NEUROLOGY Flashcards
STROKE
What is the treatment for an ischaemic stroke?
Immediate management:
- CT/MRI to exclude haemorrhagic stroke
- aspirin 300mg
Antiplatelet therapy
- aspirin 300mg for 2 weeks
- clopidogrel daily long term
Anticoagulation (e.g. warfarin) for AF
thrombolysis
- within 4.5 hrs of onset
- IV alteplase
- lots of contraindications (can cause massive bleeds)
mechanical thromboectomy
- endovascular removal of thrombus
STROKE
What other treatment can be given in ischaemic stroke either alongside alteplase or after the time frame?
- Thrombectomy (mechanical retrieval of clot)
- Proximal anterior circulation stroke within 6h (with IV alteplase if <4.5h) or within 24h if potential to salvage brain tissue
- Proximal posterior circulation stroke within 24h (with IV alteplase if <4.5h) if potential to salvage brain tissue
STROKE
What medication may be given as secondary prevention following a stroke?
- Antiplatelets (lifelong clopidogrel or aspirin + dipyridamole if cardiac disease)
- Anticoagulation if have AF but wait 2w post-stroke
- Manage co-morbidities (HTN, DM)
- Cholesterol >3.5mmol/L diet + 80mg atorvastatin
- VTE assessment + monitor for infection
SAH
What is the pathophysiology of a subarachnoid haemorrhage (SAH)?
- tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
- raised ICP - fast flowing arterial blood is pumped into the cranial space
- space occupying lesion - puts pressure on the brain
- brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
- vasospasm - bleeding irritates other vessels -> ischaemic injury
SAH
what are the investigations?
non-contrast CT head
- if CT done within 6hrs of onset + is normal = no need for LP, alternative diagnosis should be considered
- if CT done after 6hrs onset + is normal = LP required
LP should be done 12hrs after onset to allow xanthochromia to develop
SAH
What is the management of SAH?
1st line
- nimodipine 60mg 4hrly
- endovascular coiling (2nd line = surgical clipping)
- if raised ICP = IV mannitol, hyperventilation + head elevation
- conservative = bed rest, stool softeners
EDH
What is the management for EDH?
- bed position = tilted to 30 degrees
- intubation if low GCS
- maintain cerebral perfusion (hyperventilation, inotropes + vasopressors, fluids, hypertonic saline or IV MANNITOL)
- hypothermia
- burr hole
DEFINITIVE
- Craniotomy + haematoma evacuation
SDH
What is the management of SDH?
IV mannitol
ACUTE
- monitor intracranial pressure
- decompressive craniectomy
CHRONIC
- can be monitored + managed conservatively
- burr hole decompression if pt is confused, has neuro deficit or severe image findings
STATUS EPILEPTICUS
What is the step-wise management of status epilepticus?
PRE-HOSPITAL/EARLY STATUS (<10 MINS)
- in community 1st line = buccal midazolam (2nd line = rectal diazepam)
- in hospital 1st line = 4mg IV lorazepam (2nd line = IV diazepam)
two doses of benzodiazepine given 10 mins apart
ESTABLISHED STATUS (>10 MINS)
- alert on-call anaesthetist
- one of following: phenytoin, levetiracetam, sodium valproate
if one fails, try another agent on list
REFRACTORY STATUS (>30 MINS)
- phenobarbitone
- general anaesthesia with propofol, midazolam or thiopental
PARKINSON’S DISEASE
What are 4 differential diagnoses to consider in Parkinson’s disease?
Parkinson’s plus syndromes –
- Progressive supranuclear palsy
- Multiple system atrophy
- Lewy Body dementia
- Corticobasal degeneration
PARKINSON’S DISEASE
What is progressive supranuclear palsy?
- Early falls, cognitive decline or both sides being equally affected
- Occurs above nuclei of CN3, 4 + 6 so difficulty moving eyes
- Impaired vertical gaze (down worse = issues reading or descending stairs)
- Ocular cephalic reflex present (caused by supranuclear issue) where they tilt/turn their head to look at things rather than moving eyes
PARKINSON’S DISEASE
What is multiple system atrophy?
- Neurones in multiple systems in the brain degenerate
- Degeneration in basal ganglia > Parkinsonism
- Degeneration in other areas > early autonomic (postural hypotension + falls, bladder/bowel dysfunction) + cerebellar (ataxia) dysfunction
PARKINSON’S DISEASE
What is Lewy Body dementia associated with?
- Associated with Sx of visual hallucinations, delusions, REM sleep disorders, fluctuating consciousness, progressive cognitive decline + Parkinsonism
PARKINSON’S DISEASE
What is corticobasal degeneration?
- Early myoclonic jerks, gait apraxia, agnosia + alien limb
PARKINSON’S DISEASE
What is the management of Parkinson’s disease?
- Lifestyle: education, exercise, physio, MDT
1st line:
- if motor symptoms are affecting QoL = L-DOPA (CO-CARELDOPA)
- if motor symptoms not affecting QoL = dopamine agonist (ROPINIROLE) or MAO-B inhibitor (SELEGILINE or RASAGALINE)
2nd line
- COMT inhibitor (ENTACAPONE)
- amantadine
- SC apomorphine (in advanced disease with severe motor symptoms)
- deep brain stimulation
MIGRAINE
What is the pathophysiology of migraines?
- Changes in brainstem blood flow leads to unstable trigeminal nerve nucleus + nuclei in basal thalamus
- Leads to release of vasoactive neuropeptides CGRP + substance P > neurogenic inflammation > vasodilation + plasma protein extravasation leading to pain propagating all over the cerebral cortex
MIGRAINE
What are the triggers of migraines?
CHOCOLATE –
- Chocolate
- Hangovers
- Orgasms
- Cheese/caffeine
- Oral contraceptives
- Lie-ins
- Alcohol
- Travel
- Exercise
MIGRAINE
What is the acute management of migraines?
- PO (or nasal in paeds) triptan like sumatriptan plus paracetamol or NSAID
- Antiemetic like metoclopramide or prochlorperazine if vomiting occurs
MND
What is progressive bulbar palsy?
What does it affect?
What does it need to be differentiated from?
- Only affects CN 9–12 (brainstem motor nuclei) so LMN of them
- Primarily affects muscles of talking, chewing, tongue palsy + swallowing
- Progressive pseudobulbar palsy = destruction of UMN so same as bulbar but small spastic tongue with no fasciculations
MND
What is…
i) progressive muscular atrophy?
ii) primary lateral sclerosis?
i) Anterior horn cells affected so LMN signs only, distal > proximal
ii) Loss of cells in motor cortex so UMN signs only
MULTIPLE SCLEROSIS
What are some classic sites for MS?
- Periventricular white matter lesions
- Predilection for distinct sites – optic nerves, corpus callosum, brainstem + cerebellar peduncles
MULTIPLE SCLEROSIS
What is the diagnostic criteria for MS?
McDonald criteria –
- >2 relapses
- Multiple CNS lesions (≥2)
- Sx that last >24h
- Disseminated in space (Clinically or on MRI) and time (>1m apart)
MULTIPLE SCLEROSIS
What are the symptoms of MS?
SYMPTOMS
- blurred vision + red desaturation (optic neuritis)
- numbness + tingling
- weakness
- bowel + bladder dysfunction
- Uhtoff’s phenomenon (worsening symptoms following temperature rise e.g. hot bath/shower)
SIGNS
- visual (pale optic disc + inability to see red, relative afferent pupillary defect)
- internuclear ophthalmoplegia
- sensory loss
- UMN signs (spastic paraparesis)
- cerebellar signs (ataxia + tremor)
- Lhermitte’s phenomenon (electric shock sensation on neck flexion)
MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is the pattern of motor weakness?
i) Pyramidal pattern so extensors weaker than flexors in upper limb, flexors weaker than extensors in lower
MULTIPLE SCLEROSIS
What is the management of MS relapses?
How does this affect disease prognosis?
- oral/IV methylprednisolone for 5 days
- plasma exchange (for sudden, severe relapses not responding to steroids)
MULTIPLE SCLEROSIS
What is the management of MS remissions?
DMARDs
- natalizumab
- ocrelizumab
- fingolimod
- beta-interferon
- glatiramer acetate
MENINGITIS
What is the management of bacterial meningitis
1st line = ceftriaxone/cefotaxime (+ amoxicillin if <3m or >55)
IV dexamethasone (avoid in meningococcal sepsis)
if penicillin allergic = IV chloramphenicol
BRAIN ABSCESS
What are the most common causative organisms?
- Staph. aureus + strep. pnuemoniae
BRAIN ABSCESS
What is the management of brain abscess?
1ST LINE
- empirical antibiotics (IV ceftriaxone + metronidazole)
- treat underlying cause
2ND LINE
- abscess drainage/excision
BRAIN DEATH + COMA
What are the components of ‘eyes’ in GCS?
E4 = opens spontaneously
E3 = opens to verbal command
E2 = opens to pain
E1 = no response
BRAIN DEATH + COMA
What are the components of ‘verbal’ in GCS?
V5 = orientated in TPP, answers appropriately
V4 = confused conversation, odd answers
V3 = inappropriate words (random, abusive)
V2 = incomprehensible sounds (groans)
V1 = no response
BRAIN DEATH + COMA
What are the components of ‘motor’ in GCS?
M6 = obeys commands
M5 = localises pain
M4 = withdraws away from painful stimulus
M3 = flexion to pain
M2 = extension to pain
M1 = no response
MYASTHENIC CRISIS
What is the management of myasthenic crisis?
- Urgent review by neurologists + anaesthetists
- IV immunoglobulins or parapheresis
- intubation
- corticosteroids
MYASTHENIA GRAVIS
What is the management of myasthenia gravis?
1st line = acetylcholinesterase inhibitors (pyridostigmine)
2nd line = prednisolone
3rd line = azathioprine
other = methotrexate or rituximab
Thymectomy if thymoma present
GUILLAIN-BARRE
What is the pathophysiology of GBS?
- B cells produce antibodies against the antigens on the pathogen causing the preceding infection and these antibodies also match proteins on the nerve cells leading to demyelination and potentially axonal degeneration
GUILLAIN-BARRE
What is the clinical presentation of GBS?
SYMPTOMS
- tingling + numbness in hands and feet (often precedes muscle weakness)
- symmetrical ascending progresive weakness
- unsteady when walking
- back and leg pain
- SOB
- facial weakness and speech problems
SIGNS
- reduced sensation in affected limbs
- symmetrical weakness
- ataxia with hyporeflexia
- autonomic dysfunction (tachycardia, HTN, postural hypotension, urinary retention)
- respiratory distress
- cranial nerve involvement and bulbar dysfunction (diplopia, facial droop)
GUILLAIN-BARRE
What are the investigations for GBS?
BLOODS
- U&Es
- B12 + folate
- TFTs (exclude hypothyroidism)
- anti-ganglionside antibodies
CULTURES
- stool or sputum
LUMBAR PUNCTURE
- raised protein with normal WCC
To consider
- nerve conduction studies (not required for diagnosis)
- MRI brain + spinal cord
NEUROPATHY
What is Charcot-Marie-Tooth disease?
- Autosomal dominant condition.
- Characterised by high-arched feet, distal muscle weakness + atrophy (inverted champagne bottle legs), hyporeflexia, foot drop + hammer toes
CORD COMPRESSION
What are the signs of spinal cord compression?
- Motor, reflex + sensory level = normal ABOVE lesion
- LMN signs = AT level
- UMN signs = BELOW level
- Tone + reflexes usually reduced in acute cord compression
- ?Sign of infection like tender spine, pyrexia
CORD COMPRESSION
How does degenerative cervical myelopathy present?
- Pain, loss of motor or sensory function affecting neck, upper or lower limbs
- Loss of autonomic function
- Hoffman’s sign +ve
SPINAL CORD INJURY
What is Brown-Sequard syndrome?
- Lateral hemisection of spinal cord
- Ipsilateral weakness below the lesion (lateral corticospinal)
- Ipsilateral loss of fine touch, proprioception + vibration (DCML)
- Contralateral loss of pain + temp (lateral spinothalamic)
ANTERIOR CORD SYNDROME
What is anterior cord syndrome?
- Anterior spinal artery occlusion or compression
- Bilateral spastic paresis (lateral corticospinal)
- Bilateral loss of pain + temp (lateral spinothalamic)
SPINAL CORD INJURY
What is posterior cord syndrome?
- Trauma or posterior spinal artery occlusion
- Loss of fine touch, proprioception + vibration (DCML)
MYOPATHY
How do myopathies present?
- Symmetrical proximal pattern of muscle weakness (hairs, stairs + chairs)
- Weakness > wasting
- Reflexes + sensation normal, no fasciculations
IDIOPATHIC INTRACRANIAL HYPERTENSION
What is the management of IIH?
- # 1 weight loss (topiramate can be used + has benefit of weight loss)
- Acetazolamide
- Surgery = optic nerve sheath decompression + fenestration to prevent damage
- Lumboperitoneal or ventriculoperitoneal shunt
NEURO PHARMACOLOGY
What are some side effects and important information for…
i) carbamazepine?
ii) valproate?
iii) lamotrigine
i) Blurred vision, headache, drowsiness – agranulocytosis, aplastic anaemia, P450 inducer
ii) Teratogenic, hepatitis, hair loss, tremor, weight gain – some interactions with antidepressants
iii) Blurred vision, headache, drowsiness – Steven-Johnson syndrome + risk of leukopenia
NEURO PHARMACOLOGY
What are some side effects and important information for…
i) phenytoin?
ii) levetiracetam?
iii) ethosuximide?
i) Megaloblastic anaemia (folate), osteomalacia, teratogenic, P450 interactions – Steven-Johnson syndrome
ii) Headache, drowsiness – some interactions with antidepressants
iii) Night terrors, rashes
NEURO PHARMACOLOGY
What is the mechanism of action of Levodopa?
- Levodopa is dopamine precursor which can cross BBB to be converted to dopamine by dopa-decarboxylase
- Must be combined with peripheral dopa-decarboxylase inhibitor like carbidopa so levodopa can reach brain
NEURO PHARMACOLOGY
What are the side effects of Levodopa?
- Postural hypotension
- Confusion
- Dyskinesias (abnormal movements)
- Effectiveness decreases with time (even with dose increase)
- On-off effect
- Psychosis
NEURO PHARMACOLOGY
Give some examples of dopamine receptor agonists.
What is the mechanism of action?
What are some side effects?
What monitoring is required?
- Bromocriptine, cabergoline, ropinirole
- Increases amount of dopamine in CNS
- Hallucinations (more than levodopa), postural hypotension
- ECHO, ESR, creatinine + CXR prior to Rx
NEURO PHARMACOLOGY
What are some adverse effects of dopamine receptor agonists?
- Pulmonary retroperitoneal + cardiac fibrosis
- Bromocriptine associated with gambling + other inhibition disorders (e.g. sexual)
NEURO PHARMACOLOGY
What are COMT + MAO-B inhibitors?
What is the mechanism of action?
- Catechol-o-methyltransferase (COMT) inhibitor = entacapone
- Monoamine oxidase-B (MAO-B) inhibitor = selegiline
- Inhibit enzymatic breakdown of dopamine
STROKE
What is the timeframe for thrombolysis for ischaemic strokes?
- Within 4.5 hours of the onset of symptoms
STROKE
what is the mechanism of action for alteplase / streptokinase (thrombolysis drugs for ischaemic stroke)?
- Converts plasminogen > plasmin so promotes breakdown of fibrin clot
- Alteplase (tPA) or can use streptokinase
EPILEPSY
How would a partial seizure present in the parietal lobe?
paraesthesia
visual hallucinations
visual illusions
MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Lhermitte’s sign?
Neck flexion causes electric shock sensation down spine
MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Uhthoff’s phenomenon?
symptoms worsening in heat e.g. in the shower/exercise
MENINGITIS
What are the aseptic causes of meningitis?
MS.
HSV2, SLE, sarcoidosis + skull # can cause recurrent aseptic meningitis
MYASTHENIA GRAVIS
What medications can exacerbate myasthenia gravis?
Abx, CCBs, beta-blockers, lithium + statins
BRAIN TUMOURS
What focal signs would you get if the tumour was located in the temporal lobe?
Receptive dysphasia, amnesia
BRAIN TUMOURS
What focal signs would you get if the tumour was located in the parietal lobe?
Hemisensory loss, dysphasia
BELL’S PALSY
what are the symptoms?
unilateral LMN facial weakness (forehead is affected)
altered taste
post auricular pain - pain behind ears
- hyperacusis (noise sensitivity)
- dry mouth
BELL’S PALSY
what is the management?
- prednisolone
- eye protection (eye lubricants or artificial tears should be considered
NEUROFIBROMATOSIS
what are the clinical signs of NF1?
- cafe-au-lait spots on the skin
- pea-sized lumps under skin
- skeletal abnormalities
- tumour on optic nerve
NEUROFIBROMATOSIS
what are the clincial signs of NF2?
- acoustic neuromas (bilateral)
- family history
- meningioma, schwannoma, juvenile cortical cataracts or glioma
NEUROFIBROMATOSIS
what are the causes of neurofibromatosis 1 and 2?
NF1 = chromosome 17 (autosomal dominant)
NF2 = chromosome 22 (autosomal dominant)
NARCOLEPSY
what is the management?
1st line = sleep hygiene + lifestyle changes
can also consider pharmacotherapy
- modafinil
- pitolisant
- sodium oxybate
CATAPLEXY
what is the management?
sodium oxybate
tricyclic antidepressants (clomipramine)
SSRIs
EPILEPSY
what is the treatment for generalised myoclonic epilepsy?
male = sodium valproate
female = levetiracetam
PARKINSON’S DISEASE
Give 2 histopathological signs of Parkinson’s disease
- Loss of dopaminergic neurones in the substantia nigra
- Lewy bodies
MND
What is the diagnostic criteria for MND?
LMN + UMN signs in 3 regions
El Escorial criteria
Presences of LMN and UMN degeneration and progressive history
Absence of other disease processes
GUILLAIN-BARRE
When is IV immunoglobulin contraindicated in the treatment for Guillain-Barre syndrome?
If a patient has IgA deficiency - can cause severe allergic reaction
ANTERIOR CORD SYNDROME
what are the symptoms?
- acute motor dysfunction
- loss of pain and temperature sensation below level of infarction
- autonomic dysfunction - neurogenic bowel/bladder
- acute onset back pain
ANTERIOR CORD SYNDROME
what are the investigations?
MRI - ‘owls eyes’ hyperintensities in anterior horns
lumbar puncture, CSF testing, blood and urine to rule out other causes
HORNER’S SYNDROME
what are the causes of 1st order horner’s syndrome?
Stroke
Syringomyelia
MS
tumour
encephalitis
anhidrosis to face, arm and trunk
HORNER’S SYNDROME
what are the causes of 2nd order horner’s syndrome?
Pancoast’s tumour
thyroidectomy
trauma
cervical rib
anhidrosis of face
HORNER’S SYNDROME
what are the causes of 3rd order horner’s syndrome?
carotid artery dissection
carotid aneurysm
cavernous sinus thrombosis
cluster headache
no anhidrosis
HORNER’S SYNDROME
what are the clinical features of horner’s syndrome?
MAPLE
Miosis
Anhydrosis
Ptosis
Loss of ciliospinal reflex
Endophthalmos (sunken eyeball)
TIA
what are the signs of a carotid TIA?
Amaurosis fugax = retinal artery occlusion –> vision loss
Aphasia
Hemiparesis
Hemisensory loss
hemianopia
TIA
what are the signs of a vertebrobasilar TIA?
Diplopia, vertigo, vomiting
Choking and dysarthria
Ataxia
Hemisensory loss
Hemianopic/bilateral visual loss
tetraparesis
loss of consciousness
HYDROCEPHALUS
what are the causes of normal pressure hydrocephalus?
excess fluid builds up in the ventricles, which enlarge and press on nearby brain tissue
- injury
- bleeding
- infection
- brain tumour
- brain surgery
ESSENTIAL TREMOR
what is the management?
mild disease
- observation
moderate disease
- 1st line: propranolol or primidone
- 2nd line: gabapentin or benzodiazepines
- 3rd line: deep brain stimulation, MRI guided thalamotomy
HYDROCEPHALUS
What are some causes of non-obstructive hydrocephalus?
- Commonly failure of reabsorption of arachnoid granulations (meningitis, post-haemorrhage)
- increased CSF production (choroid plexus tumour) but very rare
DIABETIC NEUROPATHY
what is the management for gastroparesis?
metoclopramide, domperidone or erythromycin
HUNTINGTON’S DISEASE
where is the genetic mutation located and what type of mutation is it?
- mutation in HTT gene on chromosome 4
- trinucleotide repeat disorder (CAG)
BRAIN METASTASES
what are the most common cancers to metastasise to the brain?
- lung cancer
- breast cancer
- melanoma
- colorectal cancer
- renal cell carcinoma
CEREBELLAR DISEASE
what are the causes?
- Friedreich’s ataxia
- neoplastic (cerebellar haemangioma)
- stroke
- alcohol
- MS
- hypothyroidism
- drugs (phenytoin, lead poisoning)
- paraneoplastic (secondary to lung cancer)
RADICULOPATHY
how can you distinguish an L5 radiculopathy from a common peroneal nerve injury?
both conditions cause foot drop
L5 RADICULOPATHY
- weakness of foot on dorsiflexion
- weakness of toe on extension
- weakness during foot eversion
- lower limb tendon reflex changes
- L5 dermatomal distribution of sensory loss
COMMON PERONEAL NERVE INJURY
- weakness of foot on dorsiflexion
- weakness of toe on extension
- weakness during foot eversion
- no changes to lower limb reflexes
- sensory loss over anterior aspects of foot and leg
WERNICKE-KORSAKOFF SYNDROME
what is the clinical triad?
- confusion
- ataxia
- ophthalmoplegia + nystagmus
EPILEPSY
what is the management for different types of seizures?
GENERALISED TONIC-CLONIC
- male = sodium valproate
- female = lamotrigine or levetiracetam
FOCAL SEIZURES
- 1st line = lamotrigine or levetiracetam
- 2nd line = carbamazepine, oxcarbazepine or zonisamide
ABSENCE SEIZURES
- 1st line = ethosuximide
- 2nd line (male) = sodium valproate
- 2nd line (female) = lamotrigine or levetiracetam
MYOCLONIC SEIZURES
- male = sodium valproate
- female = levetiracetam
TONIC OR ATONIC SEIZURES
- male = sodium valproate
- female = lamotrigine
MONONEUROPATHY
what are the nerve roots for median nerve?
C5-T1
MONONEUROPATHY
what are the clinical features of median nerve palsy (carpal tunnel syndrome)?
- sensory loss and/or paraesthesia over palmar + distal aspect of thumb, index, middle and half of ring ringer
- weakness of hand
- weak thumb abduction
- thenar eminence wasting
- hand pain (worse at night)
MONONEUROPATHY
what are the nerve roots for the ulnar nerve?
C8-T1
MONONEUROPATHY
what are the clinical features of ulnar neuropathy?
- sensory loss and/or paraesthesia over little finger + medial side of ring finger
- hand weakness (loss of dexterity, grip weakness)
- muscle wasting (hypothenar eminence +/- interossei muscles)
- claw hand deformity
MONONEUROPATHY
what are the investigations for ulnar neuropathy
froments test - pinch paper between thumb + index finger
MONONEUROPATHY
what are the nerve roots for the radial nerve?
C5-T1
MONONEUROPATHY
what are the clinical features of radial neuropathy?
- sensory loss and/or paraesthesia over dorsum or hand (may extend up forearm)
- wrist drop
- weakness in finger extension
- weakness in brachioradialis
MONONEUROPATHY
what are the nerve roots of the axillary nerve?
C5-6
MONONEUROPATHY
what are the clinical features of axillary neuropathy?
sensory loss over lateral shoulder
MONONEUROPATHY
what are the nerve roots for the common peroneal nerve?
L4-S2
MONONEUROPATHY
what are the clinical features of common peroneal neuropathy?
- foot drop (weakness of dorsiflexion)
- sensory loss over dorsum of foot + lateral shin
MONONEUROPATHY
what are the nerve roots of the tibial nerve?
L4-S3
MONONEUROPATHY
what are the clinical features of tibial neuropathy?
- paraesthesia, pain or numbness over the sole of the foot (worse at night + with prolonged standing)
- foot deformities (pes planus, pronated foot, abnormal gait)
MONONEUROPATHY
what is meralgia parasthetica?
pain +/- sensory loss over anterolateral thigh due to neuropathy of lateral femoral cutaneous nerve
TIA
What is the secondary prevention following a stroke/TIA?
- 1st line = clopidogrel 75mg
- 2nd line = aspirin 75mg + MR dipyridamole
- 3rd line = MR dipyridamole
- 4th line = aspirin 75mg
all patients = high dose statin (atorvastatin 20-80mg)
manage HTN, DM, smoking and CVD risk factors
ENCEPHALITIS
what is the management?
IV acyclovir
STROKE
How would a Total Anterior Circulation Infarct (TACI) present?
(involves middle and anterior cerebral arteries)
- unilateral hemiparesis +/- hemisensory loss of face, arm and leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphagia
STROKE
how would a Partial Anterior Circulation Infarct present?
2 of the criteria are present:
- unilateral hemiparesis +/- hemisensory loss of face, arm and leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphagia
STROKE
how does a lacunar infarct (LACI) present?
presents with one of the following:
- unilateral weakness (+/- sensory deficit) of face, arm and leg or all 3
- pure sensory stroke
- ataxic hemiparesis
STROKE
what vessels are affected in a lacunar infarct?
perforating arteries around the internal capsule, thalamus and basal ganglia
STROKE
how would a posterior circulation infarct (POCI) present?
presents with one of the following:
- cerebellar or brainstem syndromes
- loss of consciousness
- isolated homonymous hemianopia
STROKE
what is the presentation of lateral medullary syndrome?
IPSILATERAL
- ataxia
- nystagmus
- dysphagia
- facial numbness
- cranial nerve palsy
CONTRALATERAL
- limb sensory loss
STROKE
what vessels are affected in lateral medullary syndrome?
posterior inferior cerebellar artery
(also known as Wallenberg’s syndrome)
STROKE
what is the presentation of Weber’s syndrome?
- ipsilateral CN III palsy
- contralateral weakness
MENINGITIS
what are the most common causes of viral meningitis?
enteroviruses e.g. coxsackie B, echovirus
APHASIA
what are the different types of aphasia?
- Wernickes (receptive)
- Brocas (expressive)
- conduction
- global
APHASIA
what is the presentation of Wernicke’s aphasia?
speech is normal but sentences do not make sense (comprehension is impaired)
APHASIA
what is Wernicke’s aphasia
receptive aphasia (can speak but do not make sense, comprehension is impaired)
APHASIA
what is the presentation of Broca’s aphasia?
comprehension is normal
speech is non-fluent
repetition is impaired
APHASIA
what is Broca’s aphasia?
expressive aphasia (can comprehend but cannot speak fluently)
APHASIA
what is the presentation of conduction aphasia?
comprehension is normal
speech is fluent
repetition is poor
APHASIA
what is the presentation of global aphasia?
- expressive + receptive aphasia
- can communicate using gestures
APHASIA
where is the lesion for Broca’s (expressive) aphasia?
inferior frontal gyrus
APHASIA
where is the lesion for Wernicke’s (receptive) aphasia?
lesion in superior temporal gyrus
APHASIA
where is the lesion for conductive aphasia?
arcuate fasciculus
APHASIA
where is the lesion for global aphasia?
lesion affecting all 3 areas:
- superior temporal gyrus
- inferior frontal gyrus
- arcuate fasciculus
MULTIPLE SCLEROSIS
what is the medical management for fatigue?
amatadine
MULTIPLE SCLEROSIS
what is the medical management of spasticity?
1st line = baclofen or gabapentin
2nd line = diazepam, dantrolene or tizanidine
MULTIPLE SCLEROSIS
what is the management of bladder dysfunction?
USS bladder first
- if significant residual volume = intermittent self catheterisation
- no residual volume = anticholinergics
CEREBELLAR LESIONS
what is the cause of finger-nose ataxia?
cerebellar hemisphere lesion
CEREBELLAR LESIONS
what is the cause of gait ataxia?
cerebellar vermis lesions
STROKE
what is the definition of a stroke?
rapidly developing neurological deficit of vascular origin lasting over 24 hours or resulting in death
