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Neurology Flashcards

1
Q

Seizure history

A

Before
-Prodromal
- Infective causes eg Headache Fever
- D&V -> electrolytes
- Drug use / alcohol
- Sleep deprivation (especially new presentation in students)
- Stress
- Blood sugars
- Any headaches with vomiting
- Head trauma

During
- Collateral
- Stiff and rigid (vs floppy and flaccid) followed by rhymic movements
- tongue biting - LATERAL
- faecal incontinence

After
- Any immediate first aid
- Post ictal at least several minutes
- Weakness (tods paresis)

PMH
- Known seizures
- Malignancy - breast renal melanoma
- Immunosuppression (infection)

Meds
Meidcation compliance
recent abx - cipro
Clozapine
Anticoagulants

Social
Profession building / HGV
Driving
Alcohol

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2
Q

Difference in prodrome of vagal vs seizure

A

Vagal
- Nausea, tunnel/darkening vision, tinnitus

Seizure
- Flashing lights, blurring of vision (rather than dimming)
-Smell or taste
- Numbness tingling

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3
Q

What is tods pareisis how long does it last

A

Unilateral weakness post seizure - often 48hrs

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4
Q

2 most common cancers mets to brain

A

Breast
RCC clear cell
melanoma

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5
Q

no driving with epilepsy / seizure?

A

1 year seizure free
6 months post 1st seizure

Ultimately case by case up to DVLA

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6
Q

What should you advice people who may have had a seizure and work eg on building site

A

Need to contact their occupational health department

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7
Q

seizure exam

A

Look
- Mouth and tongue
- Head, neck, shoulder injuries

Focal signs eg SOL
- Visual fields
- Eye movements
- Pronator drift
- Gait
- Tone and power

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8
Q

What are the causes of seizures you should present and explain to examiner why / why not in this case?

A

Genetic - idiopathic epilepsy

Structural
- SOL
- Trauma Bleeding
- CVA in elderly

Infective
- TB Malaria HIV
- Meningitis

Metabolic
-Uraemia
- Heaptic encephalopathy
- Low sodium

Autoimmune

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9
Q

Investigations first seizure

A

Baseline obs
- Temp
- LS BP
- Finger prick glucose

Bloods
FBC / CRP
Renal function
Electrolytes
LFTs - alcohol excess

CT head - any SOL

EEG

1st seizure clinic

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10
Q

Advice for new epilepsy

A

Work
- Any changes
- Occy health

Driving
- No driving until 1 year seizure free

Activities
- Shouldn’t stop doing things they enjoy but may need to modify
- No swimming alone
- High level climbing eg roofer

Shower rather than bath

Mothers
- Breast feeding -ideally sat on floor
- Changing baby.- floor mat

Pregnancy and contraception
- Antiepileptic effects on meds (COCP)
- >Barrier methods
- May need to change siezure meds
- Folic acid for at least 3 months before ( neural tube defects)
- If only option is valproate - should be on pregnancy prevent program

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11
Q

Anti epileptics in pregancy

A

Aim for single medication at lowest dose
Lamotrigine / Leveteracitam for labias

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12
Q

Difference between optic neuopathy and atrophy

A

Neuropathy - Optic nerve not working

Atrophy - Permanent damage to optic nerve

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13
Q

Optic neuritis history

A

HPC
- Describe whats happening
- Time period
- intermittent vs constant
- Both eyes or one?
- Look like looking through frosted glass - Blurred vision
- Or seeing 2 of everything - double vision
- Loss of visual field
- Any issues with acuity?
- Colour vision - RED - difference between eyes?
- Pain?

Additional symptoms
- Issues when cough or bend over = IIH
- Pulsatile tinnitus
- Any issues post hot shower / bath

PMH
- Any eye problems / glassess - Been to opticians?
- Currently pregnant?
- Migraine
- Vascular risk factors

PMH

Social

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14
Q

How does time scale relate to the aetiology of vision loss

A

Months - inherited

Weeks - possibly malignant

Days - Inflammatory

sudden - Vascular

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15
Q

Lesion at each of these spots

A
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16
Q

Curtain coming down over vision =

A

Amaurosis fugax

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17
Q

GCA causes what type of optic neuritis

A

Anterior ischemic

  • vascular
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18
Q

Visual field disturbance time period of 20 mins with headache most likely

A

Migraine

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19
Q

Visual symptoms when getting out of hot bath

A

Uhthoff’s phenomenon

[Due to bodys repair of myelin sheath not being as strong
- Doesn’t cause long term damage

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20
Q

Groups of causes of optic neuropathy

A

Ischemic - More likely in older vascular
- GCA - arteritic
- Micovascular - risk factors

Inflammatory
- More likely in younger

Infiltrative
- Sarcoid

Nutritional
- carb only
- Slow progressive symmetrical
- Thiamine, A, E, Folate

Methanol poisoning

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21
Q

What is added to mri scan in MS

A

Gadolinium

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22
Q

Pregnant patient with rapidly progressive optic neuritis

A

Nerve sheath meningioma
- hormone sensitive

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23
Q

Key sign on exam of optic neuritis

A

RAPD

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24
Q

What is Leber’s optic atrophy?

How does it present?

A

Visual loss both eyes
Or sequentially (12 months) of both eyes

Central visual loss only
- Cant read chart but good peripheral vision

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25
Q

Optic neuritis exam? To finish?

A

Measure acuity - snellen

Quick test of colour vision - red in each eye
Ishihara plates

Visual field - finger counting in 4 quadrants (1 or 2)

RAPD

**State examination with slit lamp + dilating drops

Complete and full systematic neuro exam

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26
Q

How to assess RAPD ?
What is normal?
What is abnormal?

A

In a dimly lit room, have the patient look at a distant point.

Shine a light into one eye for about three seconds.

Quickly move the light to the other eye and observe the pupils.

Repeat the steps a few times to confirm your findings.

A normal response is when both pupils constrict equally when light is shined into each eye individually. When the light is moved between the eyes, the pupils should not dilate or escape.

If the pupil dilates when the light moves from one eye to the other, a RAPD is present. This indicates that there is a difference in the afferent pathway between the two eyes.
[Supported if the good pupil constricts when light goes back to it]

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27
Q

Fundoscopy of optic neuropathy vs atrophy q

A

Neuropathy - swollen

Atrophy - Pale

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28
Q

Optic neuritis investigations

A

Vitamin D
ESR and CRP - giant cell

Consider aquaporin 4 and MOG antibodies - atypical eg neuromyelitis optica

Imaging
Orbital MRI
- longer section of signal uptate in optic nerve suggestive of atypical

[If compressive MRI brain]

Sampling
Consider LP for oligoclonal bands

If history of sarcoid
-Consider serum ACE
- CT CAP

Referral to neuroophthalmologist

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29
Q

Treatment optic neuritis

A

Typical - consider steroids
-> Plasmapheresis

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30
Q

What happens in atypical optic neuritis when you stop steroids

A

Gets worse again

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31
Q

Risk of MS if typical optic neuritis

A

about 50% in 15 years

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32
Q

TIA max length

A

24 hours

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33
Q

TIA history

A

What was going on

Motor / sesnsory
- How fast, how long
- Should be sudden onset but may wear off gradually

Speech
- Hard to get words out
- Difficulty understanding words - dysphasia

Vision
- Transient amarousis fugax
- Loss of visual field

Mimics
- Headache - GCA / Migrane / Venous sinus thrombosis / meningitis
- Seizure like activity / tongue biting / post ictal

PMH
-Diabetes - blood sugar around event
- AF / Palps
- Vascular - cardiac / Hypetension / PVD / T2DM / IHD / TIA / stroke

Drug history
AF anticoagulated?
-> Compliance

Social
- Smokling
- Alcohol -> AF
- Function at home / work
- Drive?

Family history
- Clotting issues
- heart attack / stroke at young age

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34
Q

Good way of grouping signs syptoms of strokes vs stroke mimics

A

Stroke / tia -> Loss of function

If flashing lights / floaters / tingling etc more likely something else

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35
Q

ABCD2 score

A

Score 1-3 (low)
2 day risk = 1.0%
7 day risk = 1.2%

Score 4-5 (moderate)
2 day risk = 4.1%
7 day risk = 5.9%

Score 6–7 (high)
2 day risk = 8.1%
7 day risk = 11.7%

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36
Q

TIA exam

A

Basically a cardio exam + extras
- examine what ever was the presenting complaint

Hands
- Pronator drift
- Tar staining
- Feel pulse ?AF
- BP

Head and neck
-Auscultate carotid bruis
- Xantholasma - eyes

Dsarthria - say baby hippopotamus
​
Dysphasia - name this (pen / phone)

CNs - especially if facial / visual fields
Visual acuity

Tone / power / Sensation / reflexes

Fundoscopy

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36
Q

2 TIA most common differentials

A

Migraines
- Usually spreading and gradual onset
- Headaches
- Flashing lights
- Pins and needles

Seizures
- Likely to have amnesia

Consider optic neuritis if visual only

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37
Q

What side weakness if there is speach disturbance in TIA

A

Speech disturbance = right sided weakness

\UNLESS left handed

  • All right handed people have speech centre on L side
    ie if there is speech disturbance and L sided weakness ?migrane / L handed
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38
Q

TIA investigations

A

Bloods
- FBC, U&Es
-Cholesterol
-HBA1C
-Glucose

ECG +/- 24hr tape depending if not found AF

Imaging
- CTB
- Likely to get an MRI at TIA clinic
- Carotid doppler

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39
Q

Ix if young and tia

A

Thrombophilia screen
Vasculitis screen

Echo - valvular pathology
PFO - will need bubble / TOE

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40
Q

Carotid doppler scores for endarctetomy

A

Carotid stenosis > 50% and symptoms related to that side refer to vascular surgery

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41
Q

TIA + chest pain / neck pain / occipital headache worry

A

Vertebral artery dissection
-> CT angio

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42
Q

TIA lifestyle advice

A

Low salt
Exercise
Smoking / alcohol
Healthy diet
Control BP / Diabetes

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43
Q

TIA antiplatelet treatment? Other medications?

A

Aspirin 300mg for 2 weeks then 75mg clopidogrel life long

Hypertensive managment

Statins if cholesterol high

AF

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44
Q

Driving post TIA

A

1 month
- I would check DVLA before to check

HGV - at least 1 year

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45
Q

3 main differentials of Peripheral neuropathy

A

Diabetes
Alcohol
B12 deficiency

[you have another card with lots more on - but always name these 3 first]

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46
Q

What is myasthenia gravis?

A

Antibodies to post synaptic Acetyl coline receptors
(Not all signals get down)

  • in first stage can increase ACH in receptors to treat

Over time get thickening of receptors and complement deposition - harder to treat which would lead to a fixed weakness

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47
Q

End of bed what 3 common signs of myasthenia

A

Head droop
Ptosis
Salivation

In paces most will have stable occular myasthenia

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48
Q

30 year old presents with droopy eyes at night / double vision / weakness
Take a history? Key things to check!?

A

[Myasthenia vignette]
Smoking, thyroid, breathing, swallowing

HPC
-When is weakness
- Fatigability
- Ptosis / double vision that’s worse after reading etc
- Double vision that is variable
- sometimes next to each other / sometimes on top
- struggling to finish chewing meal
- Proximal muscle weakness

Lambert eaton syndrome Cough / weight loss / haemoptysis / dry mouth / sweating / palps

**Screen red flags **
- ANY DYSPNEA
- ANY DYSPHAGIA / CHOKING

** PMH**
- Coexisting autoimmune
- Thyroid
- Lung Ca

Family history
Congenital myasthenia syndrome

DH
- Previous immune checkpoint
- inhibitors for Ca

**Social history **
Smoking alcohol
Driving - diplopia ptosis
How affecting function

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49
Q

Bar ach what is the other antibody that can occur in myasthenia? In who?

A

Black afrocaribbean
Anti muscle specific kinase antibodies

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50
Q

What is a myasthenic crisis

A

Exacerbation of underlying myasthenia which leads to respiratory/ Bulbar compromise

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51
Q

When would you want to refer to ICU in myasthenia. Name 4

A

FVC <20mls/kg

Progressive decline in FVC

Can’t complete sentences

Struggling with secretions

Can’t lift head from pillow

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52
Q

Some myasthenia patients struggle to do mouth movements for FVC? What other bedside test for monitoring

A

Count as far as possible in 1 breath

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53
Q

Key triggers for myasthenia

A

Surgery
Infection

  • Anaesthetics - non depolarising
  • Antibiotics - Including surgery antibiotics (penicilliamine rarther than penicillin) Aminoglycosides, macrolides, quinilones
  • antimalarials
  • B blockers
  • Magnesium

Non depolarising anesthetics

Penicilliamine, Gentamycin / tobramycin Macrolide, Quinolones

Quinine

EXACERBATE
Erythromycin - macrolides
Xylocaine/ lignocaine
Aminoglycosides
Ciprofloxacin - quinolones
Electrolytes - magnesium
Relaxant - none depolarising
Beta blocker and Botox
Antimalarial - Quinine
Timolol

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54
Q

Key differences between Lambert eaton and myasthenia

A

Rarely get occular / bulbar symptoms
Usually more Peripheral muscles

Autonomic features predominately
Postural hypotension
Sweating
Dry mouth

Smoking haemoptysis weight loss

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55
Q

What would make you think of botulism rather than myasthenia

A

Rapidly progressive descending Paralysis with diplopia

Also lots of autonomic symptoms

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56
Q

Things you’ll find on exam inclusion body myositis

A

Middle age man

Hip / knee and wrist/finger flexion weakness

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57
Q

Things you’ll find on exam inclusion body myositis

A

Middle age man

Hip / knee and wrist/finger flexion weakness

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58
Q

Myasthenia differentials (weakness)

A

Lambert eaton
Inclusion body myositis
Polymyositis
Drug induced
MND
Hypothyroidism
Cushings

Usually in all these the weakness is progressive rather than variable

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59
Q

Lambert eaton antibodies? What does this mean about the reflexes

A

Pre synaptic calcium channels

-> if you repeatedly stimulate eg a reflex then it slowly releases enough and might potentiate

[As the issue is pre-synaptic release essentially]

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60
Q

3rd nerve palsy findings

A

Down and out
Ptosis
Myosis

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61
Q

3rd nerve palsy findings

A

Down and out
Ptosis
Myosis

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62
Q

Myaesthenia exam

A

End of bed
Fvc machine
Ptosis / strabismus
Myasthenia snarl when smile
Thymectomy scar

Cranial nerves
In addition - make maintain update for 30 seconds see if fatigue
Can they stop you opening eyelids
Smile for snarl
Open lips against them holding shut

Ask them to count as far as possible in 1 breath WHILE looking up for 30 seconds

Ask for a cough

If ptosis -“i would like to do icepack test to see if it reverses ptosis”

FVC

Neck
CVC (plasmapheresis)
Trache scar

Neck flexion / extension

Precus for thymoma.
(Found in 10%)

Ask to hold arms out for 20 second

Check lower limbs reflexes and see if vet worse / better with repeat

Hope flexion

I would like perform the
Ice pack test to assess for fatiguabke ptosis
Check forced vital capacity
Formally asess power and fatiguability with dynometer (grip test)
Request SLT assessment
Request optometry assessment

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63
Q

What essential investigations for myaesthenia

A

Test ACH antibodies and MUSK
If LES - voltage gated calcium channel abs

Thyroid antibodies - autoimmune thyroid in about 10%

EMG - repetitive stimulaton
And for jitter
(Jitter involves testing 2 myo fibers at same time and there is slight delay between them)

CT for thymoma / hyperplasia

[Tension test - old not done]

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64
Q

What essential investigations for myaesthenia

A

EMG - repetitive stimulaton
And for jitter
(Jitter involves testing 2 myo fibers at same time and there is slight delay between them)

Teat ACH antibodies and MUSK

Thyroid antibodies - autoimmune thyroid in about 10%

If LES - voltage gated calcium channel abs

CT for thymoma / hyperplasia

Tension test - old

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65
Q

How to you manage myaesthenia

A

I would refer to neurology team

Conservative
Patient alert card
Refer to MDT inc SLT / optometry
Physio

Medical
I would treat this patient according to the Sussman protocol
Pyridostigmine
Consider buscopan for the GI side effects
Low dose oral steroids

If they relapsed despite steroids I would consider azathioprine or mycophenolate

If ICU
High dose steroids
Plasma exchange or IVIG as rescue therapy

Surgical
If under 45 and positive antibodies should be offered a thymectomy

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66
Q

Parkinsonism vs parkinsons disease

A

Parkinsonism is the signs

Rigitiy (increased tone)
Tremor
Bradykinesia

Parkinsons is most common differential of this.

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67
Q

Young vs old parkinson features

A

Young
tremor predominant slow progressive

Older
Bradykinesia predominant and usually quicker progressive

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68
Q

Parkinsons pathophysiology

A

Alpha-synuclein (α-syn) is a protein that plays a role in the development of Parkinson’s disease (PD).
In PD, α-syn misfolds and clumps together into Lewy bodies (LBs).
These clumps may be toxic and spread from neuron to neuron, potentially causing the disease to spread throughout the brain.

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69
Q

Parkinsons exam end of bed?
Progress?

A

Surrounding - mobility aids
Medication - dopa
Tremor at rest
Hypomimic face
Quiet voice when say hello

Tremor
- Resting and rotational approx 4-6Hz. Make sure relax arm
- Usually asymmetrical

Tone
- Assess all
- Usually increased tone especially on 1 side
- Cog wheel at wrist rotational

Coordination
- Bradykinesia - test finger and thumb tapping
- Lower limb - ask to stamp feet on floor

Speech
- Speed and amplitude saying Baby hippoptamus

Writing
- micrographia

Functional
- Doing up buttons

“I suspect this is parkinsonism and would like to performa more focused exam - however i can assess”

Power / reflexes / sensation usually normal

Gait
- Reduced arm swing
- Shuffling

Formally assess for anosmia

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70
Q

Who gets deep brain stimulation in parkinsons? Where is it seen?

A

People who are cognitively intact and symptoms despite 5x/day dopa therapy
Especially on/off symptopms

Seen similar site to PPM

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71
Q

therapies for complex/resistant parkinsons

A

Deep brain stimulation

Apomorphine infusion sub cut

Duodopa - gel preparation of levodopa into jejenum -.. gives continuous therapy

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72
Q

Parkinsonism Differential and features of each

A

Reduced dopamine in brain
-Idiopathic parkinsons (slow progressive usually asymmetric) - mnon scary hallucinations

Parkinsons plus = All respond poorly to levodopa
- Lew body dementia - forgetfull / early onset cognitive inpairment and scary hallucinations
- Progressive supranuclear palsy. Symetrical with tremor and falls predominant. Reduced vertical gaze. Rapid progression
- Multi system atrophy - autonomic / cerebellar features predominate
- Corticobasilar degeneration - usually rapid with ‘alien limb’ - loss of use with uncontrolled movements

Parkinsonism with NORMAL dopamine levels
- Vascular parkinsonism - essentially vascular disease affecting basal ganglia
- Drug induced
- Essential tremor
- Wilsons
- Normal pressure hydrocephalus

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73
Q

Parkinson’s investigations

A

Bloods minimal
- Consider wilsons

Imagining
- Strokes
- Vascular load in basal ganglia - MRI best
- Consider DaTSCAN

Conservative
- L/S BPs
- Cognitive assessment - Eg MOCA
- Non motor symptom questionnaire

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74
Q

What is a DaTSCAN used for

A

Can help differentiate parkinsons from Eg essential tremor

  • Looks at uptake of dopamine
  • Only helpful to differentiate parkinsonism with dopamine depletion and with normal dopamine levels
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75
Q

Management of parkinsons

A

Conservative
- Patient education - direct to parkinsons UK
- Specialist CNS nurse
- Early physio
- Speech therapy
- As progress may need dieticians

Medication - 3 options for first line
- Levodopa with peripheral decarboxylase inhibitor (dopamine doesn’t cross blood brain barrier, levodopa does) - eg co-careldopa
- MAOi - selegiline/rasagiline (can hold off need for dopamine for up to 1 year)
- Dopamine agonist - Eg Pramipexole (Mirapex)
Rotigotine (Neupro)
Ropinirole (Requip)
Apomorphine (Apokyn)

-> can add together
-> COMT inhibitor eg entacapone (reduces breakdown of L dopa)

Surgical
- Deep brain stimulation

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76
Q

Main issue with dopamine agonists

A

Impulse control issues
- Very important to council (+ document) prior to starting

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77
Q

Which dopamine agonist can you give as a patch

A

Rotigotine

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78
Q

What are the non-motor manifestations of parkinsons? How should this be assessed?

A

Non-motor symptom questionnaire

Neuropsych
- Mood disorders
- REM sleep disorder

Anosmia - loss of sense of smell

Daytime hypersomnolence

Autonomic
- Urinary retention / over active bladder
- Postural hypotension’s
- Constipation

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79
Q

Parkinsons staging

A

hoehn yahr

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80
Q

Visual loss history

A

What do you mean by visual loss

1 eye or both
Unilateral - cataract / macular degeneration
Bilateral - post chiasm / pit / infarcts

Pain - Ulcer on cornea, angle closure glaucoma, GCA (pain in temples then painless vision loss)
Painless - Macular degeneration / cataracts /

Struggle with distance or reading

Bumping into things in peripheries

PMH
- Diabetes
- Hypertension

Social history
- Smoking very bad
- Function - job / drive

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81
Q

Acute peripheral visual loss with grey shaddow progressing over vision

A

Retinal detachment

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82
Q

Floaters that coalesce -> mising of vision in diabestes

A

haemorrhage

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83
Q

Who gets angle closure glaucoma

A

People who are far sighted

Thier eyes look big with glassess on

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84
Q

Macular degeneration visual loss

A

usually 1 eye first with blurring / distortion of vision

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85
Q

Causes of cataract

A

steroids
UV
Myotonic dystophy, downs, turners

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86
Q

How to perform red reflex

A
  • Turn off the lights and darken the room
  • Use an ophthalmoscope with the lens power set to zero and light to max
  • Hold the ophthalmoscope about 18 inches from the patient’s eyes
  • Shine the light into each eye individually, then both eyes together
  • Observe the color, brightness, and symmetry of the red reflex
    What to look for

A normal red reflex is symmetrical, bright, and the same color in both eyes

An abnormal red reflex may include:
-Dark spots or black flecks
-An absence of the red reflex
-A white reflex (leukocoria)
-An asymmetric reflex

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87
Q

How to perform RAPD ? Abnormal

A

Shine light into 1 eye for 2 seconds
Both should constrict the same

Then switch and both should constrict the same

In abnormal eg glaucoma / vein / artery occlusion where partially damaged retina
-When shine light into damaged eye only constricts by half.
-When light shined into good eye both will constrict completely
-> when light switched back to eye with glaucoma it will dilate slightly

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88
Q

What is the arrow pointing to?

A

Physiological blind spot
- corresponding to optic nerve

89
Q
A

Superior / inferior arcuate defect

The reason these look like arcs and come off the blind spot is that they represent the loss of bundles of nerves as they come out of the optic nerve head.
The horizontal border is the horizontal raphe, which is an imaginary line dividing the upper and lower hemispheres of the retina.

90
Q
A

Severe constriction with a central island

end stage glaucoma.

91
Q

What is the cup to disc ratio? in glaucoma

A

Raised in glaucoma. >0.7

92
Q

Magnified vs small eyes behind glasses? risks

A

Magnified - hypermytrophic
-> glaucoma

Small - myopic
-> retinal detachment

93
Q

History of macular degeneration in 2 lines

A

Older person with slow progressive loss both distance and reading
Central visual loss with distortion being a common feature

94
Q

Mainstay of treatment of leaky vessles in diabetic retinopathy

A

VGEF inhibitors
Eg Sunitinib

95
Q

Retinitis pigmentosa presenting vingette

A

Young age with progressive peripheral visual field loss
-> bumping into things

Much worse at night

96
Q

2 things seen on fundoscopy of retinitis pigmentosa

A

Pigmented bone spicules
Waxy appearance of disc
Arteriola attenuation

97
Q

What is a focal seizure. Common symptoms in brain lobes?

A

Focal seizure is abnormally discharging neurons in a localised area

  • Either consciousness non-impaired = focal aware seizure
  • Or consciousness impaired = focal non-aware sezirue

-Occipital - flashing blobs of light
-Parietal - spreading paraesthesia / pain
-Frontal - hyperkinetic high energy motor movements
-Temporal - epigastic rising sensation . dejavu, emotion eg fear/panic, olfactory

98
Q

Occipital focal seizure vs migrane

A

Occiptal
- Short lasting seconds- blobs

Migrane
- Longer lasting minutes - jagged lines

99
Q

Focal seizure management

A

Can use any of the drugs for generalised seizures.
Lamotrigine, carbamazepaine, keppra

Valproate usally LESS effective

100
Q

Retinitis pigmentosa causes? What if you saw hearing aids?
Obesity / polydactyly? renal disease?
Progressive opthalmoplegia?
Pacemaker?
Ataxia?
Polyneuropathy?

Which has management?

A

Inheritance variable based on cause

15% Usher syndrome - recessive
- Varying severities of a sensory neural hearing loss
- (often born with moderate-severe hearing loss)

Bardet-biedel syndrome
- Obese / polydactyly
- Renal disease
[Big Boys]

Kearns-sayres
- Mitochrondrial (maternal)
- Progressibe and complex opthalmoplegia
- Cardiac conduction defects - PPM
- Ataxia

Resfem’s disease = recessive
- Ataxia
- Deafness
- Polyneuropathy
Management -> stop eating foods with phytamic

Couple of vitamin deficiencies
A and E
- Consider if

101
Q

how to assess visual acuity if vision too poor to to read top line of snellen chart

A

Can they detect movement - eg moving hand in front of face

If not
-> check for ability to detect light with pen torch

102
Q

Retinitis pigmentosa exam

A

Hands - polydactyly / scars of fingers removed
-> Bardet-biedel

Pacemaker
- Kearns-sayres

Hearing aids
- Usher, refsems, Kearns-sayres

Acuity

Eye movements
- consider Kearns-sayres if complex opthalmoplegia

Fundoscopy

103
Q

Retinitis pigmentosa investigations

A

Referral to opthalmologist

Full field electroretinography
- Response of retina to light
- would be reduced

Formal humphrey visual field testing

Ischihara plates

Retinal photography
- better than fundoscopy

If suspicion of genetic syndrome
-> geneticist

If deafness -> audiology assessment

104
Q

Management of retinitis pigmentosa

A

OT hep with visual aids

ENT - screening for hearing loss

Genetic counciling if specific diagnosis

Patient education - explaining no cure often

Discuss job / driving status

Phsycological support

105
Q

What is a stroke

A

Clot or blood in the brain

106
Q

Stroke examination?
- How does it differ if L / R sided weakness

A

Inspection - no matter if asked to examine CN / Upper / Lower
- May have splints - used for preventing fix flexed deformities
- Walking aids
- Scars on head eg hemicraniectomy
- PEG tube

Sneaky tip
- When introduce self during inspection come from left and offer to shake hands
[Assesses left side neglect and also speech
- L weakness (R brain) - assoc neglect
- R weakness (L brain) - aphasia]

Inspect
May have flaccid or flexed deformity

Tone
- Typically flexed high tone
- As examine more it will soften
- Important to differentiate high tone / contractures

Power
- Asymmetric pattern of pyramidal weakness

Reflexes - consider reinforcement eg gritting teeth / clenching hands
Clonus
Plantar

Sensation
- Light touch
- Pin prick
- Vibration

Coordination
- Heel shin
- dysdiadochokinesia

Cortical symptoms
- Test inattention
-If they have RIGHT sided weakness examine SPEECH

  • If they have LEFT sided weakness examine NEGLECT
    [ Visual fields then wiggle both fingers, Sensation L then R then Both]

To complete I would examine
- Proprioception, temperature
A full CN examination paying particular interest in visual field defects such as homonymous hemianopia and a full cortical assessment looking for neglect.

107
Q

anterior, middle and posterior cerebral arteries supply? Which parts of body generally affected ?

A

anterior cerebral arteries supply the anteromedial area of the cerebrum.
- ACA -> mainly leg

The middle cerebral arteries supply the majority of the lateral cerebrum.
- MCA -> mainly arm and face

The posterior cerebral arteries supply a mixture of the medial and lateral areas of the posterior cerebrum.

108
Q

TACS / PACS / Lacuna / POCS classification

A

Bamford

Essentially TACS and PACS involve cortical signs
- aphasia if affecting R weakness (L side brain)
- neglect if involving L weakness / R brain side.

Total anterior circulation stroke (TACS)
- Usually MCA -> mainly arm and face
- ACA -> mainly leg

All three of the following need to be present
-Unilateral weakness (and/or sensory deficit) of the face, arm and leg
-Homonymous hemianopia
-Higher cerebral dysfunction (dysphasia, visuospatial disorder)

Partial anterior circulation stroke (PACS)
- a less severe form of TACS, in which only part of the anterior circulation has been compromised.

Two of the following need to be present for a diagnosis of a PACS:
-Unilateral weakness (and/or sensory deficit) of the face, arm and leg
-Homonymous hemianopia
-Higher cerebral dysfunction (dysphasia, visuospatial disorder)*
-Higher cerebral dysfunction alone is also classified as PACS.

Posterior circulation syndrome (POCS) involves damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem).

One of the following need to be present for a diagnosis of a POCS:

-Cranial nerve palsy and a contralateral motor/sensory deficit
-Bilateral motor/sensory deficit
-Conjugate eye movement disorder (e.g. horizontal gaze palsy)
-Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia

**A lacunar stroke (LACS) ** is a subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions (e.g. dysphasia).
-> Weakness usually affects Face arm and Leg as is a more distal vessel

One of the following needs to be present for a diagnosis of a LACS:

-Pure sensory stroke
-Pure motor stroke
-Sensori-motor stroke
-Ataxic hemiparesis

109
Q

1 - In paces unilateral weakness without cerebral dysfunction is going to be someone with?

2 - If there are facial weakness you know -?

A

1 - Lacuna stroke

2 - it is a CN cause Ie. nothing to do with the spine

110
Q

In stroke what is L weakness usually associated with? R weakness ?

A

L weakness - neglect

R weakness - Speech

[The Right sided Speech Left them with Neglect]

111
Q

What is the main posterior circulation stroke syndrome to know about

A

Lateral medullary syndrome

  • Loss of pain and temperature sensation on one side of the face
    Loss of pain and temperature sensation on the opposite side of the body
112
Q

Difference between high tone and contractures in stroke

A

High tone you can overcome

Contractures - cannot either too painful or just unable
- Definitely means chronic

113
Q

What does Asymmetric pattern of pyramidal weakness mean in stroke

A

Flexor posturing in upper limb

Extensor posturing in lower limb

114
Q

MRC scale

A

0 - no movement
1 - flicker
2 - movement without gravity (eg turn arm so thumb facing up to test wrist extension)
3 - Move against gravity
4 - reduced power
5 - Against resistance

115
Q

Stroke - what features make it feel likely to be from brain and not spine?

A

Brain if face
Brain if unilateral (usually)

116
Q

Differentials for hemiparesis

A

In the Acute stroke with flaccid hemiparesis I would consider
- Tods paresis
- Migraine

However with Chronic stroke - Upper motor neurone signs i would consider
- SOL
- MS

117
Q

Stroke investigations / management

A

In the acute setting the investigations would be different from the patient who has more chronic symptoms in front of me

Acute
- Stabilisation with a focused ABCDE
- NIHH assessment
- Organise urgent CT / CTA and call the thrombolysis / thrombectomy team

Otherwise
FBC
U+Es
HBA1C
Cholesterol
Glucose

CT + CTA if within thrombolysis window

ECG - especially for AF

Carotid dopplers (if you didn’t already have the CTA in the acute setting)

Consider 24hr tape

Echo in young patient / embolic stroke

118
Q

Management of stroke

A

Check if eligible for thrombolysis (4.5hr) or thrombectomy (24hr)

Ensure medically stable and perform NIHH score then discuss with stroke team

Ischemic stroke
- Asprin 300mg for 2 weeks then clopidogrel
- Or anticoag if due to AF

Haemorrhagic
Manage hypertension to target systolic 140-150

Swallow assessment and consider NG

Full assessment from nutrition, physio and OT
Cognition assessment with MOCA

VTE prophylaxis with intermittent pneumatic compression. [NOT TEDS or enoxaparin]

Longer term
Manage cardiovascular risk factors
- Diabetes, HTN, cholesterol

  • Management of high tone eg splints / botox

Follow up ECGs and carotid dopplers

Job / driving / visual fields

119
Q

What investigations if a young person with stroke Eg <55

A

Unusual thrombosis
- Antiphospholipid screen or acquired thrombophilia

Vasculitis
- Screen ANCA / ANA

Bubble echo at 5 weeks

MRI

120
Q

Name some complications of acute stroke

A

Brain
- Swelling eg malignant MCA syndrome
- Haemorrhagic transformation
- Repeat infarcts
- Seizures

Bleeds
- Hydrocephalus

Stroke
- Swallowing / aspiration
- Incontinence
- Spasticity
- Pain

PEs, DVTs as unable to use clexane
Falls
Delirium

121
Q

MND Exam signs

A

Inspection
Wasting and fasiculation

Tone - Usually spastic but may be flaccid
Power - Weak, often footdrop is presentation
Reflexes - variable Think absent knee jerk with extensor plantar
Sensory - NORMAL

Speech - dysarthria
- Bulbar (donald duck) - palate weakness
- Pseudo bulbar (hot potato) - spastic tongue

Tongue
- Wasting and fasiculation - bulbar
- Stiff spastic with brisk jaw jerk - pseudobulbar

NO sensory, Occular or cerebellar

122
Q

What is MND? what really makes you think of it ?

A

Progressive disease of unknown aetiology which involves axonal degeneration of the upper and lower motor neurones

3 Ps
Painless, progressive paralysis

123
Q

What are the 3 main types of MND? Spastic vs flaccid predominant? Best prognosis?

A

Often overlap between them

Amyotrophic lateral sclerosis (50%)
- corticospinal tracts
- Spastic paraparesis

Progressive muscular atrophy 25%
- anterior horn cells
- Wasting fasiculation and weakness
- BEST prognosis

Progressive bulbar palsy 25%
- Lower CNs and suprabulbar nuclei -> speech and swallowing issues
- WORST prognosis

124
Q

Investigation of MND

A

Clinical diagnosis

Bloods
Consider b12 / CK

Consider genetic testing SOD1
[Poor sod]

EMG - motor neurone disfuction you struggle to detect clincially
- Denervation and renervation seen
- exclude myaesthenia etc
- look at muscle disease

MRI brain and spine
- Help exclude brain stem lesions, cervical cord compression

125
Q

MND treatment

A

Supportive
Patient education and support groups
PEG feeding / Dietician
PT mobility aids
Communication aids
OT
NIV
Advance care planning

Riluzole - glutamate antagonist

126
Q

MND prognosis / predictors

A

Die by 3 years -> pneumonia / resp failure

Poor predictors
- Onset in elderly
- Female
- Bulbar involvement

127
Q

MND differentials of hand musle wasting

A

Anterior horn cell
- MND
- Syringomyelia
- Cervical cord comrpession
- Polio

Brachial plexus
- Cervical rib
- Pancoast tumour
- trauma

Peripheral nerve
- peripheral neuropathy

Muscle
- Disuse atrophy eg rheumatoid

128
Q

What causes fasiculations? most common causes in hands

A

Axonal loss -> remaining axons recruiting and innervating more myofibrils
-> large motor units

MND
Syringomyella

129
Q

What is kennedy’s disease ? differentiate from MND

A

Lower motor neuron disease
X linked -> men

Tremor predominant
gynaecomastia
symmetrical

130
Q

differentiate MND and myotonic dystrophy on exam

A

Dystrophy has
- Myotonia
- No upper motoneurone signs
- very symmetrical
- Rarely significant wasting

131
Q

Differentiate myaesthenia and MND

A

Dysarthria - only in MG crisis
Ptosis and fatiguability of eye movements

132
Q

MND differentials

A

Myotonic dystrophy
Myaesthenia - if bulbar
Heredetary spastic paraperesis
Syringomyela
Inclusion body myosisitis - foot drop

133
Q

Where is the macula ? fovea?

A

The macula is found lateral (temporal) to the optic nerve head.
The central part of the macula, the “fovea” is about the same diameter as the optic disc and appears darker than the rest of the macula due to the presence of an additional pigment.

134
Q
A

Microaneurysms are localised outpouchings of capillaries

Look very similar to dot and blot haemorrhages - bleeding capiliaries

135
Q
A

Cotton wool spots

136
Q

What causes neovascularisation

A

Insufficient retinal perfusion results in the production of vascular endothelial growth factor -> neovascularisation

137
Q

What is bells palsy? Name 4 Features

A

Lower motorneurone palsy of CN7

Unilateral facial weakness
Inability to close eye
Hyperacusis
Pain behind ear
Loss of taste

138
Q

Bells vs stroke

A

Bells - onset over hours to days

Stroke - sudden onset
- Forehead spairing

139
Q

Why does a stroke spare the forehead

A

Forhead gets innervation from both hemispheres but only ipsilateral facial nerve

140
Q

Examination of CN 7

A

close eyes agaisnt resistance

Elevate eyebrows

Show teeth

Open mouth against resistnace

Formal taste testing

141
Q

Bells palsy red flags and what they might indicate as the cause

A

Bilateral
- Lime disease
- HIV seroconversion
- Gillian barre

Additional CN involvement
- CN8 in cerebellar pontine angle tumours

Systemic features
- Bullseye rash - lime

Sudden onset
- Vascular

Very slow onset over weeks
- ?SOL

142
Q

Bells differentials name 5

A

Ramsay hunt
- Herpes

Stroke

Lime disease

Otitis media

Acoustic neuroma

Gillian barre - common to invovle CN7 and bilat

HIV

Autoimmune
- Sjogrens
- Sarcoid
- MS

143
Q

Bells inverstigations?

A

If typical symptoms can diagnose clinically. If suspicious / not resolving after 6 weeks then consider

Lyme serology
MRI for MS
LP if thought to be inflammatory

143
Q

Bells treatment

A

50mg Pred 10 days
Eye protection - lubricating drops
[Both due to less lacrimal secretion (reduced parasympathetic) and inability to close eye

Aciclovir if evidence of ramsay hunt

If prolonged / incomplete recovery can refer to neuro

144
Q

Memory loss differentials? history?

A

Dementia
- Alz - progressive short term memory loss
- Vascular - assoc stroke / vascular disease, mood is big feature
- Lewy body - periods reduced consciousness, parkinsonism, vivid dreams
- Parkinson - usually parkinsonism before dementia
- Fronto temporal- personality / agression / language

NPH - gait, incontinence, memory loss
SOL - personality change
Depression

Hypothyroid

Alcohol related brain injury

Red flags
- Left gas on / left house open
- got lost and brought back by some body
- Feel safe in the car
- Loss of inhibition / agression

Screen systems
- Constipation
- Continence
- Gait

PMH
- Cardiovascular risk factors
- Previous psych history

DH
- Do they self manage - dossett box
- Antichoninergic - Anti psych / oxybutinin / amitrip

Family history
- Young memory problems

Social
- How is affecting
- Who is supporting
- Driving

145
Q

What are the types of memory decline

A

Short term - words dates facts

Semantic - faces

Prospective - furutre eg appointments

Working - get to the top of stairs and forget / driving and excecutive

Episodic - eg in alz no memory of last 20 years but

146
Q

Memory loss exam

A

Brief systemetic exam

Power and coordination in all limbs

Ataxia

Full set of obs

Cognitive screen Eg AMT, MMSE, MOCA

147
Q

What are the formal cognitive assessment tools

A

Screening
4AT

Tool
MMSE
MOCA
Addenbrookes ACE 3

148
Q

Memory loss investigations

A

Standard bloods
Calcium
TFTs
b12 / folate
HIV / sysphilis if any suspicion

If young
- Autoimmune encephalitis as well

Imaging
- CTB - rule out SOL, stroke, vessle disease
- Likely MRI if need more info

Formal cognitive assessment

149
Q

Management of dementia

A

Educate
- This is likely to be a slow but progressive condition
- Can discuss more later

MDT
Signposting to info like dementia services
Social services - Care / rest bite
OT - gas, car
Physio

Medication
- Alz - Ach inhibitors eg donepazil, rivastigmine (improve by less than 1 point on MMSE)
- Memantimine - behavioural symptions
- Rivastigmine.- reduces hallucinations in lewy body

150
Q

Normal pressure hydrocephalus treatment

A

Consider theraputic LP
-> vp shunting if requires regular

151
Q

Perform exam of this patient with coordination issues

A

DANISH
disdiadokinesis
Ataxia
Nystagmus
Intention tremor
Scanning dysarthria
Hypotonia / Hyporeflexia

Examine

Gait

Brief conversation
- Dysarthria

Upper limbs
- Finger nose incoordination
- Disdiadokinesis
- Hypotonia
- Hyporeflexia
- Rebound phenomenon

Eyes
- Nystagmus

Lower limbs
- Foot tapping
- Heel-shin

152
Q

Cerebella lobe lesion vs vermis vs vestibular nucleus lesion

A

Lobe
-IPSILATERAL cerebellar signs in limbs

Vermis
- Ataxic trunk / gait with normal limbs tested on bed

Vestibular nucleus
- Nystamus from Contralateral side

[L nystagmus could be due to a L (ipsilateral) cerebellar lesion or a R contralateral vestibular nucleus lesion]

153
Q

Causes of cerebellar issues

A

PASTRIES

Paraneoplastic cerebellar syndrome
Alcoholic cerebellar degeneration
Sclerosis - MS
Tumor - posterior fossa
Rare - friedricks ataxia
Iatrogenic - phenytoin toxicity
Endocrone - hypothyroid
Stroke - brainstem

154
Q

MS is? Main types?

A

Chronic inflammatory demyelinating disorder

Relapsing-remitting (85%)
Approximately half go on to develop secondary progressive MS

Primary progressive or progressive-relapsing (15%)

155
Q

Features on examination of eyes in MS

A
  • Red desaturation
  • Relative afferent pupillary defect in affected eye

Extra-ocular movements
- Internuclear ophthalmoplegia – failure of adduction of affected eye, with nystagmus on abduction of the contralateral eye
- Document preservation of convergence
- Nystagmus

Offer fundoscopy to look for pallor of the affected disc
May be normal as disease is retrobulbar in the majority of patients

156
Q

Differentials for MS

==

A

Infective
- Lime disease
- Tertiary syphilis
- HIV
- HTLV-1 -> spastic paraperisis

Inflamatory
- Vasculitis
- Acute disseminated encephalomyelitis (following viral illness / vaccination)
- Neuromyelitis optica
- Transverse myelitis
- Systemic inflammatory (SLE/ Sarcoid / sjogren

Metabolic
- B12 deficiency
- Diabetic neuopathy
- Hypothyroid

Lysosomal storage disease
- Eg Fabry

Mitochondrial diseases
- Myoclonic epilepsy with lactic acidosis and stroke-like episodes (MELAS)
Myoclonic epilepsy with ragged red fibres (MERRAF)

Heredatory spastic paraperisis

157
Q

Investigations of MS

A

Full blood count (anaemia of chronic disease)
Liver function, renal function prior to starting immunosuppression

CSF - oligoclonal bands (>80% of patients with MS, but not specific)

MRI

Visual evoked potentials looking for conduction delay (prev optic neuritis)

158
Q

MS management

A

Conservative
Patient education + support groups
Multidisciplinary team approach
Occupational and physiotherapy to preserve and maximize function
Walking aids / visual aids as necessary

Treatment of symptoms
- Spasticity: baclofen, gabapentin, tizanidine, dantrolene
- Depression: selective serotonin re-uptake inhibitors, tricyclic antidepressants
- Fatigue: amantadine
- Neuropathic pain: TCAs, pregabalin, gabapentin, carbamazepine
- Bladder dysfunction: intermittent self-catheterization, α1-antagoinists, anti-cholinergic agents

Acute attacks
- high dose IV steroids (consider plasma exchange)

Chornic Disease modifying
- Specialist input in rapidly evolving field
- Interferon b
- Natalizumab
- Fingolimod

159
Q

MS and pregnancy

A

Reduced relapse rate

-> increased post partum

160
Q

What is Gestermans syndrome

A

Gerstmann syndrome is a rare neurological disorder that affects the brain’s parietal lobe, causing a loss of certain cognitive functions:

** Writing disability **
Also known as agraphia or dysgraphia, this can include illegible writing, inconsistent letter formation, and unfinished letters
Inability to do math
Also known as acalculia or dyscalculia, this can include difficulty with adding, subtracting, multiplying, and dividing
Inability to identify fingers
Also known as finger agnosia, this can include difficulty identifying one’s own or another’s fingers
Inability to distinguish right from left

160
Q

What is the most common brainstem vascular syndrome? Pathophysiology

A

Lateral medullary syndrome (wallenberg) - Occlusion of PICA

Contralateral
- pain and temperature in limbs

Ipsilateral
- pain and temp face (trigeminal)
- Cerebella signs
- Nystagmus - vestibular nucleus
- horners - descending sympathetic tract
- palatal paralysis / loss of gag -
- nucleus ambigus

161
Q

Name 5 differentials of spastic legs

A

MS
Cord compression / cervical myelopathy
Trauma
MND (if no sensory)

Rare
- Anterior spinal artery thrombus
- sryngomyellia
- heredatory spastic paraplegia
- Subacute degeneration of spinal cord
- freidricks ataxia

162
Q

Myotomes L1-5

A

L1-2 - Hip flexion
L3 - Knee extension
L4 - ankle dorsiflexion
L5 - big toe extension

163
Q

Dermatomes lower legs

A
164
Q

Syringomyelia exam

A

Inspection
Scars from painless burns

Weakness and wasting of the small muscles of the hand

Reduced reflexes

Sensory loss
- Loss of pain and temperature (spinothalamic)
- Presevation of joint position and vibration sense (dorsal columns)

165
Q

Syringomyelia pathophysiology?

Associations?

Diagnosis

A

Expanding fluid filled cavity within the cervical cord. Compresses spinothalamic neurones first

Assoc - arnold chiari malformation

Diagnostic mri spine

166
Q

Upper limb myotomes

A

C5/6 - Biceps - Elbow flexion and suppination

C7/8 Triceps - elbow extension

T1 - finger abduction

167
Q

Upper limb dermatomes

A

c5 shoulder
c6 thumb / lateral forearm
c7 middle finger
c8 little finger
t1 medial forearm

168
Q

Parkinsonism on exam what additional features to make you suspect other cause

A

Multisysem atrophy
- Hypotension
- Cerebellar signs

Progressive supranuclear palsy
- Vertical eye movements

Forgetful
- Lewy body dementia

Medications

169
Q

Charcot-marie-tooth also called? Exam findings

A

Hereditary sensory motor neuropathy

  • Pes Cavus (also seen in freidricks ataxia)
  • Wasting of distal lower limb muscles with preservation of thigh bulk
  • Wasting of hand muscles
  • Weakness of ankle dorsiflexion and toe extension
  • Variable degree stocking sensory loss
  • High stepping gait (footdrop) and stamping (absent proprioception)
170
Q

What are the 2 types of charcot marie tooth

A

type 1 - demyelinating
Autosomal dominant - PMP22 mutation

Type 2 - axonal

171
Q

Name 8 causes of peripheral neuropathy

A

Predominant sensory
- Diabetes
- Alcohol
- Drugs - isoniazid / vincristine
- Vit B12 / B1
- Chronic inflammatory demyelinating polyradiculoneuropathy

Predominant motor
- Guillian barre
- Botulism
- lead toxicity
- Charcot marie tooth

Mononeuritis multiplex
- Diabetes
- Connective tissue - Rheum / SLE
- Vasculitis - PAN / eosinophilic granulomatosis
- HIV
- Malignancy

172
Q

friedricks ataxia exam

A

End of bed
- Young / wheelchair (or mobility aids) with scoliosis
Dysarthria when introduce self
- Bilateral cerebellar ataxia
-> Ataxiaic hand shake, dysarthria nystagmuis

Lower limb
- Leg wasting with absent reflexes and bilateral upgoing plantars
- Often mild increase in tone
- Pes cavus - high arch that doesn’t flatten when weight is applied
- Loss of vibration and proprioception sense - dorsal columns (may also have some pinprick / soft loss)
- Gross bilateral Ataxia

If time
- Assess speach / nystagmus
- Kyphoscoliosis
- Upper limb finger nose / disdiadokinesis

I would like to assess
- Fundoscopy for optic atrophy
- Finger prick marks / glucose for diabetes
- high arched palate
- Full cardiovascular exam HCOM

SN hearing loss

173
Q

Freidricks is?Pathophysiology? inheritance and onset? Key associations

A

Progressive neurodegenerative condition
(most common inherited ataxic condition in uk)

Frataxin gene on chromosome 9
Autosomal resessive
[Trinucleotide repeat with anticipation]
-> onset as a teen
-> Iron accumulation in mitochondria of cerebellum -> central ataxia
-> Iron accumulation affecting dorsal collumns -> sensory ataxia and loss of tendon reflexes

  • HOCM (cardiac myosites replaced) > most common cause of death
  • high arched palate
  • Dysphagia - CN VII, X and XII
  • Sensory neural deafness
  • diabetes
  • kyphoscoliosis
  • optic atrophy
  • Pes cavus
    • Mild dementia
174
Q

Name 5 causes of extensor (upgoing) plantars and absent ankle/knee jerk

A
  • Friedricks ataxia
  • subacute degenration of the cord - b12 def / NO2 use
  • MND
  • Conus medullaris lesions
  • Dual patology - Peripheral neuropathy (absent ankle jerk) + stroke on affected side
  • Tertiary syphilis - Taboparesis
175
Q

Name 4 causes of bilateral ptosis

A

Congenital
Senile
Myaesthnia
myotonic dystrophy
Mitochondrial eg kearns-sayre syndrome
Bilateral horners

176
Q

Recent first seizure. Examine them as you wish

A

Tuberous sclerosis

End of bed / Face
- Butterfly distrobution of adenoma sebaceum
- Antiepileptic treatment eg gum hyperplasia in phenytoin

Hands
- Periungal fibromas

Trunk
- Shagreen patch - rough leathery skin over lumbar region
- Ash leaf macules

Abdo
- Renal enlargement - PKD
- Renal transplant / dialysis

177
Q

Seen on fundoscopy tuberous sclerosis

A

Retinal phakoma
- dense white spots

178
Q

Genetics tuberous sclerosis

A

Autosomal dominant
TSC1 - chrom 9
TSC2 - chrom 16 (PKD 16 too)

179
Q

Tuberous sclerosis main 3 associations

A

Low IQ
Seizures
Renal manifestations eg PKD / angiomas

Hands
- Periungal fibromas

Trunk
- Shagreen patch - rough leathery skin over lumbar region
- Ash leaf macules

180
Q

What are the renal manifestations of tuberous sclerosis

A

Polycystic kidneys
RCC
angiomyolipomas

181
Q

Examine this patients skin and procede

A

Neurofibromatosis

Skin
- more than 2 cutaneous neurofibromas
- Six or more cafe-au lait patches
- Axillary frekling

Eyes
- Lisch nodules
- reduced acuity - optic glioma / compression

Chest
- Lung fibrosis

Neuropathy

BP - Hypertension (assoc renal artery stenosis / phaeo

182
Q

What are the 2 types of neurofibromatosis

A

Both autosomal dominant

Type 1
- chrom 17
- Peripheral form

Type 2
- Chrom 22
- Bilateral acoustic neuromas -> SN deafness

183
Q

Main complications/associations neurofibromatosis

A

Phaeo
renal artery stenosis
Epilepsy
sarcomatous change
scoliosis
Low IQ

184
Q

Name 3 causes of enlarged peripheral nerves + peripheral neuropathy

A

Neurofibromatosis
Leprosy
Amyloidosis
Acromegaly
Refsums disease

185
Q

3 causes

A

Unilateral Horners

Remember to have a look for evidence of CVCs / carotid endarctectomy
Pancoast tumour resection

Brainstem
- MS
- Stroke - wallenbergs

Spinal cord
- Syrinx

Neck
- pancoast
- aneurysm

186
Q

Bright light shone into eyes?
Additional sign

A

Holmes-aide pupil

Absent / diminished knee / ankle jerk

187
Q

4 causes

A

CN 3 palsy

Medical
- Mononeuritis multiplex (eg diabetes)
- Midbrain infarct
- Midbrain demyelination eg MS
- Migraine

Surgical
- Communicating artey aneurysm (posterior)
- Cavernous sinus pathology eg tumour / thrombosis
- Cerebral uncus herniation

188
Q

Small irregular pupil not reactiving to light? What else should you do

A

Argyll robertson - spyhilis
(may be diabetes)

Test for sensory ataxia (also sign of quaternary syphilis)

189
Q

What is marcus gunn pupil

A

Positive RAPD

189
Q

Name 5 causes of RAPD with pale disc

A

PALE DDISCS

Pressure - Gaucoma / tumour
Ataxia - freidricks
LEbers optic atrophy
Degenerative - retinitis pigmentosia
Diet - B12 deficiency
Ischemia - CRAO
Sphylis / Toxo
Cyanide /lead / alcohol poisoning
Sclerosis - MS

190
Q

Retinitis pigmentosa with
Ataxia?
Deafness?
Opthalmoplegia + PPM?
Polydactyly?
Ichyosis - Scaley skin?

A

Ataxia - Freidricks / kearns-sayre / refsum

Deafness - refsum / kearn sayre / usher

Opthalmoplegia + PPM - kearn sayre

Polydactyly - Bardet-Biedl syndrome

Ichthyosis - refsum

191
Q

upgoing plantars and absent ankle/knee jerk investigations

A

Full and familty history

Urine dip fasting glucose / HBA1C for diabetes

ECG / CXR / Echo evidence of HCOM

Nerve conduction studies - absent / reduced seonsory action potentials with increased motor velocity

MRI brain / spine - atrophic changes / rule out conus medularis or subacute degeneration of cord

  • Friedricks ataxia
  • subacute degenration of the cord - b12 def / NO2 use
  • MND
  • Conus medullaris lesions
  • Dual patology - Peripheral neuropathy (absent ankle jerk) + stroke on affected side
  • Tertiary syphilis - Taboparesis
192
Q

Management freidricks ataxia

A

MDT
- Geneticist / genetic counciler
- Neurologist
- physio
- Occupational therapist
- Orthotics
- Diabetic nurses
- Cardiologist
- GP for continuity of care

No cure
Management of complications such as spacicity / diabetes / arrythmias / joint deforment or scoliosis

193
Q

Which crainial nerves come from which bits of brainstem?

A

CN1 (olfactory) - olfactory bulb
CN2 (optic) - Retina

CN3/4 - Midbrain
CN 5-8 - Pons
CN 9-12 - Medulla

194
Q

Eye movement muscles?

A

Superior / inferior / medial / lateral Rectus muscles
Superior / inferior obliquie

Lateral rectus - CN6 (Abducens)
Superior oblique - CN4 (troclear)
Remainder - CN 3 (occulomotor)

195
Q

What is conjugate gaze

A

2 eyes moving in the same direction

195
Q

What additional structure in the pons for lateral gaze? function?

A

Paramedian pontine reticular formation

controls horizontal eye movements

196
Q

To look left which CNs are firing? what connects these?

A

L paramedian pontine reticular formation which triggers :

L sided abducens (CN6)
R sided Occulomotor (CN3)

Medial longitudinal fasiculus (heavily myelinated nerve fibres which starts at abducens and travels to occulomotor)

197
Q

What is internuclear opthalmoplegia? What do you need to then assess?

A

Disorder of horizontal conjugate gaze

Impaired ADduction of ipsilateral eye
With nystagmus of ABducting eye

Caused with a lesion in medial longitudinal fasiculus

Assess convergence to see if eye can in fact ADduct

198
Q

Looking to right

A

Left medical longitudinal fasiculus lesion

The eye which cannot move (adduct) is the side with the lesion

199
Q

If multiple eye movement issues what would you call it?

A

Complex opthalmoplegia

200
Q

What are the causes of INO? Differentials?

A

MS
- (Medial longitudinal fasiculus is highly myelinated)
- If young it is likely this

Stroke
- Small stroke affecting pons / medulla

Other
- Neoplasm / mets
- Inflammatory - cns vasculitis
- Infections - syphilis / TB
- Trauma
- Metabolic - B12 / Wernikes

Differentials
- CN3 palsy, CN4 palsy etc

INO+ syndromes
- 1 and a half syndrome - 1 eye has complete bilateral horizonal gaze palsy and the other has failure of ADduction (when abducts have nystagmus)
- Bilateral wall eyed opthalmoplegia (both eyes face out)

Mimick
- Myaesthenia gravis due to fatiguability

201
Q

Bilateral INO =?

A

MS

Stroke would have to involve large area of brainstem to cover both sides -> lots more signs

202
Q

INO investigations

A

MRI head looking at brainstem
- Infact / haemorrhage / demyelination

If young and demyelination
- MRI whole spine for cord lesions
- MRI with gadalinium (enhances with new lesions)
- Oligoclonal bands in CSF

If old and evidence of infarct
- Stroke bloods - Cholesterol / diabetes
- ECG for AF +/- 24hr tape etc

Infection
LP etc

203
Q

conjugate vision management

A

MS steroids / Disease modifying
Stroke - stroke

Eye patch etc

204
Q

Which palsys in these

A

Normal
Right occulomotor
Right Troclear
Right abducens

205
Q

Bar 4 eye muscles what else does the occulomotor nerve innervate

A
  • Superior rectus – moves the eye up.
  • Inferior rectus – moves the eye down.
  • Medial rectus – moves the eye in.
  • Inferior oblique – moves the eye up when the eye is looking in toward the nose.
  • Levator palpebrae superioris – lifts the upper eyelid. [helps to remeber the function of the inferior oblique as lifting eyelid and eye up happen together]

Conditions compromising blood flow to the inner nerve fibers controlling these muscles — without compressing the outer fibers — don’t affect the pupil.

Outer nerve fiber function

The outer fibers of CN III supply two additional muscles that are part of the parasympathetic nervous system, which controls functions when the body is in a resting state.

These muscles are the:
- Sphincter pupillae – located in the iris and makes the pupil smaller.
- Ciliary muscle – causes the lens to change shape when focusing up close.

206
Q

CN3 palsy features

A

Can be pupil sparing

207
Q

CN3 palsy medical vs surgical causes and pathophysiology

A

Surgical - Complete (with pupil involvement)
- Usually a compressive cause eg PICA
- This is a neurosurgical emergency until proven otherwise
- Others - malignancy, trauma, haemorrhage, uncal herniation
- [parasympathetic fibres which run on outside to pupil are suseptible to pressure from external structures]

Medical - Pupil sparing
- microvascular supply to neve damaged
- blood flow insufficient to reach inner fibers.
- Diabetes, hypertension

Other causes would expect more than an isolated CN3 palsy eg infection / vasculitis / cavenous sinus syndrome

208
Q

CN3 palsy investigations and management

A

If pupil involvement (surgical)
-> Urgent CT angio (or MRA) brain for PICA
With urgent neurosurgical referral dependent on result

Medical
Bedside - check BP and sugar
Bloods - FBC , HBA1C, inflam markers, [TFTs, Ach / MuSK]

Management of HTN and dieabetes and most patients recover before 12 months

  • No driving / heavy machinery while diplopia
  • prism glasses / eye patch
209
Q

Basic managenent of diplopia due to eye movement palsy

A
  • No Driving / work responsibilities
  • Prism glasses
  • Eye patch
210
Q

“double vision where the objects are split vertically” How to assess this

A

Right CN4 palsy
- Get them to ADduct (look to left) and then look down in this position

211
Q

CN4 palsy causes (make sure you get the top 3)

A
  • Congenital
  • Microvascular ischemia - DIabetes and hypertension
  • Head injury - very thin nerve - doesnt require massive trauma

[Stroke
Inflammation
Multiple sclerosis
Tumor]

212
Q

At rest

A

Right CN6 palsy
- eye sits slightly medial at rest due to unapposed action of medial recuts

213
Q

CN6 palsy causes

A
  • Congenital
  • Raised ICP( false localising sign also in IIH)
  • Microvascular ischemia - DIabetes and hypertension
  • Head injury - very thin nerve - doesnt require massive trauma
214
Q

Isloated CN syndrome investigations and management

A

Bedside
- BP and sugar

Bloods - FBC, HBa1c, inflam markers, cholesterol

New CN4 / CN6 will get an MRI head to rule out malignancy or clear structural cause

Conservative
- No driving while symptoms
- Eye patch / prism glasses

Medical
- HTN and diabetes control

214
Q

Complex opalmoplegia - What are you thinking if a few areas of brain with cn palsys

A
  • Thyroid eye disease
  • Myaesthenia
  • Myotonic dystrophy
  • Miller fisher syndrome
  • Stroke brainstem
  • Infection classically Lyme disease if multiple cranial mononeuopathies
  • Meningitis
  • Inflammatory - MS / vasculitis / sarcoid
215
Q

Infection -> ataxia complex opalmoplegia and loss of deep tendon reflexes

A

Miller fisher

215
Q

Perform a full neulogical screening exam

A

Legs
1. Rhombergs with feet together
2. Heel to toe walking
3. Walk on tip toes and then heels (plantar and dorsiflexion)
4. Hop on 1 foot

Arms
1. Pronator drift
2. Keep eyes shut and tough a finger on both hands then ask to use that finger to touch thier nose (middle and ring)
3. Play the piano in mid air
4. Tap back of each hand
5. hold hand and quick tone and cog wheel rigidity while they raise other hand in air

Head
1. Temporal visual fields “point at the fingers which move”
2. Eye movements
3. Shut eyes tight (look at pupils when open)
4. Show teeth then stick tongue out

On the couch
1. Fundoscopy
2. Tendon reflexes
3. plantars

A PACES (9 decks)

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