Phase 2a
David Gregg
David Stewart-Watson
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Two questions to ask in neurology:
1.Where is the lesion?
2.What is the pathology?
Weakness can be due to any location along the
nervous pathway – what possible locations are
there?
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Possible Sites
Muscle
•Cushing’s syndrome, thyroid disease, hyperparathyroidism, influenza, myositis, dermatomyositis, sarcoidosis, sarcoma
Neuromuscular Junction
•Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Clostridium botulinum infection
Peripheral Nerves (mono, multiplex, poly)
•Carpal tunnel syndrome, trauma
•PAN, SLE, RA, herpes zoster, HIV, sarcoid, DM, amyloid (multiplex)
•Guillian-Barre syndrome, PAN, SLE, RA, CIDP, DM, renal failure, amyloid, Vitamin B1/6/12 deficiency
Spinal nerve root
•Infection, prolapsed disc, spinal stenosis, spondylosis, tumour, vertebral fracture dislocation
Anterior horn cell
•Motor neruone disease, polio
Spinal cord
•OA, HIV, TB, MS, sarcoid, RA, Paget’s, trauma, prolapsed disc, tumour, subacute degeneration of the spinal cord, MND
Cerebral hemispheres
•MS, Stroke, TIA Meningitis, encephalitis, HIV, malaria, TB, sarcoid, SLE, Wilson’s disease, tumour,
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1.
2.
3.
4.
5.
6.
7.
8.
Myasthenia gravis
Carpal tunnel
Guillian-Barre syndrome
Spinal nerve root lesion
Motor neurone disease
Spinal cord compression (+ cauda equina)
MS
Stroke (+TIA)
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Myasthenia Gravis
Pathophysiology
In normal muscle, the amount of Ach released with each AP decreases with repetitive
activity, thus the magnitude of each end-plate potential falls. In MG, anti-Ach
antibodies have taken out Ach receptors. This means that the decreased amount of
Ach released becomes insufficient to cause sufficient end-plate potential to trigger a
muscular contraction.
Anti-MUSK antibodies are seen in a subsection of patients.
The thymus is hyperplastic in half of MG patients, and a thymoma is present in 15%. If
someone has MG look for a thymoma, and if someone has a big thymus check for MG!
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Myasthenia Gravis
Clinical Features
•Painless, fatiguable muscle weakness – particularly proximal limbs, extra-ocular,
bulbar and facial muscles
•Wasting can be seen after many years
•Respiratory difficulties can be prominent especially during a myasthenic crisis
•Average 20-40 years at presentation
•More women than men
•Associated with hyperthyroidism, RA, SLE
•Other signs and symptoms include ptosis, diplopia, voice weakening with continuous
speaking and dysphagia
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Myasthenia Gravis
Investigations
•Serum anti-AChR; serum anti-MUSK
•Electromyography (used to confirm diagnosis)
•Tensilon (edrophonium) test (rarely done nowadays – risk of cardiac arrest!)
•Mediastinal MR for thymoma
Course and Management
•Fluctuates in severity, protracted, lifelong
•Exacerbations are unpredictable, can be brought on by infections and aminoglycoside
use
•Emergency ventilation may be required
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Myasthenia Gravis
Treatment
1.Oral anticholinesterases
– Pyridostigmine is widely used, dose is determined by response
– Prolongs Ach action by inhibiting cholinesterase
– These help the weakness but do not alter the course of disease
1.Immunosuppressants
– Used in those non-responsive to above/who relapse
– Steroids are often used, azathioprine/mycophenylate are also used
2.Thymectomy
– Useful in those with positive AchR antibodies, even if no thymoma. Anti-MUSK cases do less well. If a
thymoma is present, then it is also necessary
3.Plasmapharesis/IV Ig
– Useful during exacerbations
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Carpal Tunnel Syndrome
Pathophysiology
Due to median nerve compression in the limited space of the carpal tunnel. It
is not typically associated with any disease. It can be seen in hypothyroidism,
DM, obesity, RA, acromegaly, amyloid and renal dialysis
Clinical Features
•Patient wakes with numbness, tingling and pain in a median nerve
distribution.
•The pain radiates to the forearm
•The fingers feel swollen but usually aren’t
•Wasting of the abductor pollicis brevis develops with sensory loss in the
palm and radial 3 ½ fingers
•Tinel’s or Phalen’s sign may be positive
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Carpal Tunnel Syndrome
Treatment
1.Splinting
–
Holds wrist in dorsiflexion overnight. If this relives symptoms, it is diagnostic. It can
produce full recovery if used for several weeks
2.Corticosteroid injection
–
Helps in 70% of cases, but may recur
3.Nerve conduction studies + surgical decompression
–
–
Persistent symptoms or nerve damage requires referral for nerve conduction studies
A prolonged latency across the carpal tunnel demonstrates CTS and surgical
decompression is needed
–
–
–
Weight loss helps in obese patients
CTS in pregnancy usually disappears post-partum
Other mononeuropathies occur with similar tingling and weakness distal to site of
compression (ulnar, radial, lateral cutaneous nerve of the thigh and common peroneal)
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Cranial Nerve Lesion
• Many causes
• Symptoms are easy to predict
• Learn what the cranial nerves do, the lesions
at each nerve result in a deficit of that e.g
• CN1 – Anosmia
• CN6 – Failure of eye abduction
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Mononeuritis Multiplex
• Occurs in DM, vasculitis, sarcoidosis,
amyloidosis, malignancy and HIV
• Clinical picture of multiple mononeuropathies
occurring sequentially or simultaneously
• Mononeuropathies are confirmed using nerve
conduction
• Appropriate investigation into underlying
cause (BM, inflammatory markers, serum ACE)
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Guillian-Barre Syndrome
Clinical Features
•Commonest acute polyneuropathy
•Usually demyelinating, though can cause axonal damage
•Pt complains of weakness in distal limb muscles and/or distal numbness
•Progresses proximally over days to weeks
•Areflexia is invariable; autonomic features can occur
•Follows 1-3 weeks after an infection (usually trivial)
•C.jejuni and CMV are well-recognised causes of severe GBS; the organisms
induce Ab responses against peripheral nerves. Similarity between epitopes
on the nerves and microorganisms is thought to be the mechanism
•In 20% respiratory and facial muscles become weak, sometimes to total
paralysis
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Guillian-Barre syndrome
Diagnosis
•Made clinically; confirmed by nerve conduction studies
•These studies show conduction slowing, prolonged motor latency and/or
conduction block
Course and Management
•Monitoring of vital capacity and blood gases to recognise emerging
respiratory muscle weakness – prolonged ventilatory support may be
necessary
•IV Ig reduces duration and severity of paralysis (screen for IgA deficiency due
to potential for anaphylaxis)
•Recovery begins within 6 weeks from outset
•15% are left disabled or die
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Other Polyneuropathies
Diabetic neuropathy
Several varieties
1.Symetrical sensory – starts distally, loss of vibration, pain and temperature
sensation in the feet, ‘glove and stocking’
2.Diffuse painful – burning/crawling pain in the feet, shin and anterior thighs,
typically worse at night
3.Autonomic neuropathy – postural hypotension, GI symptoms, bladder
problems, ED
Does not typically involve the motor systems at all
More common in T2DM due to long-term hyperglycaemia prior to diagnosis.
Good management can largely prevent the above in T1DM.
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Other Polyneuropathies
Toxic Neuropathies
Causes include alcohol, prescribed drugs, lead, plastic industry by-products,
arsenic and glue sniffing
Vitamin Neuropathies
Thiamine deficiency causes a polyneuropathy combined with cardiac failure.
It also lead to Wernicke-Korsakoff psychosis. The commonest cause is alcohol
abuse. Prophylactic thiamine is given to prevent Korsakoff’s
Vitamin B12 deficiency leads to sub-acute degeneration of the spinal cord.
Sensory loss, numbness and tingling and loss of reflexes distally are the usual
presenting features. Pt will be anaemic. This is an irreversible consquence.
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Plexus Lesions
Produce a variable picture that needs nerve
conduction studies to fully understand
Only one of any relevance to Phase 2 is a
Pancoast tumour – an apical bronchial
carcinoma which compresses the brachial plexus
with consequent small muscle wasting,
weakness and/or pain in the hand/arms
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Spinal Root Lesions
•
•
•
•
Also called radiculopathies
Due to mechanical compression of a nerve as it leaves the spinal cord
Commonest locations are C6+7 and L5+S1
Causes include:
–
–
–
–
Osteophytic growth
Disc degeneration and lateral protrusion
Vertebral collapse – osteoporosis, infection (TB)
Tumour growth
• Clinical features are: pain, sensory disturbance, loss of reflexes, tingling
and numbness that occurs in a dermatomal/myotomal distribution
• Treatment is rest and analgesia. If symptoms persist, then surgical
decompression may be appropriate
• MRI is required if considering for surgery; other investigations may be
indicated by history e.g. in a Pt with one of the 5 Bs that go to bone
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Motor Neurone Disease
Clinical Features
Four broad patterns – usually merge as MND progresses.
1.Amyotrophic lateral sclerosis (ALS)
– Progressive spasticity, weakness and wasting with added lower motor neurone signs and
fasciculation
– Also called Lou Gehrig’s disease
2.Progressive muscular atrophy
– Wasting begins in the small muscles of the hand. Fasciculation is common. Cramps may
occur
3.Progressive bulbar and pseudobulbar palsy
– Bulbar describes LMN signs from the 9th, 10th and 12th CN lesions i.e. wasted fibrilating
tongue; pseudobulbar palsy describes UMN lesions of the same i.e. spastic weak palate
– Presents as dysarthria, dysphagai, regurgitation and choking on fluids
– Eye movements are unaffected
4.Primary lateral sclerosis – tetraparesis, pseudobulbar palsy
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MND
Diagnosis
•Largely clinical
•Denervation (seen in all forms except primary lateral sclerosis) can be
confirmed by EMG
•Potential mimics include subacute degeneration of the spinal cord,
syringomyelia, motor neuropathy and bulbar myasthenia gravis.
Course and Management
•Survival of more than 3 years is unusual; death is often from
bronchopneumonia
•Symptomatic management and support (e.g ventialtion, gastrostomy) helps
prolong survival
•Accurate prognosis is difficult – think of Stephen Hawking!
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Multiple Sclerosis (MS)
Pathophysiology
•Caused my multiple demyelinating plaques due to T-cell mediated response
•These heal poorly causing relapsing and remitting symptoms
•Prolonged demyelination causes axonal loss and clinically progressive
symptoms
Epidemiology
•Commoner in Northern latitudes - ?Vit D
•Migrants take risk with them; 2nd generation acquires risk of where they
settled
•Commoner in women
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MS
Clinical Features
•Presentation is usually monosymptomatic – unilateral optic neuritis, leg
weakness, numbness/tingling in the limbs or brainstem/cerebellar signs
•In the long term, almost any neurological sign can become part of MS due to
the pathophysiology
•Uthoff’s sign is the worsening of MS when exposed to heat i.e. bath
•Lermitte’s sign is the ‘barber chair sign’; electrical sensation down neck and
into the limbs when flexing the neck
Diagnosis
•‘Dr Who disease’
•2 separate lesions required disseminated in time and space
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MS
Course
Three major courses
1.Relapsing and remitting (80%)
2.Primary progressive (20%) – from presentation there is a gradual decrease
in neurological function
3.Secondary progressive – R&R turning into primary progressive
There are cases of fulminant MS, where a massive demyelinating episode
causes critical illness and death over the course of days
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MS
Management
•Non-pharmaceutical – education, PT/OT, MS nurse involvement, social
services involvement, minimise disability
•MS Pts with stress-free happy lives get less attacks
•Active pharmaceutical treatment include
–
–
–
–
–
Methylpredinisolone IV, other oral – for acute relapses, use sparingly
Interferons – prevents relapses in R&R MS
Natalizumab – reduces relapses in R&R
Other treatments are being considered, many patients are willing to into research trials
Once the disease is secondary progressive, clinical trials are the sole option
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Spinal Cord Compression
Anatomy
The spinal cord runs from the medulla oblongata (C1) to the conus medulllaris
(L1).
Clinical Feature
•Wasted intercostal muscles, sensory loss, root pain (sensory level)
•Loss of contralateral pain and temperature sensation (spinothalamic tracts
decussate at cord)
•Ipsilateral UMN signs
•Diminished proprioception and light touch
•Depending on exactly where the cord is being compressed, all the above can
be bilateral i.e. total obliteration
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Spinal Cord Compression
Causes
•Primary tumour – glioma, ependymoma, meningioma, neurofibroma
•Metastases – the five Bs
•Vertebral body destruction – osteomyelitis, osteoporosis
•Trauma
•Degenerative prolapse
•Abscess
Management
1.Spinal MRI ASAP
2.Biopsy/exploration to determine nature of mass may be necessary
3.Consider bloods to rule out pathologies (e.g. PSA)
4.CXR useful for excluding lung primaries and TB lesions
5.If malignant, give IV dexamethasone.
6.Surgery is the definitive cure; may not always be possible
7.Malignancy needs an oncological input
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Cauda Equina Syndrome
• Due to a central disc protrusion, which can be acute or chronic
• Causes a syndrome of
–
–
–
–
–
–
Bilateral flaccid paralysis
Areflexia
Sacral numbness
Retention of urine
Incontinence of urine and stool
Erectile dysfunction
– Back pain
• Requires urgent MRI and surgical decompression
IF someone with back pain develops urinary retention, sacral numbness or
incontinence, this is an emergency!
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Stroke
Pathology
A sudden event in which disturbance of CNS function occurs due to vascular
disease.
This can be ischaemic (the majority) or haemorrhagic (the worst).
Ischaemic causes include arterial stenosis due to atherosclerosis, arterial
occlusion due to emboli, arterial dissection, SLE, antiphosphoplip,
thrombophilc states, and infections (TB, HIV)
Haemorrhagic causes include AVM, amyloid angiopathy, tumours, venous
thrombosis, aneurysm and hypercoaguable states
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Stroke
Risk Factors
•Age – 5x more likely over 75 than 55-64
•Hypertension – 7x more likely over 160/95 than 120/80
•Smoking – 2x more likely
•Diabetes – 2x more likely
•Ischaemic Heart Disease – 3x more likely
•Atrial Fibrilation – 5x more likely – use CHA2DS2-VASC
•Previous TIA – 5x more likely
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Stroke
Stroke Syndromes
Strokes to different parts of the brain give characteristic clinical patterns.
Here are some:
1. Partial Anterior Circulatory Stroke (PACS)
–
–
2.
Total Anterior Cicrulatory Stroke (TACS
–
3.
All of higher dysfunction, partial motor/sensory defect and homonymous hemianopia
Posterior Occiptal Circulatory Stroke (POCS)
–
–
4.
Higher dysfunction or partial unilateral motor/sensory defect
The addition of homonymous hemianopia to one of the above
Any of: cranial nerve palsy, bilateral motor/sensory defect, eye movement problems,
cerebellar dysfunction
Isolated homonymous hemianopia
Lacunar Stroke (LACS)
– 5 classic LAC sub-syndromes – pure motor stroke/hemiparesis, ataxic hemiparesis,
dysarhtria/clumsy hand, pure sensory stroke, mixed sensorimotor
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Stroke
Investigations - Imaging
1.CT to exclude haemorrhage
2.MRI for diagnosis
3.Carotid dopplers to investigate stenosis
If MRI demonstrates a stroke and dopplers show stenosis, then order CT angiogram for
confirmation of stenosis.
If CT angio shows stenosis, refer to vascular MDT for stenting/endarterectomy
If MRI demonstrates a stroke but dopplers show no stenosis, order a 72 hour tape and an
echocardiogram
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Stroke
Investigations – Bloods
1.Calcium – exclude hyper/hypocalcaemia
2.U+E – exclude hyponatraemia
3.LFTs – exclude mimics (i.e. acute liver failure)
4.FBC – exclude polycythaemia, thrombocytopenia, anaemia
5.Creatinine – exclude renal problems
6.TFTS
7.Cholesterol - risk factor for stroke
8.Clotting screen – exclude coagulopathy and check suitability for anti-clotting
agents
9.BM – exclude hypoglycaemia
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Stroke
Second Line Investigations
If 1st line bloods and dopplers have not pinpointed a cause, consider:
• Thrombophilia screen – Factor V Leiden, SLE, antiphospholipid
• Blood cultures – thinking of infective endocarditis or TB
• HIV test
• Syphilis serology – not as usual, if appropriate from history
• Homocysteine – always think of if Pt has a weird vascular presentation
• Lactate
• Cardiac enzymes
• Haemophilia/Von Willlebrand screen (haemorrhagic only) – especially if
non-HTN, non-aneurysmal and under 60.
If +ve family history for any of the above revealed in basic history, go for the
test in the first line.
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Stroke
Management in Hospital - General
1.Admit to stroke unit
2.Treat BP if >220/120 (>185/115 if haemorrhagic)
3.Oxygen if sats <92%
4.Monitor BMS as hyperglycaemia results in poorer outcomes
5.Arrange SALT assessment if any suspicion of dangerous swallow
6.PT/OT input
7.Prevent DVTs – keep hydrated, LMWH if immobilised >2 weeks,
compression stocking
8.Look out for psych problems – depression is common in old people
9.Start on a statin, especially if cholesterol is high
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Stroke
Management in Hospital – Ischaemic
1.Thrombolysis if within 4.5 hours (NICE guidelines) – possible change due to
evidence from IST-3 trial. Lots of contraindications
2.Be aware haemorrhagic transformation is a risk – especially with
thrombolysis
3.Start antiplatelet drugs once CT was excluded haemorrhage. Aspirin is
usually given for 2 weeks.
4.If patient has AF or stroke was cardioembolic, oral anticoagulation is given
after 2 weeks. Typically, this is warfarin
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Stroke
Management in Hospital – Haemorrhagic
1.Stop anticoagulants and antiplatelets
2.Correct coagulation problems
3.If hydrocephalus develops due to mass effect and midline shift, refer to
neurosurgery for decompression/shunting.
NB: This can occur in ischaemic stroke due to oedema around infarct
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What are the modifiable vascular risk factors?
Stroke
Risk Factor
Action
Infarction risk
Haemorrhagic risk
Hypertension
Treat and monitor
Major
Major
Smoking
Stop
Major
Moderate
Sedentary lifestyle
More activity
Moderate
-
High alcohol
Moderate intake
Moderate
-
High cholesterol
Statins, change diet
Moderate
-
AF
Anticoagulate
Moderate
Slight
Obesity
Weight reduction
Probable
Probable
Diabetes
Good control
Probable
-
Severe carotid
stenosis
Surgery
Major risk
-
Sleep apnoea
Treat
Moderate
-
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Stroke
Secondary Stroke Prevention
1.Post TIA – dipyrimadole + aspirin
2.Post-ischaemic stroke – clopidogrel  dipyrimadole+aspirin
If intolerant to any of the above, give either dipyrimadole or aspirin in
isolation
If prescribing aspirin, a PPI should be given as well.
Control BP to a target of 130/80
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Transient Ischaemic Attack
• Cause sudden neurological deficit, onset is over seconds and lasts less
than >24 hours
• Can be separated into anterior (carotid circulation) and posterior
(vertebrobasilar circulation)
• Investigations should be tailored towards looking for future causes of
stroke
• Follow the same investigations you would for a stroke
• Important mimic include mass lesions (spot on CT), focal epilepsy (picked
up in history), migraines (headaches rare in TIA) and Bell’s palsy (look for
forehead sparing)
• Treat any underlying conditions and reduce risk factors – 30% for TIAs
become a stroke in 5 years, 15% become MIs
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TIA
ABCD2 Score
Age
>60 – score one
Blood pressure
systolic >140/diastolic>90 – score one
Clinical features
Speech impairment – score one
Unilateral weakness – score two
NB: Use highest, don’t add
Duration
<60 minutes – score one
>60 minutes – score two
Diabetes
Present – score one
The higher the score, the higher the risk of stroke in the next 90 days – a score of >4 is good
justification for admission. Less than that should still be followed up in the community
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Exam Qs
An 82 year old female patient wakes up with weakness in the entire right side
of her body
A 56 year old patient with badly controlled diabetes has developed
numbness, pins and needles in his feet over the last 6 months
A 36 year old male patient presents with increasing unsteadiness which
started two days ago. Two years ago he had blurred vision in his left eye
which improved considerably within a few weeks, but left him with some
minor deficit. Eight years ago he had a 3 week episode of numbness in his
left arm.
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Exam Qs
A 72 year old man with uncontrolled blood sugar has presented with ulcers in
his right foot & bilateral loss of sensation below knee
A 77 year old lady with 15 year history of hypertension is brought to A&E. She
is unable to speak & cannot move her right arm & leg.
A 17 year old boy comes to the clinic with his mother. He complains of
recurrent transient episodes of tingling & weakness in his left leg. You also
notice his mother has swollen MCP joints & ulnar deviation in both hands.
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Exam Qs
A 66 year old woman presents with fatigue, breathlessness & paraesthesia in
all limbs. Examination reveals pallor, loss of position sense & impaired
vibration sense.
A 40 year old man with pulmonary tuberculosis is in the second month of
treatment with isoniazid, rifampicin & pyrazinamide. He complains of a
burning sensation in his hands & feet. There is impaired sensation to pin prick
& light touch.
A 67 year old overweight Asian woman presents with painful feet. Direct
questioning revealed that she has had nocturia for the last 3 months.
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Exam Qs
A 50 year old man develops sudden onset of weakness, numbness &
paraesthesiae on the left side of his body. His symptoms faded gradually
before disappearing 12 hours later.
A 30 year old lady presented with pain in the left eye; numbness & weakness
of her right leg. 2 months earlier she had an episode of double vision in the
left eye
A 40 year old lady with pain & tingling in the left hand, worse at night time
when she had to get out of bed to shake the hand for relief.
A 25 year old pregnant lady with increasing muscle weakness. She also
complains of double vision & drooping eye lids.
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Neuro-pharmacology
Pharmacology will come up – learn this
•
Name
•
Routes
•
Classes
•
Mechanisms
•
Common, severe, idiosyncratic side-effects
For these drugs:
•
Pyridostigmine
Seems like a lot but steroids, stroke drugs, immune
•
Immunosupressants/modulators – corticosteroids, system drugs and antibiotics all come up in other
systems as well
azathioprone, natalizumab, interferon, Ig
•
Strokes – alteplase, warfarin, aspirin, clopidogrel,
dipyrimadole
The mechanism for immunoglobulin is ‘actually magic’
according to McDermott
•
Anti-epileptics – valproate, carbamazepine,
lamotrigine, phenytoin, benzos
•
Anti-Parkinson drugs – L-Dopa, carbidopa, MAOIs
•
Triptans
•
Antibiotics – cefatexmine, benzylpenicillin
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Case 1
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Causes of Epilepsy
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Types of Epilepsy
Primary Generalised Epilepsy Location Related Epilepsy
20% of patients with epilepsy
80% of patients with epilepsy
Onset in childhood/teenage years
Can be any age, traditionally older
patients
Brain is structurally normal 
abnormality is in ion channels and
neurotransmitters
Structural abnormality of grey matter
Examples: Childhood absence epilepsy,
Juvenile myoclonic epilepsy
Example: Temporal sclerosis, Mass
lesions
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Management
• Generalized Tonic-Clonic Seizure
– Sodium Valproate
– Levetiracetam
• Location Related Epilepsy
– Carbamazepine
– Lamotrigine
• Myoclonic Epilepsy
– Sodium Valproate
– Levetiracetam
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Status Epilepticus
• Combined seizure(s) for 30 mins
• General measure
– ABC, IV access and infusions
• Early Status
– IV lorazepam, repeated after 10 mins if needed
• Established Status
– Phenytoin infusion
• Refractory Status
– Anesthesia
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Faints Vs Fits
Fits
Faints
Tongue biting and incontinent
Posture
Post-ictal period
Prodrome
Colour change
Precipitant
Stereotyped behaviours
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Case 2
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Parkinson’s Disease
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Parkinson’s Disease
• No known cause
• Can be drug induced
• Clinical Feature
– Bradykinesia
– Tremor
– Rigidity
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Huntington’s Disease
• Autosomal Dominant Neurodegenerative disease
• Due to CAG trinucleotide repeat
• Classical Triad
– Physical
– Cognitive
– Psychiatric
• Management
– No Disease modifying treatment
– Symptomatic management  BDZ, dopamine blocking
drugs, anti-psychotics
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Case 3
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Migraine
• Pathogenesis
– Aura  spreading wave of cortical depolarization and
depression
– Pain due to activation of the trigeminovascular system and
sensitization
• Pain sensing structures in the Brain
–
–
–
–
Dura
Arteries (meningeal and cerebral)
Venous Sinuses
CN 5,7,9 and 10 + the Cervical nerves
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Migraine – Diagnostic Criteria
• Headache lasting 4 hours - 3 days (untreated)
• At least one of:
–
–
–
–
Unilateral
Throbbing
Moderate to severe intensity
Motion sensitivity
• At least one of:
– Nausea/vomiting
– Photophobia/phonophobia
– Normal examination/no other obvious cause
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Migraine - Management
• Treatment of attacks
– Analgesics  Aspirin , Paracetamol, Naproxen
– Triptans  sumatriptan
• Migraine prophylaxis
–
–
–
–
Anti-epileptics  EG valproate
B-Blockers  slow release propanolol
Tricyclics
Botulinum toxins  repeated injections into scalp
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Tension Headaches
• Unknown aetiology but depression is a frequent co-morbidity
• Often attributed to cervical spondylosis, refractive errors,
hypertension
• Clinical Features
– Mild-moderate pain
– Bilateral
– Features  tight band, pressure behind eyes, bursting sensation
• Management
– Simple analgesia
– Physical  ice packs, massage
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Cluster Headaches
• Rare condition that usually affect males 20-40 yo
• Features
– Unilateral, retro-orbital pain
– Autonomic activation (inc. transient Horner's syndrome)
– Clusters typically last 1-2 years
• Management
– Only effective management is S/C sumatriptan
– Prophylaxis  lithium, verapamil
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Case 4
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Subarachnoid Hemorrhage
• Aetiology
– Berry aneurysms (can be associated with PKD)
– AVM
– Trauma/no vascular abnormalities
• Pathogeneses
– 15% immediately fatal
– Distal vasospasm  Infarction
• Risk factors
– Hypertension
– Smoking
– Excess alcohol
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Subarachnoid hemorrhage
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Subarachnoid Hemorrhage
• Features
– Thunder-clap headache
– Increase ICP
– Signs of meningism
• Investigation
– CT
– LP
– angiography
• Management
– Bed rest
– Calcium channel antagonists
• Complications
– Obstructive Hydrocephalus
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Trigeminal Neuralgia
• Aetiology
– Compression of the trigeminal nerve by a microaneurysm
– In younger pt MS
• Clinical features
– Knife like pain spreading from V3, usually unilateral
– Episodes happen multiple times a day, with innoxious
triggers
– Relapse with remission
• Management
– Carbamazepine
– Surgical – microvascular decompression
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Giant cell arteritis
• Granulomatous Inflammation of the temporal
arteries
• Clinically
– Scalp pain, jaw and tongue claudication
– Very rare in under 50s
• Diagnosis
– Raise ESR (>50)
– Temporal artery biopsy
• Management
– Prednisolone 60mg
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Case 5
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Meningitis – Organisms
• Bacterial
– Neisseria
Meningitides
– Streptococcus
pneumoniae
– Staphylococcus
aureus
– TB
– Leptospirosis  in
older patients or
occupation exposure
• Viral
– Most cases are viral
– HIV
– Enterovirus
• Fungal
– Candida albicans
– Cryptococcus
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Meningitis - Clinical features
• Meningitic triad  Headache + Neck stiffness +
Photophobia
• Fever
• Bacterial  intense malaise, fever, petechial rash
• Viral  less severe and self-limiting
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Management
• Cefotaxamine (IV)
• Benzylpenicillin (IM) – for meningococcal disease
• LP – Shows pus, increase polymorphs, decrease
glucose
• Prophylaxis
– Vaccine
– Chemoprophylaxis – Rifampicin
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Encephalitis
• 90% viral
–
–
–
–
Mumps
Rabies
HSV 1/2
Often never identified
• Clinical feature
–
–
–
–
Decrease consciousness
Confusion/personality change
Seizures
Headache + fever
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Encephalitis
• Investigation
– MRI  inflammation and swelling
– EEG
– LP  increase lymphocytes, PCR to detect virus
• Management
– If EBV acyclovir
– Supportive
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Herpes Zoster (shingles)
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Herpes Zoster (shingles)
• Reactivation of varicella zoster virus in Dorsal Root
ganglia
– Due to decrease Immunity
• Clinical features
– Dermatomal
– Cranial nerve  only sensory, particularly 5 and 7
– Post-herpic neuralgia
• Management
– Acyclovir
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Case 6
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Clinical Features
•
•
•
•
Direct effect
Raised ICP
Seizures
Investigation
– CT/MRI
– Look for Primary  CXR, CT, PET
– Biopsy
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Secondary Brain tumours
• Arise from:
 Bronchus
 Breast
 Stomach
 Prostate
 Thyroid
 Kidney
• 50% of all brain
cancers
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Glioma
• Malignant tumour of
neuroepithelia
• Astrocytoma
• Oligodendromas
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Meningioma
• Usually slow growing and
not malignant
• From arachnoid
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Acoustic Neuroma
• From Schwann cells
• Affect vestibulocochlear
nerve, can affect facial
nerve is large
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Management
•
•
•
•
•
Dexamethasone  decreases oedema
Antiepileptics  prevents seizures
Surgery  complete excision or de-bulking
Radiotherapy
Intra-thecal chemotherapy
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Brain Abscesses
• From direct or hematological spread
• Causative organisms
– S. Aureus; S. Pyogenes; anaerobes; gram –ve
• Features
– Fever
– Focal neurology
– Seizure
• Treatment
– Cefotaxime + flucloxacillin + metronidazole
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Brain Abscesses
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Intra-cranial Haematomas
• After head injury – briefly knocked out
then normal before deteriorating
• Features – decrease consciousness,
fixed, dilated pupil; focal neurology
• Treat with craniotomy
•
•
•
•
After head injury – often trivial
Associated with old age and alcoholism
Feature  headache, drowsiness, confusion
Advances to focal signs and decrease
consciousness
• Management – drainage by burr hole
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Exam Questions – Epilepsy
•
•
•
•
a. Two other causes of seizures
b. Two types of generalised seizures
c. Two drugs for generalised seizures
c. Two things to inform him of driving
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Exam Questions – SAH
•
•
•
•
•
a. How long do you wait for LP and why?
b. Why take 3 samples of LP
c. What pathological structure causes SAH?
d. Circle of Willis anatomy
e. Why headaches pre-SAH
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Exam Questions – meningitis
• 53 yo F presents with headache, fever, photophobia.
O/E nuchal rigidity. Lumbar puncture demonstrates
gram +ve cocci. Which organism?
• a. N meningitidis
• b. Listeria monocytogenes
• c. E coli
• d. Strep pneumoniae
• e. Strep agalactiae
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Exam Questions – SAH
•
•
•
•
•
a. How long do you wait for LP and why?
b. Why take 3 samples of LP
c. What pathological structure causes SAH?
d. Circle of Willis anatomy
e. Why headaches pre-SAH
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Email dtgregg1@sheffield.ac.uk
with any questions, corrections
and feedback