Lecture ILO’s Flashcards
Three types of strokes
Ischaemic
Intracranial haemorrhage, with bleeding in or
haemorrhagic stroke ,around the brain
Ischaemic vs haemorrhagic stroke
Ischaemic (I)
Haemorrhagic (H)
I CT scan normal or focal hypodense area
HCT scan shows blood
I Headache uncommon
H Headache common
I Nausea and vomiting uncommon
H Nausea and vomiting common
I Normal level of consciousness
H Decreased level of consciousness
I Older demographic
H Younger demographic
I More risk factors for atherosclerosis
H Less risk factors for atherosclerosis
I History of AF
H No history of AF
Subarachnoid haemorrhages common cause
Subarachnoid haemorrhages are often caused by berry aneurysms in the Circle of Willis
The blood fills the arachnoid space and spreads throughout the brain
The effects are often widespread, instant and devastating. Severe, sudden “thunderclap” occipital headache followed by vomiting, collapse and coma
6% have sentinel headache (this can be treated if the aneurism is found)
Intracerebral Haemmorhage
Intracerebral Haemmorhage
More localised
Focal neurological signs
Raised intracranial pressure
Reduced level of consciousness
What is a Venous sinus Thrombosis
Similar presentation to a stroke
• Occurs most often in obese young women in hypercoagulable states e.g. pregnancy, OCP
• Raised intracranial pressure
• Presents with headache, vomiting
papilloedema, blurred vision
• Focal neurology if localised infarction occurs
• Can progress to decreased consciousness, seizures
• No focal mass or blood on brain imaging
• Main differential is subarachnoid haemorrhage
Stroke vs bells palsy
• Bilateral innervation of forehead by upper and lower motor neurones
• Due to site of lesion, stroke causes partial contralateral facial paralysis but still allows for contralateral forehead muscle use (can raise eyebrows)
• Lower motor neurone lesion (Bell’s palsy) causes paralysis of all ipsilateral facial muscles (can’t raise eyebrows)
No dysphasia
No visual defects
Pressure on facial nerves due to hsv virus
What negative symptoms does a stroke cause
• Negative symptoms (depleted CNS activity)
• Motor deficit
• Sensory deficit
• Speech deficit / loss • Visual loss
• Hearing loss
• Loss of balance
Migraine
Prevalence 8%
F:M 2:1
Commonest age of presentation – 40 yrs
Cause unclear but may be due to underlying neuronal hyperexcitability, mediated by 5HT
Presents as:
Visual aura (15-30 mins) followed by unilateral throbbing headache within one hour
Isolated aura with no headache
Severe unilateral headache, often premenstrual, associated with
painful hypersensory phenomena (photophobia, phonophobia, unable to touch face), nausea and vomiting
Aura can take many forms
Visual – distortion of print lines, dots, spots, zigzags,
- hemianopia, opthalmoplegia, pupil changes
Sensory – paraesthesia spreading from fingers to face
Motor – hemiparesis
Speech – dysphasia, dysarthria,
Cerebellar - ataxia
Often history or family history of migraine
When a stroke is being identified what other conditions should be ruled out?
Sepsis / abscess
Hyper / hypoglycaemia
Migraine
Functional
Bell’s palsy
Todd’s paresis - seizure then paralysis
Tumour
Localised CNS sepsis symptoms
• Localised CNS sepsis
• Meningitis, encephalitis, brain abscess
• Signs of sepsis
• Rash
• Altered mental state
• Headache
• Reduced consciousness
• Seizures
• Focal CNS signs
Ischaemic and infarction causes
Ischaemia refers to an inadequate blood supply. Infarction refers to tissue death due to ischaemia.
The blood supply to the brain may be disrupted by:
• A thrombus or embolus
• Atherosclerosis
• Shock
• Vasculitis
Transient ischaemic attack
Transient ischaemic attack (TIA) involves temporary neurological dysfunction (lasting less than 24 hours) caused by ischaemia but without infarction. Symptoms have a rapid onset and often resolve before the patient is seen. TIAs may precede a stroke. Crescendo TIAs are two or more TIAs within a week and indicate a high risk of stroke.
Presentation of a stroke
Presentation
A sudden onset of neurological symptoms suggests a vascular cause (e.g., stroke). Stroke symptoms are typically asymmetrical. Common symptoms are:
• Limb weakness
• Facial weakness
• Dysphasia (speech disturbance)
• Visual field defects
• Sensory loss
• Ataxia and vertigo (posterior circulation infarction)
Stroke risk factors
Risk Factors
• Previous stroke or TIA
• Atrial fibrillation
• Carotid artery stenosis
• Hypertension
• Diabetes
• Raised cholesterol
• Family history
• Smoking
• Obesity
• Vasculitis
• Thrombophilia
• Combined contraceptive pill
Management of TIA
Management of TIA
Symptoms should have completely resolved within 24 hours of onset. Initial management involves:
• Aspirin 300mg daily (started immediately)
• Referral for specialist assessment within 24 hours (within 7 days if more than 7 days since the episode)
• Diffusion-weighted MRI scan is the imaging investigation of choice.
Management of ischaemic stroke
Management of Stroke
The information here is summarised from the NICE guidelines (updated 2022) on stroke. Initial management involves:
• Exclude hypoglycaemia
• Immediate CT brain to exclude haemorrhage
• Aspirin 300mg daily for two weeks (started after haemorrhage is excluded with a CT)
• Admission to a specialist stroke centre
Thrombolysis with alteplase is considered once haemorrhage is excluded (after the CT scan). Alteplase is a tissue plasminogen activator that rapidly breaks down clots.
Thrombectomy is considered in patients with a confirmed blockage of the proximal anterior circulation or proximal posterior circulation. It may be considered within 24 hours of the symptom onset and alongside IV thrombolysis.
How are stroke patients assessed for the underlying cause
Assessment for Underlying Causes
Patients with a TIA or stroke are investigated for carotid artery stenosis and atrial fibrillation with:
• Carotid imaging (e.g., carotid ultrasound, or CT or MRI angiogram)
• ECG or ambulatory ECG monitoring
Anticoagulation is initiated for atrial fibrillation (after excluding haemorrhage and finishing two weeks of aspirin).
Surgical interventions are considered where there is significant carotid artery stenosis. The options are:
• Carotid endarterectomy (recommended in the NICE guidelines)
• Angioplasty and stenting
TOM TIP: The top risk factors to remember are atrial fibrillation and carotid artery stenosis. All patients with a TIA or stroke will have carotid imaging and ECGs to identify these.
Secondary prevention of a stroke
Secondary Prevention
• Clopidogrel 75mg once daily (alternatively aspirin plus dipyridamole)
• Atorvastatin 20-80mg (not started immediately – usually delayed at least 48 hours)
• Blood pressure and diabetes control
• Addressing modifiable risk factors (e.g., smoking, obesity and exercise)
What is multiple sclerosis
Multiple sclerosis (MS) is a chronic and progressive autoimmune condition involving demyelination in the central nervous system. The immune system attacks the myelin sheath of the myelinated neurones.
Multiple sclerosis typically presents in young adults (under 50 years) and is more common in women.
Pathophysiology of MS
Pathophysiology
Myelin covers the axons of neurones and helps electrical impulses travel faster. Myelin is provided by cells that wrap themselves around the axons:
• Oligodendrocytes in the central nervous system
• Schwann cells in the peripheral nervous system
Multiple sclerosis affects the central nervous system (the oligodendrocytes). Inflammation and immune cell infiltration cause damage to the myelin, affecting the electrical signals moving along the neurones. When a patient presents with symptoms of an MS attack (e.g., an episode of optic neuritis), there are often other demyelinating lesions throughout the central nervous system, most of which are not causing symptoms. In early disease, re-myelination can occur, and the symptoms can resolve. In the later stages of the disease, re-myelination is incomplete, and the symptoms gradually become more permanent. A characteristic feature of MS is that lesions vary in location, meaning that the affected sites and symptoms change over time. The lesions are described as “disseminated in time and space”.
Causes of MS
Causes
The cause of the multiple sclerosis is unclear, but there is growing evidence that it may be influenced by:
• Multiple genes
• Epstein–Barr virus (EBV)
• Low vitamin D
• Smoking
• Obesity
Onset of multiple sclerosis
Onset
Symptoms usually progress over more than 24 hours. Symptoms tend to last days to weeks at the first presentation and then improve. There are many ways MS can present, depending on the location of the lesions.
What is the most common symptom of ms?
Optic Neuritis
Optic neuritis is the most common presentation of multiple sclerosis. It involves demyelination of the optic nerve and presents with unilateral reduced vision, developing over hours to days.
Key features are:
• Central scotoma (an enlarged central blind spot)
• Pain with eye movement
• Impaired colour vision
• Relative afferent pupillary defect
A relative afferent pupillary defect is where the pupil in the affected eye constricts more when shining a light in the contralateral eye than when shining it in the affected eye. When testing the direct pupillary reflex, there is a reduced pupil response to shining light in the eye affected by optic neuritis. However, the affected eye has a normal pupil response when testing the consensual pupillary reflex.
Other than ms, what are other causes of optic neuritis
Other causes of optic neuritis include:
○ Sarcoidosis
○ Systemic lupus erythematosus
○ Syphilis
○ Measles or mumps
○ Neuromyelitis optica
○ Lyme disease
Patients presenting with acute loss of vision need urgent ophthalmology input. Optic neuritis is treated with high-dose steroids. Changes on an MRI scan help to predict which patients will go on to develop MS.
Eye movement abnormalities in multiple sclerosis
Eye Movement Abnormalities
Lesions affecting the oculomotor (CN III), trochlear (CN IV) or abducens (CN VI) can cause double vision (diplopia) and nystagmus. Oscillopsia refers to the visual sensation of the environment moving and being unable to create a stable image.
Internuclear ophthalmoplegia is caused by a lesion in the medial longitudinal fasciculus. The nerve fibres of the medial longitudinal fasciculus connect the cranial nerve nuclei(“internuclear”) that control eye movements (the 3rd, 4th and 6th cranial nerve nuclei). These fibres are responsible for coordinating the eye movements to ensure the eyes move together. It causes impaired adduction on the same side as the lesion (the ipsilateral eye) and nystagmus in the contralateral abducting eye.
A lesion in the abducens (CN VI) causes a conjugate lateral gaze disorder. Conjugate means connected. Lateral gaze is where both eyes move to look laterally to the left or right. When looking laterally in the direction of the affected eye, the affected eye will not be able to abduct. For example, in a lesion involving the left eye, when looking to the left, the right eye will adduct (move towards the nose), and the left eye will remain in the middle.
Focal neurological symptoms of MS
Focal Neurological Symptoms
Multiple sclerosis may present with focal weakness, for example:
• Incontinence
• Horner syndrome
• Facial nerve palsy
• Limb paralysis
Multiple sclerosis may present with focal sensory symptoms, for example: ○ Trigeminal neuralgia ○ Numbness ○ Paraesthesia (pins and needles) ○ Lhermitte’s sign Lhermitte’s sign describes an electric shock sensation that travels down the spine and into the limbs when flexing the neck. It indicates disease in the cervical spinal cord in the dorsal column. It is caused by stretching the demyelinated dorsal column. Transverse myelitis refers to a site of inflammation in the spinal cord, which results in sensory and motor symptoms depending on the location of the lesion.
What is ataxia?
Ataxia
Ataxia is a problem with coordinated movement. It can be sensory or cerebellar.
Sensory ataxia is due to loss of proprioception, which is the ability to sense the position of the joint (e.g., is the joint flexed or extended). This results in a positive Romberg’s test (they lose balance when standing with their eyes closed) and can cause pseudoathetosis(involuntary writhing movements). A lesion in the dorsal columns of the spine can cause sensory ataxia.
Cerebellar ataxia results from problems with the cerebellum coordinating movement, indicating a cerebellar lesion.
Clinically isolated syndrome in MS
Clinically isolated syndrome describes the first episode of demyelination and neurological signs and symptoms. Patients with clinically isolated syndrome may never have another episode or may go on to develop MS. Lesions on an MRI scan suggest they are more likely to progress to MS.
Relapsing-remitting MS
Relapsing-remitting MS is the most common pattern when first diagnosed. It is characterised by episodes of disease and neurological symptoms followed by recovery. The symptoms tend to occur in different areas with each episode. It can be further classified based on whether the disease is active or worsening:
• Active: new symptoms are developing, or new lesions are appearing on the MRI
• Not active: no new symptoms or MRI lesions are developing
• Worsening: there is an overall worsening of disability over time
• Not worsening: there is no worsening of disability over time
Secondary progressive MS
Secondary progressive MS is where there was relapsing-remitting disease, but now there is a progressive worsening of symptoms with incomplete remissions. Symptoms become increasingly permanent. Secondary progressive MS can be further classified based on whether the disease is active or progressing.
Primary progressive MS
Primary progressive MS involves worsening disease and neurological symptoms from the point of diagnosis without relapses and remissions. This can be further classified based on whether it is active or progressing.
How is MS diagnosed?
Diagnosis
The diagnosis is made by a neurologist based on the clinical picture and symptoms suggesting lesions that change location over time. Other causes for the symptoms need to be excluded.
Investigations can support the diagnosis:
• MRI scans can demonstrate typical lesions
• Lumbar puncture can detect oligoclonal bands in the cerebrospinal fluid (CSF)
Actions of the temporal lobe
Memory, emotions, language, hearing and speech. Wernickes area (language comprehension) located here.
Actions of the occipital lobe
Visual reception and interpretation
Actions of the parietal lobe
Reception and processing of information and body orientation
Action of the cerebellum
Co ordination and control of voluntary movement
Action of the cerebellum
Co ordination and control of voluntary movement
Action of the frontal lobe
Decision making, problem solving, planning, concentration, judgement, inhibitions, personality, emotional traits.
Brocas area is here (language production)
Action of the brain stem
Breathing, digestion, heart control, blood vessel control, alertness
Signs and symptoms of a stroke
• Confusion, altered level of consciousness, and coma.
• Headache
• Unilateral weakness or paralysis in the face, arm, or leg.
• Sensory loss — paraesthesia or numbness.
• Ataxia (Co ordination and balance)
• Dysphasia.
• Dysarthria.
• Visual disturbance — homonymous hemianopia, diplopia.
• Gaze paresis — this is often horizontal and unidirectional.
• Photophobia.
• Dizziness, vertigo, or loss of balance — isolated dizziness is not usually a symptom of TIA.
• Nausea and/or vomiting.
• Specific cranial nerve deficits such as unilateral tongue weakness or Horner’s syndrome (miosis, ptosis, and facial anhidrosi s).
• Difficulty with fine motor coordination and gait.
• Neck or facial pain (associated with arterial dissection).
How to do the fast test when assessing a stroke
Facial movements:
• Ask patient to show teeth, is there an unequal smile or grimace?
• Note which side does not move well
Arm movements:
• Lift the patient’s arms together to 90 degrees if sitting, 45degrees if supine and ask them to hold the position for 5 seconds
before letting go, does one arm drift down or fall rapidly?
• If one arm drifts down or falls, note whether it is the patient’s left or right
Speech:
• Listen for new disturbance of speech
• Listen for slurred speech, get patient to say “British Constitution or Baby Hippopotamus”
• Listen for word-finding difficulties with hesitations. This can be confirmed by asking the patient to name
objects that may be nearby such as a cup, chair, table, keys, pen
• Check with any person who knows the patient, is this normal for them?
Time to ring 999
Initial management of suspected stroke
Stabilise the patient
ABCDE
abbreviated neurological examination
rapidly obtain a brain image, typically a non-contrast head CT, in order to exclude
a brain haemorrhage
The ideal time from emergency department arrival to start of CT is 25 minutes
ECG (AF)
IV Cannula inserted x 2
Serum glucose (rule out hypo)
FBC
Electrolytes
Urea and creatinine and LFTs
Partial thromboplastin time, prothrombin times with international normalised ratio
Cardiac enzymes
What is the rosier score?
Recognition of stroke in the emergency room
GCS, BP, BM
Syncope -1
Seizure -1
All +1
Asymmetrical face weakness
Asymmetrical arm weakness
Asymmetrical leg weakness
Speech disturbance
Visual field defect
Previous stroke
What is the NIHSS in assessing stroke?
NIHSS
The NIHSS is an internationally accepted tool for the systematic assessment of stroke severity.
It comprises a 15-item neurological examination stroke scale used to evaluate the effect of an acute cerebral event on the
levels of consciousness,
language,
neglect,
visual-field loss
extra-ocular movement,
motor strength,
ataxia,
dysarthria
sensory loss.
Used to assess patients prior to thrombolysis
Assesses the impact of the stroke
Score of less than 4 very goodoutcomeif thrombolysed
Score of 25 or more not suitable for thrombolysis as very poor outcome.
It can be used by appropriately trained healthcare professionals and takes approximately 10 minutes to administer.
Posterior circulation stroke
Posterior Circulation stroke
may be difficult to diagnose and should be suspected if the person presents with:
Symptoms of acute vestibular syndrome — acute, persistent, continuous vertigo or dizziness with nystagmus,
nausea or vomiting,
head motion intolerance, new gait unsteadiness.
Stroke epidemiology
Ischaemic stroke accounts for 85% of all stroke cases
Haemorrhagic stroke for 10%
Subarachnoid haemorrhage for 5%
Causes of ischaemic stroke
Embolism: an embolus originating somewhere else in the body resulting in hypoperfusion to the area of the brain the vessel supplies.
Thrombosis: a blood clot forms locally within a cerebral vessel (e.g. due to atherosclerotic plaque rupture).
Systemic hypoperfusion: blood supply to the entire brain is reduced secondary to systemic hypotension (e.g. cardiac arrest).
Cerebral venous sinus thrombosis: blood clots form in the veins that drain the brain, resulting in venous congestion and tissue hypoxia.
Alteplase / tenectase
Thrombolysis
Inclusion criteria for thrombolysis
Aged 18> with symptoms of acute stroke
Onset withing last 4.5 hours prior to rTPA infusion start
Measurable significant new deficit on NIHSS
Absence of haemorrhage or stroke mimic based on baseline CT
Absolute exclusion for thrombolysis
Absolute Exclusion
Systolic BP >185 and /or diastolic >110 despite treatment
Signs and symptoms of acute intracranial/subacrachnoid haemorrhage
history of previous intracranial haemorrhage
Evidence of active bleeding or known bleeding diathesis
Arterial puncture at non- compressible site within 7days or LP within 7 days
There is history of head trauma or prior stroke in the previous 3 months
intracranial/intraspinal surgery < 3 months
Patients with platelets <100
INR >1.7 on warfarin
dose of low-molecular-weight heparin within 48 hours
Patientistakingdirectthrombin inhibitors or direct factor Xa inhibitors within last 48 hours
Symptoms consistent with infective endocarditis
Relative exclusion criteria for a stroke
Relative Exclusion criteria
Pregnancy
Stroke with last 3 months
Major surgery or non-head trauma with last two weeks
Brain tumour , cerebral aneurysm or AVM
Gastrointestinal, urinary or gynaecological haemorrhage within the last 21 days
Recent gastro-intestinal or urinary tract haemorrhage within the previous 3 weeks
Age >80, NIHSS >25 and/or early infarct changes >one third of MCA territory
Secondary prevention of a stroke
Antiplatelet therapy
Clopidogrel 75mg OD
Alternatives : Aspirin 75mg OD and dipyridamole 200mg BD
Combined therapy can be used in severe cases
Anticoagulants
Only for those with atrial fibrillation or flutter
Anti-hypertensive
may include a thiazide-like diuretic, long-acting calcium channel blocker or angiotensin-converting enzyme inhibitor.
target systolic blood pressure below 130 mmHg (or 140–150 mmHg in people with severe bilateral carotid artery stenosis)
Haemorrhagic transformation
Frequent complication after ischaemic stroke
Bleeding into the ischaemic tissue occurs after the stroke, often
exacerbated by the thrombotic therapy we have given the patient
Can occur 1-2 days post stroke
If GCS decreases, NIHSS increases or patient deteriorates, we will rescan to check for transformation
Statins may increase the risk of HT in acute stroke, so we wait 48 hours before starting a new statin
CT scan shows Haemorrhagic Stroke
What are the next steps?
CT scan shows Haemorrhagic Stroke
Diagnosis confirms haemorrhagic stroke
Surgery - clip the aneurism
Blood pressure control
frequently elevated at presentation and requires treatment when systolic BP
(SBP) is >180 mmHg or the mean arterial pressure (MAP) is >130 mmHg
GTN, Labetalol (IV BB) or nicardipine IV
Antipyretics
Anticonvulsants in those with seizure activity
Phenytoin / levetiracetam
DVT prophylaxis
Keep comfortable and monitor closely
Control blood pressure target of 140
Stop any exacerbating drugs
Re–bleeding in 54% of ICH patients on anticoagulants occurs up to 7 days post stroke
Warfarin: may need to normalise INR - fresh frozen plasma or prothrombin complex (e.g.Beriplex) +/- vitamin K
Reversal of anti coagulation
Warfarin : Prothrombin complex (BERIPLEX) & Vitamin K IV
Dabigatran : Idarucizumab (PRAXBIND)
Apixaban, Edoxaban or Rivaroxaban : PCC & discuss with Haematology or new drugs: andexanet alpha
TIA Management > 7 Days
TIA Management > 7 Days
If the person has had a suspected TIA which occurred more than a weekpreviously:
Refer for specialist assessment as soon as possible within 7 days. Assess for atrial fibrillation and other arrhythmias
TIA management < 7 Days
TIA Management < 7 days
Suspected TIA within the last week:
Give aspirin 300 mg immediately (with proton pump inhibitor cover where appropriate)
They are taking low-dose aspirin regularly — continue the current dose of aspirin until reviewed by a specialist.
Aspirin is contraindicated — discuss management urgently with the specialist team.
and
arrange urgent assessment (within 24 hours) by a specialist stroke physician unless:
They have a bleeding disorder or are taking an anticoagulant as haemorrhage requires exclusion — arrange immediate admission for urgent assessment and imaging.
Complications post stroke
Muscle weakness
Movement, incontinence, pressure sores
Dysphagia
Aspiration pneumonia, malnutrition
CNS
Depression, pain, epilepsy, cerebral oedema
Diabetes
DVT or PE
Hypertension
UTI
Visual field defects
Speech and language difficulties
Modifiable stroke risk factors
MAJOR
Hypertension
Atrial fibrillation
Smoking
TIA
Carotid stenosis >50%
Diabetes Mellitus
High cholesterol
Peripheral arterial disease
SECONDARY
Lack of exercise
Unhealthy diet
Obesity
Excessive alcohol consumption
Drugs: HRT, oral Contraceptives, COX-2 inhibitors, atypical neuroleptics (e.g. risperidone)
Sickle cell disease
Unfortunately some risk factors can’t be changed:
Previous stroke
Age (although 25% of patients are less than 65yrs)
Gender
Race
Family history
Headache red flags
HEADACHE RED FLAGS
▪ A headache of sudden onset, reaching maximum intensity by five minutes - Thunderclap (suggestive of subarachnoid haemorrhage)
▪ Fever with a worsening headache, meningeal irritation and change in mental status (viral/bacterial meningitis)
▪ New-onset focal neurological deficit, personality change or cognitive dysfunction (intracranial haemorrhage/ischaemic stroke/space occupying lesion)
▪ Decreased level of consciousness
▪Head trauma (within the last three months)
▪ Headache which is posture dependent (e.g. worse on lying down and coughing with raised ICP).
▪Headache associated with tenderness in the temporal region (unilateral or bilateral) and jaw claudication (temporal arteritis)
▪ Headache associated with severe eye pain/blurred vision/nausea/vomiting/red eye (acute angle closure glaucoma)
NICE red flags for a headache
NICE RED FLAGS
▪ New severe/unexpected
▪ Sudden onset (maximum intensity within 5 mins)
▪ Drastic change/progressive/persistent
▪ Precipitating factors
▪ Trauma (<3months ago)
▪ Valsalva manoeuvre (cough/sneeze/bending/exertion)
▪ Worsens on posture changes
▪ Comorbidities
▪ Compromised immunity - ?infection/malignancy
▪ Current or past malignancy – esp. those that metastasize to the brain (melanoma)
▪ Current/recent pregnancy
Criteria for low risk headaches
> 30 years old
Typical features of a primary headache
History of similar episodes
No abnormal neurological findings
No high-risk co-morbidities
No new, concerning history or physical examination
No change in headaches habits
No red flags
Headache history taking
HEADACHE HX
▪ Site
▪ Location - Bilateral/unilateral/symmetrical
▪ Onset
▪ Speed of onset
▪ Aura
▪ Precipitating factors – trauma, fatigue/stress, menstr uation, medication change/withdrawal, foods
▪ Character
▪ Sharp/dull/boring/electrical/pressure
▪ Radiation
▪ Face – trigeminal neuralgia ▪ Eyes – glaucoma
▪ Neck – meningitis
▪ Associated symptoms
▪ Autonomic–tearing,dropping,swolleneyelid,painaround
one eye, congestion/rhinorrhea (cluster)
▪ Meningism symptoms – fever, neck stiffness, weakness, rash
▪ Temporal - Jaw claudication, scalp tenderness
▪ Glaucoma - Visual problems, red eyes, halos around lights
▪ RaisedICP - Vomiting/nausea,sleepdisturbance
▪ SOL – neurological deficits, weight loss, visual disturbance
▪ Neurological – fit/fall/LOC/dizziness
▪ Timings
▪ Episodic/daily/unremitting
▪ Duration
▪ Exacerbating/relieving factors
▪ Posture, Valsalva, medication, caffeine
▪ Severity
▪ Out of 10
▪ Getting better or worse
PMH, DH, SH red flags for a headache
RED FLAGS
• PMHx
• including compromised immunity, malignancy, systemic illness , current pregnancy
• Previous bleeds
• Head trauma
• DHx–include what (dose/frequency) they have taken for the headache,response,side effects of medications tried before
• Anticoagulants/antiplatelets, glucocorticoids, methamphetamines, cocaine, GTN, COCP
• Allergies
• SHx
• Effects on activities
• Avoid activity – migraine
• Pacing/restless - cluster
• Contacts with similar symptoms (CO poisoning)
Physical examination when presenting with a headache
HEADACHE EXAMINATION
▪ Basic observations (especially temperature and BP)
▪ GCS
▪ Photophobia
▪ Rash
▪ Eyes - pupils, redness
▪ Feel sinuses for tenderness (move head forward)
▪ Neck stiffness: passively turn head side to side and touch ears to shoulder
▪ Brudzinki’s sign (passive flexion of neck causes involuntary flexion of knee and hip)
▪ Kernig’s sign (pain on passive knee extension with hip fully flexed)
▪ Peripheral neruo exam: tone, power, reflexes, gait
▪ Cranial nerve exam
▪ Visual fields
▪ Fundoscopy to look for papilloedema (↑ICP) or haemorrhages (SAH)
1st degree headache investigations
Not commonly needed for 1o headaches (clinical dx)
▪ If diagnosis unclear BUT red flags have been ruled out – can use headache diary
▪ If concerned about a 2o/serious headache, refer to hospital urgently (dependent on clinical picture)
RED FLAGS- 2SNOOP
Of a headache
• 2S- Systemic symptoms (fever, weight loss, fatigue). Secondary risk factors (HIV, cancer (brain mets), immunosuppressed).
• N -Neurologic symptoms/ signs. Pins and needles ect
• O- Onset- Thunderclap, abrupt.
• O- Older-New in someone 50+.
• P- Positional (upright relieves, neck position relieves), Prior Headache (different to previous), Papilloedema
Primary headaches
PRIMARY HEADACHES
▪ Generally chronic and episodic in nature
▪ Primary headaches do not have another cause/disorder
▪Primary Headaches
▪ Classic migraine 1A
▪ Atypical/common migraine 2B
▪ Tension headache 2A
▪ Cluster headache 2A
▪ Trigeminal neuralgia*
▪‘Benign’secondary headaches
▪ Medication overuse headache
▪ Sinusitis 1A/B
Tension stress headache
TENSION (STRESS) HEADACHE
▪ Age – usually 20-50
▪ Location – usually bilateral and symmetrical – frontal/occipital
▪ Severity – mild-moderate (classically worsen during the day)
▪ Duration – 30mins – 7 days
▪ Quality – pressure, tightness, band-like - NOT pulsatile
▪ Associated symptoms – none
▪ Does not worsen with exercise
▪ Photo/phonophobia/nausea can occur (no more than 1)
▪ Risk factors
▪ Mental tension, stress, fatigue, missing meals
▪ Sternocleidomastoid, trapezius, temporalis commonly tender
Tension headache management
TENSION HEADACHE MANAGEMENT
▪ Simple analgesia is effective – NSAIDs/paracetamol/ aspirin
▪ Opioids should never be used – if required revisit diagnosis
▪ If chronic (7-9 “headache days” per month)
▪ Prophylactic low does tricyclic antidepressants (amitriptyline – off label)
▪ If no response discontinue + refer to neurology
▪ If response – attempt withdrawal after 4-6 months
▪ Acupuncture
▪ Relaxation therapy
▪ Patient information – NHS website
▪ Advise the risk of medication overuse headache
Medication overuse headache
MEDICATION OVERUSE HEADACHE
▪ “analgesic rebound”
▪ Due to regular overuse for >3/12 of
drugs used to treat headaches
▪ NSAIDs/paracetamol – if taken >15 days a month
▪ Opioids/ergotamine/triptans – if taken >10 days a month
▪ The headache must be present for >15 days a month in a patient with a pre-existing headache disorder
▪ Treatment – medication withdrawal
Common agents:
▪ Analgesics
▪ Birth control – usually during inactive days (drop in
oestrogen)
▪ Nitrates
▪ CCB
▪ Digoxin
▪ Corticosteroids
▪ HRT
▪ Alcohol/caffeine/barbiturates/narcotics ▪ Withdrawal too
Migraine
MIGRAINE
▪ Age – 10-40
▪ Location - usually unilateral (can become bilateral later)
▪ Severity - moderate-severe
▪ Duration - 4hrs-3days
▪ Quality – throbbing, pounding/pulsating
▪ Associated symptoms – prodromal symptoms (30-75% - irritable, cravings, yawning) aura (25%), during headache (N+V, photophobia, phonophobia, allodynia)
▪ Typical migraine = aura (also known as ‘classic’migraine)
▪ Can diagnose after 2 attacks
▪ Atypical migraine = no aura (also known as common migraine)
▪ Can diagnose after 5 attacks
▪ Patients may confuse a migraine headache for sinusitis
4 phases of a migraine headache
Prodrome:
Problems concentrating, fatigue, cravings, muscle weakness, nausea, sensitivity to light
Aura:
▪ Can last 5mins - 1hr before migraine onset
▪ Fully reversable
▪ Progress gradually over 5 mins
▪ Can vary a huge amount from patient to patient
▪ Visual (usually binocular) – most common
▪ Photopsia (flashes)
▪ Fortification spectra (jagged lines)
▪ Scintillating scotoma (shimmering oddly shaped area of visual deficit)
▪ Hallucinations
▪ Vertigo
▪ Peripheral sensory deficits (e.g. paresthesia)
▪ Focal loss of motor function
Headache:
Sensitivity to light, odors and noise
Nausea, vomiting, GI discomfort
Loss of appetite
Sweating, chills
Dizziness and blurred vision
Postdrome
‘Migraine hangover’
Fatigue and depression
Migraine management
▪ Lifestyle
▪ Headache diary – identify triggers
▪Stress management,sleep hygiene, hydration, regular meals, exercise, healthy BMI
▪ Optimisation of other conditions – sleep apnea/insomnia/depression/anxiety
▪ Acute attack
▪ NSAID/paracetamol + triptan (sumatriptan)
▪ Can use monotherapy
▪ Triptans can be oral, nasal or sub cut – contraindicated in cv disease/elderly
▪ Antiemetics (prochlorperazine/metoclopramide*) – even in absence of N+V
▪ Avoid opioids
▪ Acute medication should be taken early while pain is mild.
▪ If they have aura, triptans should be taken at the start of the headache and not at the star t of the aura (unless the aura and
▪ Contraindications
▪ COCP in typical migraines is absolutely contraindicated
Migraine prevention
MIGRAINE PREVENTION
▪ Aim to reduce the frequency, severity, and duration of migraine attacks, and avoid medication-overuse headache
▪ NOT to cure migraines
▪ Consider if:
▪ Significant impact on quality of life/ADL – frequent/prolonged/severe
▪ Acute management ineffective/contraindicated
▪ Medication overuse headache ruled out
▪ Medications
▪ Propranolol or,
▪ Topiramate (contraindicated in pregnancy — highly effective contraception is required prior to initiation) or,
▪ Amitriptyline (25–75 mg at night)
▪ Start low and titrate – divided doses ▪ Review regularly during titration
▪ May take 4-8 weeks to see benefit
▪ Non-pharmacological
▪ Relaxation therapy/CBT
▪ Acupuncture
▪ Riboflavin 400mg OD vitamin B2
Hemiplegic migraine
HEMIPLEGIC MIGRAINE
▪ Can mimic stroke
▪ Symptoms can vary
▪ Typical migraine symptoms
▪ Sudden or gradual onset
▪ HEMIPLEGIA ( unilateral weakness of the limbs)
▪ ATAXIA
▪ Changes in consciousness
▪ Analgesic
Motor aura - temporary one sided weakness
Sensory aura - numbness or pins and needles
Visual aura - flashing lights, zigzag lines, visual field loss
Aphasia aura - word formation and comprehension affected
Hemicrania continua
HEMICRANIA CONTINUA
3 month headache
Similar presentation to migraine although lasting >3months
Criteria
• All of the following:
• 1) unilateral pain
• Daily/continuous
• Moderate severity with exacerbations
• Plus at least one of the following: (ipsilateral)
• Conjunctival injection/lacrimation
• Nasal congestion/rhinorrhea
• Ptosis/miosis
Usually completely responsive to indomethacin (NSAID)
Cluster headaches
“Suicidal headache”
CLUSTER HEADACHE
▪ Age – 20-40
▪ Location – unilateral, peri-orbital pain
▪Severity -severe
▪ Duration – 15-180mins
▪ Quality – sharp, pulsating, boring, burning
▪ Associated symptoms – ipsilateral cranial autonomic symptoms (conjunctival injection, lacrimation, eyelid oedema)
▪ The pain characteristically makes people restless/agitated – they pace
▪ Timings of the attacks are predictable – same time of night/day
▪ Typically 1-2 hours after falling asleep
▪ May have triggers
▪ Alcohol, histamine, exercise, sleep, volatile smells (petrol/perfume)
Cluster headache aetiology
CLUSTER HEADACHE
▪ Rare
▪ Men > Women
▪ Linked to previous head trauma and smoking
▪ Episodic (80-90%)
▪ Attacks occur in periods typically between 2 weeks and 3 months
▪ Can occur in periods of 7 days to one year
▪ Attacks separated by pain-free periods of at least 1 month
▪ Chronic (10-20%)
▪ Attacks occur for more than one year without remission (or remission lasts less than 1 month)
▪ Can present initially or convert from episodic (10%)
▪ 30% convert to episodic
Cluster headache management
CLUSTER MANAGEMENT
▪ First presentation
▪ Urgent referral/discuss with neurologist/specialist GP
▪ Requires specialist diagnosis (may need neuroimaging)
▪ Acute
▪ Subcutaneous triptan
▪ 1 injection 6mg sumatriptan
▪ Can have second injection after 1 hour (unless no response)
▪ Maximum 12mg/day
▪ Nasal triptan
▪ 1 nostril 10-20mg sumatriptan
▪ Can have second dose after 2 hours (unless no response)
▪ Maximum 40mg/day
▪ Oxygen therapy
▪ 100% 15L non-rebreather for 15-20mins
▪ Preventative
▪ Verapamil 40mg/day (up to 960mg) – ECG monitoring
>120mg/every increase(AV block)
▪ Prednisolone (60-100mg) – short periods (2-3 weeks) - wean off after 2-5 days
▪ Do not use paracetamol/NSAIDs/opioids
Trigeminal Neuralgia
TRIGEMINAL NEURALGIA
▪ Not a true primary headache – “painful cranial neuropathy’
▪ Disorder of 5th cranial nerve (trigeminal)
▪ Most commonly maxillary/mandibular branches involved
▪ Chronic, debilitating
▪ Intense and extreme electric shock pain – unilateral
▪ Lasts seconds to minutes – can have hundreds of attacks per day
▪ Can have remission for weeks/months – shortens gradually shorten between episodes
▪ Can be triggered by – light touch, eating, cold wind, vibrations, brushing teeth
▪ Refer to specialist
▪ May require an MRI to rule out other causes
Trigeminal Neuralgia management
TRIGEMINAL NEURALGIA MANAGEMENT
▪ Medical
▪ Carbamazepine 1st line
▪ Withdraw gradually after 1 month of remission
▪ Gabapentin
▪ Botox
▪Surgery
▪ Sever trigeminal nerve root
▪ Microvascular decompression
Sinus headaches
SINUS HEADACHES
▪ Headache due to inflammation of the mucosal lining of the nasal cavity and paranasal sinuses
▪ Tender to palpation over sinuses when leaning head forward
▪ Can be viral or bacterial
▪ Usually 2o to URTI (viral)
▪ If symptoms last >10 days think bacterial infection
▪ Purulent nasal discharge, nasal obstruction, dental pain, or facial pain/pressure/headache are more common with acute bacterial sinusitis
Sinusitis management
SINUSITIS MANAGEMENT
▪ Viral is self-limiting (usually within 10 days)
▪ NSAIDs/paracetamol/codeine
▪ Decongestants
▪ Nasal corticosteroids
▪ Bacterial
▪ Symptomatic treatment
▪ Watchful waiting (up to 10 days unless immunocompromised)
▪ Antibiotics can be used to shorten symptoms (penicillin / Co amox)
▪ Or if severe/worsening symptoms
Examples of second degree headaches
• Subarachnoid Haemorrhage 1A
• Acute Bacterial Meningitis 1A
• TIA/Stroke 1A
• Raised intracranial pressure 1B
• Accelerated hypertension 1B
• Acute Angle Closure Glaucoma 1B
• Hypotension 1B
• Temporal Arteritis 2A
• Pre-eclampsia 2A
• Viral Encephalitis 2B
• Venous sinus thrombosis 2B
• Cavernous sinus thrombosis 2B
• Internal carotid dissection 2B
• Space occupying lesion
• Post-lumbar puncture headache
