Neurology and neurosurg Flashcards
Difference between a stroke and a TIA
TIA: episode <24hours without brain damage on imaging or neurological deficits
Stroke: brief episode with brain injury or neurological deficits still existing at 72 hours.
When do you call a code stroke and what does this mean?
If <4.5hours from symptom onset -> thrombolysis (if ischaemic)
What does fast stand for?
Facial weakness (can they smile? Any mouth or eye droop?)
Arm weakness (can they raise both arms and hold it there)
Speech difficulity
Time to act fast!
What are some DDX that can mimic stroke? (list 5)
Seizure
Sepsis
Syncope/pre-syncope
Space occupying lesion (haemmhorage or tumour)
Toxic/metabolic derangement (hypoglycaemia, hyponatraemia)
Initial management (in ED) of stroke
ABCs and vitals BSL, FBE, UEC CODE STROKE -> mobilise stroke team ECG (AF?) CT brain Medications (aspirin 100mg, ACEi, statin)
What are the 2 main types of stroke and their sub categories?
- Ischaemic
- intracerebral
- subarachnoid - Haemmhoragic
- Large artery thromboembolism
- Cardiogenic embolism (AF)
- Lacunar infarct
Which type of stroke is most lethal?
Intracerebral
What is the hallmark of a SA haemmhorage?
What is this due to?
CT findings
Thunderclap headache
-ruptured berry
Aneurism (around circle of willis) or AV malformation
CT: Hyperdense blood in fissures, commonly around COW.
What type of stroke is associted w HTN?
Deep intracerebral haemmhorage (putamen, thalamus, brainstem, cerebellum)
Should patients be able to recall what they were doing at the moment their stroke SX began, or is this is a sign of a mimic?
Yes they should with a stroke.
In stroke MX, what agent do you use for thrombolysis? What is the aim of thrombolysis?
Recominant tpa
Aim to salvage the ischaemic penumbra (tissue surrounding the dead core, not yet but will die if left without treatment)
Contraindications for thrombolysis (4)
Haemmhorage (stroke or elsewhere)
Recent surgery
Known aneurysm
Stroke mimics (must rule these out first!)
What further investigations would you do if the stroke is ischaemic?
ECG +/- echo (AF/clot of cardiac origin?)
Carotid doppler U/S +/- CTA (internal carotid stenosis?)
What medications do you give in ED for stroke?
ASPIRIN 100mg
ACE inhibitor
Statin
+/-Warfarin/NOAC if in AF
Primary prevention of stroke (before any stroke has occurred)
- Reduce stroke risk factors
-weight loss (diet and exercise)
-smoking cessation
Statin (reduce cholesterol)
Good blood sugar control
ACE-inhibitior (BP control)
What is the CHADS2 score?
Stroke risk for people in AF:
- Congestive cardiac failure (1 point)
- HTN (1)
- Age (>75) (1)
- Diabetes (1)
- Prior TIA or stroke (2 points)
□ 0 = very low risk -> antiplatelet
□ 1 = 1 low risk -> anticoag or antiplatelet
□ >2 = mod-high risk -> anticoag
Secondary prevention of stroke (after stroke/TIA)
- Antiplatelet (Aspirin) is FIRST LINE
- BP lowering (ACEi, thiazide diuretics)
- Cholesterol: Statins
- If in AFIB: CHADS2 score to determine antiplatelet and/or anticoagulant
+/- Carotid revascularisation (endarterectomy and stenting if symptomatic and stenosis >70%)
MX of haemmhoragic stroke
Keep BP low (SBP 120-130
Control raised ICP
Admit to neurosurg -> may need craniotomy
What are the different types of brain bleeds?
Which is associated w old age and alcoholism?
Which with trauma?
Which with ruptured berry aneurysm?
Which with HTN?
Epidural -> trauma
Subdural -> old age, alcohol, anticoag
Subarachnoid -> ruptured berry aneurysm/AVM
Intracranial -> HTN (aneurysm/AVM to lesser degree)
Characteristic présentation of an epidural haematoma and CT finding
Lucid interval before altered conscioussness
Hyperdense lenticular (lemon shaped) mass limited by suture lines
Characteristic présentation of an subdural haematoma and CT finding
No lucid period
Altered consciousness
Pupil irregularities
Hemiparesis
Hyperdense concave crescentic (crescent moon shaped) mass
Crosses suture lines
How do intracranial bleeds present?
TIA like SX and signs of raised ICP
DDX for headache
Tension-type
Migraine
Cluster
Analgesic overuse
Encephalitis/meningitis SAH Subdural haemmhorage Giant cell arteritis Raised ICP Glaucoma Stroke/TIA Space occupying lesion - tumour of abscess Systemic disorders -thyroid, THN, pheochromocytoma
Clinical presentation of meningitis vs encephalitis
Meningitis: severe headache
+/- neck stiffness, photophobia, rash, fever, systemic illness
Encephalitis: confusion, drowsiness, altered LOC, focal neurological signs, seizures, headaches, signs of systemic illness and fever
Causes of meningitis - how do signs and treatment differ?
Acute Bacterial
+/- Altered mental state and focal neurological signs
- Strep pneumonia, neisseria meningiditis, listeria, meningococcus (commonly in teens)
- Needs antibiotics
Viral
- no altered conscious state or focal neurological signs
- benign except in cases of HSV, VZV
- Self-limiting within 1-2 weeks
Investigating suspected meningitis
Blood tests and blood culture
Empiracle dexamethasone and empiracle antibiotics before CT
CT followed by LP (ensures no increased ICP which is a CI for LP)
** probably can skip CT if they don’t have risk factors for incr ICP and go straight to LP
What is empiracle treatment for bacterial meningitis
Ceftriazone (covers S. pneumonia and N. miningiditis)
How does CSF content differ between acute bacterial meningitis and viral meningitis?
Appearance
WCC
Protein
Glucose
Bacterial
- Cloudy
- > 1000 WBC/microL
- > 95% PMN
- Protein >1g/L
- Glucose decr (used up)
Viral
- Clear
- <500 WBC/microL
- Mostly lymphocytes
- Protein 0.4-1g/L
- Glucose normal
Where does HSV encephalitis typically affect?
Temporal lobe
Causes of altered mental state + Fever
Encephalitis Meningitis Brain abscess Intracranial tumour or haemmhorage Seizures
MX of brain abscess
Drainage by neurosurgery
Prolonged antibiotics
Anticonvulsants
Follow up CT
Source of bacteria from brain abscess
Continuous (sinusitis, dental abscess, mastoiditis etc)
Haematogenous
Direct implantation (post-op, post LP etc)
How can sinusitis lead to headaches and sepsis?
Focus of inflammation is in the sphenoid sinus, with para-meningeal involvement, immediately adjacent to CSF space.
Inflammation has incr vascular permeability and polymorphs have leaked across into CSF space. Bacteria may also leak across into CSF and/or blood via this method, causing encephalitis and/or sepsis.
Social implications of eplilepsy
Lose license (impacts ability to work, socialise, ADLs etc)
Reduced libido, depression, anxiety
Limited relationships, friendships etc
Simple vs complex partial seizures
Partial - limited to one hemisphere or lobe.
Simple: awareness/consciousness not affected (they are awake and alert- often remember)
Complex: consciousness/awareness affected (may not remember
Focal vs generalised seizures (how do they begin, and what is the underlying cause)
Focal
- begins w focal features referral to part of one hemisphere (aura)
- often w underlying structural disease
General
- no aura, comes without warning
- electrical discharge throughout cortex bilaterally, not localising to one hemisphere
What are the subtypes of focal vs general seizures
Focal (partial)
- Simple partial
- complex partial/dyscognitive
- secondary generalised
General
- Generalised tonic clonic
- myoclonus
- Absence seizures (spaced out)
How does epilepsy differ from seizure?
Seizure: sudden hyper synchronous neural activity
Epilepsy: tendency to stereotypical, repeated spontaneous seizures (2 +)
DDX to first seizure presentation
Seizure
Syncope - awaken rapidly, no post-ictal period/confusion
TIA - sudden focal neurological deficit
Psychogenic/psedo seizure
- consciousness retained
- long duration of seizure
- respond to you
-substance use/withdrawal
Triggers of seizures
Alcohol
Lack of sleep
Antidepressants and anticonvulsants
MX of seizures
Don’t treat the first seizure - await recurrence UNLESS you see and epileptiform EEG or MRI lesion
Treatment:
- Terminate status epilepticus in ED w benzodiazepine (carbamazepine)
- Prophylaxis: benzo and phenytoin
- Surgery in some cases to remove cause (tumour etc)
How do you diagnose epilepsy?
Interictal EEG + MRI /CT (anatomical cause)
Ictal EEG not of use because almost almost abnormal in seizure of any type
Pathophys of PD and post-mortem findings
Degeneration of DA-ergic neurone in substantial nigra -> decr DA in striatum -> lewy bodies present at post-mortem
Clinical Ft of PD
- Resting tremor (pill-rolling tremor occurs between thumb and index finger)
- Rigidity (cog-wheel when moved passively)
- Bradykinesia, hypokinesia, akinesia.
- Postural instability
Weakness is not a feature of PD
\+ Depression Trouble smelling Trouble sleeping Dementia
Different tremor types
Resting tremor - worse with rest, better with movement (PD)
Acting/Essential tremor - worse with movement, not present at rest (cerebellar diseases)
Treatment of PD
Levodopa + Carbidopa
Amantadine (produces endogenous DA production)
Bromocryptine (DA R agonist)
Entecapone (COMT inhibitor, inhibits DA breakdown)
Selegiline (Mao-B inhibitor)
Deep brain stimulation
Anticholinergics treat the tremor
Why is L-DOPA given with Carbidopa
Carbidopa is a Dopa decarboxylase inhibitor that can’t cross the BBB, so it inhibits conversion of LDOPA to DA in the periphery.
This limits the peripheral side-effects of levodopa conversion to Da or adrenaline (GI upset, arrhythmias)
What are things/conditions that cause ‘Parkinsonism’
Lewy body dementia, Wilson disease
Haloperidol (blocks DA receptors)
Metaclopromide (Da antagonist treats nausea, vomiting)
Pathophysiology of Alzheimers
Neurodegeneration in the cortex caused by: plaques and tangles
Outside neuron
- Amyloid precursor protein (APP) helps neuron grow and repair after injury. Gets used, broken down and recycled. Broken down into monomers called beta amyloid which forms clumps -> Beta amyloid plaque -> disrupt signalling
beta amyloid also deposit in walls of vessels in brain -> Amyloid angiopathy -> incr risk of haemmhorage
INSIDE neuron: tangles (tau protein inside neuron forms neurofibrillary tangles)
Macro changes to brain in AD
Brain atrophies
- ventricles and sulci widen
- gyrus narrow
Genetic predispositions to AD
- Apo-E
- Presenelin 1 and 2 (PSEN1/2)
- Down syndrome (trisomy 21)
Symptoms of AD (in order of progression)
Short-term memory loss
Loss of some motor skills and language
Long-term memory loss
Disorientation, wandering
Bed ridden
Definitive diagnosis of AD
Exclude other causes of dementia
Definitive diagnosis is post-mortem biopsy
Symptoms following seizure
Todd’s paralysis
Post-ictal confusion
What is MS?
What is the underlying pathophys?
A progressive, demyelinating disease of the CNS causing relapsing and remitting or clinically progressive CNS symptoms.
Discreet plaques of demyelination occur at multiple CNS sites, caused inflammation and/or degeneration
Presentation of MS
Usually get one of the following that is relapsing and remitting (with full recovery) not assoc w fever or other illness.
-May be stress induced:
- Unilateral optic neuritis (pain on eye movement and decr central vision)
- transverse myelitis - (Numb/tingling in limbs or Limb weakness)
- Brainstem/cerebellar (Diplopia, ataxia, nystagmus, vertigo)
Over time recovery becomes incomplete and disability accumulates.
Investigations for MS
MRI brain and spine with gadolinium contrast: shows lesions and excludes other causes (T2 -fluid- shows plaques as hyperintense areas)
CSF evaluation - presence of oligoclonal bands
Basic bloods (+TSH, B12) normal
Diagnosis of MS
Dissemination in space (clinical evidence of 2 or more lesions) and in time (2 or more attacks, > 1 month apart) as based on the revised McDonald criteria
Backed up by MRI findings
Management of MS
- acute
- chronic (long-term therapy)
Treat acute exacerbations
- IV methylprednisilone 3-5 days followed by oral prednisilone
Long-term therapy slows disease progression (but can’t reverse pre-existing plaques)
- IFNs (SE: Depression)
- Monoclonal antibodies (Natalizumab and alemtuzumab but SE: JC virus)
- Azathioprine
- Non-immunosuppressives
- Monitor with MRI
- psychosocial and physio support
+ Treat SX (palliative) + REHAB
What functions reside in the anterolateral spinothalamic tract?
Pain and temperature laterally
Crude touch anterior
What resides in the dorsal root ganglion?
Sensory cell bodies
What modalities reside in the dorsal column medial lemniscus pathway?
Proprioception, light touch and vibration
How does diabetes cause nerve palsies?
Vasanavorum are affected -> ischaemia of neutrons -> nerve palsy
What nerve does carpal tunnel syndrome affect?
Median nerve compression
Neuromuscular conditions in which you get diplopia and ptosis
MG
CNIII palsy
Thyroid eye disease
NOT MND
Neuromuscular conditions with proximal weakness
Myopathy (Duchennes muscular dystrophy) Myasthenia graves (fatiguability)
Neuromuscular conditions with distal weakness?
Neuropathy
MND
Neuromuscular conditions ft. dysphagia and dysarthria?
MG
MND
Pathophys of MG
Post-synaptic anti-AchR Ab inhibit transmission at NMJ
What is the presentation of MG?
FATIGUABLE WEAKNESS is main finding. Prox -> distal Early involvement of EOM and lid-opening muscles (Ptosis and diplopia) Dysarthria
(no change in sensation, reflex, coordination)
Investigations for Diagnosis of MG
Tensilon Test (Ach-esterase antagonist) GOLD STANDARD
EMG
Bloods: anti-Ach R antibody, MUSK Ab
CT chest (assoc w thymoma)
Investigations to diagnose a myopathy
Electrophysiology studies (needle EMG)
Serum CK
Genetic tests (myotonic and duchenne’s dystrophy)
Muscle biopsy
What will you see on a biopsy of a myopathic muscle
Varying muscle fibre size
Increasing fibrosis
HX features suggestive of NMD
Muscle weakness/wasting
Fasciculation’s
Stiffness
Fatigue
Sensory loss/numbness
Burning/tingling
Clumsiness
Poor balance, falls
Diplopia/blurred vision
Dysphagia
Dyspnoea
What causes foot drop
Focal single nerve root neuropathy
- L5 radiculopathy
- Perineal neuropathy
Examples of NMJ disease
Pre-synaptic
- Botulism (degrades the SNARE complex so Ach can’t be released into NMJ)
- LEMS: Lambert Eaton Myasthenia Syndrome (Ab against pre-synaptic Ca channels)
Post-synaptic
- MG
- MuSK Myasthenia
What is LEMS associated with 50% of the time?
Neoplasm (small cell lung cancer often)
Examples of myopathies
Duchennes
Beckers
Myotonic dystrophy
Investigations of neuromuscular conditions
Electrophysiology
Laboratory blood tests
LP
Muscle biopsy/MRI if myopathy suspected
What is the main side-effect of Levodopa?
Motor fluctuations and dyskinesia develop in 50% of patients after 5-10 years on drug, so start L-DOPA later in disease progress when SX start to seriously interfere w life
- wearing off earlier
- on/off syndrome
- failure to turn ‘on’
- acute akinesia
Potential causes of raised ICP
Cerebral oedema (reactive swelling that occurs with trauma, tumour, infarct, haemmhorage, infection)
Overproduction of CSF
Decreased absorption of CSF
What type of cerebral oedema and causes responds to steroid therapy?
Vasogenic oedema secondary to tumours, trauma.
Steps of herniation
Steps
- Internal herniations first in attempt to compensate
- Subfalcine
- Transtentorial (penetration of brain into where cerebellum are meant to be) - Coning -> death because squashes and injures brainstem
+/- Basilar artery tears and you get haemmhorage within brainstem
What is hydrocephalus?
Enlarged ventricles
2 main types of cerebral oedema
- Vasogenic (BBB disruption with incr permeability due to tumours, trauma)
- responds to steroids - Cytotoxic (brain swells due to electrolyte imbalance, often due to infarcts)
- no response to steroids
Cushing’s triad - what does this indicate?
Near brain herniation and imminent death
- Bradycardia
- High SBP (wide Pulse pressure)
- Irregular respiration
What is Guillan Barre and what is the basic pathophys?
Trigger
Acute rapidly evolving polyneuropathy starting distally and ascending proximally.
Autoimmune attack and damage to peripheral nerve myelin, sometimes preceded by viral/bacterial infection.
Management of GBS
IvIg or plasmapheresis +/- analgesia
Presentation of GBS
Sensory: distal, symmetric parasthesia and neuropathic pain
Motor: distal weakness, areflexia
Autonomic dysregulation of BP, heart rhythm, bladder
MX of myasthenia gravis
Steroids or immunosuppressants (azathioprine, cyclophosphamide, mycophenolate)
Thymectomy (85% patients show improvement/remission)
Ach-Esterase inhibitors (SX relief)
Short-term IVIg and plasmapheresis for crises
Brain tumours
Primary:
- Most common: Astrocytoma
- Glioblastoma (high grade astrocytoma)
- oligodenroglioma
- schwannoma
- meningioma
- pituitary adenoma
Secondary
- Lung
- BReast
- RCC
- GI
- Melanoma
DDX for ring enhancing lesion on CT with contrast
MAGICAL DR
Metastases Abscess Glioblastoma Infarct Contusion AIDS Lymphoma Demyelination Resolving hematoma
Treatment for Brain tumours
Monitor - serial imaging
Steroids (reduce cytotoxic oedema)
Surgery - decompressive, palliative
Radiotherapy
Chemotherapy
Presentation of prolactinoma
Young woman
Amenorrhea
Galactorrhea
Investigation of galactorrhea
Prolactin levels and MRI
BetaHCG, TSH/T4 (r/o pregnancy and hypothyroid)
Presentation of pituitary apoplexy
Headache (episodic, severe)
Visual Loss
Endocrine Issues (hypotension)
Associated SX with migraine
Pulsative, photophobia Over 4-72 hours Unilateral Nausea and Vomiting Disabling intensity
aggravated by stress, food, wine, sleep deprivation, hormones, fatigue, exercise
Treatment for migraine
- acute
- prophylactic
Acute: Acetaminophen, ASA
or NSAIDs
+/- antiemetic
Prophylactic: beta blockers or TCAs
Treatment for tension type headache
Rest and relaxation
NSAIDs
Exercise (prophylactic)
Facial nerve palsy symptoms
Complete ipsilateral facial weakness:
- Facial droop
- Flattened forehead
- Flattened nasolabial fold
- Inability to close eyes
Supra nuclear facial nerve palsy SX (UMN)
forehead sparing with contralateral facial weakness (opposite side)
Causes of facial nerve palsy
80-90% Bell’s palsy (idiopathic)
but often related to HSV
May also be related to CMV, HZV, EBV, temporal bone fracture, otitis media/mastoiditis
Differentials of MS
Neuromyelitis optica Other systemic autoimmune diseases Acute disseminated encephalomyelitis Sarcoidosis Infections Tumours Conversion Disorder
Common permanent MS symptoms
Fatigue Walking problems Bowel and bladder symptoms Pain and paraesthesias Cognitive problems Visual disturbances
