Neurology Flashcards
Presentation of a tension headache
Mild ache / pressure in a band like pattern around the head
Management of tension headache
- Reassurance
- Simple analgesia (e.g., ibuprofen or paracetamol)
4 associations with tension headahces
Stress
Depression
Alcohol
Skipping meals
Dehydration
Presentation of sinusitis and it’s management
- Recent URTI
- Tenderness and swelling on palpation
- Prolonged cases (>10 days) = steroid nasal spray or Abx (phenoxymethylpenicillin)
Presentation of cervical spondylosis
- Neck pain, worse with movements
- Headahces
Presentation of trigeminal neuralgia and 1st line management ?
- Electric shock like pain
- Triggered by touch, talking, eating, shaving or cold
- First line = carbamazepine
Presentation of a cluster headache
- Unilateral severe pain
- Red, swollen and watering eye
- Miosis
- Ptosis
- Nasal discharge
- Facial sweating
Management of acute cluster headache attacke
-> Triptans (e.g., subcutaneous or intranasal sumatriptan)
-> High-flow 100% oxygen (may be kept at home)
1st line prophylaxis of cluster headaches
Verapamil
Typical symptoms of a migraine
Last between 4 and 72 hrs
- Usually unilateral
- Moderate-severe intensity
- Pounding or throbbing in nature
- Photophobia (discomfort with lights)
- Phonophobia (discomfort with loud noises)
- Osmophobia (discomfort with strong smells)
- Aura (visual changes)
- N&V
common migraine triggers
- Stress
- Bright lights
- Strong smells
- Certain foods (e.g., chocolate, cheese and caffeine)
- Dehydration
- Menstruation
- Disrupted sleep
- Trauma
Presentation of hemiplegic migraine
- Hemiplegia
- Ataxia
- Impaired consciousness
Acute management of migraine
- NSAIDs (e.g., ibuprofen or naproxen)
- Paracetamol
- Triptans (e.g., sumatriptan)
- Antiemetics if vomiting occurs (e.g., metoclopramide or prochlorperazine)
How do triptans work >
-> 5-HT receptor agonist, binding to serotonin receptors.
- > Cranial vasoconstriction, inhibit transmission of pain signals and inhibit release of inflammatory neuropeptides
3 prophylactic options for migraines
- Propranolol (a non-selective beta blocker)
- Amitriptyline (a tricyclic antidepressant)
- Topiramate (teratogenic and very effective contraception is needed)
Prophylaxis of menstrual migraines
Prophylactic triptans (e.g., frovatriptan or zolmitriptan)
definition of tuberous sclerosis and mutations involved
- AD condition causing development of hamartomas
- TSC1 gene on chromosome 9, which codes for hamartin
- TSC2 gene on chromosome 16, which codes for tuberin
- Leads to abnormal cell size and growth
skin features of tuberous sclerosis
-> Ash leaf spots (depigmented areas of skin shaped like an ash leaf)
-> Shagreen patches (thickened, dimpled, pigmented patches of skin)
-> Angiofibromas (small skin-coloured or pigmented papules that occur over the nose and cheeks)
-> Ungual fibromas (circular painless lumps that slowly grow from the nail bed and displace the nail)
-> Cafe-au-lait spots (light brown “coffee and milk” coloured flat pigmented lesions on the skin)
-> Poliosis (an isolated patch of white hair on the head, eyebrows, eyelashes or beard)
Neurological features of tuberous sclerosis
Epilepsy
Learning disability
Brain tumours - glioma
Define MS
- Autoimmune demyelination of the CNS
What cells produce myelin in the CNS and in the PNS ?
-CNS : oligodendrocytes
-PNS : schwann
How do the episodes of demyelination present in MS?
-Episodes disseminated in time and space
What is optic neuritis ?
-Unilateral painful reduced vision developing over hrs to days.
Give 4 key features of optic neuritis
-Central scotoma (blind spot)
-Pain on eye movement
-Impaired colour vision
-Relative afferent pupillary defect
Give 7 other causes of optic neuritis other than MS
-Sarcoidosis
-SLE
-DM
-Syphilis
-Measles
-Mumps
-Lyme disease
What investigations can support a diagnosis of MS
- MRI with contrast -> demyelinating lesions
- LP -> oligoclonal bans in CSF
- McDonald criteria for diagnosing
Give the 4 disease patterns of MS
-Clinically isolated syndrome
-Relapsing-Remitting
-Secondary progressive
-Primary progressive
Explain the relapsing-remitting pattern of MS
-Episodes of disease followed by recovery. Classified on whether active and/or worsening
-Active : new symptoms developing
-Not active : no new symptoms developing
-Worsening : overall worsening of disability over time
-Not worsening : no worsening of disability over time
Explain secondary progressive pattern of MS
-Was relapsing/remitting but now a progressive worsening of symptoms
-Can also be classified as active and/or worsening
Explain primary progressive pattern of MS
-Worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions
Give two common characteristics of MS
-Lhermitte’s sign : tingling electric shock shooting up the spine when flexing the neck
-Uhthoff’s phenomenon : symptoms are worse when hpt (e.g. in bath, hot weather, exercise).
What can be used to treat relapses in MS?
-Methylprednisolone
-500mg orally for 5 days or 1g IV for 3-5 days if treatment fails
What is the pathophysiology behind MND?
-Progressive degeneration of both upper and lower motor neurones
-Sensory neurones are spared
What can increase the risk of MND?
-Smoking
-Exposure to heavy metals
-Certain persticides
What is a typical presentation of MND
- Late middle aged man
- Insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech
- Weakness often first noticed in upper limbs
- Fatigue when exercising
Give 4 signs of lower MND
-Muscle wasting
-Reduced tone
-Fasciculations
-Reduced reflexes
GIve 3 signs of upper MND
-Increased tone or spasticity
-Brisk reflexes
-Upgoing plantar responses
What is the most common presentation of MND ?
-Amyotrophic lateral sclerosis (ALS)
- Typically LMN signs in the arms and UMN signs in the legs
What can be used to slow the progression of MND ?
-Riluzole : prevents stimulation of glutamate receptors
Signs seen in primary lateral sclerosis (MND)
UMN signs only
Signs seen in progressive muscular atrophy (MND)
LMN signs only
affects distal muscles before proximal
carries best prognosis
Signs seen in progressive bulbar palsy
- Palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
- Carries worst prognosis
What is myasthenia Gravis ?
-Autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest
- Affects the NMJ
What is strongly associated with myasthenia Gravis?
-Thyoma : tumour of the thymus gland
Explain the pathophysiology behind myasthenia gravis
-In most cases, acetylcholine receptor antibodies are produced
-These bind to the postsynaptic receptors
-This prevents the stimulation of the receptor and so prevents muscle contraction
-The antibodies also activate the complement system, leading to damage to the cells of the postsynaptic membrane further worsening the symptoms
Why do the symptoms of myasthenia gravis get worse with exercise ?
-The receptors are used more during muscle activity and so more of them become blocked up.
-This leads to less effective stimulation of the muscle with increased activity
-There is more muscle weakness the more the muscles are used
-This improves with rest as more receptors are freed up again for use
What are 2 other antibodies involved in myasthenia gravis?
-Muscle-specific kinase (MuSK)
-Low density lipoprotein receptor-related protein (LRP4)
-These proteins are imprtant for the creation of acetylcholine receptor
-Destruction of these by the antibodies leads to inadequate acetylcholine receptors
What is a characteristic feature of myasthenia gravis
-Weakness that gets worse with muscle use and improves with rest
What muscles are most affected in myasthenia gravis ?
-Proximal muscles and small muscles of the head and neck
Give 8 common symptoms of myasthenia gravis
- Diplopia : extraocular muscle weakness
- Ptosis
- Weak upwards gaze
- Weakness in facial movements
- Difficulty with swallowing
- Fatigue in the jaw when chewing
- Slurred speech
- Progressive weakness with repetitive movements
Give 3 things to assess of examination for myasthenia gravis
-Thymectomy scar
-FVC
-Elicit fatiguability of muscles : repeated blinking will exacerbate ptosis ; prolonged upward gaze with exacerbate diplopia ; repeated abduction of one arm 20 times with result in unilateral weaknes when comparing both sides
Give 3 investigations for diagnosing myasthenia gravis
- Test for antibodies
- CT/MRI of the thymus to check for thymoma
- Edrophonium test if in doubt (tensilon)
What is the edrophonium test
-Used to aid diagnosis of myasthenia gravis
-IV edrophonium chloride is given which will prevent the breakdown of acetylcholine
-Acetycholine levels will rise giving temporary relief from the weakness
Give 3 treatment options for myasthenia gravis
-Pyridostigmine -> reversible acetylcholinesterase inhibitors -> increase the amount of acetylcholine at the junction (or rivastigmine)
-Immunosuppression with prednislone or azathioprine : suppress antibody production
-Thymectomy
What 2 monoclonal antibodies can be used in myasthenia gravis ?
-Rituximab -> targets b cells reducing antibody production
-Eculizumab -> targets complement protein C5.
What is a myasthenic crisis?
-Acute worsening of symptoms often triggered by a viral infection
-Can lead to resp failure due to weakness in the muscle of respiration
- FVC needs monitoring
What is used in the management of a myasthenic crisis?
- IV immunoglobulins
- Plasmapheresis
If needed :
- BiPAP
- Intubation and ventilation
what drugs can exacerbate myasthenia ?
- penicillamine
- quinidine, procainamide
- beta-blockers
- lithium
- phenytoin
- antibiotics: gentamicin, macrolides, quinolones, tetracyclines
What is Lambert-Eaton myasthenic syndrome ?
autoimmune condition affecting the neuromuscular junction
Who is usually affected by Lambert-Eaton myasthenic syndrome ?
-Patients with small cell lung cancer
Explain the pathophysiology behind Lambert-Eaton myasthenic syndrome
- Antibodies against voltage-gated calcium channels in the SCLC are produced.
- These target and damage the same channels in the presynaptic terminals of the neuromuscular junction
- This results in less acetylcholine being released into the synapse
How does lambert-eaton syndrome present ?
-Proximal muscles most affected -> leg muscle weakness (difficulty climbing stairs)
- Reduced or absent tendon reflexes
-Autonomic dysfunction : dry mouth, blurred vision, impotence and dizziness
-Double vision
-Ptosis
-Dysphagia
What is post-tetanic potentiation ?
-In lambert-eaton syndrome, tendon reflexes are normally reduced
-They can become temporarily normal for a short period following a period of strong muscle contraction
How is lambert-eaton syndrome managed?
-Treat underlying malignancy if present
-Amifampridine
-Immunosuppressants
-IV immunoglobulins
-Plasmaphersis
How does amifampridine work in the treatment of Lambert-Eaton?
-It blocks voltage-gated potassium channels in the presynaptic cells
-This prolongs the depolarisation of the cell membrane and assists calcium channels in carrying out their action
Define Gullian-Barre syndrome (GBS)
-Acute paralytic polyneuropathy affecting the peripheral nervous system
What usually triggers GBS ?
-Infection
-Campylobacter jejuni (food poisoning), cytomegalovirus, EBV
How does GBS present ?
- Back/leg pain in initial stages
- Symmetrical ascending weakness
- Reduced reflexes
-+/- peripheral loss of sensation or neuropathic pain - May progress to cranial nerves and cause diplopia, bilateral facial nerve palsy and oropharyngeal weakness
What is the clinical course of GBS?
-Preceding infection
-Symptoms begin 4 wks later
-Symptoms peak after 2-4 wks
-Recovery period lasting mnths to years
What investigations support the diagnosis of GBS?
-Once clinically diagnosed using Brighton criteria :
-Nerve conduction studies showing reduced signal through the nerves
-LP : raised protein with normal cell count and glucose
How is GBS managed ?
- IV immunoglobulins
- Plasmapheresis can be an alternative to IVIG
- VTE prophylaxis with LMWH
What are the features of a benign essential tremor ? (6)
-Fine tremor
-Symmetrical
- 6-12 Hz
-MORE prominent on VOLUNTARY movement
-Worse when tired, stressed or after caffeine
-Improved by alcohol
-Absent during sleep
Give 6 differentials of a tremor
-Parkinson’s
-MS
-Huntington’s chorea
-Hyperthyroidism
-Fever
-Medications (e.g. antipsychotics)
What 2 medications can improve the symptoms of a benign essential tremor ?
- First line = Propranolol
- Primidone
What is the cause of parkinson’s ?
- Progressive reduction of dopamine in the basal ganglia
- Leads to disorders of movement
- Symptoms are ASYMMETRICAL
What is the classic triad of parkinson’s
- Cogwheel rigidity
- Pill-rolling resting tremor (4-6Hz)
- Bradykinesia : smaller handwriting, shuffling gate, difficulty initiating movements, reduced facial expressions (hypomimia)
postural instability is an extra
Where is dopamine produced ?
-Substantia nigra of the basal ganglia
Give 5 other features of parkinson’s
-Depression
-Sleep disturbance and insomnia
-Anosmia
-Postural instability (caused by autonomic failure)
-Cognitive impairment and memory problems
Describe a parkinson’s tremor
-Asymmetrical / unilateral
-WORSE at REST
-IMPROVES with INTENTIONAL movement
-No change with alcohol
Give 4 treatment options for parkinson’s
- Co-benyldopa or co-careldopa
- COMT inhibitors
- Dopamine agonists
- Monoamine Oxidase-B Inhibitors
Explain how levodopa works
-Synthetic dopamine
-Most effective but becomes less effective over time
What is usually given with levodopa and why?
-Peripheral decarboxylase inhibitor
-Stops is being broken down before it reaches the brain
-Examples : carbidopa, benserazide
What is the main side effect of levodopa?
- Too high dopamine = dyskinesias = abnormal movements associated with excessive motor activity.
- E.g. dystonia, chorea, athetosis
How do COMT inhibitors work?
-Example : entacapone
-Inhibits catechol-o-methyltransferase which is responsible for metabolising levodopa
-Extends to duration of levodopa
How do dopamine agonists work ?
- Mimic dopamine in the basal ganglia and stimulate dopamine receptors
- Less effective than levodopa
- Examples : bromocryptine, pergolide, cabergoline
What is the most notable side effect of dopamine agonists with prolonged use ?
- Pulmonary fibrosis
How do monoamine Oxidase-B Inhibitors work?
-They block Monoamine Oxidase-B enzyme which is responsible for breaking down dopamine
-Examples are selegiline and rasagiline
what can be given with levodopa to help with the dyskinesia ?
-> Amantadine (glutamate antagonist)
what causes multiple system atrophy and how does it present
-> Neurones in various areas of brain degenerate
-> Parkinsonism
-> Autonomic disturbance : erectile dysfunction: often an early feature, postural hypotension, atonic bladder
-> Cerebellar signs : ataxia
Presentation of lewy body dementia
-> Progressive cognitive impairment FOLLOWED BY parkinsonism
-> Visual hallucinations
-> Delusions
- > REM sleep disorders
-> Fluctuating consciousness
Features of progressive supranuclear palsy
-> postural instability and falls
-> Impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficultly reading or descending stairs)
-> Parkinsonism : bradykinesia is prominent
-> Cognitive impairment : primarily frontal lobe dysfunction
what usually causes an extradural haemorrhage
- Rupture of the middle meningeal artery in the temporoparietal region
- Often associated with fracture of temporal bone
What does an extradural haemorrhage look on a CT ?
- Bi-convex shape
- Limited by cranial sutures
- Hyperdense
Typical history of an extradural haematoma
- Pt with traumatic head injury
- Period of improved neurological Sx and consciousness
- Followed by rapid decline over hrs
Cause of a subdural haematoma
Rupture of bridging veins in outermost layer
Appearance of subdural haemorrhage on CT
Crescent shaped
Can cross suture lines
Who often presents with subdural haemorrhages
- Elderly or alcoholic patients
- Atrophy in their brains make the vessels more prone to rupture
Presentation of subarachnoid haemorrhage
- Sudden onset occipital headache during strenuous activity
- N&V
- Meningism (photophobia, neck stiffness)
- Coma
- Seizures
first line investigation for subarachnoid haemorrhage
Non contrast CT
Investigation required if CT is done >6 hrs after onset of SAH symptoms and is normal
- LP
- Needs to be done 12 hrs after start of symptoms
LP results in SAH
-> Raised red cell count (a decreasing red cell count on successive bottles may be due to a traumatic procedure)
-> Xanthochromia (a yellow colour to the CSF caused by bilirubin)
usual cause of SAH
Cerebral aneurysm
Management options of SAH
- Endovascular coiling OR
- Neurosurgical clipping
3 common complications of SAH and necessary treatment options
- Vasospasm -> Nimodipine (CCB)
- Seizures -> anti-epileptic meds
- Hydrocephalus -> LP, external ventricular drain, ventriculoperitoneal (VP)V shunt.
Presentation of intracerebral haemorrhage
- Sudden onset focal neurological symptoms (e.g. limb or facial weakness, dysphasia or vision loss)
What is Charcot-Marie-Tooth disease and what is the usual inheritance pattern?
- Hereditary motor and sensory neuropathy
- Autosomal dominant
Give 7 features of Charcot-Marie-Tooth ?
-High foot arches (pes cavus)
-Distal muscle wasting causing ‘inverted champagne bottle legs’
-Weakness in lower legs, particularly loss of ankle dorsifelxion (with high stepping gait due to foot drop)
-Weakness in the hands
-Reduced muscle tone
-Reduced tendon reflexes
-Peripheral sensory loss
Give 5 causes of peripheral neuropathy
-A : alcohol
-B : B12 deficiency
-C : cancer and chronic kidney disease
-D : diabetes and drugs (e.g isoniazid, amiodarone & cisplatin)
-E : every vasculitis
Explain the facial nerve pathway
-> Exits brainstem at cerebellopontine angle
-> Passes through the temporal bone and parotid gland
-> Divides into 5 branches :
~ Temporal
~ Zygomatic
~ Buccal
~ Marginal mandibular
~ Cervical
Motor function of the facial nerve
- Facial expression
- Stapedius in the inner ear
- Posterior digastric, stylohyoid and platysma muscles
Sensory function of facial nerve
Taste from anterior 2/3 of the tongue
Parasympathetic function of the facial nerve
-> Submandibular and sublingual salivary glands
-> Lacrimal gland (stimulating tear production)
Explain the differing presentations of UMN and LMN lesions after the facial nerve
-> UMN = forehead sparing
-> LMN = NO forehead sparing
- Each side of the forehead has UMN innervation from BOTH sides of the brain but LMN innervation from ONE side
what is Bell’s palsy
-> Acute idiopathic unilateral LMN facial palsy
-> Forehead affected, drooping of eyelide, loss of nasolabial fold
Management of Bell’s palsy
If pt presents with 72 hrs : PREDNISOLONE either :
-> 50mg for 10 days
-> 60mg for 5 days followed by a 5-day reducing regime, dropping the dose by 10mg per day
+
-> Artificial tears
Cause of Ramsay-Hunt syndrome
Varicella Zoster Virus (VZV)
Presentation of Ramsay-Hunt Syndrome
- Unilateral LMN faical nerve palsy
- Painful and tender vesicular rash in the ear canal, pinna and around the ear on affected side
Management of ramsay-Hunt syndrome
-> Oral aciclovir and prednisolone.
-> Patients also require lubricating eye drops.
Role and inheritance of neurofibromatosis type 1 gene
- Found on chromosome 17
- Codes for neurofibromin -> tumour suppressor protein
- Inherited in AD pattern
Diagnostic criteria for neurofibromatosis type 1
CRABBING :
- C – Café-au-lait spots (more than 15mm diameter is significant in adults)
- R – Relative with NF1
- A – Axillary or inguinal freckling
- BB – Bony dysplasia, such as Bowing of a long bone or sphenoid wing dysplasia
- I – Iris hamartomas (Lisch nodules), which are yellow-brown spots on the iris
- N – Neurofibromas
- G – Glioma of the optic pathway
2 unique complications of NF1
- Malignant peripheral nerve sheath (MPNST)
- Gastrointestinal stromal tumours (GIST)
Role and inheritance of neurofibromatosis type 2
- Chromosome 22
- Codes for merlin -> tumour suppressor protein important in Schwann cells
Common finding in neurofibromatosis type 2
- Bilateral vestibular schwannomas (tumours of the auditory nerve)
- Unilateral sensorineural hearing loss (often the first symptom)
- Unilateral tinnitus
- Dizziness or imbalance
- Sensation of fullness in the ear
- Facial nerve palsy (if the tumour grows large enough to compress the facial nerve)
Cause of Huntington’s disease
- AD genetic condition
- Caused by trinucleotide repeat disorder affecting the HTT gene on chromosome 4
Define anticipation and what disease is it seen in ?
- Successive generations have more repeats resulting in “
- Earlier age of onset
- Increased severity of disease
Presentation of Huntington’s
Usually cognitive / psychiatric / mood problems FOLLOWED by movement disorders :
- Chorea (involuntary, random, irregular and abnormal body movements)
- Dystonia (abnormal muscle tone, leading to abnormal postures)
- Rigidity (increased resistance to the passive movement of a joint)
- Eye movement disorders
- Dysarthria (speech difficulties)
- Dysphagia (swallowing difficulties)
Explain generalised seizures and the different specific types
- Involve both sides of the brain
- > Tonic-clonic (grand mal)
- > Tonic
- > Clonic
- > Typical absence (petit mal)
- > Atonic
Explain focal seizures
- Involve specific area, on one side of the brain
- Simple/focal aware
- Complex/ focal impaired awareness
Seizure type seen in those affecting temporal lobe
-> Typically a rising epigastric sensation
- > Deja vu
- > Hallucinations
-> Automatisms (lip smacking/grabbing/plucking)
-> Post-ictal dyspahsia
Seizure type seen in frontal lobe seizures
- Head/leg movements
- Post-ictal weakness
- Jacksonian march
Features of parietal lobe seizure
Paraesthesia
Features of occipital lobe seizure
Floaters / flashes
Management of generalised tonic clonic seizures
- Male : SV
- Female : Lamotrigine / Levetiracetam
Management of focal seizures
1st : Lamotrigine / levetiracetam
2nd : Carbamazepine
Management of absence seizures
1st : ethosuximide
Management of myoclonic seizures
- Male : SV
- Female : levetiracetam
Management of tonic or atonic seizures
- Male : SV
- Female : Lamotrigine
How does sodium valporate work ?
- Increasing activity of gamma-aminobutyric acid (GABA) -> which has a calming effect on the brain
5 notable SE of sodium valporate
- Teratogenic
- Liver damage and hepatitis
- Hair loss
- Tremor
- Reduce fertility
what advice should be given to women planning on becoming pregnancy with epilepsy
Take 5mg folic acid
Definition of status epilepticus
- A seizure lasting more than 5 minutes
- Multiple seizures without regaining consciousness in the interim
Medical management of status epilepticus
-> A benzodiazepine (IV lorazepam) first-line, repeated after 5-10 minutes if the seizure continues
-> Second-line options (after two doses of benzodiazepine) are IV levetiracetam, phenytoin or sodium valproate
-> Third-line options are phenobarbital or general anaesthesia
Dosage of rectal diazepam for status epilepticus based on age
- Neonate : 1.25 - 2.5 mg
- Child 1 month - 1 year : 5 mg
- Child 2 years - 11 years : 5 - 10 mg
- Child 12 years - 17 years : 10 mg
- Adult : 10 - 20 mg (max. 30 mg)
- Elderly : 10 mg (max. 15 mg)
Explain the analgesic ladder
- > Step 1: Non-opioid medications such as paracetamol and NSAIDs
-> Step 2: Weak opioids such as codeine and tramadol
-> Step 3: Strong opioids such as morphine, oxycodone, fentanyl and buprenorphine
Key SE of NSAIDs
- Gastritis with dyspepsia (indigestion)
- Stomach ulcers
- Exacerbation of asthma
- Hypertension
- Renal impairment
- Coronary artery disease, heart failure and strokes (rarely)
PPI co-prescribed to reduce GI effects
CI to NSAIDs
Asthma
Renal impairment
Heart disease
Uncontrolled hypertension
Stomach ulcers
5 SE of opioids
- Constipation
- Pruritus
- Nausea
- Altered mental state (sedation, cognitive impairment or confusion)
- Respiratory depression (usually only with larger doses in opioid-naive patients)
What is used for opioid overdose
Naloxone
Explain the combination of opioids used to control pain in palliative patients
-> Background opioids
-> Rescue doses for breakthrough pain
- The dose of the rescue opioid should be 1/6th of the background dose
what do the NICE guidelines clearly state in regards to chronic primary pain
- Avoid essentially all forms of analgesia in chronic primary pain, except antidepressants.
Typical features of neuropathic pain
Burning
Tingling
Pins and needles
Electric shock like sensation
Causes of neuropathic pain
- Post-herpetic neuralgia from shingles is in the distribution of a dermatome and usually on the trunk
- Nerve damage from surgery
- Multiple sclerosis
- Diabetic neuralgia (typically affecting the feet)
-Trigeminal neuralgia - Complex regional pain syndrome
four first line treatments for neuropathic pain
- Amitriptyline – a tricyclic antidepressant
- Duloxetine – an SNRI antidepressant
- Gabapentin – an anticonvulsant
- Pregabalin – an anticonvulsant
Should be used as monotherapy, if one doesn’t work SWITCH don’t add
which tumours most commonly spread to the brain
lung (most common)
breast
bowel
skin (namely melanoma)
kidney (renal cell carcinoma)
What is the most common primary brain tumour in adults and how do they appear on imaging
- Glioblastoma
- Solid tumours with central necrosis and a rim that enhances with contrast
How do brain tumours present ?
- Progressive focal neurological symptoms
- Signs and symptoms of raised ICP
What concerning features of a headache might suggest raised ICP
Constant headache
Nocturnal (occurring at night)
Worse on waking
Worse on coughing, straining or bending forward
Vomiting
Papilloedema on fundoscopy
Other than a headache, what are the other features of raised ICP
Altered mental state
Visual field defects
Seizures (particularly partial seizures)
Unilateral ptosis (drooping upper eyelid)
Third and sixth nerve palsies
First line investigation for a brain tumur
MRI
what criteria is used to assess the type of stroke ?
Bamford classification, assesses :
- unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
Total anterior circulation infarct
- Involves middle and anterior cerebral arteries
- All 3 of bamford criteria
Partial anterior circulation infarct
- Involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
- 2 of the bamford classification
Lacunar infarcts
- Involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
- unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
- pure sensory stroke.
- Ataxic hemiparesis
Posterior circulation stroke
- Involves vertebrobasilar arteries presents with 1 of the following:
- cerebellar or brainstem syndromes
- loss of consciousness
- isolated homonymous hemianopia
Lateral medullary syndrome stroke
-> Involves posterior inferior cerebellar artery (Wallenberg’s syndrome)
- Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
- Contralateral: limb sensory loss
Weber’s syndrome (stroke)
- Ipsilateral CN III palsy
- Contralateral weakness of upper and lower extremity
Stroke in the branches of the posterior cerebral artery that supply the midbrain
Management of TIA
- > Aspirin 300mg daily (started immediately)
-> Referral for specialist assessment within 24 hours (within 7 days if more than 7 days since the episode)
-> Diffusion-weighted MRI scan is the imaging investigation of choice.
What score is used to assess probablity of a stroke ?
ROSIER (one or more = stroke is possible)
Initial management of suspected stroke
- Exclude hypoglycaemia
- Immediate non contrast CT head to exclude haemorrhage
- Aspirin 300mg daily for two weeks (started after haemorrhage is excluded with a CT)
- Admission to a specialist stroke centre
when should thrombolysis with alteplase and thrombectomy be considered for acute stroke management
-> If it can be administered within 4.5 hours of onset of stroke symptoms
-> Haemorrhage has been definitively excluded (i.e. Imaging has been performed)
when can thrombectomy be offered for the management of acute stroke
- In patients with a confirmed blockage of the proximal anterior circulation or proximal posterior circulation.
-> It may be considered within 24 hours of the symptom onset and alongside IV thrombolysis.
What underlying conditions are all patients with a TIA or stroke investigated for ?
-> Carotid artery stenosis : Carotid imaging (e.g., carotid ultrasound, or CT or MRI angiogram)
-> AF : ECG or ambulatory ECG monitoring
Secondary prevention following a stroke
-> Clopidogrel 75mg once daily (alternatively aspirin plus dipyridamole)
-> Atorvastatin 20-80mg (not started immediately – usually delayed at least 48 hours)
-> Blood pressure and diabetes control
-> Addressing modifiable risk factors (e.g., smoking, obesity and exercise)
Anterior cerebral artery stroke
- Contralateral hemiparesis and sensory loss, - - Lower extremity > upper
Middle cerebral artery stroke
- Contralateral hemiparesis and sensory loss, - - Upper extremity > lower
- Contralateral homonymous hemianopia
- Aphasia
Posterior cerebral artery stroke
- Contralateral homonymous hemianopia with macular sparing
- Visual agnosia
Most important causes of status epilepticus to rule our first
Hypoxia
Hypoglycaemia
Management of status epilepticus in a pre hospital setting
PR diazepam or buccal midazolam
Underlying condition that can cause prolonged reliance on a ventilator following anaesthesia
Myasthenia gravis
What other symptom could be elicited on cranial nerve examination in Bell’s palsy
- Loss of taste on anterior two-thirds of the tongue (one same side as facial weakness).
simple initial management of raised ICP
Elevate the bed to 30 degrees
long term prophylaxis of stroke / TIA ?
Antiplatelet therapy -> clopidogrel
Common trigger for cluster headaches
Alochol
Headache associated with valsalva manoeuvres suggests what underlying cause and what would be the investigation of choice
- Raised ICP
- Ix = CT head (LP is CI until raised ICP excluded).
Explain the therapeutic guidelines for what anti-emetic is used depending on the underlying cause
- Ondansetron for chemotherapy-induced nausea
- Haloperidol for intracranial causes (raised ICP, direct effect of tumour)
- Prochlorperazine for vestibular causes
- Metoclopramide for gastrointestinal causes
How does onsansetron work
5-HT-3 receptor antagonist (serotonin receptor)
Points in glasgow coma scale
M : motor response /6
V : verbal response /5
E : eye opening /4
Motor response in GCS
6 : Obeys commands
5 : Localises to pain
4 : Withdraws from pain
3 : flexes to pain
2 : extends to pain
1 : none
Verbal response in GCS
5 : Orientated
4 : Confused
3 : words
2 : sounds
1 : none
Eye opening in GCS
4 : spontaneous
3 : to voice
2 : to pain
1 : none
what is often spared in MND
Eye movements
what medication should be avoided in myasthenia gravis and why
Bisoprolol
Can worsen MG and cause drop in FVC
Signs of a fourth nerve palsy (Trochlear)
- Vertical diplopia (WORSE ON GOING DOWNSTAIRS).
- When looking straight, the affected eye may deviate upwards and rotate outwards
- May develop head tilt
Action of fourth nerve on eyeb
Trochlear = superior oblique
Depresses eye and move inwards
example of a medication that should be stopped following dementia diagnosis
Amitriptyline - can worsen cognitive impairment
Illicit drug, blood condition and kidney condition associated with SAH
- Drug = cocaine
- Blood condition = sickle cell
- Kidney condition = ADPKD
Presentation of complex regional pain syndrome
- Previous injury (e.g. fracture)
- Pain, skin flushing, swelling and abnormal hair growth in the area
Name for experiencing pain from stimuli that are not normally painful
Allodynia
Most malignant brain tumour
Glioblastoma
4 secondary mets of a brain tumour
Renal cell carcinoma
Breast
Lung
Melanoma
3 presenting symptoms of acoustic neuroma
Tinnitus
Unilateral hearing loss
Balance problems
pathology in the heart, brains, kidneys, retina and lungs in tuberous slerosis
- Heart : rhabdomyomas
- Brain : gliomas
- Kidneys : polycystic kidneys
- Retina : hamartomas
- Lungs : Lymphangioleimyomatosis
Management of idiopathic intracranial hypertension
- Weight loss
- Topiramate
- Acetazolamide
- LP and drainage
- CN II decompression
Mechanism of action of acetazolamide
Carbonic anhydrase inhibitor
Presentation of a third nerve palsy
- ‘Down and out’ eye
- Ptosis
- Dilated pupil
- Absent light reflex but intact consensual constriction (third nerve carries efferent fibres hence absent light reflex but afferent still in tact = consensual)
most common long term complication of bacterial meningitis
Sensorinerual hearing loss
Typical presentation of a brain abscess
- Triad : fever, headache and focal neurological deficit
- Can also present with seizure
likely nerve injury followung mid-shaft humeral fracture and how to test it
- Radial
- Extend the wrist
Signs and symptoms of a pontine haemorrhage
- Reduced GCS
- Paralysis
- Bilateral small / pin point pupils
- Hx of long standing HTN
3 investigations you would do in someone with suspected TIA
ECG : AF
Head CT / MRI
Carotid artery doppler USS
3 TIA RF
Smoking
DM
HTHN
