Neuro Flashcards
PACS criteria?
- 2/3 of TACS
or
- Higher cortical dysfunction alone
or
- Isolated motor deficit not meeting LACS criteria
Higher cortical problems in stroke?
LEFT = Language dysfunction
RIGHT = Neglect of contralateral limbs Apraxia
POCS criteria?
- Ipsilateral cranial nerve palsy + contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Disordered conjugate eye movement
- Cerebellar dysfunction
- Isolated hemianopia or cortical blindness
Investigations in stroke?
- Bloods
- ECG
- CXR
- CT head
- Echo/carotid doppler/24h ECG
Criteria for thromboylsis in stroke?
- Age <80 - <4.5 hours from start of symptoms
- Age >80 - <3 hours from start of symptoms
- Non-haemorrhagic stroke (excluded by CT)
- Significant symptoms and not improving
Contraindications to thrombolysis?
- Active bleeding
- CNS trauma
- Neoplasms or arteriovenous malformations
- Previous intracerebral haemorrhage
- Ischaemic stroke in previous 6mths
- Major trauma/surgery in past 3wk
- Non-compressible punctures in past 24hrs (LP etc).
Management of haemorrhagic stroke?
FFP/prothrombin complex concentrate, vitamin K and surgical review.
ABCD2 score?
- Age >60
- Blood pressure >140/90
- Clinical features = unilateral weakness (2) and speech disturbance without weakness (1)
- Duration = >60 mins (2), 10-60 mins (1)
- Diabetes
>4 = high risk
>5 = 8% risk of stroke in 48 hours
Causes of bacterial meningitis in different age groups?
NEONATES
- E.coli,
- GBS
- listeria
- S.aureus
- Pneumococcal
1m-15yrs
- HIB
- meningococcus
- pneumococcus
ADULTS 15+
- Pneumococcus
- meningococcus
ELDERLY
- Staph aureus
- Gram -ve organisms
Causes of non-bacterial meningitis?
VIRAL
- Mumps
- coxsackie
FUNGAL
- Immunosuppressed - cryptococcus
Contraindications to LP?
- Focal neurological signs (seizures)
- Raised ICP (low HR, high BP, papilloedema)
- Shock/CV instability
- Bleeding risk
Bacterial LP appearance?
- Turbid
- High polymorphs (neutrophils)
- High protein
- Low glucose
Viral LP appearance?
- Clear
- High lymphocytes
- Low/normal protein
- Low/normal glucose
TB LP appearance?
- Turbid/clear/viscous
- High lymphocytes
- V high protein
- V low glucose
Abx in meningitis?
- 2nd/3rd gen ceph (IV)
- <3 months or >55 years - amoxicillin to cover listeria
- Further abx directed by MC+S
Supporting therapy in meningitis?
- Corticosteroids
- Analgesics
- Antipyretics
Management of viral meningitis?
Supportive therapy – analgesia, antipyretics, nutritional support, hydration
Vaccinations that protect against meningitis?
Vaccination against H. influenzae type b, meningococcus groups B and C and S. pneumoniae.
Quadrivalent vaccine (A, C, W, Y) for 17-18 year olds.
Pharmacological sedation?
Haloperidol 0.5mg PO, 1-2 hourly PRN – daily max = 5mg – avoid atypicals in elderly.
Can add lorazepam but try to avoid as tolerance and dependence may occurs (hangover effect)
Delirium screen investigations?
- FBC, U&Es and creatinine, glucose, calcium, magnesium, LFTs, TFTs, cardiac enzymes, vitamin B12 levels
- Syphilis serology, autoantibody screen
- PSA, eGFR
- Blood cultures/serology
- ABG
- CT head
- Urine dipstick/MC+S,
- ECG
- Lumbar puncture
Risk factors for SAH?
- Hypertension
- Smoking
- Cocaine use
- Excessive alcohol intake
- Family history (1st degree)
- Genetic disorders (autosomal dominant adult polycystic disease, Ehlers-Danlos syndrome, neurofibromatosis, Marfan’s)
Signs in SAH?
- Coma/depressed level of consciousness (direct effect of haemorrhage or mass effect)
- Focal neurological signs (limb weakness, dysphagia)
- Reactive hypertension III nerve palsy – indicates direct nerve damage from posterior communicating artery or basilar artery aneurysm
Imaging in SAH?
- CT first line - hyperdense appearance in basal cisterns
- If +ve –> angiography
- If -ve –> MRI or lumbar puncture
- Angiography determines the origin of the bleed - catheter angiography offers possibility of coiling the aneurysm.
ECG changes in SAH?
- QT prolongation
- Q waves
- Dysrhythmias
- ST elevation
Management of SAH?
GENERAL
- Continuous observation, IV access, analgesia
PREVENTING ISCHAEMIA
- Nimodipine (calcium antagonist)
DEFINITIVE
- Surgical - clipping (11-14 days after) Antifibrinolytics reduce bleeding
Definition of status?
Seizure lasting for >30 minutes, or repeated seizures without intervening consciousness
Management of status?
- Open and maintain airway
- Recovery position
- Oral/nasal airway
- Oxygen
- IV access if possible
-
Lorazepam
- IV 2-4mg (2nd dose if no response in 10 min)
-
Phenytoin
- 15-20mg/kg IVI at <50mg/min
- Maintenance - 100mg/6-8h
- OR Diazepam 100mg in 500mL of 5% glucose - infuse at 40mL/h
Pre hospital drugs for status?
Diazepam 10-20mg PR
Midazolam 10mg buccal
Causes of cranial nerve lesions?
Common = aneurysm, diabetes, MS, tumour, trauma/surgery, stroke
Rare = vasculitidies, sarcoidosis
Infection = Lyme disease, syphilis, HIV, Wernicke’s encephalopathy
Causes of altered visual fields?
glacucoma, retinitis pigmentosa, stoke, retinal occulsion, detached retina
Cause of enlarged blind spot?
Papilloedema
CN III - what does it innervate and what happens in palsy?
- Medial, superior, and inferior recti, and inferior oblique muscles
- Lateral rectus and superior oblique take over –> down and out.
- Ptosis – due to ↓response of levator palpebrae superioris
CN IV - what does it innervate and what happens in palsy?
- Superior oblique
- Eye turns up and out, and elevates more as it moves medially
CN XI - what does it innervate and what happens in palsy?
- Lateral Rectus
- Eye medially deviated and movement lateral from midline is not possible
What happens in facial nerve palsy?
- Inability to raise eyebrows, open eyes against resistance, do facial movements etc.
- Forehead sparing in UMN lesion, not so in Bell’s palsy.
- Lacrimation, salivation impaired (lesion proximal to geniculate ganglion)
- Taste impaired (anterior 2/3 tongue – lesion above chorda tympani)
- Hyperacusis (lesion above nerve to stapedius)
What does Weber’s test do?
Sensorineural deafness
- Patient will report a quieter sound in the ear with the sensorineuronal hearing loss
Conductive hearing loss
- Sound lateralises to affected ear - ear with the conductive hearing loss is only receiving input from the bone conduction and no air conduction, and the sound is perceived as louder in that ear
Glossopharyngeal taste distribution?
Posterior 1/3 of the tongue
Causes of acquired sensorineural deafness?
MINDMATT
- Meniere’s
- Infective
- Neoplastic (acoustic neuroma)
- Degenerative
- Metabolic
- Autoimmune
- Toxic
- Trauma
Features of median nerve palsy
- Hand of benediction on trying to make a fist
- Paraesthesiae in thumb, index and middle fingers – relieved by dangling hand over edge of bed and shaking it (‘wake and shake’)
- Sensory loss and weakness of abductor pollicics brevis +/- wasting of thenar eminence
Management of median nerve pasly?
Splinting; local steroid injection +/- decompression surgery.
Cause of ulnar nerve palsy?
Trauma
Cause of median nerve palsy?
(C6-T1)
Swelling/compression in tunnel myxoedema, prolonged flexion (Colle’s splint), acromegaly, myeloma, local tumours (lipoma, ganglion), RA, amyloidosis, pregnancy, sarcoidosis.
Signs of ulnar nerve palsy?
(C7-T1)
- Weakness/wasting of medial (ulnar) wrist flexors, interossei and medial two lumbricals
- Cannot cross fingers in good luck sign/claw hand
- Hypothenar eminence wasting, weak 5th digit abduction, 4th/5th DIP joint flexion
- Sensory loss over medial 1½ fingers and ulnar side of hand
What does radial nerve innervate?
C5-T1
- Opens the fist
- muscles involved = BEAST –> brachioradialis, extensors, abductor pollicis longus, supinator & triceps.
Cause of radial nerve palsy?
Compression against humerus
Signs of radial nerve palsy?
Wrist/finger drop with elbow flexed and arm pronated
Sensory loss variable – anatomical snuff box mostly
Main 2 signs of brachial plexus injury?
Klumpke’s palsy (lower) and Erb’s palsy (upper)
Signs of Phrenic nerve palsy?
(C3-5)
Orthopnoea & raised hemidiaphragm on CXR
Signs of common peroneal nerve palsy?
(L4-S1)
- Foot drop, weak ankle dorsiflexion/eversion
- Sensory loss over dorsal foot.
Signs of tibial nerve palsy?
(L4-S3)
Inability to stand on tiptoe (plantarflexion), invert the foot, or flex the toes, with sensory loss over the sole.
Features of sensory neuropathy?
- Numbness; pins and needles/paraesthesiae; ‘glove and stocking’ distribution,
- Difficulty handling small objects like buttons
- Signs of trauma (finger burns) or joint deformation may indicate sensory loss
- Diabetic and alcoholic neuropathies are typically painful
Causes of peripheral neuropathy?
A = alcohol
B = B12/folate deciciency
C = Cancer/Connective Tissue/Collagen
D = Diabetes
E = Endocrine e.g. hypothyroid

Features of motor neuropathy?
Guillain-Barré, Lead Poisoning, Charcot-Marie-Tooth
- Often progressive (may be rapid)
- Weak or clumsy hands; difficulty in walking (falls, stumbling)
- Difficulty in breathing (↓vital capacity)
- Signs = LMN lesion - wasting/weakness in distal muscles of hands/feet – reflexes are reduced/absent
Features of autonomic neuropathy?
DM, amyloidosis, Guillain Barré, Sjogren’s Syndrome, HIV, Leprosy, SLE
- Postural hypotension, decreased sweating, ejaculatory failure, Horner’s syndrome
- Constipation, nocturnal diarrhoea, urinary retention, erectile dysfunction
Investigations to do in peripheral neuropathy?
- Bloods
- FBC, ESR, glucose, U+E, LFT, TSH, B12, electrophoresis, ANA, ANCA
- Urinalysis
- Imaging
- CXR
- Other
- LP +/- specific genetic tests; nerve conduction studies
Management in peripheral neuropathy?
- Treat cause; involve physio and OT.
- Foot care and shoe choice [Symbol] minimise trauma.
- Splinting
- IV immunoglobulin in Guillain-Barré and demyelinating polyradiculoneuropathy
- Steroids/immunosuppressants may help in vasculitic causes
- Neuropathic pain –> amitriptyline, duloxetine, gabapentin and pregabalin
What vessels rupture in subdural?
- Cortical bridging veins
- Connect the venous system of the brain to the large intradural venous sinuses and lie relatively unprotected in the subdural space
Risk factors for subdural?
- Any factor that stretches bridging veins –> cerebral atrophy, low CSF pressure after shunting
- Alcoholism
- Coagulation disorder/anticoagulation
Signs in subdural?
-
Fluctuating conscious level
- History of gradual onset headahces, memory loss, personality change, dementia, confusion, drowsiness
- Symptoms vary from day to day with intervening lucid periods
-
Focal neurological signs
- Often hemiparesis on the side ipsilateral to the lesion (false localising sign)
-
Aphasia
- If lesion on the left side
CT/MRI findings in subdural?
Shows clot +/- midline shift.
Crescent-shaped collection of blood (increased density) over 1 hemisphere.
Management of subdural?
Irrigation/evacuation (via burr twist drill and burr hole craniostomy) = 1st line
Craniotomy = 2nd line
Artery that ruptures in extradural?
Middle meningeal - typically after trauma to temple
Extradural signs?
- Hemiparesis +/- brisk reflexes and upgoing plantars
- Ipsilateral pupil dilates –> coma deepens –> bilateral limb weakness
- Breathing becomes deep and irregular (brainstem compression)
- Bradycardia and raised BP (Cushing’s response) are late signs
CT findings in extradural?
Haematoma (biconvex/lens-shaped are of increased density); blood forms more rounded shape (dural attachments to skull keep it more localised.
Drug you can give to decrease ICP? (e.g. in Extradural etc)
Mannitol
Types of MS?

Definition of MS?
Presence of multiple neurological deficits which are separated in time and space.
Features of MS?
- Optic neuritis – usually unilateral
- Transverse myelitis - acute episode of bilateral weakness of legs, with loss of control of bowels and bladder.
- Neurogenic bladder dysfunction – urgency +/- incontinence and frequency
- Impotence
- Sensory deficits – tingling in restricted distribution, trigeminal neuralgia, Lhermitte’s phenomenon (electricity sensation down spine on neck flexion)
- UMN deficit – spastic weakness of legs
- Cerebellar damage – ataxia, dysarthria, nystagmus
- Vertigo
- Dementia in later stage
Investigations in MS?
-
Bloods
- FBC, CRP, ESR, U&Es, LFTs, TFTs, glucose, HIV, calcium and B12 levels
-
MRI
- 95% have periventricular lesions
- 90% discrete white matter abnormalities
- Focal demyelination – plaques in optic nerve, brainstem and spinal cord
- Gadolinium enhancement improves sensitivity
-
CSF
- Oligoclonal bands of IgG on electrophoresis that are not present in serum suggest CNS inflammation.
-
Visual Evoked Potentials
- Show conduction changes consistent with demyelination – increased latency in patients with optic neuritis.
3 categories of treatment in MS?
- Steroids
- Disease-modifying
- Symptomatic
Steroids in MS?
Methylprednisolone – shortens acute relapses (use sparingly) – doesn’t alter overall prognosis.
Disease-modifying therapy in MS?
Interferons (IFN-1β and IFN-1α)
- ↓Relapses 30% and ↓lesion accumulation on MRI. Modest role in delaying disability.
MABs
- Alemtuzumab/Natalizumab – better than interferons.
Non-immunosuppressive
- Glatiramer, mioxantrone
Others
- Azathioprine is good for relapsing remitting.
Symptomatic treatment in MS?
Spasticity
- Baclofen, diazepam, dantrolene, tizanidine.
Tremor
- Botulinum toxin A
Urgency/Frequency
- Intermittent self-catheterisation/tolterodine
Triad of features in Parkinson’s Disease?
-
Tremor
- Worse at rest; often ‘pill rolling’
-
Rigidity/↑Tone
- ‘Cogwheel ridigity’ - jerky resistance to passive movement- felt by rapid pronation/supination
- ‘Lead pipe rigidity’ - sustained resistance to passive movement throughout the whole range of motion, with no fluctuations
-
Bradykinesia/Hypokinesis
- Slow to initiate movement and slow, low amplitude repetitive actions (low blink rate, monotonous hypophonic speech, migrographia).
- Gait: ↓arm swing, festinance, freezing at obstacles or doors
- Expressionless face (hypomimesis)
Non-motor features of Parkinson’s disease?
- Sense of smell reduced
- Constipation
- Visual hallucinations
- Frequency/urgency
- Dribbling of saliva
- Depression and dementia
Investigations in Parkinson’s Disease?
Usually clinical diagnosis
SPECT scan
Medical management of Parkinson’s Disease?
Levodopa
- Co-beneldopa/Co-careldopa (combined with dopa-decarboxylase inhibitor)
- Variable response (unpredictable freezing) and reduced end of dose response.
- Key decision = when to start. Cons = ↓efficacy over time, dopamine-induced dyskinesias (5-10 years), psychosis, visual hallucinations, N+V (domperidone)
Dopamine Agonists
- Ropinirole/pramipexole (transdermal).
- Drowsiness, nausea, hallucinations, compulsive behaviour
- Apomorphine = potent DA (continuous SC infusion) – evens out end-of-dose effects
Anticholinergics, MAO-B inhibitors, COMT inhibitors
Neuropsychiatric and surgical management of Parkinon’s Disease?
Neuropsychiatric
- Deep brain stimulation
Surgical
- Surgical ablation of overactive basal ganglia circuits (subthalamic nuclei)
Definition of…
- Prodrome
- Aura
- Partial (focal)
- Primary generalised
- Simple
- Complex
- Secondary Generalised
- Prodrome = Change in mood/ behaviour (hrs -days)
- Aura = Simple partial seizure (temporal) which may precede
- Partial (focal) = Features referable to part of one hemisphere
- Primary generalised = No warning/aura. Discharge throughout cortex w/o localising features
- Simple = awareness unimpaired
- Complex = awareness impaired
- Secondary generalised = focal seziure –> generalised (e.g. aura –> ton-clon)
Causes of epilepsy/seizures?
2/3 are idiopathic (often familial)
-
Congenital
- NF, tuberous sclerosis, TORCH, perinatal anoxia
-
Acquired
- Vascular (CVA), cortical scarring (trauma, infection), SOL, SLE, PAN, MS, sarcoidosis
-
Non-Epileptic Seizures
- Withdrawal (EtOH, opiates, benzos), metabolic (glucose, Na, Ca, urea, NH3), ↑ICP, infection, eclampsia, pseudoseizures
Features of simple partial seizures?
Focal motor, sensory, autonomic or psychic symptoms
Features of compex partial seizures?
5 As (usually from temporal lobe)
- Aura
- Autonomic (skin colour change, temperature, palpitations)
- Awareness lost (motor arrest, motionless state)
- Automatisms (lip-smacking, fumbling, chewing, swallowing)
- Amnesia
Features of Absence seizures?
ABSCENCES
- ABrupt onset/offset
- Short (<10s)
- Eyes (glazed, blank stare)
- Normal (intelligence, examination, brain scan)
- Clonus (or automatisms)
- EEG (3Hz spike and wave)
- Stimulated by hyperventilation and photics
Features of tonic-clonic seizures?
- LoC
- Tonic = limbs stiffen; Clonic = rhythmic jerking of limbs
- Cyanosis; incontinence; tongue biting (lateral)
- Post-ictal confusion and drowsiness
Features of myoclonic seizures?
Sudden jerk of limb, face or trunk
Features of atonic seizures?
Sudden loss of muscle tone à fall (no LoC)
What is West Syndrome?
Clusters of head nodding and arm jerks (EEG shows hypasarrhythmia)
Investigations in seizures/epilepsy?
- Bloods – FBC, U+E, LFT, calcium, glucose
- Urine toxicology
- ECG
- Imaging – MRI (focal onset, adult epilepsy, seizures in spite of treatment)
- EEG – to support diagnosis and help classification
General advice for epileptics/potential epileptics?
Advise against driving, swimming, bathing alone until Dx is established
Diagnosis –> no driving until seizure free for 1 year (HGV 10 years seizure and medication free)
Drugs for different types of epilepsy?

Women and AEDs?
- Avoid valproate (lamotrigine or CBZ instead)
- 5mg folic acid daily if child-bearing age
- CBZ and phenytoin are inducers and ↓efficacy of OCP
Enzyme effects of AEDs?
INDUCERS (reduce concentration)
- Carbamezapine
- Phenytoin
- Barbituates
INHIBITORS (increase concentration)
- Valproate
Side effects of lamotrigine?
- Skin rash
- Rash
- Diplopia/blurred vision
- Levels affected by inducers/inhibitors
Side effects of carbamazepine?
- Leukopenia
- Skin reactions
- Diplopia/blurred vision
- SIADH –> hyponatraemia
Side effects of valproate?
ALPROAT3E
- Appetite↑
- Liver failure
- Pancreatitis
- Reversible hair loss
- Oedema
- Ataxia
- Teratogenicity, Tremor, Thrombocytopenia
- Encephalopathy (due to ammonia)
Side effects of phenytoin?
- Gingival hypertrophy
- Hirsutism
- Cerebellar signs (ataxia, nystagmus, dysarthria)
- Peripheral sensory neuropathy
- Diplopia
- Tremor
+ve and -ve features of tension headahce?
Bilateral - may have photophobia and phonophobia
No nausea/vomiting or significant systemic upset/neurological deficit
Lifestyle changes in management of tension headahce?
- Avoid overwork/stress, excess alcohol, lack of exercise. Strategies to counteract stress.
- Treat clinical depression.
- Avoid analgesic abuse – max 12 doses per week.
- Headache diary
- Reassurance
Drug therapy/alternative therapies for tension headache?
If <2 days a week – OTC analgesics.
- Paracetamol – not great
- NSAID or aspirin
- Avoid codeine
If frequent/chronic –> aim for long term remission (prophylaxis)
- Low dose amitriptyline
- 3 week course of naproxen BD
Alternative = acupuncture
Definition of migraine? Two theories of aetiology?
Syndrome characterised by periodic headaches with complete resolution between attacks.
- Vascular theory = aura due to vasoconstriction, headache due to vasodilation
- Neuronal theory = aura associated with spreading neuronal inhibition
Who gets migraines? When in life? Which type is most common?
25% prevalence in women, 8% in men
Usually first attack before age 30
Migraine without aura 3x more common than migraine without aura
Diagnostic criteria for common migraine (without aura)?
At least 5 attacks, all fulfilling following criteria
-
Frontotemporal headahce lasting 4-72 hours with at least 2 of the following characteristics
- Unilateral location
- Pulsating/throbbing quality
- Moderate to severe pain intensity
- Causing problems/avoidance of routine physical activity
- With at least one of
- N+V
- Photophobia/phonophobia
- Not attributable to another disorder
Onset of simple migraine?
Usually gradual - peak after 2-12 hours, gradually subsiding.
Often begin in morning, possibly waking them from sleep
Non-obvious symptoms/signs of simple migraine?
- Symptoms
- Anorexia, blurred vision, impaired concentration, nasal stuffiness, hunger, tenesmus, diarrhoea, abdominal pain, polyuria, pallor, sweating, and sensations of heat or cold
- Signs
- Localized oedema of the scalp, face, or under the eyes; scalp tenderness; prominence of temporal blood vessels; or neck stiffness and tenderness
Diagnosis of classical migraine (with aura)?
Diagnosis = at least 2 attacks. Aura has at least one of the following characteristics (but no motor weakness)
- Fully reversible visual symptoms (flickering lights, spots or lines, loss of vision)
- Fully reversible sensory symptoms (paraesthesiae, numbness)
- Less common –> usually starts in the hand, migrates up the arm, then involves the face, lips, and tongue. Numbness may follow the paraesthesia.
- Sensory auras rarely occur alone, and usually follow visual auras
When does headahce occur in classical migraine?
During the aura or follows the aura within 60 mins
Complications of migraine?
- ↑Risk of ischaemic stroke (RR = 2.16)
- More so in migraine with aura – OCP + migraine with aura = NO (8x risk)
- ↑Risk of depression, BAD, anxiety, panic disorder
- Status migranosus – debilitating migraine that lasts more than 72 hours
- Migrainous infarction – cerebral infarction occurring during course of typical attack of migraine with aura.
Differentials for migraine?
- Primary headache - tension, cluster
- Secondary - intracranial tumour
- Others = depression, sinusitis, dental caries, epilepsy, TIA, arteriovenous malformations, phaeochromocytoma
Acute management of migraine?
Pharmacological
- Combination Therapy
- Oral triptan (5HT agonist - rizatriptan, sumatriptan) + NSAID or paracetamol
- Antiemetics (metoclopramide) – relieves nausea and enhances efficacy of analgesics
General
- Identify and avoid trigger factors
- Regular sleep and dietary measures
In whom are triptans contraindicated?
- IHD
- Coronary spasm
- Uncontrolled BP
- Recent lithium
- SSRIs
How do triptans work?
5HT agonists
Constrict cranial arteries and inhibit release of substance P/pro-inflammatory neuropeptides –> block transmission from trigeminal nerve.
Prevention of migraines?
General
- Identify and avoid trigger factors = most important.
- If migraine recurring 4 or more times per month –> treat prophylactically
1st Line
- Topiramate or Propranolol
- Amitriptyline
2nd Line
- Pizotifen (can cause weight gain) - triptan
- Gabapentin, pregabalin
- Valproate
Problems with topiramate?
Can cause foetal malformations and impair effectiveness of hormonal contraceptives
Combined motor and senory disorders?

What is Brown Sequard?
- Ipsilateral upper motor neurone signs (weakness)
- Contralateral spinothalamic signs (no pain/temp)
- ipsilateral dorsal column signs (no vibration/proprioception)
Results from an injury to one side of the spinal cord resulting in hemisection of the cord - damage to corticospinal tract, spinothalamic tract and dorsal columns

What is Anterior cord syndrome?

What is posterior cord syndrome?

What is central cord syndrome?

Risk factors for fibromyalgia?
female sex, middle age, low income household, divorced, low educational status
Features of fibromyalgia?
-
Pain – chronic (>3 months) and widespread (involves left and right sides, above and below the waist, and the axial skeleton.
- Allodynia = pain in response to non-painful stimulus.
- Hyperaesthesia = exaggerated perception of pain in respon=se to a mildly painful stimulus.
- Profound fatigue – unrefreshing sleep, significant fatigue and pain with small increases in physical exertion.
- Additional Features – morning stiffness, paraesthesiae (without underlying cause), headaches (migraine and tension), poor concentration, low mood, sleep disturbance.
All investigations normal.
What is Myasthenia Gravis? What is it associated with?
Autoimmune disease mediated by antibodies to nicotinic acetylcholine receptors on post-synaptic membrane of neuromuscular junction.
Associated with AI disease (RA, SLE)
Symptoms of Myasthenia Gravis?
Slowly increasing or relapsing muscular fatigue. Muscle groups affected (in order):
- Extraocular
- bulbar (swallowing, chewing)
- face
- neck
- limb girdle
- trunk
Symptoms exacerbated by:
- Pregnancy, hypokalaemia, infection, over-treatment, change of climate, emotion, exercise, gentamicin, opiates, tetracycline, quinine, beta-blockers
Signs of myasthenia gravis?
- Ptosis; diplopia;
- Myasthenic snarl on smiling;
- ‘Peek sign’ or orbicularis fatigability (eyelids begin to separate after manual opposition to sustained closure)
- On couning to 50, the voice fades
- Tendon reflexes normal
Tests for myasthenia?
Anti-AChR antibodies (90%)
Ptosis improves by >2mm after ice application to eyelid for >2 min
How is myasthenia treated?
Treated with anticholinesterases, immunosuppression (steroids, azathioprine, ciclosporin)
Causes of hydrocephalus?
- Post-meningitis
- SAH
- Trauma
- Neoplastic
- Dural sinus thrombosis
Presentation of adult hydrocephalus?
- Features of raised ICP
- Impaired upward gaze
- Mental impairment
- Gait apraxia; up going plantars, tendon jerks exaggerated
- Urinary incontinence due to sphincter dysfunction
- Hypopituitarism due to enlargement of 3rd ventricle into posterior fossa.
Presentation of infantile hydrocephalus?
- Macrocephaly – anterior fontanelle enlarged and tense
- Scalp veins are prominent
- Irritability
- Poor feeding/FTT
- Developmental delay
- Convulsions/mental impairment
- Setting sun appearance - lids retracted, eyes depressed forwards and downwards, upward gaze is impaired
Management of hydrocephalus?
- Treat cause
- Ventriculoperitoneal shunt – burr hole à silicone tube in lateral ventricle –> drains CSF subcutaneously into peritoneum.
Most common type of MND? What is its pathophysiology?
Amyotrophic Lateral Sclerosis (ALS)
- Selective loss of neurons in motor cortex, cranial nerve nuclei and anterior horn cells
- Combined UMN and LMN signs - no sensory loss or sphincter disturbance - different from MS/polyneuropathies
- Never affects eye movements - different from Myasthenia
- Closely linked with FTD
Symptoms of MND?
- >40 yrs
- Stumbling spastic gait
- Foot drop +/- proximal myopathy
- Weak grip (door-handles don’t turn) and shoulder abduction (hair washing is hard)
Signs of MND?
UMN
- Spasticity, brisk reflexes, ↑plantars
LMN
- Wasting, fasciculation of tongue, abdomen, back, thigh.
- Speech and swallowing sometimes affected (bulbar signs)
Causes of encephalitis?
- Usually viral = HSV1/2, CMV, EBV, VZV, arboviruses, HIV
- Non-viral = any bacterial meningitis, TB, malaria, Lyme disease
Presentation of encephalitis?
- Infectious prodrome à fever, rash, LNs, cold sores, conjunctivitis, meningeal signs
- Bizarre behaviour or personality change
- Confusion, ↓GCS –> coma
- Fever, headache
- Focal neurology –> seizures
- Hx of travel or animal bite
Cerebellar Signs?
Lesions cause ipsilateral signs
DANISH
- Dysdiadochokinesis, Dysmetria (past-pointing)
- Ataxia (limb, truncal)
- Nystagmus
- Intention tremor
- Slurred speech, Scanning dysarthria
- Hypotonia
Causes of cerebellar signs?
PASTRIES
- Posterior fossa tumours
- Alcohol
- Stroke
- Trauma
- Rare (paraneoplastic syndromes)
- Inherited (Freidrich’s ataxia)
- Epilepsy drugs (phenytoin)
- Sclerosis (multiple)
Name some primary brain tumours?
General presentation of tumours?
Astrocytoma, Glioblastoma, Oligodendrocytoma, Ependyoma, Meningioma
- Signs of raised ICP
- Seizures
- Evolving focal neurology (localising signs)
- Personality change
What is this and what does it indicate?

Peek sign - Myasthenia Gravis
Investigations/management of encephalitis?
- Bloods – cultures, viral PCR, malaria film
- Contrast CT – focal bilateral temporal involvement = HSV
- LP - ↑protein, lymphocytes, PCR
Treat with IV Aciclovir; supportive management in HDU/ICU.
Stroke mimics?
- With abnormal scans
- Tumours – fluctuating gradual onset
- Abscess – fever, fluctuating onset
- Haematomas – subdural, extradural
- With normal scans
- Todd’s paresis – focal weakness in a part of the body after a seizure. This weakness typically affects appendages and is localized to either the left or right side of the body. It usually subsides completely within 48 hour
- Migraine
- Neuroglyopenia (low blood sugars)
Seizures, spreading depolarisation, subdural, sugars, sepsis
Stroke management?
- Aspirin 300mg PO (600mg PR) 14 days à switch to clopidogrel 75mg afterwards
- Admit to stroke unit care
- Monitor BP <150/90
- O2 >93%
- Early SALT assessment
- 40-80mg atorvastatin
- If anterior circulation – carotid endarterectomy (doppler à if 50% stenosed within 2 weeks, or >70% stenosed within 12 weeks, consider surgery).
Anticoagulation in AF/stroke?
- Not until TWO WEEKS AFTER – consider if AF.
- Warfarin, DOACs
- CHADVASc in AF/HASBLED
- Relative risk reduction in stroke is 2/3
- Questions about lifestyle and other drugs and liver disease
- Counsel on lifestyle!! – 5 a day, fishy oils, less salt, cut down on booze, cut out the fags.
- Vocational stuff – can you return to work? Driving?
Things to mention in bad stokes?
-
Problems after stroke
- Immobility
- Pressure sores
- Contractures – physio, botulinum, baclofen
- PE/DVT – compression stockings
- UTI/aspiration pneumonitis
- Immobility
-
Prognosis
- Haemorrhage = poor prognosis (long term disability if survive)
- Ischaemic = if dense, poor (50% mortality at 30 days, long term disability) if smaller, is better (lower recurrence)
-
Difficult decisions
- Long term feeding (NG, PEG etc)
- EOL care – palliation, second opinions, withholding/withdrawing care

