Primary Care Live -Neurology

Dr Estelle McFadden

MBChB, MRCP, MRCGP

GPwSI, Bradford

Headaches

www.mipca.org.uk

Why is this important?

• Prevalence of headache is very high (96%)– Most common headaches are tension-type headache

(TTH), migraine and chronic primary headaches– Migraine is associated with high economic costs

• Headaches are a frequent reason for GP consultation– However, migraine is under-diagnosed and under-

treated in the UK

What should I already know about this condition?

• Most headaches are benign• Migraine can occur with or without an aura• Chronic primary headaches usually evolve from

episodic headaches (migraine or TTH)• Differential diagnosis of TTH, migraine, chronic

primary headaches and cluster headache• Types of secondary (sinister) headaches and

diagnostic features (RED FLAGS)

What new evidence so I need to know about?

• Features of medication overuse headache (MOH)

• Topiramate is an effective and generally well tolerated new preventive drug for migraine

Practical management tips

• Seven step process for managing headache1. Screening

2. Patient education and eliciting commitment

3. Differential diagnosis

4. Assessment of illness severity

5. Tailoring management to the needs of the individual patient

6. Proactive, long-term follow up

7. A team approach to care

When should I refer my patient?

• <5 years or >60 years• New-onset or acute headaches

– Single, sudden severe headache

• Progressive headaches• History of cancer• Symptoms: rash, non-resolving neurological deficit,

vomiting outside of the headache, scalp pain/tenderness, accident/head injury, infection, worrisome hypertension

• Uncertain diagnosis• Refractory to repeated acute and preventive treatments• Very anxious despite reassurance

Commonly asked questions

• Will my patient benefit from having a scan, even if I do not think there is intracranial pathology?

Common pitfalls

• Misdiagnosing chronic headache as migraine

• Over-treating chronic headaches leading to MOH

• Under-treating migraine – relying on analgesics

• Missing unusual primary headache variants

• Blaming headaches solely on stress

Important messages

• Most headaches can be managed effectively in primary care

• Headaches are a major cause of morbidity

• Specific management of headaches can help

Epilepsy

Principles of epidemiology

• Incidence rate = new cases per year [n per 100,000 per year]

• For epilepsy is around 50 per 100,000

• Point prevalence = All cases with active epilepsy at a point in time [n per 1000].

• For epilepsy is 4-7 per 1000

• Active epilepsy = to have had a seizure or treatment in the last 5 yrs

Epilepsy seizure types

• Focal Seizures• 60% of epilepsy• Focal Cortical

Disturbance• Their origin usually

determines the clinical picture

• Focal Spikes on EEG

Primary Generalised Seizures

• Origin unclear either sleep spindles or hyper-synchrony

• Commence bilaterally• Spike and wave • No aura

Focal epilepsy – the site of the focus determines the seizure morphology

Focal vs Primary Generalised Epilepsy

Focal Epilepsy• Aura• Simple Sz.’s• Complex Partial Sz’s• Secondary

Generalised Sz.’s

P.G.E.• Myoclonic Jerks• Absence• Atonic Sz’s• Tonic Sz’s• Tonic-clonic Sz.’s

Mortality in epilepsy

– Up to 1000 deaths a year. – 20% more men than women. No change in figures for over a

decade– SUDEP = 350-400 a yr in the UK– Possible cardiac arrhythmias caused by channelopathies,

bradycardia 2’ to apnoea, endogenous opioids/endorphins– External obstruction likely to be a factor in up to 70%– May effect up to 1 per 1000 with epilepsy– 1 per 250 attending a tertiary epilepsy clinic– If seizures are fully controlled, SMR falls to close to normal

for the population– Has been studied in small numbers – one was during video

telemetry

Epilepsy is not just about seizures• Social implications are varied and very much lie within

the remit of General Practice e.g. the impact of epilepsy on sexuality

• Hypo sexuality. Surveys suggest 22-67% reduction in sexual interest

• Erectile dysfunction – occurs in 57% [Toone et al 1989], up to 83% in TLE

• Sexual Functioning in Males [1989]– Previous SI 56% [compared to 98% controls]– S.I. in the previous month 43% [compared to 91% in controls]– Previous erectile dysfunction 57% [compared to 18% controls]

Psychosocial impact of epilepsy

• Psychiatric– Depression – Up to 2/3 of PWE are depressed, with

2’ reduced libido and effects of antidepressants– Anxiety – self medicate with alcohol

• Psychosocial• In one study [1988] of 92 patients with poorly

controlled epilepsy– 68% Had no friends– 34% Never had a “true” friendship– 57% Never had a steady relationship

Dizziness: the management of vertigo: the illusion of

movement

The Labyrinth

NB vertigo is perceived by the brain - ± Mismatch of visual, vestibular & proprioceptive cues- ± Abnormality of central vestibular processing

Epidemiology

• 6-25% UK population complain of dizziness at some point

• After viral vestibular neuronitis (idiopathic) benign paroxysmal positional vertigo is most common cause

VertigoDifferential diagnosis for acute onset of first attack – cardiac or brain or ear

• Viral vestibular neuronitis (idiopathic)– common, usually self limiting– acute – symptomatic management with rest, avoidance of provocative

manoeuvres, short course of vestibular sedatives–

• Benign Paroxysmal Positional Vertigo– Increase physical activity, Epley, precipitate vertigo, core stability

muscle activity

• Iatrogenic, e.g. diuretics

• Cardiovascular, Hypotension, Myocardial Infarction, Cardiac dysrhythmia

• Cerebrovascular Vertebrobasilar TIA, posterior fossa CVA, migraine

• Psychogenic

Red Flags

• If history inadequate– Presume cardiovascular till proven otherwise

• ECG, cardiac enzymes, cardiac monitor, ECHO, tilt table, carotid sinus massage

• If cardiac symptoms present before, during or after arrange cardiac tests especially while symptomatic

• Altered consciousness, behavioural change– Exclude epilepsy– Exclude cardiac/cardiovascular causes– The Blackouts Checklist (refs)

• Vomiting

Vertigo and the neck

• Compression of vertebral arteriesexpect multiple neurological symptoms;tinnitus & hearing loss– very rare cause of recurrent vertigo

• Carotid sinus hypersensitivity– Relatively common, but causes falls NOT vertigo

• Cervicogenic vertigo proprioceptive dysfunction desensitization to neck stimuli vestibular failure

Not common

Nystagmus

• Transient Positional nystagmus WITH vertigo – think BPV

• Positional nystagmus NO vertigo – brain stem lesion

• If present when patient sitting up – Usually indicates cerebellar involvement– Rarely present with ACUTE peripheral

vestibular lesion• Viral labyrinthitis first 1-3 days• During attack of Meniere’s, migraine-

associated vertigo (positional = laying back)

Benign Positional Vertigo

• Diagnosed ONLY by the Hallpike manoeuvre or by the lateral canal manoeuvre– Must be performed in the acute phase

• Curative manoeuvres– Epley– Barrel

Epley manoeuvre and Barrel manoeuvre

Positional manoeuvres move debris around the semicircular canals (diameter 0.3 mm) back to the utricule

Hallpike manoeuvre1-2Epley manoeuvre1-6

1 2

3 4

5 6

> 30 s in eachposition

The best policy: A team approach

• General practice, elderly medicine, neurology, cardiology, audiological medicine

• Rehabilitation team: physiotherapy, cognitive behaviour therapy, occupational therapy, exercise therapy, activities in the community

• Open access to Audiological Physician by patients already seen – to finalise diagnosis and expedite treatment

Web links

• www.vestibular.org website of vestibular disorders association

• www.dizziness-and-balance.com• Google - images – Epley• www.youtube.com

– Epley manoeuvre

• www.stars.org.uk– The Blackouts Checklist

Transient ischaemic attacks

Definition

• Transient ischaemic attack (TIA) is defined as an acute loss of focal cerebral or ocular function with symptoms lasting less than 24 hours and which is thought to be due to inadequate cerebral or ocular blood supply as a result of low blood flow, thrombosis, or embolism associated with diseases of the blood vessels, heart, or blood (Hankey and Warlow 1994)

TIA or stroke?

• Brief episode of rapidly developing neurological dysfunction with no apparent cause other than of vascular origin with symptoms resolving completely within 24 hours

• MR scans have shown that those with symptoms lasting more than 1 hour show cerebral infarction i.e. a stroke– Definition may be changed to symptoms resolving

completely within 1 hour• TIA is the only warning that a stroke is imminent• Estimated 30,000 new TIAs per year

Risk of stroke following TIA

• Most patients who have a TIA have a short benign course but up to 20% will have a stroke within the next 90 days

• Half of those who will have a stroke will do so in the first seven days after their TIA(Coull A, Lovett JK & Rothwell PM on behalf of the Oxofrd VAscualr Study, 2004, Early risk of stroke after a TIA or minor stroke in population-based incidence study, BMJ, 328, 326-8)

• Risk of a stroke following a TIA varies• ABCD2 risk stratification tool helps identify those

at highest risk of a stroke(Johnston SC, Rothwell PM et al The Lancet 2007; (369) 283-292)

ABCD2 score to identify individuals with high early risk of stroke after TIA

SCORE AGE BLOOD PRESSURE

CLINICAL FEATURES

DURATION OF SYMPTOMS

DIABETES MELLITUS

0 < 60 years

<140/90 Other <10 mins

1 ≥ 60 years

Systolic >140 and/orDiastolic ≥ 90

Speechdisturbancewithoutweakness

10-59 mins Yes

2 Unilateralweakness

≥ 60 mins

Risk of stroke following TIA

• HIGH Score 6-7 = 8.1% 2 day risk

• MODERATE Score 4-5 = 4.1% 2 day risk

• LOW Score 0-3 = 1.0% 2 day risk

• More than one TIA in seven days also at high risk of stroke

ANTERIOR VS POSTERIOR ISCHAEMIA

Carotid (80% TIAs)

Vertebrobasilar (20%TIAs)

Motor Contralateral weaknessParalysisClumsiness

Bilateral or shifting weaknessParalysisClumsinessAtaxiaImbalance without vertigo

Sensory Contra lateral numbness,Pins and needlesSensory loss

Bilateral or shifting numbnessPins and needlesSensory loss

Speech Dysphasiadysarthria

Dysarthria

Visual Ipsilateral monocularblindnessContralateral homonymoushemianopia

DiplopiaPartial or complete blindness in bothvisual fields

Other Combination of above VertigoDysphagia

Presentation of TIA

Management of TIAurgent medical admission

• As TIA is a retrospective diagnosis then if they are symptomatic at the time of presentation then refer for emergency admission to an acute stroke unit

• In a centre offering thrombolysis, those still symptomatic at 3 hours may be eligible for thrombolysis

Management of TIA: High risk

• High risk of subsequent stroke in < 2 days if:– ABCD2 score ≥4 – More than one TIA in seven days

• Require assessment and treatment within 24 hours– ?admit as urgent medical admission– Refer to rapid access neurovascular clinic, one stop

shop with strong advice to seek urgent medical referral (via 999) in the event of symptoms returning or new symptoms i.e. develop a stroke AND give 300mg aspirin if not already on regular aspirin

– To be treated or referred if presenting to Out Of Hours services or A&E (not referred back to GP)

Management of TIA: Low risk

• All other TIAs • Should be given 300mg aspirin (if not taking regular

aspirin already)• Those attending out of hours must be treated and not

referred back to their GP to avoid delays• Need prompt referral to a rapid access neurovascular

clinic (referrals for TIA are excluded from Choose and Book as considered to be a medical emergency) and to be seen within SEVEN days

• UNLESS– Presenting several weeks after event (still refer)– Treatment not felt to be in patient’s best interest e.g. bed bound

with dementia

Assessment of TIA

• Carotid imaging should be performed at initial assessment (and not delayed for more than 24 hours in high risk patients and those with carotid territory minor stroke) – Doppler ultrasound– MR including angiography, diffusion weighted

imaging, gradient echo imaging– CT

• Where indicated– ECG– Echocardiogram

Treatment of TIA

• Carotid endarterectomy for >70% stenosis– Recommendation this becomes a surgical emergency– Stroke prevention benefits lost if treatment delayed– Should be performed within

• 48 hours in high risk patient• 28 days to prevent stroke

• Atrial fibrillation and other arrhythmias– Anticoagulation unless contra-indications– Aspirin 75 – 300mg daily– Treatment of arrhythmia

Secondary prevention

• Antiplatelet – Aspirin 75mg – 300mg plus dipyridamole MR

200mg bd for 2 years following event then aspirin alone

– Clopidogrel alone if aspirin intolerance or sensitivity

• Anticoagulation– Anticoagulant if arrhythmia unless

contraindication (high risk of falls, recent GI bleed)

Secondary prevention

• Hypertension– Risk of stroke halves with every 10mmHg fall

in diastolic blood pressure even in normotensive patients

• Cholesterol– Equal benefit of simvastatin 40mg across all

those who had had a stroke or TIA down to baseline 3.5mmol/l total cholesterol

Lifestyle advice

• Smoking cessation

• Alcohol intake– Binge drinking associated with increase in

blood pressure

• Exercise

• Obesity