Neuro

Question 1

Bell’s palsy (facial nerve paralysis)

Prognosis
most people with Bell’s palsy make a full recovery within 3-4 months
if untreated around 15% of patients have permanent moderate to severe weakness

Answer 1

Ix:

lower motor neuron facial nerve palsy → forehead affected

Also,
post-auricular pain (may precede paralysis)
altered taste
dry eyes
hyperacusis

Mx = oral prednisolone within 72 hours of onset

Eye care = lube, tape and artificial tears

For a patient with a Bell’s palsy, if the paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT!

Query add antivirals?

Question 2

Cluster headache (intense sharp, stabbing pain around one eye, occurs once or twice a day, each episode lasting 15 mins - 2 hours, for 4-12 weeks accompanied by redness, lacrimation, lid swelling nasal stuffiness
miosis and ptosis in a minority)

RF’s?

Answer 2

Ix = MRI with gadolinium contrast

RF’s = young male smoker with positive family history

Mx = refer to neurologist

Acute = triptan + O2
prophylaxis = verapamil

Question 3

Encephalitis (caused by HSV-1!

meningitis vs enceph? - enceph has psychiatric sx or altered mental status - e.g. focal/absence seizure)

Answer 3

Ix:

CSF
lymphocytosis
elevated protein
PCR for HSV, VZV and enteroviruses

MRI = medial temporal and inferior frontal changes (e.g. petechial haemorrhages)

normal in one-third of patients

EEG = lateralised periodic discharges at 2 Hz

Mx = IV aciclovir should be started in all cases of suspected encephalitis

Question 4

Epilepsy (t/c, focal, absence, myoclonic, a/tonic)

Focal can present with aura
simple = aware, complex = no memory of the seizure + automatisms

After this focal(aura) seizure this can then develop into a full generalised seizure!

Answer 4

Generalised tonic-clonic seizures
m = sodium valproate*
f = lamotrigine or levetiracetam

girls < 10yo or women who are unable to have children = sodium valproate

Focal seizures (previously called partial)

1st = lamotrigine or levetiracetam
2nd = carbamazepine, oxcarbazepine or zonisamide

Absence seizures (Petit mal)
1st = ethosuximide
2nd = same as gen-ton-clon
m = sodium valproate
f = lamotrigine or levetiracetam

carbamazepine may exacerbate absence seizures

Myoclonic seizures
m = sodium valproate
f = levetiracetam

Tonic or atonic seizures
m = sodium valproate
f = lamotrigine

men take sodium valproate for everything apart from focal
Women take leve/lamo for everything apart from (myo = leve, a/tonic = lamo)

“myo-lev!, miya-ha-ha” drinking a tonic in a lambo

Focal and absence are the only special ones

*Caution should be exercised when combining sodium valproate and lamotrigine as serious skin rashes such as Steven-Johnson’s syndrome may be provoked

Question 5

Extradural haemorrhage

Answer 5

Ix = CT head
Mx = ?

Question 6

Guillain-Barré syndrome

Caused by an immune attack on the
nerve cells of the peripheral nervous system and their support structures

Answer 6

Ix = Multifocal decreased motor conduction speed with/without conduction block

Miller Fisher syndrome = variant of Guillain-Barre syndrome
associated with ophthalmoplegia, areflexia and ataxia.

The eye muscles are typically affected first
usually presents as a descending paralysis rather than ascending as seen in other forms of Guillain-Barre syndrome

anti-GQ1b antibodies are present in 90% of cases

Mx: 1st = IV Ig 2nd = plasmapharesis

Question 7

Horner’s Syndrome

Answer 7

Ix = miosis (small pupil), ptosis, anhidrosis (loss of sweating one side)

enophthalmos* (sunken eye)

apraclonidine drops (an alpha-adrenergic agonist) can be used.

causes pupillary dilation in Horner’s syndrome due to denervation supersensitivity but produces mild pupillary constriction in the normal pupil by down-regulating the norepinephrine release at the synaptic cleft

Question 8

Huntington’s disease

Answer 8

Ix:

Genetics
autosomal dominant - trinucleotide repeat disorder: repeat expansion of CAG (n huntingtin gene on chromosome 4) - results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia leading to hyperkinetic movements.

Anticipation - as Huntington’s disease is a trinucleotide repeat disorder, the disease presents at an earlier age in successive generations

Features typical develop after 35 years of age
- chorea
- personality changes (e.g. irritability, apathy, depression) and intellectual impairment
- dystonia
- saccadic eye movements

Question 9

Hydrocephalus

Normal pressure hydrocephalus is a unique form of non-obstructive hydrocephalus characterised by large ventricles but normal intracranial pressure. The classic triad of symptoms is wet wacky and wobbly (incontinence, dementia, and disturbed gait)

Answer 9

Ix:
1st line = CT head

MRI may be used to investigate hydrocephalus in more detail, particularly if there is a suspected underlying lesion

Lumbar puncture* is both diagnostic and therapeutic since it allows you to sample CSF, measure the opening pressure, but also to drain CSF to reduce the pressure

*Lumbar puncture must not be used in obstructive hydrocephalus! Since the difference of cranial and spinal pressures induced by the drainage of CSF will cause brain herniation.

Mx = external ventricular drain (EVD) into the right lateral ventricle and drains into a bag at the bedside

A ventriculoperitoneal shunt (VPS) is a long-term CSF diversion technique that drains CSF from the ventricles to the peritoneum

Obstructive hydrocephalus = surgery on the obstruction

Question 10

Idiopathic intracranial hypertension - fat, female, on COMAAR;

Ciclosporin
Ocp,
Mineralocorticoids,
Amiodarone,
Antibiotics (tetracyclines)
Retinoids,

Answer 10

Ix = (headache + papilloedema) blurred vision, enlarged blind spot, sixth nerve palsy may be present

Mx = weight loss

diuretics e.g. acetazolamide (carbonic anhydrase inhibitor)

topiramate is also used (causes weight loss)

repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management

surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure

Question 11

Meningitis (Fever, neck pain, confusion (bacterial=hours, viral=days)

meningitis becomes meningococcal septicaemia when the pathogen spreads into the blood and causes systemic sx

Sensorineural hearing loss is the most common complication following meningitis

Answer 11

Ix = Lumbar puncture
LP is delayed if;

Signs of sepsis/rash
Resp/cardiac compromise
Bleeding risk
Raised ICP
focal neurological signs
papilloedema
Seizures
GCS ≤ 12

Mx: ab’s given as a priority if LP isn’t possible, to treat potential septicaemia!

<50yo = IV cefotaxime* + IV dexameth
>50yo = cefotaxime+amox+dexameth

Contacts of patients with meningococcal meningitis = Oral ciprofloxacin or rifampicin

over 50s men(ingitees) are CADs

• benpen in the community!

Question 12

Migraine (Unilateral, severe headache, phonophobia 4-72hrs)

Answer 12

Ix:
UMN = (URTI) increased tone+reflexes, decreased power
LMN = everythings lower (tone, reflexes, power)

MRI, LP, FBC,

Mx:

Acute = oral triptan, NSAID/paracetemol
prophylaxis(>2attacks/month) = topiramate/propranolol

Question 13

Motor neurone disease (ie. ALS and bulbar palsies - mixed UMN+LMN sx but no sensory deficit)

Brisk reflexes in a wasted limb is classic for MND

Answer 13

Ix:

MRI, EMG (fasiculations), LP

Mx = Riluzole

Amytriptyline (drooling)
baclofen/botulin (spasticity)
NG/PEG (dysphagia)
Analgesia (pain)
ventilate (resp)

AL’s wearing a R.A.B coat - Riluzole, amytriptyline, baclofen

UMN can be tested by hoffmans reflex - flicking the middle finger and if the thumb twitches, its an UMN lesion

or Babinskis - upgoing plantar reflex = UMN

Question 14

Multiple sclerosis (AI attack causing demyelination in the cns, leading to relapsing and remitting)

UMN/LMN?

Also, which cells are affected?

Factors influencing severity of disease?

Answer 14

Ix = Lesions disseminated in time and space. MS TEAMS - Tingling, Eye*, Ataxia, Motor

May involve UMN, senosry loss and cerebellar ataxia but NEVER involves LMN

MRI =
high signal T2 lesions
periventricular plaques
Dawson fingers: often seen on FLAIR images - hyperintense lesions penpendicular to the corpus callosum

LP
oligoclonal bands (and not in serum)
increased intrathecal synthesis of IgG

Visual evoked potentials
delayed, but well preserved waveform

Mx:

Acute = methylpred (predators on MS TEAMS)
Chronic = DMARD’s (IFN-B, glatiramer) + natali/alemtu-zumab

Cells affected = Oligodendrocytes

Factors predicting a less severe disease;

1.Female,
2. <25 yo,
3. Optic neuritis/ sensory, rather than
cerebellar symptoms on initial presentation,
4. A long interval (>1 year)
between relapses
5. Few lesions on MRI

*Often presents with opthalmoplegia - diplopia when asked to look right,
the left eye stays in the midline but the right eye moves right and starts jerking

Question 15

Myasthenia gravis

Interestingly, MG is hypersensitive to rocuranium (as it antaganises post-synaptic nicotinic receptors which are already reduced in MG)

and is resistant to suxamethonium (which works by over-depolarising nicotinic receptors, of which there are few in MG)

Answer 15

Ix = single fibre electromyography: high sensitivity (92-100%)

CT thorax to exclude thymoma

CK normal

anti-Ach-r ab’s
anti-muscle-specific tyrosine kinase ab’s

Mx:
1st = pyridostigmine (long-acting acetylcholinesterase inhibitors)

immunosuppression (pred) is usually not started at diagnosis, but the majority of patients eventually require it in addition to long-acting acetylcholinesterase inhibitors:
azathioprine, cyclosporine, mycophenolate mofetil may also be used

Thymectomy

Management of myasthenic crisis = plasmapheresis + IV IG’s

Maya working at the pyramids surrounded by (pred)ators

Question 16

Neurofibromatosis

Answer 16

Ix: NF2 has vestibular schwannomas

Question 17

Parkinson’s disease

Answer 17

Parkinson’s disease should only be diagnosed and managed by a specialist. Therefore, the GP must make a neurology referral.

Ix:

MRI (to rule out vascular causes)

DAT-scan - to trace DA

Mx:

1st = Levodopa, MAO-Bi (selegiline), DA agonists (ropinirole)

2nd = COMTi (entacapone)

Question 18

Raised intracranial pressure

Answer 18

Ix:

neuroimaging (CT/MRI)

Invasive ICP monitoring

Catheter in lateral ventricles to monitor the pressure is used to (collect+drain CSF)

A cut-off of > 20 mmHg is often used to determine if further treatment is needed to reduce the ICP

Mx:
Investigate and treat the underlying cause

head elevation to 30º

IV mannitol may be used as an osmotic diuretic

controlled hyperventilation - aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP

leads to rapid, temporary lowering of ICP. However, caution needed as may reduce blood flow to already ischaemic parts of the brain

CSF removal (catheter, LP’s, ventriculoperitoneal shunt (for hydrocephalus))

Question 19

Spinal cord compression (incl. cauda equina)

Answer 19

Ix = MRI spine within 24 hours of presentation

Mx = high-dose oral dexamethasone

Urgent oncological assessment for consideration of radiotherapy or surgery

If there are multiple lesions and pt is too frail for surgery. Radiotherapy is
the best treatment option!

Question 20

Spine: Radiculopathy

Question 21

Stroke (ischaemic and haemorrhagic)

Low GCS or HIGH BP precludes thrombolytic treatment

Answer 21

Ix = A non-contrast CT head scan - Iooking for is it ischaemic/haemorrhagic?

Acute ischaemic strokes = areas of low density in the grey and white matter of the territory. These changes may take time to develop

other signs include the ‘hyperdense artery’ sign corresponding with the responsible arterial clot - this tends to visible immediately

Acute haemorrhagic strokes = areas of hyperdense material (blood) surrounded by low density (oedema)

Mx:

Acute = 300mg aspirin

<4.5hrs = alteplase
<4.5hrs + PCA = alteplase + thrombectomy
<6hrs thrombectomy

Secondary prevention:

No AF = Clop (if clop is CI, then aspirin+dipyridamole, if aspirin is CI then just dipyridamole)

AF = apixaban/warf

If they’re eating put them NBM immediately

Question 22

Subarachnoid haemorrhage

Answer 22

Ix:
1st - non-contrast CT

Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.

if CT head is done within 6 hours of symptom onset and is normal

new guidelines suggest NOT doing a lumbar puncture and consider an alternative diagnosis

if CT head >6hrs after symptom onset and is normal -> do an LP

Timing wise the LP should be performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown)

Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).

As well as xanthochromia, CSF findings consistent with subarachnoid haemorrhage include a normal or raised opening pressure

If the CT shows evidence of a SAH = Referral to surgery as soon as SAH is confirmed

After spontaneous SAH is confirmed, the aim of investigation is to identify a causative pathology that needs urgent treatment:

CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)

+/- digital subtraction angiogram (catheter angiogram)

Mx = supportive + Nimodipine (prevents vasospasm/aneurysm)
bed rest + analgesia

Venous thromboembolism prophylaxis

discontinuation of antithrombotics (reversal of anticoagulation if present)

Aneurysm treated using coil/clipping by a neurosurgeon

Question 23

Subdural haemorrhage

Question 24

Tension headache (bilateral tight band)

Answer 24

Ix:
Not associated with aura, nausea/vomiting or aggravated by routine physical activity
may be related to stress
may co-exist with migraine

Chronic tension-type headache = 15+ days per month

Mx 1st = aspirin, paracetamol/NSAID

Prophylaxis: = ‘up to 10 sessions of acupuncture over 5-8 weeks’

Question 25

Transient ischaemic attacks (TIA)

Answer 25

Ix = MRI on the same day as the assessment

Carotid doppler = to view atherosclerosis emboli to see if they’re a candidate for carotid endarterectomy!

Mx:

acute = 300mg aspirin

prevention: 1st= Clop

2nd = Dipyridamole
3rd = Aspirin (75mg)

lipid modification = atorvastatin 20–80 mg daily - the aim of statin therapy is to reduce non-HDL cholesterol by more than 40%

Carotid stenosis > 70% = endartectomy

Question 26

Trigeminal neuralgia (a unilateral disorder characterised by brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve)

Answer 26

The pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously

small areas in the nasolabial fold or chin may be particularly susceptible to the precipitation of pain (trigger areas)

the pains usually remit for variable periods

Red flag symptoms and signs suggesting a serious underlying cause:

Sensory changes
Deafness or other ear problems
History of skin/oral lesions that could spread perineurally
Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
Optic neuritis
A family history of multiple sclerosis
Age of onset before 40 years

Mx = Carbamazepine

failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology

Question 27

Wernicke’s encephalopathy

Answer 27

Ix = decreased red cell transketolase + MRI

Mx = thiamine

Question 28

Rinne and Webers Test

Answer 28

Weber = middle of the head
Rinne = mastoid process

1st = Weber

Localises to louder side

2nd = Rinne

Air>Bone = normal
Bone>air = conductive loss

Question 28

Rinne and Webers Test

Answer 28

Weber = middle of the head
Rinne = mastoid process

1st = Weber

Localises to louder side

2nd = Rinne

Air>Bone = normal
Bone>air = conductive loss

Question 29

Alzheimers (make card)

Which part of the brain is most affected in early alzheimers?

Answer 29

temporal lobe!

Question 30

Vestibular neuronitis = a cause of vertigo that often develops following a viral infection.

Answer 30

Features
recurrent vertigo attacks lasting hours or days
nausea and vomiting may be present
horizontal nystagmus is usually present
NO hearing loss or tinnitus

Differential diagnosis
viral labyrinthitis
posterior circulation stroke: the HiNTs exam can be used to distinguish vestibular neuronitis from posterior circulation stroke

Mx:

Severe = buccal or IM prochlorperazine

Less severe = a short oral course of prochlorperazine, or an antihistamine (cinnarizine, cyclizine, or promethazine)

Chronic = vestibular rehabilitation exercises

Question 31

BPPV (Benign paroxysmal positional vertigo)

Answer 31

(BPPV) is one of the most common causes of vertigo encountered. It is characterised by the sudden onset of dizziness and vertigo triggered by changes in head position. The average age of onset is 55 years and it is less common in younger patients.

Features
vertigo triggered by change in head position (e.g. rolling over in bed or gazing upwards)
may be associated with nausea
each episode typically lasts 10-20 seconds
positive Dix-Hallpike manoeuvre, indicated by:
patient experiences vertigo
rotatory nystagmus

BPPV has a good prognosis and usually resolves spontaneously after a few weeks to months. Symptomatic relief may be gained by:
Epley manoeuvre (successful in around 80% of cases)
teaching the patient exercises they can do themselves at home, termed vestibular rehabilitation, for example Brandt-Daroff exercises

Question 32

Reversal of Neuro-muscular blocking drugs used in muscle paralysis for mechanical ventilation in surgery? (Non-depolarising)

Answer 32

Neostigmine!

Question 33

What signs indicate a lesion in the;

Basal ganglia
Cerebellum
Internal capsule
Motor cortex
Pyramidal tracts

?

Answer 33

Basal ganglia – to initiate and stop movement

Cerebellum – fine movement, gait, proprioception

Internal capsule – will give purely motor or purely sensory

Motor cortex -

Pyramidal tracts – tracts of the spine?

Question 34

What is Brown Sequard syndrome?

Answer 34

Hemisection of the cord is also known as Brown–Séquard syndome.

This results in ipsilateral paralysis and loss of light touch and vibration
sensation and contralateral loss in pain and temperature below the point
of the lesion.

The spinothalamic tracts cross at the level of the cord, so
sensation to pain and temperature is lost in the contralateral limbs

Question 35

Whats the differentiator for orthostatic vs vasovagal syncope?

Answer 35

Orthostatic = reduced cerebral
perfusion as the patient moves from lying to standing. Symptoms are
similar to vasovagal in that the patient may become pale and describe ‘the
lights or sound dimming’. Perfusion is restored after the patient collapses
and unconsciousness lasts no more than seconds or a couple of minutes
with full recovery.

However, vasovagal epsiodes can be brought on by
sleep or food deprivation, hot or emotional environments, Valsalva
manoeuvre (such as straining) and are not as closely related to position!

Question 36

What are the 9 contraindications for thrombolysis?

Answer 36

contraindications for thrombolysis are:

1. onset of symptoms more than 3
   hours ago,
2. seizures at presentation,
3. uncontrolled blood pressure (over
   180/110),
4. previous intracranial bleed,
5. lumbar puncture in the last week,
6. ischaemic stroke or head injury in the last three months,
7. active bleeding (not menstruation),
8. surgery/major trauma (including CPR) within the last 2 weeks
9. non-compressible arterial puncture within the last week.

Question 37

Status epilepticus

What is it?
Mx?

Answer 37

Status epilepticus is defined as:

a single seizure lasting >5 minutes, or
>= 2 seizures within a 5-minute period without the person returning to normal between them

This is a medical emergency. The priority is the termination of seizure activity, which if prolonged will lead to irreversible brain damage.

Management
ABC
airway adjunct
oxygen
check blood glucose

1st = IV benzodiazepines such as diazepam or lorazepam

2nd = phenytoin or phenobarbital infusion

3rd = general anaesthesia

in the prehospital setting PR diazepam or buccal midazolam may be given

in hospital IV lorazepam is generally used. This may be repeated once after 10-20 minutes

If ongoing (or ‘established’) status it is appropriate to start a second-line agent

If no response to phenytoin (‘refractory status’) within 45 minutes from onset, then the best way to achieve rapid control of seizure activity is induction of general anaesthesia.

Question 38

4 Causes of combined UMN+LMN symptoms?

Answer 38

B12 deficiency

Cord compression (chord+roots) spondylitis/syringomyelia

Motor neurone disease

Freidreich’s ataxia - both cord and peripheral nerve involvement accompany cerebellar degeneration. These patients also have sensory loss, pes cavus and may have complications such as diabetes and hypertrophic cardiomyopathy

Question 39

3 scenarios for the 3 intracranial haemmorrhage types

Answer 39

1. Convex (lenticular) haematomas are seen in extradural haemorrhages
   as the blood is trapped between the dura and the skull. These most
   commonly occur as a result of trauma and rupture of the middle meningeal
   artery.
2. Crescent-shaped haematomas indicate the blood is between the dura and arachnoid. Subdural haemorrhages occur as a result of bleeding from bridging veins, more commonly seen in the elderly and alcoholics as the veins are stretched from cerebral atrophy.
3. Blood along the sulci and fissure indicates that it is located between the arachnoid and the pia. Subarachnoid haemorrhages present clinically as a thunderclap headache which may be associated with reduced GCS and seizures

Question 40

Herpes Simplex encephelitis px?

AI enceph hx?

Answer 40

CT head showing temporal lobe changes (hypodensities) - think herpes simplex encephalitis

Autoimmune encephalitis is typically the result of a paraneoplastic syndrome (usually secondary to small cell lung cancer or ovarian teratoma).

Question 41

Phenytoin SE’s?

Answer 41

Acute
initially: dizziness, diplopia, nystagmus, slurred speech, ataxia
later: confusion, seizures

Chronic
common: gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness
megaloblastic anaemia (secondary to altered folate metabolism)
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia

Idiosyncratic
fever
rashes, including severe reactions such as toxic epidermal necrolysis
hepatitis
aplastic anaemia
drug-induced lupus

Question 42

Lesions and their signs on examination

Answer 42

Cerebellar hemisphere - finger-nose ataxia

Basal ganglia - Hypokinetic (e.g. Parkinsonism) or hyperkinetic (e.g. Huntington’s)

Parietal lobe - sensory symptoms, dyslexia, dysgraphia

Frontal lobe - motor symptoms, expressive aphasia, disinhibition

Cerebellar vermis lesions = Gait ataxia

Question 43

Lateral medullary syndrome cause and px?

Basilar artery?

Webers syndrome?

Answer 43

The Posterior Inferior Cerebellar Artery (PICA) supplies the lateral medulla and occlusion of the left vessel will cause;

1. Left-sided Horner’s syndrome,
2. ataxia,
3. facial numbness with contralateral body numbness

Basilar artery = locked in syndrome

Webers = Branches if the PCA supplying the midbrain, occlusion causes;

Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity

Question 44

Lambert-Eaton sx + mx?

Caused by an antibody directed against presynaptic voltage-gated calcium channel in the peripheral nervous system.

Also which cancer is it associated with?

Answer 44

Opposite to MG - repeated muscle contractions lead to increased muscle strength

Autonomic symptoms(dry mouth, impotence, difficulty micturating),

Limb-girdle weakness (manifesting as a waddling gait),

Hyporeflexia

cancer = Small cell lung cancer

mx = pred/aza immunosuppression

Question 45

Difference between posterior and pontine stroke?

Answer 45

Pontine haemorrhage commonly presents with reduced GCS, paralysis and bilateral pin point pupils

Posterior = (ipsilateral?) cranial nerve palsy and contralateral motor and/or sensory deficits, nystagmus, cerebellar dysfunction, vertigo, or isolated homonymous hemianopia

Question 46

Difference between Wernickes and Korsakoffs?

Answer 46

Wernickes = classic triad of;

1. ophthalmoplegia/nystagmus, 2. ataxia
2. encephalopathy

Korsakoffs = amnesia + confabulation without any neurological signs!

Question 47

What clinical sign could be examined to further evaluate whether a lower leg weakness is an organic or functional presentation?

To rule in/out conversion disorder

Answer 47

Hoover’s sign of leg paresis is a specific manoeuvre used to distinguish between an organic and non-organic paresis of a particular leg. This is based on the concept of synergistic contraction.

If a patient is genuinely making an effort, the examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg. Noticing this is indicative of an underlying organic cause of the paresis.

If the examiner, however, fails to feel the ‘normal’ limb pushing downwards as the patient tries to raise their ‘weak’ leg, then this is suggestive of an underlying functional weakness, also known as ‘conversion disorder’.

Question 48

5 types of a/dysphasia?

wernickes
Brocas
Global
Anomic
Conduction

Answer 48

Broca’s aphasia results in non-fluent, laboured and halting speech.

Wernicke’s aphasia results in neologisms and nonsense sentences which is fluent.

Global aphasia causes severe expressive and receptive deficits.

Anomic aphasia is a deficit of expressive language which results primarily in word finding difficulties

Conduction dysphasia: speech fluent, but repetition poor. Comprehension is relatively intact

Question 49

When there is a mix of UMN and LMN signs in a patient, always consider Subacute degeneration of the chord. What is SCDC?

Answer 49

Subacute combined degeneration of the cord involves degeneration of the posterior and lateral columns of the spinal cord, often due to vitamin B12 deficiency.

Damage to the posterior columns - loss of proprioception, light touch and vibration sense (sensory ataxia and a positive Romberg’s test).

Damage to lateral columns - spastic weakness and upgoing plantars (UMN signs).

Damage to peripheral nerves - absent ankle and knee jerks (LMN signs).

Question 50

Cerebral abscess

Answer 50

Ix = CT scan

Mx:

surgery
a craniotomy is performed and the abscess cavity debrided

the abscess may reform because the head is closed following abscess drainage.

IV antibiotics: IV 3rd-generation cephalosporin(cefotaxime) + metronidazole

strep = cefuroxime + metro
staph = cefuroxime + floclox

intracranial pressure management: e.g. dexamethasone

Question 51

Syringomyelia

Answer 51

In Syringomyelia a fluid filled cyst forms in spinal cord and expands over time. This causes slowly progressive neurological symptoms. Syringomyelia is also associated with the Arnold-Chiari malformation (congenital issue where the lower part of the brain pushes down on the spinal chord)

Syringomyelia starts with the lack of pain sensation in the arms before giving
more prominent lower motor neuron weakness in the arms, and then later upper motor neuron weakness in the legs

Features
a ‘cape-like’ (neck, shoulders and arms)
loss of sensation to temperature but the preservation of light touch, proprioception and vibration

classic examples are of patients who accidentally burn their hands without realising
this is due to the crossing spinothalamic tracts in the anterior commissure of the spinal cord being the first tracts to be affected

spastic weakness (predominantly of the lower limbs)
neuropathic pain
upgoing plantars
autonomic features:
Horner’s syndrome due to compression of the sympathetic chain, but this is rare
bowel and bladder dysfunction
scoliosis will occur over a matter of years if the syrinx is not treated

Ix = full spine MRI with contrast to exclude a tumour or tethered cord

a brain MRI is also needed to exclude a Chiari malformation

Treatment will be directed at treating the cause of the syrinx.

In patients with a persistent or symptomatic syrinx, a shunt into the syrinx can be placed.

Question 52

How to tell the difference between bacterial and viral meningitis

Answer 52

Everything is more mild in viral meningitis!

Onset and Progression of Symptoms:

Bacterial Meningitis: Symptoms typically develop rapidly and progress quickly, often within hours. The condition can be severe and life-threatening.
Viral Meningitis: Symptoms generally have a more gradual onset, evolving over a period of days. The progression is usually less severe compared to bacterial meningitis.

Fever:

Bacterial Meningitis: High fever is commonly present, often exceeding 38.5°C (101.3°F).
Viral Meningitis: Fever is generally lower grade, often below 38.5°C (101.3°F).

Presence of Neck Stiffness:

Bacterial Meningitis: Neck stiffness (nuchal rigidity) is frequently observed and may be severe.
Viral Meningitis: Neck stiffness can be present but is typically milder compared to bacterial meningitis.

Severity of Headache and Other Symptoms:

Bacterial Meningitis: Headache is usually severe and persistent. Other symptoms may include nausea, vomiting, photophobia (sensitivity to light), and altered mental status.
Viral Meningitis: Headache is generally milder compared to bacterial meningitis. Other symptoms may include mild nausea, vomiting, and sensitivity to light.

CSF Analysis:

Bacterial Meningitis: Cerebrospinal fluid (CSF) analysis typically reveals elevated white blood cell count (predominantly neutrophils), increased protein levels, and low glucose levels.
Viral Meningitis: CSF analysis typically shows increased lymphocytes (lymphocytic pleocytosis), normal or slightly elevated protein levels, and normal glucose levels.

Other Clinical Signs and Symptoms:

Bacterial Meningitis: Patients may present with more severe signs, such as seizures, focal neurological deficits, altered consciousness, and petechial or purpuric rash.
Viral Meningitis: These severe signs are less common, and a rash, if present, is usually maculopapular and non-purpuric.