Psych / Neuro Flashcards

Question 1

Q

Neuroanatomy - blood supply to the brain

Answer

A

Circle of Willis - perfuses brain

Cerebral arteries - anterior, middle, posterior (all bordering the circle)
- ACA - supplies anterior & medial brain (frontal lobe + medial motor & somatosensory cortices) –> behavioural changes, weakness legs > arms, mild sensory defect
- MCA - supplies the lateral brain (lateral motor & somatosensory cortices, language - Broca & Wernicke’s, optic tracts) –> weakness face > arms > legs, aphasia (expressive/receptive), hemisensory defect, homonymous hemianopia
- PCA - supplies inferior & posterior brain (affecting visual cortex and tracts) –> homonymous hemianopia, visual agnosia/prosopagnosia
Major arteries giving rise to the circle of Willis:
- Vertebral artery (from the spine)
- Internal carotid artery (gives rise to A & M cerebral arteries)

Question 2

Q

UMN vs LMN:

Motorpathway name + route
UMN & LMN lesion causes and signs

Answer

A

Corticospinal tract = voluntary motor pathway for body:

Cortex - primary motor cortex (posterior frontal cortex)
Medulla - tracts from PMC converge and cross over = pyramids
Spinal cord - UMN synapases with LMN
Peripheral nerves - LMN innervates muscle

UMN lesions

Causes (anything affecting brain itself): stroke, SOL, MND, MS
Signs: hypertonia, hyperreflexia, spasticity (velocity/direction-dependent), upgoing plantars, pronator drift
NOTE: increased tone/reflexes as -ve feedback loop from the brain is removed

LMN lesions

Causes (affect peripheral nerves): MND, trauma, polio, GBS
Signs: hypotonia, hyporeflexia, muscle atrophy, fasciculations, fibrillations
NOTE: reduced tone/reflexes because no nerve supply

Question 3

Q

Intracranial bleeds - layers of the outer brain? types? Appearance on CT-head? Presentations?

Answer

A

Outer layers of the brain:

Skull > dura mater (adherent to inside of skull) > arachnoid mater > pia mater > brain parenchyma

Types:

Extradural haemorrhage- bleed between dura mater & skull
- Most common = skull fracture of pterion (temple) –> trauma to middle meningeal artery
- Hx: clear trauma –> transient LoC –> lucid interval –> ongoing headache –> reduced consciousness
- Convex (EGG) appearance on CT-head as blood sealed in by dura ± soft-tissue oedema outside skull (trauma site)
- Mx: A-E approach, refer to neurosurgery
  - Monitor GCS = deterioration
Subdural haemorrhage - bleed between dura & arachnoid mater
- Tearing of bridging veins going from outer surface of brain to dura mater
- Common in elderly + alcoholics (both have cerebral atrophy)
- Types: both concave (SICKLE) appearance on CT-head
  - Acute - assoc w/ trauma + blood white (hyperdense) on CT-head
  - Chronic - little/no Hx of head trauma e.g. fall several weeks ago and then not been normal since (elderly) + dark (hypodense) blood on CT-head
  - Reduced consciousness, if severe = focal neurology (esp. if midline shift)
- Mx: A-E, neurosurgery referral
  - Monitor GCS, reverse Warfarin
Subarachnoid haemorrhage - between arachnoid & pia matter
- Caused by an aneurysm (berry) or trauma
- Presentation: sudden-onset worst headache ever, photophobia, neck stiffness, kernig’s +ve
- CT (if + angio, -ve for MRI), LP 12hrs after Sx-onset (xanthochromia, not if raised ICP)
- Mx: A-E approach
  - Monitor GCS and neuro obs
  - Discuss with neurosurgery
  - Other – fluids, monitor Na, nimodipine
- Complications:
  - Vasospasm – presents like a stroke
  - Hyponatraemia – can be SIADH
  - Rebleed - coil ASAP if possible

Question 4

Q

Headache - types? Ix? Mx?

Answer

A

Types:

Tension - band-like, front of forehead, causes: dehydration, stress
Cluster - intense pain behind/around eye (worse @night + lacrimation & ptosis during attack), daily clusters for 4-6wks then nothing for months, M>F
- Mx: 100% O2 + nasal triptans
Migraine - intense/throbbing, focal, aura, photophobia
- Triggers: alcohol, chocolate, cheese, oestrogens (OCP)
- Mx:
  - Acute - simple analgesia, dark room + Triptans (take as soon as Sx start)
  - Prevent - trigger avoidance + propranolol/ topiramate (anticonvulsant, terratogenic) /amitriptytline (TCA)
Meningitis - generalised, moves down neck, neck stiffness + fever + rash (meningococcal)
- Ix: CT-head, LP (type of meningitis), BC (causative organism)
- Mx:
  - Suspected in primary care - IM/IV Benzypenicillin
  - Secondary care - IV Ceftriaxone ± Amoxicillin (infants/>50yrs)
  - If could be encephalitis (seizure/behavioural) - IV Aciclovir
SAH - sudden-onset, worst headache ever ± neck stiffness, can get preceding sentinel bleed (minor), assoc w/ PCKD (Berry aneurysm in Circle of Willis)/Marfan’s
- Ix: non-contrast CT –> LP for xanthochromia (after 12hrs)
- Mx: nimodipine (CCB, give every 4hrs, reduces vasospasm in cerebral arteries)
Giant cell (temporal) arteritis - vasculitis –> scalp tenderness, jaw claudication, vision loss, assoc w/ polymyalgia rheumatica (>50yrs)
- Ix: ESR, temporal artery biopsy
- Mx: high-dose Prednisolone (to prevent blindness, do not wait for biopsy)
Trigeminal neuralgia - electric shock-like pain on touching face (extremely tender)
- Divisions of trigeminal nerve (V2&3)
- Ix: MRI brain
- Mx: Carbamazepine (for pain), neurology referral
Raised ICP - worse at night/on waking/coughing/straining ± N&V, visual disturbances
- Mx: osmotic diuresis - mannitol/hypertonic saline
Cerebral Venous Sinus Thrombosis (VTE in the brain) - papilloedema, 6th nerve palsy, seizures, Cushing’s reflex (HTN, bradycardia, Cheyne-Stokes breathing)
- Ix: MRI w/ MR venography
- Mx: LMWH
Idiopathic intracranial HTN (IIH) - Obese, female, papilloedema, postural headache worse with straining/morning, assoc w/ OCP +/- visual changes & N/V.
- Ix: visual field testing, fundoscopy, MRI brain, LP (≥25 opening pressure)
- Mx: acetazolamide (carbonic anhydrase inh), weight loss, LPs + VP/LP shunt, ophthalmology follow-up

Question 5

Q

Cardiovascular accident (CVA) - Def? Presentation? DDx? Classification? Ix? Mx?

Answer

A

Def: better to use cardiovascular accident (CVA)

Stroke ≥24hrs, TIA ≤24hrs

Presentation:

Pyramidal weakness (flexors stronger than extensors in upper limb, opposite in lower limb), hypertonia, hyperreflexia
Hemiplegic/scissor gait –> circumduction
TIA: Amaurosis Fugax (black curtain)
- If ≥2 in 1wk = high risk of stroke –> ADMIT
- Aspirin 300mg + secondary prevention (as for stroke)

DDx:

Cerebral lesion - 80% ischaemic, 20% haemorrhagic (reduced GCS & raised ICP)
Neoplastic - SOL
Rare: syphilis, Todd’s paralysis (post-ictal), migraine, MS, cerebral abscess, rheumatological (arteritis)

Classification: Bamford aka Oxford

Total anterior circulation stroke: hemiplegia, homonymous hemianopia, higher cortical dysfunction
Partial anterior circulation stroke: 2/3
Lacunar circulation stroke: hemi-motor OR hemi-sensory stroke only
Posterior stroke: cranial nerve problems, eye-movement disorder, cerebella presentation
- Weber’s & Wallenberg’s (lateral medullary syndrome = posterior cerebellar artery infarct)

Ix:

BEFORE Tx = CT-head - 80% strokes ischaemic, 20% haemorrhagic (wrong Tx will make it much worse) –> haemorrhage has an area of hyperdense (white) bleeding
After initial Mx –> identify cause:
- Structural heart defect - echocardiogram
- AF - ambulatory ECG (24hr tape if no obv sign of AF as outpatient)
- Carotid atherosclerosis - carotid doppler –> carotid artery stenosis (70-99%) = carotid endarterectomy

Mx: A-E approach + URGENTLY contact stroke team –> dedicated stroke unit, if ischaemic:

Immediately:
- Aspirin 300mg OD + STOP anticoagulants (high risk of haemorrhagic transformation in first 2wks)
- <4.5hrs since Sx onset: thrombolysis (Alteplase = tPA)
  - C/I: any sign of active bleeding, very high BP, recent surgery, raised ICP
- >4.5hrs since Sx onset: conservative Mx:
  - BM - keep controlled <11 (sliding scale insulin)
  - NG tube (nutrition)
  - MDT - dietician, SALT, PT/OT
- < 6hrs (sometimes up to 24hrs, depending on size, area, damage) –> thrombectomy (neurosurgery)
After 2wks:
- STOP aspirin –> start clopidogrel 75mg OD + consider anticoagulation (e.g. if AF) - DOAC/Warfarin
- Manage vascular RFs (DM, HTN, QRISK etc.)

Question 6

Q

Parkinson’s disease definition? Cardinal Sx? DDx? Ix? Mx? Complications?

Answer

A

Def: a neurodegenerative disease of dopaminergic neurones of substantia nigra (part of basal ganglia in the midbrain)

Cardinal Sx (from extrapyramidal involuntary dysfunction): resting tremor, rigidity (cogwheeling due to superimposed tremor), bradykinesia, postural instability

+ insomnia, hypomimia (mask face), depression, autonomic dysfunction

DDx:

Benign essential tremor - bilateral, postural, FHx, alcohol improves it (in 50%)
Drug-induced (anti-psychotic, metoclopramide) - drug chart
MSA (multisystem atrophy) incl Shy-Drager (autonomic) - cerebellar signs
PSP (progressive supranuclear palsy) - loss of downward gaze
LBD (Lewy body dementia) - visual hallucinations + extrapyrimidal Sx & dementia present at same time (vs in Parkinson’s motor Sx 1yr before dementia)
Normal-pressure hydrocephalus - gait disturbance, cognitive impairment, impaired bladder control
Other:
- Corticobasal degeneration - single-arm signs, alien limb syndrome (myoclonus)
- Wilson’s disease (copper) - motor

Ix: clinical Dx –> dopaminergic agent trial ± MRI scan/DAT scan

Mx: problem = lack of dopamine in substantia nigra –> aim of Tx is to increase dopamine here

Dopamine agonist (cross BBB):
- Good for younger patients to reduce time on levodopa (as get very sensitised)
- Types:
  - Non-ergot - ropinirole, pramipexole - avoid below SEs = 1st line but still get dopamine dysregulation syndrome (hypersexuality & gambling)
    - SC Apomorphine for advanced disease
  - Ergot - cabergoline, bromocriptine –> retroperitoneal/pulmonary fibrosis
‘L-DOPA (levodopa) AND peripheral DOPA-decarboxylase inhibitor (Carbidopa)’ = Sinemet/Medapar
- Relevant physiology:
  - Substantia nigra contains dopaminergic neurones with DOPA decarboxylase (converts L-DOPA –> dopamine) - not happening as normal in Parkinson’s
  - Peripheral DOPA-decarboxylase in body
  - Chemoreceptor trigger zone (CTZ) –> triggers nausea & vomiting
- Drug explanation:
  - If give L-DOPA by itself it will be broken down by peripheral DOPA-decarboxylase into dopamine - this can’t cross BBB to reach substantia nigra but can reach CTZ –> nausea/vomiting
  - Instead, give L-DOPA with peripheral DOPA-decarboxylase inhibitor to allow more L-DOPA to cross BBB to reach dopaminergic neurones in substantial nigra to be converted to dopamine (some still reaches CTZ –> SE of nausea/vomiting)
- Other SEs: dyskinesia, on-off phenomena, postural hypotension
  - Amantadine - for dyskinesia secondary to levodopa
  - COMT inhibitors e.g. entacapone for tailing off betw/ doses of levodopa

Complications:

Falls, cognitive impairment, depression
Drool (SALT/glycopyrronium)
Meds SEs (e.g. vomiting)

Question 7

Q

Rigidity vs Spasticity

Answer

A

Rigidity (in Parkinson’s disease) = increased muscle tone, that is not velocity or direction-dependent

In Parkinson’s get Cogwheeling = rigidity overlayed by tremor

Spasticity (in Stroke) = increased muscle tone, that is velocity or direction-dependent

Flexors/extensors become imbalanced in strength - certain directions have increased muscle tone (not all) AND worse stiffness if move arm more quickly

Question 8

Q

Dementia - Types? Mx?

Answer

A

Types:

Alzheimer’s disease
- Progressive decline in cognitive function
- Mx: MMSE 23/30 diagnostic (Donepezil/Rivastigmine, <10 - Memantine)
Vascular dementia
- A stepwise decline in cognitive function
- Background of vascular disease (IHD, PVD)
Dementia with Lewy Bodies
- Triad - dementia, hallucinations, parkinsonism
- Balance - Parkinsonism = dopamine def vs hallucinations = dopamine excess - AChE for Sx control
Frontotemporal (Pick’s disease) - personality changes, early onset - Mx w/ benzos for behaviour/SSRI for depression
Depressive pseudodementia - disinterested, low mood

Other medications:
○ Antipsychotics if acutely agitated in dementia (be careful in Lewy body/Parkinson’s –> worsen EPSEs –> instead try PRN lorazepam)
○ Behavioural & Psychosocial Symptoms of Dementia (BPSD) –> Trazedone (antidepressant, sedative, increases appetite)

Question 9

Q

What are the nerve innovations for deep tendon reflexes in upper and lower limb neuro examination?

Answer

A

Nerve innovations:

S1,2 - buckle my shoe - ankle jerk (Achilles tendon)
L3,4 - kick the door - knee jerk (patellar tendon)
C5,6 - pick up sticks - biceps, brachioradialis reflex
C7,8 - lay them straight - triceps reflex

Question 10

Q

MRC Power Scale

Answer

A

1 flicker
2 is moves with gravity removed
3 is movement against gravity
4 is reduced power against resistance
5 is normal

Question 11

Q

Gait abnormalities vs normal

Answer

A

SUMMARY:

Normal gait cycle: 1) heel strike 2) foot flat 3) mid stance 4) heel off 5) toe-off
Antalgic gait - limping due to pain e.g. osteoarthritis, inflammatory joint disease, fracture, sciatica
Hemi/Diplegic gait - uni/bilateral circumduction of leg - CNS lesion (bilateral is called a ‘scissoring gait’)
Parkinsonian gait - shuffling gait, no arm swing - Parkinson’s/DLB/Antipsychotics
Ataxic gait - wide/broad-based stance & imbalance - Cerebellar/Vestibular/Sensory neuropathy
- NOTE: can’t do tandem walk
Neuropathic gait - high-step gait (from foot drop) - motor neuropathy e.g. L5 radiculopathy (e.g. herniated disc), common peroneal neuropathy, MS, Charcot-Marie-Tooth disease
- Can’t walk on heels
Myopathic gait - waddling/Trendelenburg gait (hip sways to one/both sides - hip abductor muscles weak) - muscular dystrophy/myopathy
Choreiform gait - involuntary movements - Basal ganglia disease e.g. Parkinson’s meds, Huntington’s, Wilson’s, Cerebral Palsy
Stomping gait - sensory neuropathy (loss of proprioception & vibration sense = dorsal column disease)
- Vibration –> proprioception (Romberg’s +ve) –> light touch (in order lost)
- Causes: SACD (subacute combined degen cord - B12), Friedrich’s ataxia, Tabes/taboparesis & tabes dorsalis (syphilis),
Marche à petit pas - small steps = normal pressure hydrocephalus

IN-DEPTH:

Normal gait cycle: 1) heel strike 2) foot flat 3) mid stance 4) heel off 5) toe off

Antalgic gait - limping due to pain

Causes: osteoarthritis, inflammatory joint disease, lower limb fracture, nerve entrapment (sciatica)

Hemiplegic gait - unilateral circumduction of leg to prevent dragging foot

CNS lesion –> unilateral weakness & spasticity (spastic flexion of upper limb vs extension of lower limb)
Causes - UMN lesion:
- Unilateral cerebral lesion e.g. stroke, SOL, trauma, MS
- Hemisection of spinal cord (trauma)

Diplegic gait - bilateral circumduction of legs (scissoring gait_)_

CNS lesion as above but bilateral clinical findings - spasticity worse in lower limbs vs upper limbs ± hyperreflexia, clonus, Babinski +ve, reduced power, sensory level if spinal cord pathology
Causes:
- Spinal cord lesion e.g. prolapsed intervertebral disc, spinal spondylosis, spinal tumour/infarct, transverse myelitis
- Bilateral brain lesion - cerebral palsy, MS, bilateral brain infarcts, midline tumour (paraspinal meningioma)
- MND - if also LMN findings (wasting, fasciculations)

Parkinsonian gait - shuffling gait

Loss of dopaminergic neurones in substantia nigra of basal ganglia –> extrapyramidal dysregulation = rigidity, bradykinesia, resting tremor, postural instability
Features of parkinsonian gait:
- Initiation - slow to start walking
- Step length - shuffling gait (short steps) & festinant gait (progressively smaller steps)
- Arm swing - reduced (early feature)
- Posture - flexed trunk & neck = stooped
- Turning - postural instability
Causes: Parkinson’s, Dementia w/ LBs, Parkinson’s plus syndromes (Multisystem atrophy & progressive supranuclear palsy), drug-induced (antipsychotics/emetics)

Ataxic gait - wide/broad-based stance (to maintain balance)

Assoc w/:
- Midline cerebellar disease (alcoholism/B12 def, MS, cerebellar stroke) - DANISH (dysdiadokokinesia, ataxia, nystagmus, intention tremor, slurred speech, hypotonia)
- Vestibular disease (labyrinthitis, Meniere’s, acoustic neuroma) - vertigo, N&V
- Sensory ataxia (peripheral neuropathy e.g. DM) - +ve Romberg’s, impaired proprioception, impaired vibration sense, lack of other cerebellar signs
Features of ataxic gaint:
- Stance - broad-based ataxic gait
- Stability - staggering, slow, unsteady –> veer towards side of lesion
- Turning - very difficult

Neuropathic gait - high-step gait (from foot drop)

Weakness in muscles of distal limb (foot dorsiflexors) - damage to peripheral nerves providing motor innervation –> foot drop & dragging toes –> knee & hip flex excessively to compensate
Other features: peripheral vascular disease, peripheral sensory impairment, reduced/absent reflexes
Causes: motor neuropathy
- Isolated common peroneal nerve palsy (trauma/compression)
- L5 radiculopathy (disc prolapse)
- Generalised polyneuropathy involving multiple nerves (DM, MND, Charcot-Marie Tooth disease)

Myopathic gait - waddling/Trendelenburg gait (hip sways to one/both sides)

Weakness of hip abductors –> can’t stabilise pelvis –> tilts down towards unsupported side
Assoc features: hard to stand from seat/squat/lying without arms, +ve trendelenburg’s sign (stand on one leg - if the hip on the side of the raised leg drops = +ve)
Causes: muscular dystrophy, myopathy (e.g. in hyperthyroidism, Cushing’s, acromegaly, Polymyalgia rheumatica)

Choreiform gait - involuntary movements

Oro-facial dyskinesia (grimacing/lip-smacking) & choreic mov of upper/lower limbs = dance-like/writhing @rest/mov
Causes: Basal ganglia disease
- Huntington’s, Sydenham’s chorea, Cerebal palsy (Choreiform type), WIlson’s disease, Dopaminergic meds (e.g. Parkinson’s)

Question 12

Q

Cerebellar syndrome causes?

Answer

A

MAVIS:

MS - eye (RAPD, INO), spastic paraparesis, catheterised
Alcohol - peripheral neuropathy, liver signs
Vascular (thromboembolic/haemorrhagic)
Inherited (Friedrich’s ataxia)
SOL
Other: hypothyroidism & paraneoplastic syndrome

Question 13

Q

MS - def? key features? DDx? Clinical courses? Ix? Mx? Poor prognostic features?

Answer

A

Def: evidence of damage to CNS that is separated in time & space

Key features:

Profile: young, female (catheter & walking aid/wheelchair), eye & cerebellar signs
Initial:
- Ipsilateral visual disturbance - greying/blurring ± pain on eye mov/loss of red colours
- Sensory phenomena - wetness/burning, uncomfortable band around the chest
  - Lhermitte’s sign - electric shock down neck and along spine & may radiate along limbs
  - Uthoff’s - neuro Sx worsen with increased temperature (hoff = hot)
UMN Sx: hyperreflexia, hypertonia, pyramidal pattern (arm flexors stronger, leg extensors stronger)
Dorsal column disease - reduced vibration, proprioception, Romberg’s +ve
Eyes:
- Internuclear ophthalmoplegia
  - Adduction paralysis and abduction nystagmus
  - From lesion in medial longitudinal fasciculus
- Optic nerve damage:
  - Colour & visual acuity loss, RAPD
  - Central scotoma (central blindspot), optic atrophy
- CN palsy (most commonly 6th - as longest)
Cerebellar signs (imbalance, can’t tandem walk)

DDx:

Cervical spondylosis - wo/ UMN signs but no cerebellar signs
Subacute combined degeneration of the cord (SACD) - dorsal columns & cerebellar - if low B12
Neuromyelitis optica aka Devic’s disease (IgG against aquaporin-4 channel) - optic neuritis & transverse myelitis but no cerebellar Sx

Clinical courses/patterns:

Relapsing-remitting - steady decline + strong flair
Primary progressive - steady decline without attacks
Secondary progressive - initial relapsing-remitting becoming primary progressive
Marburg variant - very severe, rapidly progressive

Ix:

Bedside:
- Fundoscopy (optic neuritis), full functional assessment (physio, OT)
- Nerve conduction studies - visual evoked potentials (VEPs) - if single nerve lesion, delayed response
Bloods - B12 (SACD), TFTs
Imaging:
- MRI (T2) head (lesions disseminated in time & space) - McDonald’s criteria
  - Periventricular white matter lesions
- LP: IgG oligoclonal bands, high protein

Mx:

Acute relapse: high-dose methylprednisolone (shortens acute attack) e.g. optic neuritis (painful eye mov + reduced visual acuity)
Long-term - MDT approach (physio, OT, SALT)
- Mobility - mobility aids, physio, OT
- INF-beta = disease modifying
- Spasticity –> Baclofen/Gabapentin (Dantrolene if CKD)
- Bowel (laxatives) & bladder (oxybutynin, LT catheter)
- Fatigue –> Amantadine
- Emotional lability –> Amitriptyline

Poor prognostic features:

Brainstem/cerebellar disease at onset
>40yrs at onset
Primary progressive MS (no resolution

Question 14

Q

Wernicke’s encephalopathy - Def? Sx triad? Mx - in hypoglycaemia and without? Complication?

How does delirium tremens present?

Answer

A

Def: Acute presentation of thiamine (B1) def
* Triad: confusion, ataxia, nystagmus
* NOTE: giving glucose without thiamine replacement can trigger Wernicke’s encephalopathy
* Complication = Korsakoff syndrome (chronic & permanent memory problems)

Delirium tremens: confusion, visual hallucinations, tachycardia, pyrexia

Question 15

Q

Spinal cord injury - RFs? Ix? First Mx?

Answer

A

RFs: atherosclerosis, hypotension, aortic aneurysm, aortic dissection

Ix:

Traumatic - CT-spine (bony injury/fracture)
Non-traumatic - MRI spine (soft tissue injury)

Mx: spinal immobilisation, manage in tertiary neurosurgical centre

Question 16

Q

What is Cushing’s triad? Indicates? Mx?

Answer

A

HTN, bradycardia, Cheyne-Stokes breathing

Indicates raised ICP (likely form herniation through foramen magnum)

Urgent referral to tertiary neurosurgical centre

Question 17

Q

Most common cause of SAH?

High SAH suspicion but normal CT - Ix?

How do you reduce risk of ischaemia afterwards?

Answer

A

Berry aneurysm (85%)

LP in 12hrs for xanthochromia (yellow from bilirubin in CSF - RBC breakdown)

Nimodipine

Question 18

Q

Neurology Ix depending on UMN/LMN signs?

Answer

A

ALL: involve MDT for full functional assessment (physio & OT)

UMN:

Imaging (brain ± spinal cord)
CSF (LP)
Brain biopsy

LMN:

Nerve conduction studies & electromyography (NCS & EMG)
Bloods (metabolic, abs)
Muscle/nerve biopsy

Question 19

Q

GBS Ix? Mx?

Answer

A

Ix:

Bloods (metabolic, abs), CT –> LP ± MRI spine (exclude other causes)
Nerve conduction studies

Mx: ADMIT suspected cases - normally self-limiting course

MDT - psychologist, SALT (if speech muscles affected)
Plasmapheresis (plasma exchange)
High-dose IVIG
DVT prophylaxis

Question 20

Q

MND - Presentation? DDx? Types of MND? Dx? Mx? Complications?

Answer

A

Presentation: mixed UMN/LMN (no sensory deficits, no eye involvement)

UMN in lower limbs (spasticity, hyperreflexia, upgoing plantars)
LMN in upper limbs (hypotonia, hyporeflexia, fasciculations, wasting)
Bulbar/pseudo-bulbar tongue/speech (tongue fasciculations, palatal paralysis, nasal speech)
NORMAL SENSORY EXAM

DDx mixed signs:

Dual pathology (stroke + peripheral neuropathy)
Conus medullaris lesion - painful, assoc with traumatic spinal injury/higher up mets)
B12 def (subacute combined degen of spinal cord) = cofactor in myelination (as is folate)

Types:

Amyotrophic lateral sclerosis (60%) - classic (UMN & LMN)
Progressive Bulbar Palsy (30%) - CN 9-12 –> dysarthria (speech), dysphagia (swallowing)
Primary Lateral Sclerosis - pure UMN onset
Progressive Muscular Atrophy - pure LMN onset, ‘flail limb’ appearance

Dx: clinical, exclude other causes

EMG/NCS (nerve conduction study) - chronic nerve root denervation
Imaging - MRI (cervical, thoracic, lumbar spine) - exclude other causes

Mx: no cure - MDT approach

Conservative - SALT (swallowing), physio & OT
Sx-control:
- Quinine - muscle cramp
- Anticholinergics e.g. hyoscine patches - drooling
- Exercise & nutrition
Prognostic:
- Riluzole - glutamate antagonist (extend life expectancy by 3-5 months)
- NIV - if respiratory muscles no longer functioning

Complications: resp compromise, frontal lobe dementia (2%)

Question 21

Q

How to remember nerve innervation of the diaphragm? Nerve associated?

Answer

A

C3,4,5 keep the diaphragm alive

Phrenic nerve

Question 22

Q

Raised ICP - what is the Monro-Kellie Doctrine? Causes? Signs? Mx?

Answer

A

Monro-Kellie Doctrine: skull is a closed box, the sum of volumes of brain, CSF & IC blood is constant - increase in one should cause a decrease in one/both of others

In brain there is little wiggle-room, the only weak point is the foramen magnum –> herniation = coning –> death

Causes: IC haemorrhage (IC blood), tumour, (brain vol), cerebral oedema (CSF)

Signs:

Acute (pressure on brainstem): CUSHING’S TRIAD (HTN, bradycardia, irregular breathing) + reduced GCS
Chronic: long-term headache

Mx:

Conservative: sit up, hyperventilated (if intubated –> reduce pCO2 –> reduce vasodilation in brain)
Medical: mannitol (osmotic diuretic), hypertonic saline –> both draw fluid out of brain –> reduce ICP
URGENT neurosurgical input –> Burr hole surgery

Question 23

Q

Cauda equina - def? Sx? Causes? Key Ix? Mx?

Answer

A

Def: compression of Cauda Equina (nerve fibres below L1-2)

Sx: can you feel it while you urinate/when you tug on catheter?

Severe back pain
Saddle anaesthesia (numb around the anus)
Bladder/bowel dysfunction (urinary retention, faecal incontinence)
Lower limb weakness
Reduced anal tone (on PR exam)

Causes: large disc herniation, cancer, trauma, abscess, haematoma

NOTE: if likely mets e.g. background of prostate cancer –> 16mg Dexamethasone (reduces swelling)

Ix: urgent MRI scan (+ PR exam)

Mx:

In normal disc herniation (above cauda equina):
- Get the patient to keep moving (or muscles will seize up)
- Analgesia - PR Diclofenac (neuropathic pain) + Diazepam
In cauda equina –> urgent referral to neurosurgery for decompression/laminectomy

Question 24

Q

Spinal cord compression Ix & Mx for malignancy?

Answer

A

Ix: MRI whole spine (often multifocal lesions)

Mx:

1st line = surgical decompression (if localised, fit enough)
2nd line = radiotherapy (external beam radiotherapy)

Question 25

Q

Meningitis & encephalitis - presentation? causes? Ix? Mx?

Answer

A

Meningitis:

Presentation: headache, fever, photophobia, neck stiffness
Causes:
- Bacterial – N. meningitides, S. pneumo (TB; neonates/elderly – GBS/Listeria/E.coli) – Listeria also more common in alcoholics
- Viral – enterovirus (Coxsackie, echovirus), mumps, HSV2
- Fungal – cryptococcus neoformans (chr)
Ix: A-E, BC, CT head, LP (CT first, if raised ICP –> LP would cause coning)
- Kernig sign - flex knee & hip to 90 degrees –> extend knee (painful & limited extension)
- Brudzinski sign - raise head while flat –> hip & knee flexion
Mx: bacterial – IV ceftriaxone ± amoxicillin (Listeria - neonate/elderly)
- IM BenPen for possible meningococcal infection (rash) in GP setting before sending to the hospital
- Viral – supportive (self-limiting)
- Altered consciousness (encephalitis?) –> add IV acyclovir

Encephalitis:

Presentation: headache, fever, seizures, drowsiness, confusion (viral HSV1 affects temporal lobes –> affecting consciousness)
Ix: BC, CT head, LP
Mx: IV acyclovir ± anti-convulsants

Question 26

Q

Sensory ataxia vs Cerebellar ataxia based on Romberg’s test?

Answer

A

Postural imbalance/swaying:

When eyes open & closed = Cerebellar ataxia
When eyes are closed = sensory ataxia (somatosensory nerve affected)
- Dorsal column loss: Tabes dorsalis (syphilis), SCDC (B12), MS
- Sensory peripheral neuropathy

Question 27

Q

Spinal cord anatomy

Answer

A

Dark matter middle (cell bodies = synapses) –> white matter on the outside (neurone tracts)

Sensory pathways (ascending - goes up):

Dorsal columns (posterior) - fine touch, vibration, proprioception
- Sensory receptors - 1st order neurone up spinal column along ipsilateral side
- At the medulla oblongata - synapses with 2nd order neurone that crosses the midline (decussation)
- At the thalamus synapses with 3rd order neurone to the Primary Somatosensory cortex
Spinothalamic tracts (anterior) - pain & temperature
- Nociceptors (pain) - 1st order neurone to Substantia Gelatinosa within grey matter of spinal cord
- Synapses with 2nd order neurone & immediately crosses midline (decussation) to ascend spinothalamic tract
  - NOTE: spinothalamic tracts decussate at the level the neurone enters the spinal cord
- At the thalamus synapses with 3rd order neurone to the Primary Somatosensory cortex
(Spinocerebellar tracts (lateral) - proprioceptive info to cerebellum)

Motor pathways (descending - goes down):

Corticospinal tracts (anterior = trunk, neck, shoulders; lateral - limbs) - voluntary motor control (from primary motor cortex)
- From the Primary Motor Cortex - UMN goes to the Medulla and crosses over (decussation)
- At the anterior horn for each spinal level synapses with LMN–> muscle
- NOTE: at any spinal level will be LMNs exiting the spine and UMNs that travel down further before synapsing with their respective LMN
  - SO cord pathology above the level of Cauda Equina –> some UMN & LMN signs

Question 28

Q

Epilepsy - def? types & Tx? Status epilepticus def & Mx?

Answer

A

Def: tendency to have recurrent, unprovoked seizures

Seizure = episodes of abnormal uncoordinated excessive brain activity
- Provoked seizures = consequence of inf/drugs
- Unprovoked = epilepsy
Definition of epilepsy: ≥2 unprovoked seizures >24hrs apart OR ≥1 unprovoked seizure AND probability of further seizures OR Dx epilepsy syndrome

Types:
* Generalised (whole brain):
* Tonic-clonic, Tonic, Atonic, Myoclonic –> Tx: Na Valproate (AVOID in girls/women of childbearing age)
* Absence (EEG - spike & wave pattern, Jeavons syndrome - myoclonic absence/eyelid myoclonia) –> Tx: Ethosuximide/Na Valproate
* Focal - aware (conscious) OR impaired awareness (impaired consciousness)
* Tx: Lamotrigine

General management:
* First seizure clinic - while waiting avoid trigger factors (sleep, caffeine, alchohol), stop driving and avoid dangerous activities + shower > bath
* Drugs see above
* For women:
* Contraception - medroxyprogesterone acetate inj or IU methods (Cu-IUD or LNG-IUS), other methods interact with epilepsy meds
* Pregnant - risk to child but dangerous to stop meds - avoid Na Val if at all possible

Status epilepticus = >5mins/repeated seizures without full recovery in between
* 1st - IV lorazepam 4mg –> repeat
* 2nd - phenytoin infusion
* 3rd - general anaesthesia
* If no IV access –> buccal midazolam (or rectal diazepam)
* Recovery position once seizure stop

Question 29

Q

Lumbar disc herniation vs lumbar spinal stenosis - presentation? Ix? Mx?

Answer

A

Presentation

Disc herniation - acute unilateral radiculopathy (pain & numb in specific dermatome/weakness in muscle group)
- Straight leg raise +ve
- Worse on flexion (bending over/sitting)
Spinal stenosis - insidious neurogenic claudication (intermittent back pain worse on walking/standing) ± pain radiating down leg/leg paraesthesia
- RFs: rev back injury/surgery, manual labour
- Worse on extension (standing/walking)

Ix:

Disc herniation - erect lumbar x-ray & MRI spine
Spinal stenosis - plane x-ray, MRI (T2-weighted)

Mx: surgical decompression

Question 30

Q

Brain anatomy “rules” summary - cerebellar, motor nerves, dorsal columns, spinothalamic tract

Clues to localisation - cortical, basal ganglia, cerebellar, nerve root

Answer

A

Cerebellar signs ipsilateral

Motor nerves travel laterally in brainstem & cross @medulla

Dorsal columns are posterior & cross @medulla

Spinothalamic tract is anterior in spinal cord & cross in spinal cord

Localisation:

Cortical - UMN pyramidal signs (hypertonia, hyperreflexia, babinski)
Basal ganglia - rigidity, tremor, bradykinesia
Cerebellar - DANISH (dysdiadokokinesia, ataxia, nystagmus, intention tremor, slurred speech, hypotonia)
Nerve root (dermatome/myotome)/single nerve - LMN signs (hypotonia, hyporeflexia, fasciculations, wasting, sensory loss)

Question 31

Q

Myotonic dystrophy - presentation? Assoc? Ix? Mx?

Answer

A

LMN presentation = muscle pathology

Face:
- Myopathic facies (sunken cheeks, bilateral ptosis, expressionless)
  - Wasting of facial & muscles of mastication
- Frontotemporal balding
Distal wasting, weakness w/ loss of ankle jerks
Associations: cataracts, dysphagia, cardiac (cardiomyopathy, heart block), DM, hypogonadism (gynaecomastia/testicular atrophy)
Exam - failure of immediate relaxation after voluntary contraction
- Percussion myotonia - tap thenar eminence and thumb contracts
- Slow-releasing grip - SHAKE HANDS (or make a fist and then spread fingers quickly or squeeze eyes shut and open quickly)

Ix:

Conservative: full functional assessment (incl. SALT), lung function tests (NM resp insufficiency), ECG/echo (CMO/HB), slit lamp (cataracts)
Bloods - BM (DM assoc), CK, genetic testing
Imaging & invasive:
- Electromyography (EMG) - ‘dive-bomber’ potentials
- Muscle/nerve biopsy

Mx: MDT approach

Phenytoin for myotonia, weakness has no Tx
Genetic counselling - AD w/ genetic anticipation (trinucleotide repeat - worse severity/earlier presentation with each generation)
Avoid statins (can cause myopathy)

Question 32

Q

Ptosis causes?

Answer

A

Bilateral:

MG
Myotonic dystrophy
Tabes dorsalis (syphilis) = Argyll-Robertson pupil

Unilateral:

3rd nerve palsy (down & out, dilated, ptosis)
Horner’s syndrome (ptosis, meiosis, anhydrosis)

Question 33

Q

Myasthenia Gravis Vs Lambert-Eaton Myasthenic Syndrome (LEMS)

Def? presentation? Assoc? Ix? Mx?

Answer

A

Myasthenia Gravis

Def:
- Chr AI disorder of post-synaptic membrane of NMJ in skeletal muscle
- Abs to AChR on post-synaptic membrane
Presentation:
- Muscle fatiguability incl dysphagia, rarely SoB
- Eyes - bilateral ptosis (and compensatory increased frontalis muscle activity = raised eyebrows), diplopia
- Face - dysarthria (slurred speech), facial paresis
- Curtain sign - when raising one upper eyelid the other one drops down
- Assoc: thymomas (in the chest)
Ix:
- Abs: AChR (on post-synaptic membrane), MUSK abs
- Serial pul funct tests (FVC & negative inspiratory force)
  - NOTE: do not wait for ABG findings - late in course
- CT-chest (for thymoma)
Mx:
- Acetylcholinesterase inhibitors (Pyridostigmine) + IS (azathioprine)
- IVIG/Plasmapheresis
- Surgery - thymectomy
Myasthenic crisis = acute respiratory failure - FVC <1L, negative inspiratory force (NIF) ≤20cm H2O, need mechanical ventilatory support
- Accessory muscle use indicates sign inspiratory muscle weakness
- Weak cough indicates sign expiratory muscle weakness
- ABG often shows hypercapnia before hypoxia
- Low threshold for endotracheal intubation (rapid deterioration of bulbar & resp muscles)
- Mx: intubation + mechanical ventilation (& Mx above)

Lambert-Eaton Myasthenic Syndrome (LEMS)

Def: rare AI disorder of NMJ
- Pre-synaptic membrane Ab to voltage-gated Ca-channel receptors
- 40% occur as paraneoplastic disorder assoc w/ SCLC
Presentation:
- Limb weakness - proximal legs –> proximal arms e.g. waddling gait
  - STRONGER WITH USE (vs MG get’s weaker with use)
- Hyporeflexia, NO eye involvement (compared to MG)
- Autonomic disturbance - dry mouth (& orthostatic hypotension, sweating, GI & urinary problems, visual blurring, sexual dysfunction)
- Associated with: small cell lung cancer (SCLC)
Ix:
- Nerve conduction studies, EMG, serial PFTs
- Ab testing (Voltage-gated Ca-channels & AChR-abs)
- CT chest (SCLC)
Mx: MDT support
- Tx underlying cause, Amifampridine
- IVIg/plasma exchange
- Supportive care

Question 34

Q

Hammertoes can be seen in what condition? Presentation? What do I need to check for to exclude DDx? DDx? Types? Ix? Mx?

Answer

A

Hammertoes - bilateral, symmetrical, distal wasting of small muscles of feet

Advanced = dorsal guttering from distal wasting, wasting of extensor digitorum brevis at inferior border of lateral malleolus
Similar can be seen in the hands = wasting of first dorsal interosseus

Sign of Charcot-Marie-Tooth disease aka hereditary motor & sensory neuropathy (HMSN)/peroneal muscular atrophy (PMA)

Hx ankle sprains & scoliosis
Motor & sensory losses (sensory milder) = classic peripheral neuropathy
- LMN pattern of weakness:
  - Motor loss in anterolateral compartments of legs (ankle dorsiflexion & toe extension)
  - Absent reflexes (plantar reflexes show no response)
- Sensory loss in glove & stocking distribution bilaterally
Pes cavus ± palpable common peroneal nerve, thickened nerves @medial malleolus
High stepping (foot drop) & ataxic gait
- Test for foot drop = heel walking

What do I need to check for? NO scars over fibula (would indicate peroneal nerve damage from trauma e.g. car accident)

DDx:

Common peroneal nerve palsy (inversion of foot normal)
Sensory peripheral neuropathy: B12-def (SACD), Alcohol, DM, Hypothyroid (vitiligo?), HIV, drugs
Motor peripheral neuropathy: lead poisoning

Types:

Type 1 - demyelination, AD
Type 2 - axonal, AD/AR
Type 3 - demyelination, AR & presents as infant

Ix: full functional assessment, FHx, nerve conduction studies, genetic testing

Mx:

Physio, walking aids with ankle & foot supports (e.g. foot splint)

Question 35

Q

Wasting of hand muscles - distinguishing different nerves?

Answer

A

Hand muscle wasting - dorsal guttering = first to be affected in ulnar lesions

First dorsal interosseous (next to thumb) = ulnar nerve
Abductor policies brevis (thenar eminence) = median nerve
Weakness of both - suspect T1 radiculopathy
NOTE: ulnar nerve innervates most of the intrinsic muscles of hand except median nerve serves LOAF: 2 radial Lumbricals, Opponenes pollicis, Abductor pollicis brevis & Flexor pollicis brevis

Ulnar nerve palsy = claw hand @rest (4th & 5th fingers in extension at MCP, flexion at PIP/DIP)

Commonest site of lesion = elbow (arthritis @wrist & elbow)
Froment’s sign (weak adductor pollicis brevis –> thumb flexion) = +ve if thumb arches to hold paper = ulnar nerve palsy
Ulnar paradox - higher lesion causes lesser deformity as lower lesions spares flexor digitorum profundus (causes flexion at DIP)

Median nerve palsy = sign of benediction on asking to close hand (thumb, index finger can’t close, middle finger can close partially)

Look for sensation over thenar eminence –> if lost can’t be carpal tunnel syndrome (still median nerve palsy but arises proximally to carpal tunnel)
Bilateral carpal tunnel syndrome causes: Acromegaly, Amyloid (periorbital purpura after sneezing), DM, Hypothyroid, pregnancy

Question 36

Q

Muscle weakness causes by location?

Answer

A

Brain: stroke, SOL, MS

Spinal cord: MS, trauma, disc herniation/spinal stenosis, spinal cord infarct, syringomyelia

MS - weakness & paraesthesia based on UMN demyelination, disseminated in time & space
- Optic neuritis, periorbital pain, RAPD, INO (damage to medial longitudinal fasciculus)
- Ataxia, vertigo, chr constipation, blaadder dysfunct
- Lhermitte’s sign - electric shock down back on neck flexion
- Unhthoff’s phenomenon - worsening of Sx with increased body temp e.g. exercise, hot shower
- Ix: MRI (brain & spinal cord) + LP (oligoclonal bands), nerve conduction study (evoked potential)
- Mx: methypred for flare, INF-b long-term
Trauma - extremity weakness wo/ cortical signs/facial weakness e.g. hemisection of spinal cord (Brown-Sequard syndrome) - below level of lesion:
- Ipsilateral hemiparesis & loss of vibration/proprioception
- Contralateral loss of pain & temperature
- At level of lesion - loss of sensation + flaccid paralysis of muscles supplied by this spinal cord segment
Herniated disc/spinal stenosis - weakness at level of lesion & lower extremities + bladder/bowel dysfunction + sciatica
Spinal cord infarct - occlusion of anterior spinal artery (complication of aortic surgery)
- Affects anterior 2/3 spinal cord in affected segment
  - Sudden-onset bilateral flaccid paralysis –> developing into spastic paralysis after several days
  - Loss of pain & temp
  - Light-touch, vibration & proprioception-sense spared (dorsal columns not involved)
Syringomyelia - developmental disorder
- Syrinx (cavity) grows from centre of spinal cord & spreads outwards
- Normally affects cervical cord but can extend into brainstem
- Early - bilateral loss of pain & temp in cape-like distribution affecting neck, shoulders, upper arms
- Late - as syrinx expands anterior horn cells affected –> bilateral flaccid paralysis

Anterior horn (motor neurone lesions): MND, poliomyelitis

Poliomyelitis - enterovirus infection attacking anterior horn cells
- 1-2wks prodrome (fever, headache, N&V)
- Asymmetrical weakness + can develop years after inf (post-polio syndrome) + can take place after taking live-attenuated polio vaccine
MND
- Mixed UMN/LMN presentation
- Ix (exclude other causes): EMG/NCS, MRI - whole spine
- Mx: no cure - MDT approach (SALT (swallowing), physio & OT)
- Sx-control:
  - Quinine - muscle cramp
  - Anticholinergics e.g. hyoscine patches - drooling
- Prognostic:
  - Riluzole - glutamate antagonist (extend life expectancy by 3-5 months)
  - NIV - if respiratory muscles no longer functioning

Neuropathy: diabetic neuropathy

Polyneuropathy (multiple nerves): DANG My THeRAPIST
- Diabetic neuropathy (most common, T1/2)
  - Sensory - glove & stocking loss of sensation/paraesthesia
  - Motor - same distribution as above + CN palsies (3rd - pupil-sparing)
  - Autonomic - orthostatic hypotension, constipation, erectile dysfunction
- Alcoholic neuropathy (2nd most common)
- Nutritional (B1/6/12 def)
- GBS (AIDP - acute inflam demyelin polyneuropathy)
  - AI demyelination of peripheral nerves
  - 2-4wks post-inf e.g. diarrhoea with C. jejuni
  - Ascending weakness in distal lower extremities over hrs/days (worst after 4wks)
  - Flaccid paralysis with reduced/absent deep tendon reflexes
    - Can involve diaphragm –> resp failure
    - Bilateral facial nerve palsy
    - Difficulty swallowing –> aspiration
  - Autonomic dysfunction - sweating, orthostatic hypotension, urinary retention
  - NOTE: sensory Sx rare
  - Ix:
    - LP (high protein, normal WCC)
    - NCS & EMG (reduced conduction velocity)
    - Serum abs (anti-glycolipid abs)
  - Mx:
    - Monitor FVC <1L, NIF <20cm H2O –> intubate + mechanical ventilation
    - Monitor BP –> IV fluids for hypo, Labetalol for hyper
    - IVIG, plasma exchange
- M(y)-edications (colchicine, cisplatin, isoniazid –> niacin def)
- Toxins (lead)
- Hereditary - HMSN (CMT)
  - Progressive hereditary (AD) motor & sensory neuropathy (HMSN)
  - Distal back & lower extremity weakness:
    - Foot drop (damage to common peroneal nerve)
    - High-arch foot (pes cavus) - does not flatten with weight-bearing
    - Scoliosis
  - ± pain & sensory loss (can lead to foot ulcers)
  - Ix: nerve conduction study + EMG, genetic testing (electrophoresis/FISH)
  - Mx: physio, walking aids, foot & heel-support
- Renal failure (uraemic nephropathy)
- Amyloidosis
- Porphyrias
- Inf (HIV, syphilis)
- Systemic (hypothyroidism)
- Tumours (multiple myeloma)
Mononeuropathy (one nerve):
- Facial nerve palsy - not forehead-sparing, crying/sensitive to noise/abnormal taste (ant 2/3 tongue)
  - Idiopathic = Bell’s palsy
  - Secondary:
    - Lyme disease
    - Ramsay-Hunt syndrome - HZV reactivation in the geniculate ganglion, causes painful eruption in auditory canal
    - Tumours - acoustic neuroma, parotid
    - Bilateral palsy - Sarcoidosis, GBS
  - Tx: treat cause or if Bell’s palsy –> pred within 72hrs Sx onset + eye protection
- Carpal tunnel syndrome - entrapment of median nerve in flexor retinaculum
  - Repetitive use of wrist –> numbness & tingling in lateral 3 fingers (& 1/2 4th finger) –> weakness of thenar muscles
  - Tinel’s sign - tap nerve at wrist
  - Phalen’s sign - reverse prayer sign for 60s
  - Ix: EMG, wrist USS, MRI wrist (imaging to detect SOL e.g. ganglion cyst)
  - Tx: immobiliser wrist (splint), CS injection, carpal tunnel release

Neuromuscular junction: MG/LEMS

Myasthenia gravis (MG) - AI condition where Abs attach to NMJ post-synaptic nicotinic AChR in skeletal muscle
- FATIGUABILITY with use
- Initial - oculobulbar weakness (diplopia, ptosis, dysphagia, nasal voice)
- Chr:
  - Asymmetrical proximal limb muscle weakness
  - Resp muscle failure
- Assoc w/ thymic hyperplasia/thymoma
- NOTE: normal sensation, normal deep tendon & pupillary reflexes
- Ix:
  - Serological testing: AChR, MUSK abs
  - Repetitive nerve stimulation (CMAPs decrease)
  - CT chest - thymoma
  - Monitoring with serial pul funct tests (FVC & negative inspiratory force) if suspect myasthenic crisis
- Mx:
  - Acetylcholinesterase inhibitors (Pyridostigmine) + IS (azathioprine)
  - Surgery - thymectomy
- Myasthenic crisis = acute respiratory failure - FVC <1L, negative inspiratory force (NIF) ≤20cm H2O
  - Often trigger - meds/inf
  - Accessory muscle use/weak cough = sign. exp muscle weakness
  - Mx: intubation + mechanical ventilation (& Mx above)
    - IVIG/Plasmapheresis
    - Stop pyridostigmine (increases secretions –> aspiration risk), stop trigger (meds)
- Cholinergic crisis - same presentation as above (resp muscle weakness) BUT cause = excess pyridostigmine –> overstimulation of AChR –> eventually stop working
  - Pyridostigmine also binds to nicotinic receptors –> cholinergic Sx - SLUDGE (Salivation, Lacrimation, Urination, Diarrhoea, GI cramps, Emesis)
  - Mx: intubation + mechanical ventilation
    - Atropine (anti-muscarinic) for Sx but does not address resp weakness
    - Reduce dose of pyridostigmine
Lambert-Eaton myasthenic syndrome (LEMS) - AI condition where Abs target pre-synaptic voltage-gated Ca channels –> reduces release of ACh from presynaptic vesicles
- Proximal muscle weakness - IMPROVES with use
- Reflexes reduced/absent, ± autonomic Sx
- Assoc w/ SCLC, Hodgkin’s lymphoma
- Ix:
  - NCS, repetitive nerve stimulation (CMAPs increase)
  - Serological testing: VGCC abs
  - CT chest (SCLC)
- Mx: Tx underlying cause, Amifampridine
  - IVIg/plasma exchange
  - Supportive care incl. intubation + mech ventilation (if resp compromise)

Myopathy: dermatomyositis

Inflammatory: proximal muscle weakness & pain
- Dermatomyositis - skin rash (heliotropic rash & Gottron’s papules)
- Polymyositis
- Assoc: ILD - in 10% patients
- Ix: CK, ab panel (anti-Jo-1, ANA)
  - EMG, muscle MRI + muscle biopsy
- Mx:
  - Induction: CS (PO/IV) ± IVIg
  - Maintenance: IS (methotrexate/azathioprine) ± IVIg
Inherited:
- X-linked - Duchenne’s & Becker’s muscular dystrophy
- AD - Myotonic dystrophy
  - Myopathic facies (facial wasting) + frontal balding
  - Distal wasting & weakness + loss of ankle jerk
  - Assoc: cataracts, dysphagia, cardiac, DM, hypogonadism
  - Exam - failure of immediate relaxation after voluntary contraction
    - Percussion myotonia - thumb contracts tapping thenar eminence
    - Slow releasing grip on shaking hands
  - Ix: CK, genetic testing, EMG ‘dive-bomber’ potentials, muscle biopsy
  - Mx: MDT approach
    - Phenytoin for myotonia, weakness has no Tx
    - Genetic counselling - trinucleotide repeat -severity/earlier with each generation
    - Avoid statins (can cause myopathy)
Endocrine:
- Hypothyroidism - proximal muscle weakness & pain, deep tendon reflexes decreased, myoedema (swelling on percussion)
- Also possible in Addison’s Cushing’s, Vit D def
Meds - statins (proximal muscle weakness & pain), glucocorticoids (muscle weakness)
Ix: serum CK, TSH lvls, EMG

Question 37

Q

Idiopathic inflammatory myopathies (IIMs) - RFs? Presentation by type? Ix? Mx?

Answer

A

RFs:

Exposure to high-intensity global UV radiation
Treatment w/ lipid-lowering agents, D-penicillamine (Tx for RA)
HIV, prev inf/vaccine

Presentation:

Overall: insidious/acute symmetrical muscle weakness of proximal arm & leg –> difficulty getting out of chair/climbing stairs
Dermatomyositis - acute, proximal muscle weakness + rash:
- Heliotropic rash (purple discolouration of upper-eyelids)
- Gottron’s papules (erythema over knuckles)
Polymyositis - subacute, proximal muscle weakness, no rash
Inclusion body myositis (IBM) - slowly, proximal & distal muscle weakness + muscle atrophy (quadriceps, distal wrist & finger flexor)
Assoc:
- ILD - in 10% patients with dermatomyositis/polymyositis
- Malignancy (ovarian, pancreatic, NH lymphoma, lung, bladder)
- AI disease

Ix:

Bloods: CK, ANA/myositis ab panel (anti-Jo-1)
Imaging: MRI of involved muscle, electromyogram (EMG), muscle biopsy

Mx:

Induction: CS (PO/IV) ± IVIg
Maintenance: IS (methotrexate/azathioprine) ± IVIg

Question 38

Q

Proximal muscle weakness causes?

Answer

A

CONGENITAL MIND

CONGENITAL - mitochondrial
Metabolic - Cushing’s, hypothyroidism
Inflammatory - dermato/poly/inclusion body myositis
Neuromuscular - MG/LEMS
Dystrophy - Becker

Question 39

Q

UMN pattern of weakness - causes?

Answer

A

Bilateral = 3Ms

MS
MND (normal sensation)
Myelopathy (sensory level) - SOL, cervical myelopathy, disc prolapse, transverse myelitis, syringomyelia

Unilateral:

Intracranial - CVA, SOL, MS
Brainstem - MS
Spinal cord - trauma, SOL, haemorrhage

Question 40

Q

Mononeuritis multiplex causes?

Answer

A

Vasculitis - GPA, EGPA, microscopic polyangiitis, polyarteritis nodosa

Rheum - RA, SLE, Sjogren’s, Sarcoidosis

Question 41

Q

Causes of absent ankle jerk reflex AND extensor plantar response?

Answer

A

MND

B12 - SCDC (subacute combined degeneration of the spinal cord)

Friedrich’s ataxia (cause of cerebellar syndrome)
* Most common inherited AR ataxia in UK
* Degen disease affecting heart and nervous system - assoc w/ DM & cardiomyopathies
* Onset before 20yrs
* PC: unsteady gait +/- pes cavus/scoliosis -> prog ataxia, dysarthria (slurred speech), decreased proprioception/vibration-sense/muscle weakness

Syphilitic tabo-paresis

Question 42

Q

Normal Pressure Hydrocephalus Overview

Answer

A

Normal Pressure Hydrocephalus - distended ventricles distort central corona radiata (incl sacral motor fibres innervating legs/bladder)

PC: elderly pt with slow progressing triad - unsteady gait, urinary incontinence, potentially reversible dementia
* Unsteady gait - like parkinson’s (bradykinetic, broad-based, shuffling)
* Urinary incontinence (can be faecal)
* Potentially reversible dementia - from distortion of perivetricular limbic system -> memory loss/bradyphrenia (slowing)

NOTE: no papilloedema, normal opening pressure on LP

Mx:
1. LP + clinical response to removing CSF
2. CT/MRI (enlarged ventricles with convolutional atrophy) + continuous external lumbar CSF drrainage over 3-4 days
3. VP shunt to drain excess CSF to abdomen where it can be absorbed

Question 43

Q

Depression overview
Starting and stopping anti-depressants Mx?

Answer

A

Depression
* PC:
* >2wks Sx, affecting functionality
* DSM-5: 5/9 Sx including ≥1 core Sx (low mood, anhedonia)
* Ix: PHQ-9/HADS
* Mx: self-help books -> self-CBT/computerised CBT -> SSRI (Sertraline)/In-person CBT +/- CMHT/crisis team/IP
* Mx for kids: CBT -> fluoxetine

Anti-depressant medication Mx:
* Start meds –> review in 2wks:
* If no effect after further 4wks –> increase/change
* If effective – continue for 6 months past no depressive Sx –> wean off over 4wks
* After started meds – monitor depression w/ PHQ-9
* Switching anti-depressants - direct switch/cross-taper

Question 44

Q

Psychiatric Legal Overview: 1) MHA 2) MCA/DOLS 3) Sectioning

Answer

A

MHA assessment: patient risk to themselves/others due to MH issue. 3-person decision-making (can’t do for family/friends):
* Approved mental health professional (AMHP) – 95% social workers (not doctors), only person that can run/start assessment
* One treating doctor (full license, previous acquaintance w/ patient e.g. GP OR S12 approved)
* Independent doctor S12 approved

Mental capacity act:
* Understand, retain, weigh up and communicate decision
* Decision-specific, in best interest, least restrictive of persons rights/freedom
* Capacity assumed in general, unwise choices ≠ lacking capacity

Deprivation of Liberties Safeguarding (DOLS):
* For people in care homes/hospitals
* Checks to ensure protection of those with DoL - appropriate/best interests
* Commonly dementia-related

Legal sections SUMMARY:
* S2 – 28d detention for assessment (& treatment), 2 doctors (1 psychiatrist, 1 knows patient) + 1 AMHP –> can be appealed within 14 days
* S3 – 6-month detention for forceful treatment (can extend), 2 doctors (1 psychiatrist, 1 knows patient) + 1 AMHP –> can be appealed within 14 days
* S4 – outside hospital, emergency admission for 72hrs by 1 doctor + AMHP – no appeal
* S5(2) – voluntary hospital patient, hold inpatient for 72hrs for assessment by doctor
* S5(4) – hold inpatient for 6hrs for assessment by nurse
* S17 – conditional leave from ward as inpatient at MH unit
* S136 – police to remove patient from public space (requires warrant – 24hrs)
* S135 – police to remove from home to place of safety (24hrs)
* CTO (community treatment order) – after discharge from S3 with conditions in place for treatment

Question 45

Q

Perinatal psychiatry overview

Question 46

Q

Personality disorder overview

Question 47

Q

What causes hemiballismus?

Answer

A

Hemiballismus - invol flinging motions of extremeties

Caused by infarct/haemorrhage in contralateral subthalmic nucleus

Question 48

Q

Types of psychosis

Answer

A

Schizophrenia - most common form of psychosis (perceive/believe/interpret differently)

PC:
* Positive Sx - auditory hallucinations, delusions, disrupted speech
* Negative Sx - self-neglect, social withdrawal, flat affect, demotivation

Types:
* Paranoid (most common) - hallucinations/delusions prominent
* Hebephrenic - 15-25yrs, poor prognosis, fluctuating affect + fleeting fragmented delusions/hallucinations
* Catatonic - stupor, posturing, wavy flexibility, negativism
* Simple & residual - negative Sx predominant

ICD-11:
* ≥1 first rank Sx (thought echo/thought insert/withdrawal/broadcasting/delusions of control/influence/passivity/delusional perception/auditory/sensory hallucinations)
* Delusion - false/fixed/irrational belief firmly held despite evidence to contrary (not explained by pt’s cultural/religious BG)
* Hallucination e.g. auditory - sensory perception without stimulus
* Passivity - external control of thoughts/feeling/actions
* Thought disorder - insertion/withdrawal/broadcasting
* OR ≥2 other Sx

Mx:
* ALL adults –> EIS (intense specialist outpatient service for 3yrs)
* ALL get care-coordinator = main contact
* Therapy: CBTp (psychosis CBT)
* Meds & Physical health checks - bloods, ECG, weight – med SEs (T2DM, weight gain, BM supression)
* 1st - atypical antipsychotic e.g. aripiprazole, olanzapine, risperidone
* 2nd - typical antipsychotic e.g. haloperidol, chlorpromazine (EPSEs + hyperprolactinaemia common)
* Tx-resistent (failure to respond to ≥2 antipsychotics, one atypical, each at therapeutic dose for ≥6wks) - Clozapine/combo

Schizoaffective disorder - mood disorder + schizophrenia within days/same intensity
* Delusions/hallucinations need to be present for ≥2wks without mood Sx + NOT DUE TO ORGANIC CAUSE/MEDS
* Tx: Anti-psychotics + anti-depressants + therapy +/- ECT

**Delusional disorder **- ≥1 delusion ≥1 month (DSM5)/≥3 months (ICD10) - not due to schizophrenia/organic/drugs
* NOTE: Normal psychosocial functioning/ordered thinking
* Emotional response/behaviour consistent with delusions
* No auditory/visual hallucinations (can have olfactory/tactile)
* No thought/mood disorder or flat affect
* Tx: individual CBT, social skills training

Question 49

Q

Unusual psychotic syndromes

Question 50

Q

Anti-psychotic medication overview

Question 51

Q

Acute stress reaction vs adjustment disorder vs PTSD

Answer

A

ASR - transient disorder without other apparent mental disorder in response to exceptional physical/mental stress (if >1month ?PTSD)
* Daze -> withdrawal/agitation
* Mx: short course benzos, social support, reassurance

Adjustment disorder (incl prolonged grief reaction) - subjective emotional distress affecting functioning during sign life chang (prolonged grief following death >6 months)
* Mx: psych support +/- SSRIs

PTSD - delayed/protracted response to catastrophic event, >1 month
* PC:
* Re-experiencing (flashbacks/nightmares)
* Avoidance (reminiscent activities)
* Autonomic hyperarousal (vigilent for threat, insomnia, difficulty concentrating)
* Other: emotional numbing/depression/substance use/unexplained physical Sx
* Ix: trauma screen questionnaire, referral to mental health services
* Mx: DO NOT DEBRIEF
* Mild (<4wks) - watchful waiting
* >1 month - trauma-focused CBT
* >3 months after non-combat trauma (severe) - eye movement desensitisation and reprocessing (EMDR)
* 2nd line - NaSSA (mirtazapine)/SSRI/SNRI, 3rd line - anti-psychotic

Question 52

Q

What is pseudo-hallucination?

Answer

A

Pseudo-hallucinations - false sensory perception in absence of external stimuli when affected has insight (is it is a hallucination)
* Hypnagogic hallucination - transitioning from wakefulness to sleep
* As part of grief response (e.g. seeing the deceased)

Mx: reassure = normal + will not develop mental illness

Question 53

Q

How long presentation of OCD for Dx?

Answer

A

> 2wks, >1hr per day

Question 54

Q

Screen questions for depressions vs anxiety

Answer

A

Depression - PHQ9
Anxiety - GAD7
Both - HADS score

Question 55

Q

Childhood psychiatry DDx

Answer

A

ASD - persistent deficits in social communication and social interaction across multiple contexts, starts <3yrs
* Refer to CAMHS for Dx: impaired social communication & interaction, inflexible thinking/ritualistic behaviour, sensory hyperstimulation (loud noise/textures)
* Spectrum: autism (triad, IQ <70, impaired language dev), high-functioning autism (IQ >70), asperger’s (IQ>70, normal language dev)
* Mx:
* Young children (2-3y) - Applied behav analysis (ABA), picture exchange comm systems (PECS)
* Older children - comm skills/psychoeducation + ABA (sexual/aggresion)

ADHD - <12yrs, ≥2 settings, reduced functioning, ≥6 months
* PC: inattention, hyperactivity, impulsive
* Ix: ADHD assessment
* Mx:
* Watchful waiting for 10 days if persistent refer for ADHD assessment
* Severe/failed Tx & ≥5yrs - methylphenidate 6wk trial (2nd - Lisdexamphetamine, all cardio toxic - baseline ECG)
* NOTE: methylphenidate SEs - reduced hunger, difficulty sleeping, mood/seizures/cardiac complications (CIs: glaucoma, phaeo, hyperthyroid, psych hx, CV/cerebrovasc abn, FHx: cardiac issue/arrythmia/tourette’s/epilepsy)

Learning disability spectrum - mild (IQ 50-69), mod (IQ 35-49), severe (IQ <35)
* Scores: WAIS for adults, WISC for children

Tic disorder - Mx: clonidine (alpha 2 antag/atypical antipsychotic)

Chronic insomnia - difficulty getting to/maintaining sleep on >3 nights/wk for ≥3 months
* Ix: sleep diary
* Mx: sleep hygeine, CBT-I, benzos short-term if daylight impairment

Question 56

Q

Unexplained symptom disorders

Question 57

Q

Alcohol questionnaires & Mx for assisted withdrawal

Answer

A

CAGE questionnaire (≥ excessive drinking): cut down, annoyed, guilt, eye opener

Formal assessment tools:
* AUDIT (alcohol use disorders identification test) - 16-19 harmful, ≥20 possible alcohol dependence
* SADQ (severity of alcohol dependence questionnaire) - do if >15 on AUDIT -> 16-30 moderate, ≥31 severe
* CIWA-Ar (Clinical institute withdrawal assessment for alcohol) - determines severity of withdrawal (determine next stage of Tx)
* APQ - alcohol problems questionnaire (nature + extent of problems arisen from alcohol misuse)

Assisted alcohol withdrawal - worst Sx in first 48hrs –>3-7 days to disappear
* If >15 units/day OR >20 on AUDIT -> community-based assisted withdrawal
* INPATIENT withdrawal if 30+ units/day OR ≥30 on SADQ, Hx of delirium tremens/withdrawal-related seizures, children (≤17yrs)
* Meds:
* Acute - Chlordiazepoxide/diazepam (if liver impaired - lorazepam) –> reduce dose over 7-10 days
* After successful withdrawal - 6months of Acamprosate/Naltrexone (2nd - disulfiram)

Question 58

Q

Eating disorder DDx & screening tool

Answer

A

SCOFF Questionnaire - ≥2 = possible ED
* Sick (self-induced vom), Control (lost control of eating), One (lost >1 stone in 3m), Fat (think fat others think thin), Food (food dominates life)

Anorexia nervosa
* PC:
* Restricted food intake > WL/low BMI
* Fear of gaining weight/fat
* Distorted view (think fat)
* Ix: preg test, bloods (hormone profile, ESR, general), ECG +/- DEXA
* Mx:
* Admit if BMI <13/extreme WL/physical complications/high suicide risk (refeeding syndrome - low PO4/Mg/K/thiamine, Na/H2O retention)
* Urgent referral to community ED service (CEDS) if BMI <15 (routine referral if 15-17)
* Weight restoration target - 0.5-1kg weight gain/wk
* Psychotherapy: MANTRA (Maudsley AN treatment in adults), CBT-ED, SSCM
* Child - family therapy (2nd - CBT-ED)

NOTE: Bulimia nervosa > binge eating if purging (being sick, laxatives, thyroid drugs)
* Recurrent binge eating ≥1/wk ≥3 months
* Mx: CBT-ED +/- SSRI

Question 59

Q

What are best mental health meds during pregnancy? Breastfeeding?

Answer

A

Antidepressants: Sertraline best
* TCAs = cardiotoxic (in/out of pregnancy) but low-dose amitriptyline likely ok

Antipsychotics - not teratogenic but may need induction of labour
* Clozapine risk of neonatal agranulocytosis

Mood stabilisers - low dose carbamazepine / lamotrigine safe
* Lithium – neonatal thyroid, arrythmia, Ebstein’s anomaly
* Na Valproate – neural tube defects (pregnancy protection programme to prevent)

BENZOS – oral cleft, floppy baby syndrome

Breastfeeding:
* Recommended antidepressant = sertraline
* Recommended antipsychotic/mood stabilisers = olanzapine/quetiapine (but sedating)
* For sleeping = promethazine > benzos
* Consider ECT

Question 60

Q

CNS TB overview

Answer

A

CNS TB - commonly caused by mycobacterium TB secondary to disease elsewhere in the body
* PC: meningitis (headache, neck stiffness +/- focal neuro/tremor/vision changes over 2-3wks) or IC tuberculomas (slow growing focal lesion/raised ICP)
* Ix: CSF analysis, CT/MRI head (oedema, hydrocephalus, basilar meningeal thickening, tuberculomas), 50% CXR abn

Tx:
* TB without CNS - RIPE (2 months) -> RI (4 months)
* TB with CNS - RIPE (2m) -> RI (10 months)

Question 61

Q

Optic neuritis

Answer

A

ON - demyelinating inflam of optic nerve assoc w/ MS
* PC: preceeding viral illness -> unilateral acute visual deterioration, change in colour perception, retro-orbital pain (worse on eye mov)
* NOTE: Uhthoff’s phenomenon - pain worse on exercise/heat, Pulfrich phenomenon - straight mov appears curved
* O/E: pupilary light defect +RAPD (Marcus-Gunn pupil) + 1/3 have swollen optic disc
* Ix: myelin basic protein, oligoclonal bands, high IgG index/synthesis rate in CSF = MS + MRI/visual evoked potentials can show optic nerve inflam
* Tx: high-dose steroids

Question 62

Q

CSF interpretation

Question 63

Q

Cranial nerve palsy presentations

Question 64

Q

Progressive difficulty whistling and sucking through straw spot Dx?

Answer

A

Facioscapulohumeral muscular dystrophy
* Disease progresses from face downwards
* Winging of scapula is characteristic sign

Answer 58

A

Definition: chr mental health disorder characterised by mania/hypomania + episodes of depression
* Manic episode - ≥1wk abn elevated mood/irritability –> severe functional impairment/psychotic Sx (delusions of grandeur/aud hallucinations)
* Hypomanic episode - ≥4d abn elevated mood/irritability –> decreased/increased function
* Mixed episode - alternating mania/depression - ≥1wk (hypo)mania + 3 depressive Sx OR ≥2wk depression + 3 (hypo)manic Sx

Classification - ≥2 episodes mood/activity disturbed:
* Type 1 BAD (most common) - manic episodes + major depressive episodes
* Type 2 BAD - recurrent depressive episodes + periods of hypomania
* Rapid-cycling bipolar disorder - 4 depressive/manic/mixed episodes in 1 year

DDx: cyclothymia (rapid mood swings)

Mx:
* Urgent referral to CMHT (non-urgent ref if hypomania)
* CBT/family therapy
* Mania pharm: stop anti-depressant, anti-psychotic (olanzapine), 2nd - alternative/dose change, 3rd - lithium/Na Val, 4th - ECT
* Short-term benzos if severe behav issues
* Bipolar depression pharm: if not on other meds fluoxetine + olanzapine (2nd - Quetiapine, 3rd - lamotrigine)
* Long-term Mx: lithium - switch from acute meds 4wks post manic episode (2nd - Na Val/Olanzapine/Quetiapine)

Drug monitoring:
* Lithium - 0.4-1 therapeutic margin (>1.2 is toxic, 1.5 Sx, >2-life-threatening) - check lvls 5d after starting/changing dose (12hr after last dose), weekly until stable then 3m for first year then 6 monthly
* Na Val - LFTs every 6 months
* Lamotrigine - 10% benign rash, some develop SJS