myasthenia_gravis_carpal_tunnel_gbs_mnd_cord_compression_ms_stroke.ppt

Phase 2a
David Gregg
David Stewart-Watson
The Peer Teaching Society is not liable for false or misleading information…

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?

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,
Possible Sites

1. Myasthenia gravis
2. Carpal tunnel
3. Guillian-Barre syndrome
4. Spinal nerve root lesion
5. Motor neurone disease
6. Spinal cord compression (+ cauda equina)
7. MS
8. Stroke (+TIA)

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!
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
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
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
Myasthenia Gravis

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
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)
Carpal Tunnel Syndrome

• 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
Cranial Nerve Lesion

• 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)
Mononeuritis Multiplex

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
Guillian-Barre Syndrome

Diagnosis
•Made clinically; confirmed by nerve conduction studies
•These studies show conduction slowing, prolonged motor latency and/or
conduction block
•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
Guillian-Barre syndrome

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.
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.
Other Polyneuropathies

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
Plexus 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
Spinal Root Lesions

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
Motor Neurone Disease

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.
•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!
MND

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
Multiple Sclerosis (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
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
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
MS

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
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
Spinal Cord Compression

• 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!
Cauda Equina Syndrome

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
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
Stroke

Stroke Syndromes
Strokes to different parts of the brain give characteristic clinical patterns.
Here are some:
1. Partial Anterior Circulatory Stroke (PACS)
– Higher dysfunction or partial unilateral motor/sensory defect
– The addition of homonymous hemianopia to one of the above
2. Total Anterior Cicrulatory Stroke (TACS
– All of higher dysfunction, partial motor/sensory defect and homonymous hemianopia
3. Posterior Occiptal Circulatory Stroke (POCS)
– Any of: cranial nerve palsy, bilateral motor/sensory defect, eye movement problems,
cerebellar dysfunction
– Isolated homonymous hemianopia
4. Lacunar Stroke (LACS)
– 5 classic LAC sub-syndromes – pure motor stroke/hemiparesis, ataxic hemiparesis,
dysarhtria/clumsy hand, pure sensory stroke, mixed sensorimotor
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
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
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.
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
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
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
Stroke

What are the modifiable vascular risk factors?

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 -
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
Stroke

• 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
Transient Ischaemic Attack

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
TIA

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.
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.
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.
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.
Exam Qs

Pharmacology will come up – learn this
• Name
• Routes
• Classes
• Mechanisms
• Common, severe, idiosyncratic side-effects
Neuro-pharmacology
For these drugs:
• Pyridostigmine
• Immunosupressants/modulators – corticosteroids,
azathioprone, natalizumab, interferon, Ig
• Strokes – alteplase, warfarin, aspirin, clopidogrel,
dipyrimadole
• Anti-epileptics – valproate, carbamazepine,
lamotrigine, phenytoin, benzos
• Anti-Parkinson drugs – L-Dopa, carbidopa, MAOIs
• Triptans
• Antibiotics – cefatexmine, benzylpenicillin
Seems like a lot but steroids, stroke drugs, immune
system drugs and antibiotics all come up in other
systems as well
The mechanism for immunoglobulin is ‘actually magic’
according to McDermott

Case 1

Causes of Epilepsy

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

• Generalized Tonic-Clonic Seizure
– Sodium Valproate
– Levetiracetam
• Location Related Epilepsy
– Carbamazepine
– Lamotrigine
• Myoclonic Epilepsy
– Sodium Valproate
– Levetiracetam
Management

• 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
Status Epilepticus

Fits Faints
Tongue biting and incontinent Posture
Post-ictal period Prodrome
Colour change Precipitant
Stereotyped behaviours
Faints Vs Fits

Case 2

Parkinson’s Disease

• No known cause
• Can be drug induced
• Clinical Feature
– Bradykinesia
– Tremor
– Rigidity
Parkinson’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
Huntington’s Disease

Case 3

• 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
Migraine

• 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
Migraine – Diagnostic Criteria

• 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
Migraine - Management

• 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
Tension 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
Cluster Headaches

Case 4

• 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
Subarachnoid Hemorrhage

Subarachnoid hemorrhage

• Features
– Thunder-clap headache
– Increase ICP
– Signs of meningism
• Investigation
– CT
– LP
– angiography
Subarachnoid Hemorrhage
• Management
– Bed rest
– Calcium channel antagonists
• Complications
– Obstructive Hydrocephalus

• 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
Trigeminal Neuralgia

• 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
Giant cell arteritis

Case 5

• Bacterial
– Neisseria
Meningitides
– Streptococcus
pneumoniae
– Staphylococcus
aureus
– TB
– Leptospirosis  in
older patients or
occupation exposure
Meningitis – Organisms
• Viral
– Most cases are viral
– HIV
– Enterovirus
• Fungal
– Candida albicans
– Cryptococcus

• Meningitic triad  Headache + Neck stiffness +
Photophobia
• Fever
• Bacterial  intense malaise, fever, petechial rash
• Viral  less severe and self-limiting
Meningitis - Clinical features

• Cefotaxamine (IV)
• Benzylpenicillin (IM) – for meningococcal disease
• LP – Shows pus, increase polymorphs, decrease
glucose
• Prophylaxis
– Vaccine
– Chemoprophylaxis – Rifampicin
Management

• 90% viral
– Mumps
– Rabies
– HSV 1/2
– Often never identified
• Clinical feature
– Decrease consciousness
– Confusion/personality change
– Seizures
– Headache + fever
Encephalitis

• Investigation
– MRI  inflammation and swelling
– EEG
– LP  increase lymphocytes, PCR to detect virus
• Management
– If EBV acyclovir
– Supportive
Encephalitis

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
Herpes Zoster (shingles)

Case 6

• Direct effect
• Raised ICP
• Seizures
• Investigation
– CT/MRI
– Look for Primary  CXR, CT, PET
– Biopsy
Clinical Features

Secondary Brain tumours
• Arise from:
 Bronchus
 Breast
 Stomach
 Prostate
 Thyroid
 Kidney
• 50% of all brain
cancers

• Malignant tumour of
neuroepithelia
• Astrocytoma
• Oligodendromas
Glioma

• Usually slow growing and
not malignant
• From arachnoid
Meningioma

• From Schwann cells
• Affect vestibulocochlear
nerve, can affect facial
nerve is large
Acoustic Neuroma

• Dexamethasone  decreases oedema
• Antiepileptics  prevents seizures
• Surgery  complete excision or de-bulking
• Radiotherapy
• Intra-thecal chemotherapy
Management

• From direct or hematological spread
• Causative organisms
– S. Aureus; S. Pyogenes; anaerobes; gram –ve
• Features
– Fever
– Focal neurology
– Seizure
• Treatment
– Cefotaxime + flucloxacillin + metronidazole
Brain Abscesses

Brain Abscesses

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

• 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
Exam Questions – Epilepsy

• 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
Exam Questions – SAH

• 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
Exam Questions – meningitis

Email dtgregg1@sheffield.ac.uk
with any questions, corrections
and feedback

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