Harrison's Question Bank Flashcards
What is postural orthostatic tachycardia syndrome?
A change from the supine position to an upright position causes an abnormally large increase in heart rate (and causes symptoms, usually presyncopy) It is thought to be related to mutations in the noradrenaline transporter
What is Stiff-Person syndrome?
Paraneoplastic syndrome with Anti-amphiphysin antibodies associated with SCLC and breast cancer. These antibodies are pretty much anti-GABA-pathway. Causes progressive rigidity and spasms (particularly trunk in early days)
Can you explain anything about EEG lead placement? hint: there are numbers and letters. Do odds = left or right?
The International 10:20 system - usually details to the left of the wave A, earlobe; C, central; F, frontal; Fp, frontal polar; P, parietal; T, temporal; O, occipital. Right-sided placements are indicated by even numbers, left-sided placements by odd numbers, and midline placements by Z.
What happens to an EEG during metabolic encephalopathy? Can you comment about what might happen in space occupying lesion?
he EEG generally slows in metabolic encephalopathies, and triphasic waves may be present. Periodic lateralizing epileptiform discharges (PLEDs) are commonly found with acute hemispheric pathology such as a hematoma, abscess, or rapidly expanding tumor
What are the major findings seen on EMG? What are the characteristics of myopathic changes vs neuropathic?
TL;DR: 1. myopathic is short, small amp contraction. 2. neuropathic is long, diffuse contraction (think that some nerve fibres are fast, some slow - all over the shop). 3. fibrillations, which are NOT the same as myotonic discharges
Activity recorded during EMG.
A. Spontaneous fibrillation potentials and positive sharp waves.
B. Complex repetitive discharges recorded in partially denervated muscle at rest.
C. Normal triphasic motor unit action potential.
D. Small, short-duration, polyphasic motor unit action potential such as is commonly encountered in myopathic disorders.
E. Long-duration polyphasic motor unit action potential such as may be seen in neuropathic disorders
Case from Harrison’s:
37 year old man, first ever seizure. Now post-ictal with nuchal rigidity. Drug screen positive for cocaine.
What’s your investigation sequence?
Harrison’s argues that exclusion of meningitis is most important. CT head may be indicated if there are concerns with elevated ICP, but MRI is not the primary investigation.
This is a LOW YIELD QUESTION:
Approximately what percentage of adults can discontinue AEDs? What percent of patients with mesial temporal lobe epilepsy respond to surgery?
60% for discontinuation
70% respond to temp lobe surgery in MTLE
Which of the following does NOT have a role in primary or secondary prevention of atherothrombotic stroke ? (from Harrison’s)
- aspirin
- BP control
- clopidogrel
- statins
- warfarin
Warfarin.
The WARSS study found no benefit of warfarin over aspirin for 2ndary prevention in atherothrombotic disease. Warfarin’s role is apparently only in AF/cardiocerebral emboli-related stroke.
Restless legs syndrome requires four main symptoms for diagnosis. Can you list a few? (all four if you can, champ!)
Are there any investigations we should do for RLS? (any causes of secondary)
- an urge to move legs accompanied by unpleasant sensation in legs
- symptoms begin or worsen when at rest
- feel better after movement
- worse during evening/night
Harrison’s recommends testing for ferritin (anaemia) and renal failure. Can also be associated with peripheral neuropathy
By the way - Primary RLS has a genetic component.
Do you know what complex regional pain syndrome (CRPS) is?
Could you explain a little about the pathogenesis and the symptomatology please.
Used to be known as “Reflex sympathetic dystrophy”.
There are two types. CRPS type I: regional pain syndrome usually after tissue trauma - but not necessarily the same tissue as is affected by the condition (e.g. after MI, stroke, minor shoulder injury). In this version, pain is not confined to a single peripheral nerve area.
CRPS type II: occurs after injury to a specific nerve - and initially symptoms are localised to that nerve, but may eventually spread.
Symptoms of both: spontaneous pain, vasomotor dysfunction, sweat gland abnorm, focal oedema.
Eventually can lead to skin atrophy and contractures
Should trigeminal neuralgia have sensory loss associated with it?
Does the absence or presence of sensory loss lead to any other investigation?
Typically trigeminal neuralgia does not have sensory loss. Only pain along the sensory divisions.
Sensory loss would inspire the need for MRI/neuroimaging
What diagnosis do you think of with:
progressive lower limb weakness and a less of sensation “below the belly button” and incontinence?
Myelopathy is the thing we were going for in this case.
The next step of the differential is compressive vs non-compressive myelopathy.
What are the major causes of compressive myelopathy?
(the answer has 4 things)
tumour
epidural abscess or haematoma
herniated disc
vertebral pathology
what are the major causes of non-compressive myelopathy?
5 main types
spinal cord infarction
systemic disorders like vasculitis, SLE, sarcoid
infections (particularly viral)
demyelinating disease
idiopathic
What is the typical clinical presentation of syringomyelia?
(also give a little about demographics and predisposing features)
over 50% is associated with a Chiari malformation
usually symptoms start in teen
can be acquired though
classic presentation is central cord syndrome - pain and temperature loss, and upper limb weakness (because the motor nerves cross near the central canal - and the syrinx is usually in the cervical cord)
eventually progresses and patient gets UMN signs in legs
