapsing-remitting multiple sclerosis
Most common pattern in initial stages
Episodes of disease, then recovery
Symptoms in different areas in different episodes
Active - new symptoms/lesions on MRI
Not active - no new symptoms/lesions on MRI
Worsening - overall worsening disability over time
Not worsening - no worsening disability over time
Explain what is meant by primary progressive multiple sclerosis
Worsening from point of diagnosis
No remissions
What is meant by secondary progressive multiple sclerosis
Relapsing-remitting at first then progressive worsening with incomplete remission
Symptoms become more and more permanent
Classifications: active/not active, progressing/not progressing
How is multiple sclerosis diagnosed
By a neurologist
Based on clinical picture over time (need to have progressive symptoms for > 1 year)
MRI lesions
Oligoclonal bands in CSF on lumbar puncture
What is the management for multiple sclerosis
MDT support
Disease modification: disease modification drugs/biological therapies, aim to induce long term remission
Treating relapses: steroids (methylprednisolone)
Symptomatic treatment: exercise, analgesia (amitriptyline, gabapentin), manage depression, manage urge incontinence (oxybutynin), manage spasticity (baclofen, gabapentin)
What is motor neurone disease
Umbrella term
Progressive, ultimately fatal condition where motor neurones stop functioning
No effect on sensory neurones
Upper and lower motor neurones affected
Most common type: amyotrophic lateral sclerosis
Progressive bulbar palsy: affects muscles of talking and swallowing
Present in late middle age
M>F
Usually die of respiratory failure or pneumonia
How might motor neurone disease present
Insidious, progressive weakness of muscles throughout body
Increased fatigue on exercise
Drop things
Tripping
Dysarthria
Upper motor neurone signs
Lower motor neurone signs
What are some lower motor neurone signs
Muscle wasting
Reduced tone
Fasciculations
Reduced reflexes
What are some upper motor neurone signs
Increased tone
Spasticity
Brisk reflexes
Up-going plantars
How is motor neurone disease diagnosed
Based on clinical presentation and exclusion of differentials
What is the management for motor neurone disease
No effective treatment for halting/reversing progression
Riluzole: slows progressing, extends survival
NIV
End of life care planning
What is Parkinson’s disease
Progressive reduction of dopamine in basal ganglia
Get disorders of movement
Usually asymmetrical
Classic triad: resting tremor, rigidity, bradykinesia
Typically presents in older men
How might Parkinson’s disease present
Unilateral tremor
Cogwheel rigidity
Bradykinesia
Depression
Sleep disturbances
Anosmia (loss of sense of smell)
Postural instability
Cognitive impairment
Memory problems
Describe the unilateral tremor of Parkinson’s disease
4-6 Hz frequency
Pill-rolling tremor
More pronounced when resting
Improves with voluntary movement
Worse when distracted
Describe the cogwheel rigidity of Parkinson’s disease
Resistance to passive movement
Tension in limbs, gives way to movement in small increments
Describe the bradykinesia of Parkinson’s disease
Movements get slower and smaller
Handwriting gets smaller
Shuffling gait
Difficulty initiating movements
Difficulty turning around when standing
Reduced facial movements and expressions
What is Parkinson’s plus syndrome
Multiple system atrophy: Parkinson’s symptoms, autonomic dysfunction, cerebellar dysfunction
Dementia with Lewy bodies: dementia with features of Parkinson’s, progressive cognitive decline, visual hallucinations, delusions, fluctuating consciousness
Progressive supranuclear palsy
Corticobasal degeneration
How is Parkinson’s disease diagnosed
By a specialist
Based on clinical features
What is the management for Parkinson’s disease
Aim to control symptoms and minimise side effects
Levodopa
COMT inhibitors
Dopamine agonists
Monoamine oxidase-B inhibitors
Explain the role of levodopa in the management of Parkinson’s
Synthetic dopamine (boosts levels)
Combines with a drug that stops it being broken down before it reaches the brain (carbidopa, benserazide)
Less effective over time (reserved for when other things stop working)
Side effects: dyskinesia (if dose too high)
Explain the role of COMT inhibitors in the management of Parkinson’s
Entacapone
Slow breakdown of levodopa (longer duration of effect)
Explain the role of dopamine agonists in the management of Parkinson’s
Mimic dopamine, stimulate dopamine receptors
Less effective than levodopa
Side effects: pulmonary fibrosis
Explain the role of monoamine oxidase-B inhibitors in the management of Parkinson’s
Selegiline, rasagiline
Prevent breakdown of dopamine
What is benign essential tremor
Common condition associated with older age
Fine tremor
Affects all voluntary muscles (most noticeable in hands)
How might benign essential tremor present
Fine tremor
Symmetrical features
More prominent on voluntary movements
Worse when tired/stressed/caffeinated
Improves with alcohol
Absent during sleep
What are the differentials for benign essential tremor
Parkinson’s disease
Multiple sclerosis
Huntington’s chorea
Hyperthyroidism
Fever
Medications (especially antipsychotics)
What is the management for benign essential tremor
No definitive treatment
Only need treatment if causing functional/psychological problems
Propranolol (beta blocker)
Primidone (barbiturate anti-epileptic)
What is epilepsy
Umbrella term for conditions where there is a tendency to have seizures
What are seizures
Transient episodes of abnormal electrical activity in the brain
What are the investigations for epilepsy
EEG (typical patterns in different forms)
MRI brain (diagnose structural problems/tumours)
ECG (exclude cardiac conditions)
What are generalised tonic-clonic seizures
Loss of consciousness
Muscle tensing, muscle jerking
Associated features: tongue biting, incontinence, groaning, irregular breathing
Prolonged post-ictal period (confused, drowsy, irritable, depressed)
Management
- First line: sodium valproate
- Second line: lamotrigine, carbamazepine
What are focal seizures
Start in temporal lobe
Affect hearing, speech, memory, emotions
Presentation: hallucinations, flashbacks, deja vu, doing strange things on autopilot
Management:
- First line: carbamazepine, lamotrigine
- Second line: sodium valproate, levetiracetam
What are absence seizures
Usually in children, stop as get older
Blank, stare into space, abruptly return to normal
Unaware of surrounding and don’t respond during episodes
Usually last 10-20 seconds
Management:
- First line: sodium valproate, ethosuximide
What are atonic seizures
Drop attacks
Brief lapses in muscle tone
Last < 3 minutes
Usually begin in childhood
Often indicative of Lennox-Gastaut syndrome
Management:
- First line: sodium valproate
- Second line: lamotrigine
What are myoclonic seizures
Sudden brief muscle contractions
Patient awake during episode
Often part of juvenile myoclonic epilepsy
Management:
- First line: sodium valproate
- Second line: lamotrigine, levetiracetam, topiramate
What are infantile spasms
Start at around 6 months
Get clusters of body spasms
Poor prognosis (1/3 die by 25)
Management:
- First line: prednisolone, vigabatrin
What are the maintenance medications for epilepsy
Sodium valproate
- First line for most types of epilepsy
- Increase activity of GABA
- Side effects: teratogenic, liver damage, hepatitis, hair loss, tremor
Carbamazepine:
- First line for focal seizures
- Side effects: agranulocytosis, aplastic anaemia, induces P450 system
Phenytoin:
- Side effects: vitamin D/folate deficiency, megaloblastic anaemia, osteomalacia
Ethosuximide:
- Side effects: night terrors, rashes
Lamotrigine:
- Side effects: Steven-Johnson syndrome, leukopenia
What is status epilepticus
Medical emergency
Seizure lasting >5 mins
3 seizures in 1 hour
Management: ABCDE, IV lorazepam (4mg, repeat if needed), if persistent - IV phenobarbital/IV phenytoin
Community management: buccal midazolam, rectal diazepam
What is neuropathic pain
Abnormal function of sensory nerves
Get abnormal painful signals to brain
What are the causes of neuropathic pain
Postherpetic neuralgia (from shingles)
Nerve damage from surgery
Multiple sclerosis
Diabetic neuralgia
Complex regional pain syndrome
What are the typical features of neuropathic pain
Burning
Tingling
Pins and needles
Electric shocks
Loss of sensation to touch
What are the investigations for neuropathic pain
DN4 questionnaire
Score > 4 indicates neuropathic pain
What is the management for neuropathic pain
Amitriptyline
Duloxetine
Gabapentin
Pregabalin
Try all 4 in turn if not responding
Other options: tramadol, capsicin cream, physio, psychology input
What is complex regional pain syndrome
Often triggered by injury to a localised area
Neuropathic pain
Skin flushing
Swelling
Abnormal hair growth
Solar changes
Temperature changes
Abnormal sweating
What is facial nerve palsy
Isolated dysfunction of facial nerve
Usually presents with unilateral facial weakness
What are the branches of the facial nerve
Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical
How might facial nerve palsies present
Upper motor neurone lesions - forehead sparing
Lower motor neurone lesions - forehead affected
What is Bell’s palsy
Idiopathic cause of facial nerve palsy
Relatively common
Unilateral lower motor neurone lesion
Most recover in a few weeks (can take a year)
Management:
- If present within 72 hours: prednisolone
- Lubricating eye drops
- If develop eye pain, urgent ophthalmology review (exposure keratopathy)
What is Ramsay-Hunt syndrome
Due to varicella zoster virus
Unilateral lower motor neurone facial nerve palsy
Painful and tender rash in ear canal pinna, around ear
Management:
- If present within 72 hours: prednisolone, aciclovir, lubricating eye drops
What are the less common causes of facial nerve palsy
Infection: otitis media, malignant otitis externa, HIV, Lyme disease
Systemic disease: diabetes, sarcoidosis, leukaemia, multiple sclerosis, Guillain-Barre syndrome
Tumours: acoustic neuroma, parotid tumours, cholesteatomas
Trauma: direct nerve trauma, damage during surgery, basal skull fracture
How might brain tumours present
Often asymptomatic
Focal neurological symptoms
Signs of raised ICP (papilloedema, altered mental state, visual field defects, seizures, 3rd/6th nerve palsy)
Headaches (constant, nocturnal, worse on waking, worse on straining/coughing/bending, vomiting)
What are the types of brain tumours
Secondary metastasis:
- Commonly from lung, breast, renal cell carcinoma, melanoma
Glioma:
- Tumour of glial cells in spinal cord
- Subtypes: astrocytoma, oligodendroglioma, ependymoma
Meningioma:
- Tumour of meninges
- Takes up lots of space, so raised ICP symptoms
Pituitary tumours:
- Usually benign
- Can compress optic chiasma (bitemporal hemianopia)
- Hormonal imbalance: acromegaly, hyperprolactinoma, Cushing’s, thyrotoxicosis
Acoustic neuroma:
- Tumour of schwann cells surrounding auditory nerve
- Classic symptoms: hearing loss, tinnitus, balance issues
- May have facial nerve palsy
What is the management for brain tumours
Surgery
Chemotherapy
Radiotherapy
Palliative care
What is Huntington’s chorea
Autosomal dominant condition
Progressive deterioration of nervous system
Symptoms start at 30 - 50
Genetic mutation in HHT gene
Anticipation effect: each generation gets more repeats of faulty gene
How might Huntington’s chorea present
Insidious, progressive worsening of symptoms
Cognitive problems
Psychiatric issues
Mood issues
Chorea (involuntary, abnormal movements)
Eye movement disorders
Speech difficulties
Dysphagia
What is the management for Huntington’s chorea
No treatment to stop/slow progression
Supportive MDT care
Medications to stop abnormal movements (olanzapine, diazepam, tetrabenazine)
What is the prognosis for Huntington’s chorea
Life expectancy 15-20 years from onset
Death often due to pneumonia
High risk of suicide
What is myasthenia gravis
Autoimmune condition
Antibodies against ACh receptor (stop action potentials)
Muscle specific kinase (MuSK) antibodies
Progressive muscle weakness with activity
Improves with rest
Women < 40
Men > 60
Strongly linked to thymoma
How might myasthenia gravis present
Muscle weakness - worse with activity, improves with rest
Proximal muscles affected
Diplopia
Ptosis
Weak facial movements
Dysphagia
Fatigue in jaw when chewing
Slurred speech
Progressive weakness
How can the signs of myasthenia gravis be elicited
Ptosis on repeated blinking
Diplopia on prolonged upward gaze
Unilateral weakness on abducting arm 20 times
What are the investigations for myasthenia gravis
Specific antibodies:
- ACh receptor (ACh R)
- Muscle-specific kinase antibody (MuSK)
- Low-density lipoprotein receptor-related protein 4 antibody (LRP4)
CT/MRI thymus
Edrophonium test (give edrophonium chloride, stops breakdown of ACh, levels of ACh in neuromuscular junction increase, temporary relief)
What is the management for myasthenia gravis
Reversible ACh inhibitors (increase amount of ACh in neuromuscular junctions)
Steroids (suppress production of antibodies)
Thymectomy (even if don’t have thymoma)
Monoclonal antibodies (rituximab)
Plasmapheresis
What is myasthenia crisis
Severe complication of myasthenia gravis
Slack facial muscles, weak neck, drooling, nasal speech, general weakness, unsafe swallow
Acute worsening of symptoms
Often triggered by infection
Management:
- NIV/intubation
- Immunomodulatory therapies (IV immunoglobulins, plasma exchange)
What is Lambert-Eaton myasthenic syndrome
Progressive muscle weakness with increased use
Damage to neuromuscular junctions
In patients with small cell lung cancer (get antibodies against voltage-gated calcium channels, so impaired release of ACh)
How might Lambert-Eaton myasthenic syndrome present
Proximal muscle weakness (diplopia, ptosis, slurred speech, dysphagia)
Autonomic dysfunction (dry mouth, blurred vision, impotence, dizziness)
Reduced tendon reflexes (can have post-tetanic potentiation - normal reflexes after strong muscle contractions)
What is the management for Lambert-Eaton myasthenic syndrome
Amifampridine (more ACh released into neuromuscular junctions)
Immunosuppressants
IV immunoglobulins
Plasmapheresis
What is Charcot-Marie-Tooth disease
Inherited condition (autosomal dominant)
Affects peripheral motor and sensory nerves
Lots of subtypes
Symptoms start at 10 - 40
What are the classical features of Charcot-Marie-Tooth disease
High foot arches
Distal muscle wasting
Weakness in lower legs
Loss of ankle dorsiflexion
Weakness in hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss
What are the causes of peripheral neuropathy
Alcohol
B12 deficiency
Cancer
CKD
Diabetes
Vasculitis
What is the management for Charcot-Marie-Tooth disease
Nothing to stop/slow progression
MDT support
What is Guillain-Barre syndrome
Acute paralytic polyneuropathy
Affects peripheral nervous system
Get acute, symmetrical, ascending muscle weakness
Usually triggered by infection
Body makes antibodies that attack myelin sheath of nerve cells
Clinical course: symptoms within 4 weeks of infection, peak after 2-4 weeks, resolve over months-years
How might Guillain-Barre syndrome present
Symmetrical ascending weakness
Reduced reflexes
Peripheral loss of sensation
Peripheral neuropathic pain
Facial weakness
What are the investigations for Guillain-Barre syndrome
Clinical diagnosis based on Brighton criteria
Nerve conduction studies (reduced signal)
Lumbar puncture (raised protein, normal cell count, normal glucose)
What is the management for Guillain-Barre syndrome
IV immunoglobulins
Plasma exchange
Supportive care
VTE prophylaxis (PE leading cause of death)
What are the complications of Guillain-Barre syndrome
Respiratory failure
Pain
VTE
SIADH
Renal failure
Hypercalcaemia
What is the prognosis for Guillain-Barre syndrome
80% recover
15% left with neurological disability
5% die
What is neurofibromatosis
Benign nerve tumours throughout nervous system
Autosomal dominant
Defect in gene coding for neurofibromin protein
Types 1 (more common) and 2
What is the diagnostic criteria for neurofibromatosis 1
Need 2 of 7
CRABBING
Cafe au lait spots
Relative with NF1
Axillary/inguinal freckles
Bony dysplasia
Iris haematomas
Neurofibromas
Glioma of optic nerve
What are the investigations for neurofibromatosis
Clinical diagnosis
Genetic testing
X-ray of long bones
What is the management for neurofibromatosis
No treatment
Aim to control symptoms
What are the complications of neurofibromatosis
Migraines
Epilepsy
Renal artery stenosis
Hypertension
Learning disability
Scoliosis
Loss of vision
Malignant peripheral nerve sheath tumours
GI stromal tumours
Brain tumours
Spinal cord tumours
Increased risk of cancer
What is neurofibromatosis 2
Development of schwannomas
Get acoustic neuromas
What is tubular sclerosis
Get hamartomas (benign neoplastic growths of tissues that they come from)
Can affect skin, brain, lung, heart, kidney, eye
Due to mutations in TSC1 or TSC2 genes (get uncontrolled cell size and growth)
How might tuberous sclerosis present
Mostly children with epilepsy and skin features
Skin signs
Neurological features
Rhabdomyomas in heart
Gliomas
Polycystic kidneys
Retinal hamartomas
What are the skin signs of tuberous sclerosis
Ash leaf spots (depigmented areas)
Shagreen patches (thickened, dimpled, pigmented patches)
Angiofibromas (skin coloured/pigmented papules)
Subungual fibromata (lumps under nails)
Cafe au lait spots (mild pigmented lesions)
Poliosis (isolated patch of white in head/facial hair)
What are the neurological features of tuberous sclerosis
Epilepsy
Learning disability
Developmental delay
What is the management for tuberous sclerosis
Supportive
Monitor and treat complications
What are the red flags for headaches
Fever, photophobia, stiff neck (meningitis, encephalitis)
New neurological symptoms (haemorrhage, malignancy, stroke)
Dizziness (stroke)
Visual disturbances (temporal arteritis, glaucoma)
Sudden onset occipital headache (subarachnoid haemorrhage)
Worse on coughing or straining (raised ICP)
Postural, worse on lying/bending (raised ICP)
Severe enough to wake from sleep
Vomiting (raised ICP, CO poisoning)
History of trauma (intracranial haemorrhage)
Pregnancy (pre-eclampsia)
What are the investigations for headaches
Fundoscopy (look for papilloedema)
Explain tension headaches
Bank-like pattern around head
Frontalis, temporalis, occipital pain
Come on and resolve gradually
Associated with: stress, depression, alcohol, skipping meals, dehydration
Management: reassurance, basic analgesia, relaxation techniques, hot towel to area
Explain secondary headaches
Non-specific
Due to:
- Underlying medical condition
- Alcohol
- Head injury
- CO poisoning
Explain sinusitis headaches
Headaches associated with inflammation of sinuses
Facial pain (behind nose/forehead/eyes)
Tenderness over sinuses
Resolves in 2-3 weeks
Usually viral
Management: steroid nasal spray (if prolonged), consider antibiotics
Explain analgesic headaches
Due to long term analgesia use
Non-specific features
Management: withdraw analgesia
Explain hormonal headaches
Related to low oestrogen
Generic, non-specific
Typical timing: 2/3 days before period, around menopause, pregnancy
Improve with COCP use
Explain cervical spondylosis
Degenerative changes in cervical spine
Get headache and neck pain
Explain trigeminal neuralgia
Compression of trigeminal nerve
90% unilateral
Linked to multiple sclerosis
Intense facial pain (seconds to hours)
Shooting pains
Triggers: cold weather, spicy food, caffeine, citrus fruits
Management: carbamazepine, surgery to decompress nerve
What are the different types of migraines
Migraine with aura
Migraine without aura
Silent migraines (with aura, without headache)
Hemiplegic migraine
How might migraines present
Headache for 4-72 hours
Moderate to severe
Pounding/throbbing sensation
Usually unilateral
Photophobia
Phonophobia
May have nausea and vomiting
What is an aura
Visual changes associated with migraines
Sparks, blurring, lines, loss of visual fields
What are hemiplegic migraines
Mimic strokes
Sudden or gradual onset
Hemiplegia
Ataxia
Changes in consciousness
What are the triggers for migraines
Stress
Bright lights
Strong smells
Certain foods (chocolate, cheese, caffeine)
Dehydration
Menstruation
Abnormal sleep pattern
Trauma
What are the stages of a migraine
Prodromal: 3 days before headache, yawning, fatigue, mood changes
Aura: up to 60 mins
Headache: 4-72 hours
Resolution: headache fades, relieved by vomiting/sleeping
Postdromal: recovery
What is the acute management for migraines
Lie down in dark room
Paracetamol
Triptans (sumatriptan as migraine starts)
NSAIDs
Antiemetics
What is the prophylactic management for migraines
Avoid triggers
Acupuncture
B2 supplements
To reduce frequency and severity: propranolol, topiramate, amitriptyline
What are cluster headaches
Severe, unbearable, unilateral headaches
Usually around eye
Come in clusters of attacks
Last 15 mins - 3 hours
How might cluster headaches present
Unilateral symptoms
Red, swollen, watery eye
Pupil constriction
Eyelid drooping
Nasal discharge
Facial sweating
What is the management for cluster headaches
Acute: triptans (subcut), high flow oxygen
Prophylaxis: verapamil, lithium, prednisolone (breaks cycle during clusters)
What are the upper motor neurone lesion signs
Increased tone
Clonus
Weakness
Brisk tendon reflexes
Extensor plantars
What are the lower motor neurone lesion signs
Muscle wasting
Fasciculations
Reduced tone
Reduced/absent tendon reflexes
Flexor plantars
What are the side effects of anticholinergics
Miosis
SSLUDGE syndrome: salivation, sweating, lacrimation, urinary incontinence, diarrhoea, GI upset, emesis
Explain CN 1
Olfactory
Sense of smell
Explain CN 2
Optic
Visual acuity
Explain CN 3
Oculomotor
Extrinsic eye muscles, LPS, sphincter pupillae
Explain CN 4
Trochlear
Superior oblique
Explain CN 5
Trigeminal (branches: ophthalmic, maxillary, mandibular)
Facial sensation
Muscles of mastication
Explain CN 6
Abducens
Lateral rectus
Explain CN 7
Facial
Muscles of facial expression
Taste anterior 2/3 tongue
Explain CN 8
Vestibulocochlear
Hearing
Balance
Explain CN 9
Glossopharyngeal
Pharyngeal sensation
Taste posterior 1/3 tongue
Explain CN 10
Vagus
Movement of soft palate, pharynx, laryns
Explain CN 11
Accessory
Movement of SCM and trapezius
Explain CN 12
Hypoglossal
Tongue movement
