Neuro (3a Cards) Flashcards

1
Q

what is a cluster headache?

A

severely disabling episodic headaches.

more common in men and smokers.

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2
Q

how do cluster headaches present?

A

rapid onset excruciating pain around one eye
eye becomes watery, bloodshot, lids swollen, lacrimation
facial flushing
rhinorrhoea
pain is strictly unilateral, will usually affect one side only
course - headaches last 15-60min, once or twice a day, often nocturnal
clusters last 4-12 weeks, then they might have months/years before next cluster

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3
Q

how do you treat cluster headaches?

A

acute attack - 100% oxygen for 15 mins via non-rebreathe, sumitriptan SC or nasal spray at onset (nasal spray not licensed).
preventative - verapamil (start at 40mg and build up to 960mg max, requires ECG monitoring for AV block once at high doses/whilst raising dose)
prednisolone (second line, but can be preferred as started at top dose - then quickly wean off! may relapse)
lithium - if verapamil not tolerated, requires lots of monitoring
other options:
melatonin
topiramate
sodium valproate

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4
Q

give some possible triggers for cluster headaches

A
  • alcohol precipitates attacks when in a cluster, but can be drunk between clusters
  • histamine and nitroglycerine
  • for some patients - heat, exercise and solvents
  • disruption to sleep patterns (e.g. by shift work, jet lag, etc)
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5
Q

list some headache red flags that should prompt further investigation

A
  • change in pattern of headache.
  • new headache at age > 50.
  • onset of seizures.
  • headache with systemic illness.
  • personality change.
  • symps suggestive of raised ICP (morning headache, headache with coughing, sneezing, straining).
  • acute onset of the worst headache ever (possible intracranial aneurysm).
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6
Q

list some differentials to consider for an acute single episode of headache

A
with meningism (stiff neck etc):
  - meningitis
  - encephalitis
  - subarachnoid haemorrhage
head injury
sinusitis
glaucoma (acute closed-angle)
tropical illness e.g. malaria, typhus
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7
Q

what features of an acute single episode of headache would make you consider meningitis?

A

meningism - acute, severe headache felt all over with neck stiffness.
fever, photophobia, purpuric rash (although not always!)

admit urgently for CT head/LP if CT negative

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8
Q

what features of an acute single episode of headache would make you consider encephalitis?

A

neck stiffness, fever, odd behaviour, fits, reduced consciousness
admit urgently for CT head/LP if CT negative

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9
Q

what features of an acute single episode of headache would make you consider subarachnoid headache?

A

SUDDEN ONSET, ‘worst ever’ headache, often occipital (been kicked in back of head), stiff neck, focal signs, reduced consciousness
admit urgently for CT head/LP if CT negative

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10
Q

what features of an acute single episode of headache would make you consider head injury? what would prompt you to consider further investigations?

A

hx of trauma!
pain usually around site of trauma, but can be generalised.
CT head to exclude subdural/extradural haemorrhage if drowsiness ± lucid interval or focal signs.

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11
Q

what features of an acute single episode of headache would make you consider sinusitis? how do you treat it?

A
dull, constant ache over frontal or maxillary sinuses, with tenderness ± postnasal drip. pain worse on bending over. preceding coryzal symptoms. lasts 1-2 weeks.
if bacterial (likely Strep pneumoniae, haemophilus influenzae, moraxella catarrhalis) treat with abx - amoxicillin - although some evidence says this doesn't achieve anything.
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12
Q

give some home treatment measurers you would advise for a patient with acute sinusitis

A
  • paracetamol/ibuprofen for pain/fever.
  • intranasal decongestant (oral is not recommended for sinusitis) for a max of a week.
  • nasal irrigation with warm saline solution.
  • warm face packs, which may provide localised pain relief.
  • adequate fluids and rest.
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13
Q

what features of an acute single episode of headache would make you consider acute angle-closure glaucoma?

A

elderly, long-sighted people
constant, aching pain develops round one eye, radiating to forehead.
markedly reduced vision, visual haloes, N&V.
red congested eye, cloudy cornea, dilated non-responsive pupil (may be oval), reduced acuity.

seek urgent expert help, if delay in treatment >1hr likely start acetazolmide 500mg IV, plus lay supine and give any topical agents not contra-indicated in the patient
topical agents inlude:
Beta-blockers - eg, timolol, cautioned in asthma.
Steroids - prednisolone 15 every 15 minutes for an hour, then hourly.
Pilocarpine 1-2% (in patients with their natural lens).
Phenylephrine 2.5% (in patients who do not have their own lens).

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14
Q

what are tension headaches?

A

main cause of bilateral, non-pulsatile headache ± scalp muscle tenderness, with no vomiting/sensitivity to movement. often described as band round scalp, pressure, tightness.

divided into

  • episodic TTH. This occurs on fewer than 15 days each month. It can evolve into the chronic variety.
  • chronic TTH. This occurs on more than 15 days each month and has all the features of the episodic TTH.

chronic is more likely due to medication overuse.

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15
Q

how should you manage tension type headache?

A

reassurance, advise on stress management, hydration, risk of medicines overuse.
drug therapy - avoid codeine, ibuprofen first line (OTC), naproxen second. can try paracetamol but usually not as effective.
if nothing’s working - try amitriptyline.

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16
Q

what are the characteristic features of headache due to raised ICP?

A

worse on waking, lying, bending forward, coughing.
vomiting, papilloedema, odd behaviour, false localising signs.
must image before do LP - contraindicated otherwise!

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17
Q

what is a medication overuse headache?

A

chronic daily headache (> 15 days per month, with opiate/triptan use on >10 or paracetamol/NSAIDs on >15) due to overuse of analgesics - mixed opiates and paracetamol (Cocodamol) common culprit.

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18
Q

how do you manage a medication overuse headache?

A

reassurance/education.
withdrawal of analgesia - warn patient headache will worsen initially.
headache should resolve in 10 days or so.

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19
Q

what are the symptoms of trigeminal neuralgia? what are the common triggers?

A

paroxysms of intense stabbing pain, lasting seconds, in trigeminal nerve distribution (facial).
unilateral, typically maxillary/mandibular.
may have preceding symptoms e.g. tingling, numbness.
triggers - washing affected area, shaving, eating, talking, dental prostheses.
typical pt >50yo, woman (F:M = 2:1)

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20
Q

what are some red flags in a trigeminal neuralgia history that should prompt referral/further investigation?

A

Sensory changes, deafness or other ear problems.
Difficulty achieving pain control, poor response to carbamazepine.
History of any skin lesions or oral lesions that could lead to perineural spread.
Ophthalmic division only or bilateral as suggestive of benign or malignant lesions or multiple sclerosis.
Age of onset under 40 years.
Optic neuritis.
Family history of multiple sclerosis.

if investigation needed it’d normally be a brain MRI.

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21
Q

list some possible causes of secondary trigeminal neuralgia

A
  • compression by anomalous or aneurysmal intracranial vessels or a tumour
  • chronic meningeal inflammation
  • MS
  • varicella zoster
  • skull base malformation e.g. Chiari malformation

MRI needed to exclude these causes.

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22
Q

how do you treat trigeminal neuralgia?

A

carbamazepine PO at 100mg every 12hrs, max 400mg/6hrs.

then try lamotrigine, phenytoin or gabapentin.
if drugs fail, surgery - rhizotomy, microvascular decompression, stereotactic gamma knife surgery can work.

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23
Q

list some differential diagnoses for facial pain

A
migraine
trigeminal neuralgia
post-herpetic neuralgia - shingles
cervical disk pathology
sinusitis
bone neoplasia
temperomandibular joint dysfunction
dental problems
giant cell arteritis
cluster headaches
MS
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24
Q

what is giant cell arteritis?

A

needs excluding in anyone >50yrs with headache lasting a few weeks.
systemic immune-mediated vasculitis affecting medium-sized and large-sized arteries, particularly the carotid artery and its extracranial branches. associated with PMR in 50%.
can cause sudden bilateral vision loss so considered an emergency.

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25
Q

how does giant cell arteritis present?

A

recent onset temporal headache, myalgia, fever. temporal artery and scalp tenderness (e.g. when combing hair), jaw claudication (pain comes on gradually when chewing), amaurosis fugax or sudden blindness.
extracranial symps - dyspnoea, morning stiffness, unequal/weak pulses.

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26
Q

how do you manage a patient presenting with possible giant cell arteritis?

A

do an ESR blood test and give high dose (40mg) prednisolone immediately - if claudication give 60mg, if visual symptoms admit for IV methylpred.
other Ix - CRP, platelets, alk phos all raised, might see anaemia. get a temporal artery biopsy within 7 days of starting treatment.
typically a 2 yr course before it resolves - reduce pred once symps controlled and ESR reduced, but don’t be afraid to bump it back up as necessary.

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27
Q

how do migraines present?

A
  • visual (or other) aura for 15-30 mins before onset within 1hr of severe, throbbing, unilateral headache
  • headache without aura
  • aura without headache
  • headache is incredible severe with N&V, photo/phonophobia
  • lasts 4-72h
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28
Q

what are the criteria for diagnosing a headache as migraine if there’s no aura?

A

5+ headaches lasting 4-72hrs plus N&V or photo/phonophobia plus any 2 of the following:

  • unilateral
  • pulsating
  • impairs usual activity
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29
Q

what are the possible triggers for migraine?

A
CHOCOLATE:
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie-ins
Alcohol
Tumult
Exercise
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30
Q

what kinds of aura may be experienced in migraine?

A

visual - chaotic distorting lines/shapes/patterns, hemianopia
somatosensory - paraesthesiae spreading from fingers to face
motor - dysarthria and ataxia (basilar migraine), ophthalmoplegia or hemiparesis
speech - dysphasia or paraphasia

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31
Q

how do you manage/treat migraines? (not prophylaxis)

A
  • reassurance, education, encourage headache diary and identification of triggers, lifestyle (stress, diet and exercise, sleep)
    1) soluble aspirin or ibuprofen, prochlorperazine buccal for anti-emetic if needed
    2) rectal diclofenac and domperidone (anti-emetic) - not often used due to patient preference!
    3) triptans or ergotamine - ‘abortive’ so must be taken immediately after onset of headache/aura

MUST stop COCP - stroke risk

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32
Q

list some contra-indications for triptans

A

People with uncontrolled hypertension.
People with coronary heart disease or cerebrovascular disease
People with risk factors for coronary heart disease or cerebrovascular disease
People with coronary vasospasm (Prinzmetal’s angina)*.

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33
Q

what are the options for migraine prophylaxis?

A

offer if 2+ per month, impacting daily activity for 3+ days each time

1) beta blockers e.g. atenolol
2) amitriptyline
3) topiramate, sodium valproate (these are started in specialist care)
4) pizotifen
5) 12 weekly botulinum toxin A injections

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34
Q

list some differentials for stroke (there’s bloody loads)

A
head injury
hypo/hyperglycaemia
subdural haemorrhage
intracranial tumours
hemiplegic migraine
epilepsy (Todd's palsy)
CNS lymphoma
pneumocephalus
Wernicke's encephalopathy
hepatic encephalopathy
herpes encephalitis
abscesses
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35
Q

what are the two main types/mechanisms of stroke?

A

haemorrhagic vs infarction

arterial embolism (infarction) – from a distant site; e.g. carotids, vertebral or basilar arteries. embolus occludes an artery of brain resulting in infarction. may also come from heart valves in endocarditis.
Haemorrhage – can be in the cerebrum itself, or also a subarachnoid haemorrhage may cause a similar effect
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36
Q

list some uncommon causes of stroke

A
Venous infarct
Carotid/vertebral artery dissection (spontaneous or from neck trauma)
Polycythemia
Fat / air embolism – e.g. in divers
MS – demyelinating plaque may act as an embolus
Mass lesions (e.g. tumour)
Migraine
Thrombocythaemia and thrombophilia
Venous sinus thrombosis
Vasculitis
Amyloidosis
Drugs – particularly cocaine and OTC cold remedies that contain vasoconstrictors.
Sepsis - sudden BP drop
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37
Q

list some modifiable risk factors that can reduce the risk of a stroke

A
mostly affect risk of infarctive stroke:
HTN
smoking
DM
heart disease - valvular, ischaemic, AF
peripheral vascular disease
past TIA
carotid bruit
COCP
hypercholesterolaemia
alcohol misuse
clotting disorders
syphilis
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38
Q

what is CADASIL?

A

rare, inherited cause of stroke and vascular dementia.
Caused by a defective NOTCH3 gene
multiple small infarcts in the brain.
Often presents as migraine and depression in teenagers, and by the 20’s and 30’s there are often TIA’s and strokes.
Dementia may follow after age 40-50

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39
Q

list the main causes of infarctive stroke

A

60% – Atherosclerosis of the carotid arteries and aortic arch
20% – valvular heart disease
20% – disease of the vessels in the brain itself

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40
Q

what symptoms would you expect to see for a middle cerebral artery infarction?

A

most common stroke presentation!
Contralateral:

Hemiparesis
Hemiplegia (initially flaccid, becomes spastic)
Limbs usually floppy, and reflexes reduced/absent
Facial weakness (not always)
Hemianopia – visual field defect in which vision is lost in half of the visual field in one/both eyes.
Aphasia – when the dominant hemisphere is affected - ask about left and right handedness!

symptoms develop rapidly, over a period of minutes, or less commonly they can develop over a few hours.

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41
Q

what symptoms/signs indicate a cerebral infarct rather than brainstem/lacunar?

A
depending on site - 
contralateral sensory loss
contralateral hemiplegia - initially flaccid (floppy limb falls like dead weight when lifted), then spastic (UMN signs)
dysphasia
homonymous hemianopia
visuo-spatial deficit
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42
Q

what symptoms/signs indicate a brainstem infarct rather than cerebral/lacunar?

A

wide range of effects, incl (features - location):
Hemi/tetraparesis - Corticospinal tracts
Sensory Loss - Medical lemniscus / spinothalamic tract
Diplopia - Occulomotor nuclei
Facial Numbness - 5th nerve nuclei
Facial weakness - 7th Nerve nucleus
Nystagmus and vertigo - Vestibular connections
Dysphagia / dysarthria - 9th/10th nuclei
Horner’s syndrome - Sympathetic fibres
Altered consciousness - Reticular formation

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43
Q

what symptoms/signs indicated lacunar infarct rather than cerebral/brainstem? where are these infarct occurring?

A
occurring in brainstem, internal capsule, thalamus, pons
5 main syndromes:
1) ataxic hemiparesis
2) pure motor
3) pure sensory
4) sensorimotor
5) dysarthria (clumsy hand)

may be symptomless, or present with very localised symptoms (as in pure motor/sensory) due to the very localised effect it has.
consciousness/cognition stay intact (except in thalamic stroke)

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44
Q

give some info on the use of thrombolysis in acute stroke

A

must be sure it’s non-haemorrhagic (imaging) and that you are acting within 4.5 hours of onset of symptoms (so if they woke up with it, you can’t do it!) and there’s no CIs.

IV recombinant tissue plasminogen activator (tPA) e.g. alteplase.
must do CT 24hrs post-thrombolysis to check for bleeds.

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45
Q

give some absolute contra-indications for thrombolysis

A

Previous intra-cranial haemorrhage / haemorrhagic stroke
Major surgery or trauma <2 weeks
Active internal bleed (excluding menses)
Prolonged / traumatic CPR
Pregnancy, or <18 weeks postnatal
Severe liver disease / known oesophageal varices
Hypertension >200/120
Cerebral neoplasm
Previous allergy
Head/face trauma < 3months
Previous ischaemic stroke < 3 months (except current episode)

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46
Q

give some relative contra-indications for thrombolysis

A
Hx of severe (>200/120 hypertension)
Peptic Ulcer
Anticoagulant therapy
Infective Endocarditis
Known coagulation disorder
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47
Q

what symptoms indicate an anterior cerebral artery infarct?

A

Weak leg (± shoulder), on the contralateral side

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48
Q

what symptoms indicate a MCA infarct?

A

Weak arm and face on the contralateral side.

Hemiplegia
Hemianopia
Asphasia
Visuospatial problems

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49
Q

what symptoms indicate a posterior cerebral artery infarct?

A

Eye Problems

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50
Q

what features of a history might indicate carotid/vertebral artery dissection as the cause of a stroke?

A

Accounts for 20% of strokes in those under 40
often the result of trauma - but may be spontaneous

symptoms resembling stroke, TIA, or migraine, with pain at the site of the dissection

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51
Q

what is locked in syndrome and what causes it?

A

patient is aware and awake, but virtually all motor neurons are paralysed, and thus the patient cannot move. Usually the eyes are the only structures not affected. Caused by an upper brainstem infarct.

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52
Q

what is pseudo-bulbar palsy and what causes it?

A

the result of a lower brainstem infarct. Results in bilateral impairment of the 9-12thcranial nerves. There is dysarthria and dysphagia

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53
Q

what is Wallenberg’s syndrome / lateral medullary syndrome / posterior inferior cerebellar artery thrombosis (PICA)? - these all mean the same!

A

Syndrome resulting from brainstem infarction.
presents with acute vertigo and other cerebellar signs. Due to the nature of the cerebellar pathways, there are the following signs:

Contralateral
Spinothalamic sensory loss
Hemiparesis (usually mild, quite rare)
Ipsilateral
Facial numbness (V)
Diplopia (VI)
Nystagmus
Ataxia
Horner’s syndrome
9th and 10th nerve lesions
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54
Q

explain the appearance of stroke on CT and MRI

A

Infarctions will always show up as a wedge shape on both CT and MRI.
Haemorrhage – blood appears bright white (dense) on CT – but the longer it has been present, the darker it becomes. After 1-2 weeks it may look the same as normal brain tissue.

can roughly estimate the length of time the haemorrhage has been present by density of blood on a scan.
Depending on the site of the bleed, it will have a different shape on the scan
The damage is easier to see the longer it has been present

For example, a ‘new’ stroke (e.g. <2 hours old) may not show up at all, but after 6-12 hours will be clearly visible. This has clinical consequences – because the sooner you can see the stroke, the sooner you can treat it.

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55
Q

how do you investigate a stroke

A

send for urgent CT/MRI if considering thrombolysis, or high risk for haemorrhage, otherwise aim to do within 24hrs
diffusion weighted MRI most sensitive for acute infarct, CT helps rule out primary haemorrhage.
further tests:
BP / examine for signs of HTN e.g. retinopathy.
look for cardiac source of emboli - 24h ECG (for AF), might do an echo.
check for carotid artery stenosis - carotid Doppler USS ± CT/MRI angiography - 70+ % stenosis = consider carotid endartectomy.
bloods - ESR (for vasculitis), FBC/platelets/clotting, glucose, cholesterol/lipids

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56
Q

how do you manage a suspected infarctive stroke if thrombolysis not an option? - also cover secondary prevention after stroke.

A

give everyone aspirin 300mg/day for 2 weeks
THEN
clopidogrel - long-term secondary prevention.
if not tolerated give:
aspirin 75mg day, plus dipyridamole (antiplatelet)

if AF - start on NOAC.

Carotid endartectomy – carotid stenosis of either >70% or >50% (NICE quotes two criteria??) should be referred for assessment for this within 1 week, and have procedure within 2.

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57
Q

explain the oxford stroke classification system

A

The following criteria should be assessed:

  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia

Total anterior circulation infarcts (TACI, c. 15%) -
involves middle and anterior cerebral arteries
all 3 of the above criteria are present

Partial anterior circulation infarcts (PACI, c. 25%) -
involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
2 of the above criteria are present

Lacunar infarcts (LACI, c. 25%) -
involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

Posterior circulation infarcts (POCI, c. 25%) - 
involves vertebrobasilar arteries
presents with 1 of the following:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia
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58
Q

explain the ROSIER criteria for assessing likelihood of stroke

A

like a grown up version of FAST.

Exclude hypoglycaemia first, then assess the following:
(assessment –> score)
Loss of consciousness or syncope –> - 1 point
Seizure activity –> - 1 point
New, acute onset of:
• asymmetric facial weakness –> + 1 point
• asymmetric arm weakness –> + 1 point
• asymmetric leg weakness –> + 1 point
• speech disturbance –> + 1 point
• visual field defect –> + 1 point

A stroke is likely if > 0

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59
Q

how is haemorrhagic stroke managed?

A

Treatment is essentially supportive. If anticoagulants and antiplatlets have been given, then the effect can be reversed with vitamin K, fresh frozen plasma (FFP) and platelet transfusions.

Hypertension should only be treated if systolic is >185
If the haemorrhage causes a mass of >3cm diameter, then surgery can be lifesaving.

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60
Q

what is a transient ischaemic attack (TIA)?

A

mini stroke! symptoms resolve completely within 24hrs
80% are due to thromboembolus.
“sudden onset of focal CNS symptoms/signs due to temporary occlusion of part of the cerebral circulation”

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61
Q

what symptoms/signs in a TIA indicate an anterior circulation lesion? where is the thrombus likely to be from?

A

Likely thrombus from carotid system
Most likely affecting cerebral function

Symptoms/signs:
Aphasia/dysphasia	
Hemiparesis	
Amaurosis fugax
Sensory loss (hemi)	
Hemianopic visual loss
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62
Q

what symptoms/signs in a TIA indicate a posterior circulation lesion? where is the thrombus likely to be from?

A

Posterior Circulation
Likely thrombus from vertebrobasilar system
Most likely affecting cerebellar/brainstem function

Symptoms/signs:
Diplopia, vertigo, vomiting
Chocking / dysarthria
Hemianopic visual loss
Sensory loss (hemi)
Transient global amnesia
Tetraparesis
LOC (rare)
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63
Q

what is amaurosis fugax?

A

sudden loss of vision in one or both eye(s), caused by an infarct in the retinal artery(ies).
classically - curtain coming down.

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64
Q

how do you decide how to manage someone presenting with a possible TIA?

A
assess risk of stroke using ABCD2 - score of 4+ needs urgent referral to TIA clinic (within 24h - everyone with TIA should be seen within 7 days):
Age 60+ --> 1 pt
BP >140/90 --> 1pt
Clinical features
  - unilateral weakness --> 2 pts
  - speech disturbance only --> 1 pt
Duration of symptoms
  - 1+ hrs --> 2 pts
  - 10-59 mins --> 1pt
Diabetes --> 1 pt

start everyone on 300mg aspirin daily (unless current bleeding disorder, already on it, or otherwise CI’ed).

then switch to clopidogrel (or aspirin + dipyridamol as per stroke secondary prevention)
investigate/treat for cause, esp carotid artery doppler/carotid endartectomy

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65
Q

give info on driving and stroke/TIAs

A

avoid for 1 month, DVLA doesn’t need informing unless multiple attacks (for TIA) or residual deficit (for stroke) after 1 month.
if HGV/passenger carrying vehicle - must inform DVLA.

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66
Q

explain MRC muscle weakness grading

A

grade 0 - no muscle contraction
grade 1 - flicker of contraction
grade 2 - some active movement when gravity removed (e.g. swinging leg sideways across bed)
grade 3 - active movement against gravity
grade 4 - active movement against resistance (can be split into 4-, 4 and 4+)
grade 5 - normal power (allowing for age)

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67
Q

what are upper motor neurone lesions? signs/symptoms?

A

damage to motor pathways (corticospinal tracts) anywhere from motor nerve cells in prefrontal gyrus of frontal cortex –> internal capsule –> brainstem –> cord –> synapse with anterior horn cells.

pyramidal weakness
loss of skilled fine finger movements to greater extent than you’d expect from weakness
spasticity in stronger muscles (arm flexors, leg extensors)
hyperreflexia - brisk reflexes
upgoing plantars (+ve babinksi sign) ± clonus ± positive Hoffman’s reflex

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68
Q

what is pyramidal weakness?

A

seen in UMN lesions
distribution of weakness, typically involving arm extensors, small muscles of hand, lower limb flexors.

weakness of extension in upper limb, and flexion in lower limb
no muscle wasting

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69
Q

what is spasticity?

A

increased tone that is velocity-dependent and non-uniform i.e. faster you move the muscle, the greater the resistance - usually seen with brisk reflexes as well.

compare to rigidity, which is constant throughout the movement

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70
Q

what is the Babinski reflex?

A

draw thumbnail from heel to toes - upgoing plantar response = positive Babinski

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71
Q

what is Hoffman’s sign/reflex?

A

flick the pulp of middle finger away from palm –> brief flexion of thumb and index finger in pincer movement
may be more pronounced if neck extended.

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72
Q

what is clonus?

A

elicited by rapid dorsiflexion of foot - 3 or less downward, rhythmic beats is normal, any more suggests UMN lesion

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73
Q

what are lower motor neurone lesions? signs/symptoms?

A

damage anywhere from anterior horn cells in cord –> nerve roots –> plexi –> peripheral nerves

weakness distribution is according to muscles supplied by the involved nerve/cord segment etc.
affected muscles show wasting ± fasciculation
hypotonia/flaccidity
reduced/absent reflexes
Babinski negative (flexor plantars)

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74
Q

what is fasciculation?

A

spontaneous involuntary twitching of a muscle, might be seen in a LMN lesion.

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75
Q

what is idiopathic intracranial hypertension?

A

occurs typically in young, obese women.
symps/signs of raised ICP but no mass lesion on CT/MRI.
thought to be due to impaired CSF absorption.

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76
Q

how does idiopathic intracranial hypertension present?

A

young, obese woman complaining of morning headache, vomiting and sometimes visual disturbance (e.g. diplopia, visual obscurations). tinnitus common.
uni/bilateral sixth nerve palsies = ‘false localising sign’ of raised ICP.
scans normal, LP confirms raised pressure but otherwise normal.

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77
Q

what are visual obscurations?

A

sudden, transient bilateral visual loss with changes in posture

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78
Q

how do you manage a patient with idiopathic intracranial hypertension? what are you worried about?

A

in some, it’ll self-resolve, or go with weight loss/a few LPs.
if progresses to more chronic - threat to vision from secondary optic atrophy.
Rx with acetazolamide, diuretics or corticosteroids, or surgery to insert lumboperiotneal shunt draining CSF.

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79
Q

what is Kernig’s sign?

A

pain and resistance to passive knee extension with hip flexed - demonstrates meningism (NB - can be negative even in presence of meningism!)

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80
Q

give some differentials for facial pain

A
trigeminal neuralgia
post-herpetic neuralgia
giant cell arteritis - if presenting with jaw claudication
sinusitis
dental/oral disease
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81
Q

what is post-herpetic neuralgia? how can you treat it?

A

patient who’ve had shingles in a branch of the optic nerve may end up with persistent facial pain after the rash.
may be very severe and intractable, lasting 2-3yrs after rash.
might respond to TCAs, carbamazepine, topical capsaicin.

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82
Q

outline the GCS scoring system

A

Motor response

  1. Obeys commands
  2. Localises to pain
  3. Withdraws from pain
  4. Abnormal flexion to pain (decorticate posture)
  5. Extending to pain
  6. None

Verbal response

  1. Orientated
  2. Confused
  3. Words
  4. Sounds
  5. None

Eye opening

  1. Spontaneous
  2. To speech
  3. To pain
  4. None

score = 3-15

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83
Q

outline motor scoring in the GCS

A
6 = obeys command
5 = localises to pain
4 = withdraws from pain
3 = abnormal flexion to pain
2 = extending to pain
1 = none
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84
Q

outline verbal response scoring in GCS

A
5 = orientated
4 = confused
3 = inappropriate words
2 = incomprehensible sounds
1 = none
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85
Q

outline eye opening scoring in GCS

A
4 = spontaneously
3 = to speech
2 = to pain
1 = none
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86
Q

list some causes of altered level of consciousness

A

Structural

  • infratentorial (directly involving brain stem) e.g. trauma, infarction, haemorrhage, tumour, demyelination
  • supratentorial (compressing brainstem) e.g. as above, esp if affect R hemisphere

Diffuse

  • hypoxia
  • hypoglycaemia
  • renal/liver failure
  • hypothermia
  • vitamin deficiencies
  • epilepsy
  • inflammation - meningitis, encephalitis
  • drugs and toxins - opiates, antidepressants, hypnotic, alcohol
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87
Q

explain criteria for brainstem death

A

Criteria for brain stem death testing:

  • Deep coma of known aetiology.
  • Reversible causes excluded
  • No sedation
  • Normal electrolytes

Testing for brain death:

  • Fixed pupils which do not respond to sharp changes in the intensity of incident light
  • No corneal reflex
  • Absent oculo-vestibular reflexes
  • No response to supraorbital pressure
  • No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation
  • No observed respiratory effort in response to disconnection of the ventilator

Notes:
The test should be undertaken by two appropriately experienced doctors on two separate occasions. Both should be experienced in performing brain stem death testing and have at least 5 years post graduate experience. One of them must be a consultant. Neither can be a member of the transplant team (if organ donation contemplated).

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88
Q

give some causes of syncope - also what is it?

A

syncope = LOC due to transient reduction in blood flow to brain

  • cardiac arrhythmias
  • prolonged standing, esp in warm surroundings
  • psychogenic e.g. around needles
  • excessive reflex vagal stimulation e.g. micturition syncope, cough syncope
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89
Q

what features in a LOC hx suggest syncope?

A

prodrome - lightheadedness, nausea, blurred/tunnel vision, pallor, sweating
rapid recovery - once supine, will recover in seconds to 1-2 mins.
situation e.g. standing in hot room, around needles

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90
Q

list some differentials for LOC

A
  • epilepsy
  • syncope
  • hypoglycaemia (warnings = anxiety, tremor, unsteadiness, sweating, hunger)
  • drop attacks (in middle aged and elderly woman - random falls)
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91
Q

what are the 4 clinical features you might see in narcolepsy?

A

1) daytime sleep attacks - lasting 10-20 mins, pt awake refreshed. irresistible and occur inappropriately e.g. during meals, driving, mid-convo
2) cataplexy - episodes of loss of postural control + limb weakness, with preserved consciousness - often provoked by emotional events e.g. laughter
3) sleep paralysis - inability to move while falling asleep/waking
4) hypnagogic hallucinations - frightening visual hallucinations on falling asleep

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92
Q

what is cataplexy?

A

episodes of loss of postural control and limb weakness, with preserved consciousness - often provoked by emotional events e.g. laughter

Ix - sleep studies, EEG, MRI (for SOLs)

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93
Q

how can you treat narcolepsy/cataplexy?

A

narcolepsy - amphetamines, but be sure you’ve got the diagnosis right before starting due to addictive properties! also modafinil.
cataplexy - clomipramine, other antidepressants.

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94
Q

what brain functions is the frontal lobe responsible for?

A
  • higher intellectual function
  • personality, mood
  • social conduct, behaviour
  • posterior frontal region contains motor areas
  • frontal eye fields (conjugate eye movements)
  • language (in dominant hemisphere)
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95
Q

what brain functions is the temporal lobe responsible for?

A
  • memory
  • language (in dominant hemisphere)
  • visual pathway (optic radiation)
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96
Q

what higher brain functions is the parietal lobe responsible for?

A
dominant hemisphere:
- language, reading, writing
- calculation
- praxis (learning complex motor skills)
non-dominant:
- visuo-spatial function
both:
- higher sensory function
- visual pathway (optic radiation)
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97
Q

what higher brain functions is the occipital lobe responsible for?

A
  • visual cortex and visual association areas
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98
Q

what is aphasia/dysphasia?

A

impairment of language function as a result of brain damage

distinguish from dysarthria - impairment of articulation due to disease of muscles/neves involved with speech production

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99
Q

what is dyspraxia/apraxia?

A

inability to perform complex motor acts despite normal muscle power, sensation and coordination, with good comprehension and cooperation.
results from parietal lobe damage

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100
Q

what is Broca’s aphasia?

A

aka expressive aphasia
due to a lesion of the inferior frontal gyrus
speech is non-fluent, laboured, and halting
comprehension is normal

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101
Q

what is Wernicke’s aphasia?

A

due to a lesion of the superior temporal gyrus
this area ‘forms’ the speech before ‘sending it’ to Broca’s area. Lesions result in sentences that make no sense, word substitution and neologisms but speech remains fluent
comprehension is impaired

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102
Q

what is conduction aphasia?

A

classically due to a stroke affecting the arcuate fasiculus - the connection between Wernicke’s and Broca’s area
speech is fluent but repetition is poor. Aware of the errors they are making
comprehension is normal

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103
Q

what clinical features would you expect to see in a parietal lobe lesion?

A
sensory inattention
apraxias
astereognosis (tactile agnosia)
inferior homonymous quadrantanopia
Gerstmann's syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation
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104
Q

what clinical features would you expect to see in an occipital lobe lesion?

A

homonymous hemianopia (with macula sparing)
cortical blindness
visual agnosia

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105
Q

what clinical features would you expect to see in a temporal lobe lesion?

A

Wernicke’s aphasia: this area ‘forms’ the speech before ‘sending it’ to Brocas area. Lesions result in word substituion, neologisms but speech remains fluent
superior homonymous quadrantanopia
auditory agnosia
prosopagnosia (difficulty recognising faces)

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106
Q

what clinical features would you expect to see in a frontal lobe lesion?

A
expressive (Broca's) aphasia: located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus. Speech is non-fluent, laboured, and halting
disinhibition
perseveration
anosmia
inability to generate a list
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107
Q

what clinical features would you expect to see in a cerebellar lesion?

A

midline lesions: gait and truncal ataxia

hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus

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108
Q

what’s CN I called and what does it do?

A

olfactory nerve –> sense of smell.

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109
Q

what’s CN II called and what does it do?

A

optic nerve –> vision:

visual acuity, visual fields, colour vision, pupillary responses.

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110
Q

what kind of vision loss is seen in a lesion of the optic nerve?

A

monocular visual loss - essentially ‘blind’ in one eye (ipsilateral to lesion)

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111
Q

what kind of vision loss is seen in a lesion of the optic chiasm?

A

bitemporal hemianopia - loss of temporal halves of vision on both sides.
due to damage to decussating fibres from the nasal halves of retinae, as light from the temporal half-field is processed by nasal part of the retina.

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112
Q

what kind of vision loss is seen in a lesion of the optic tract?

A

homonymous hemianopia e.g. left half-fields in each eye missing (lesion would then be in R optic tract i.e. contralateral).
damage is to fibres from temporal half of one retina (in this e.g. the L one) and the decussated fibres from nasal half of the other (R one).

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113
Q

which lobes are damaged in homonymous inferior vs superior quadrantanopias?

A

PITS
Parietal = inferior
Temporal = superior

contralateral!

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114
Q

what is a central scotoma and what might cause it?

A

loss of central vision, usually associated with reduction in visual acuity
diseases of optic nerve and macular region of retina

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115
Q

what causes enlargement of the physiological blind spot?

A

papilloedema - swelling of the optic disc - due to raised ICP.
usually have preserved visual acuity.

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116
Q

what is macular sparing and what kind of lesion could cause it?

A

preservation of macular (central) region in patients with homonymous hemianopia
lesion of visual cortex sparing occipital pole

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117
Q

what is tunnel vision and what can cause it?

A

loss of peripheral fields, with preservation of central region

  • ophthalmological disease - chronic simple glaucoma
  • retinal disease - retinitis pigmentosa
  • cortical disease
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118
Q

what does an afferent pupillary defect look like?

A

when torch shines in affected eye, the light isn’t perceived so neither pupil constricts (direct or consensual).
when torch is shined in the normal eye, they both constrict.

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119
Q

what does an efferent pupillary defect look like?

A

light is perceived by affected eye but pupil can’t respond - the other pupil constricts consensually but direct reflect absent.
when light shined on unaffected eye, you get direct response but not consensual

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120
Q

what is a relative afferent pupillary defect? what condition is it strongly linked with?

A

affected eye can still respond directly to light but not as well as the other side
important sign of optic neuritis - persists after symptoms resolve.
aka the Marcus-Gunn pupil

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121
Q

what is a Holmes-Adie pupil?

A

benign cause of dilated pupil, commonly seen in women:

unilateral in 80% of cases
dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slowly reactive to accommodation but very poorly (if at all) to light

aka myotonic pupil

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122
Q

what is a Argyll Robertson pupil?

A

sometimes seen in neurosyphilis
mnemonic = Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)

Features:
small, irregular pupils
no response to light but there is a response to accommodate

Causes:
diabetes mellitus
syphilis

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123
Q

what are the names of CNs III, IV and VI - what do they do?

A

occulomotor, trochlear, abducens nerves

trochlear (IV) supplies superior oblique
abducens (VI) supplies lateral rectus
the rest are supplied by occulomotor, which also supplies levator palpebrae superioris (opens eye lid)

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124
Q

what is ptosis?

A

drooping of eyelid (partial) or unable to open eye (complete) - weakness of levator palpebrae suprioris

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125
Q

what is diplopia? what causes it?

A
double vision - neurologically, arises from malalignment of eyes
distinguish binocular (occurs when both eyes open) from monocular (persists when one eye covered) - monocular = ophthalmological rather than neurological
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126
Q

what would you see in a third nerve palsy?

A

ptosis due to paralysis of levator palpebrae superioris
when examiner opens eyelid, eye is in ‘down-and-out’ position due to unopposed action of superior oblique and lateral rectus muscles
pupil may be ‘fixed’ (no reflex responses) or dilated (‘surgical’ 3rd nerve palsy) or spared (‘medical’ third nerve palsy)

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127
Q

list some causes of third nerve palsies

A

diabetes mellitus
vasculitis e.g. temporal arteritis, SLE
false localizing sign due to uncal herniation through tentorium if raised ICP
posterior communicating artery aneurysm (pupil dilated)
cavernous sinus thrombosis
Weber’s syndrome: ipsilateral third nerve palsy with contralateral hemiplegia - caused by midbrain strokes
other possible causes: amyloid, multiple sclerosis

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128
Q

what would you see in a fourth nerve palsy?

A

unilateral paralysis of superior oblique, causing vertical diplopia noticed when descending stairs or looking down at a book - may tilt head towards normal side to correct.
causes - mild head trauma

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129
Q

what would you seen in a sixth nerve palsy?

A

unable to abduct affected eye because of unopposed action of medial rectus.
diplopia on looking to affected side with horizontal separation of images.
if isolated sixth nerve palsy - vascular prob, secondary to diabetes/HTN
also can be false localising sign of raised ICP due to long, tortuous intracranial course

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130
Q

what is Horner’s syndrome?

A
Features - 
miosis (constricted pupil)
ptosis (partial)
enophthalmos (sunken eye)
anhidrosis (loss of sweating on affected side of face)

lesion of sympathetic nerve supply to eye - hypothalamus –> brainstem –> cervical cord –> T1 nerve root –> cervical sympathetic chain –> eye

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131
Q

what is nystagmus?

A

involuntary rhythmic oscillatory movement of eyes, might be present on attempted sustained horizontal/vertical gaze.

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132
Q

what is CN V called? what does it do?

A

trigeminal nerve - facial sensation and masticatory muscles
divided into ophthalmic, maxillary, mandibular.
corneal reflex
lesions - loss of facial sensation and corneal reflex, problems chewing, jaw deviation - all depends which branch is affected.

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133
Q

what is CN VII called? what does it do?

A

facial nerve - muscles of facial expression, taste sensation to anterior 2/3rds of tongue, lacrimation, salivation.

lesions:
flaccid paralysis of upper + lower face
loss of corneal reflex (efferent)
loss of taste
hyperacusis
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134
Q

what is Bell’s palsy? features?

A

acute, unilateral, idiopathic, facial nerve paralysis - cause unknown, might be to do with HSV.

Features - rapid sudden onset:
lower motor neuron facial nerve palsy - forehead affected*
patients may also notice post-auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis

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135
Q

how do you manage Bell’s palsy?

A

10 day course of pred if within 72hrs of onset

advise artificial tears, eye lubricants and taping eyelid down to protect the cornea

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136
Q

what is CN VIII called? what does it do?

A

vestibulocochlear nerve - hearing and balance.

lesions cause:
Hearing loss
Vertigo, nystagmus
Acoustic neuromas are Schwann cell tumours of the cochlear nerve

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137
Q

explain Rinne’s and Weber’s tests

A

Performing both Rinne’s and Weber’s test allows differentiation of conductive and sensorineural deafness.

Rinne’s test:
512 Hz tuning fork is placed over the mastoid process until the sound is no longer heard, followed by repositioning just over external acoustic meatus
air conduction (AC) is normally better than bone conduction (BC)
if BC > AC then conductive deafness

Weber’s test:
512 Hz tuning fork is placed in the middle of the forehead equidistant from the patient’s ears
the patient is then asked which side is loudest
in unilateral sensorineural deafness, sound is localised to the unaffected side
in unilateral conductive deafness, sound is localised to the affected side

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138
Q

what is CN IX called? functions?

A

glossopharyngeal nerve

taste (posterior 1/3rd of tongue)
Salivation
Swallowing
Mediates input from carotid body & sinus

lesions - loss of gag reflex, hypersensitive carotid sinus reflex (afferent)

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139
Q

what is CN X called? functions?

A

vagus

functions:
Phonation
Swallowing
Innervates viscera

lesions:
uvula deviates away from site of lesion
loss of gag reflex (efferent)
swallowing difficulties, dysarthria
vocine cough
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140
Q

what is CN XI called? functions?

A

accessory nerve
supplies sternomastoid and trapezius muscles
sternomastoid - turning head against resistance
trapezius - shrugging shoulders

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141
Q

what is CN XII called? functions?

A

hypoglossal
tongue muscles!
lesion (if LMN) - uni/bilateral wasting and fasciculation.
if unilateral - tongue deviates to affected side on protrusion.

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142
Q

differentiate between bulbar and pseudobulbar palsies

A

bulbar palsy = LMN lesion of CN IX, X and XII.

pseudobulbar palsy = UMN of CN IX, X and XII.

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143
Q

list some causes of bulbar palsy

A
brainstem vascular disease
MND
syringobulbia
tumour
brainstem encephalitis e.g. polio
Guillain-Barre syndrome
skull base or meningeal infiltration
myasthenia gravis
some muscular dystrophies
polyomyositis
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144
Q

what are the features of a bulbar palsy?

A
nasal speech
absent jaw jerk
palatal weakness, nasal regurg of food
reduced or absent gag reflex
wasted, fasciculating tongue
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145
Q

list some causes of pseudobulbar palsy

A
bihemispheric vascular disease
MND
MS
tumour
extrapyramidal disease
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146
Q

what are the features of pseudobulbar palsy?

A

slow, monotonous speech, sometimes explosive
brisk jaw jerk
dysphagia
brisk gag reflex
shrunken, immobile tongue
emotional lability - spontaneous laughing/crying

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147
Q

describe the gait you would see in a spastic paraparesis

A

spastic paraparesis = UMN lesion affecting both legs

described as scissoring, ‘wading through mud’

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148
Q

describe the gait you would see in a spastic hemiparesis

A

spastic hemiparesis = UMN lesion affecting one leg

leg is rigid and circumducts - described as semicircle rotating at hip

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149
Q

describe the gait you would see in a bilateral foot drop

A

bilateral foot drop = LMN lesion of both legs

steppage gait - legs lifted high to avoid scraping toes

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150
Q

describe the gait you would see in a cerebellar lesion

A

wide-based gait, staggering, unable to walk heel-toe

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151
Q

describe the gait you would see in a Parkinsons

A

stooping posture, rigid shuffling gait, no arm swing

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152
Q

describe the gait you would see in a proximal myopathy

A

waddling

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153
Q

what is epilepsy?

A

tendency to recurrent seizures - paroxysmal cerebral cortical neuronal discharges result in intermittent, stereotyped attacks of altered consciousness, motor or sensory function, behaviour or emotion

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154
Q

explain how epileptic seizures are classified

A

focal vs generalised
focal aware = consciousness maintained through
focal impaired awareness = consciousness impaired at any stage
generalised onset involved both sides of / whole brain, LOC occurs immediately
note focal seizures may become secondary generalised (aka bilateral tonic-clonic) - pt loses consciousness and there’s clinical evidence of more generalised involvement

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155
Q

give some info on generalised onset seizures and the subtypes

A
these engage or involve networks on both sides of the brain at the onset
consciousness lost immediately. 
further subdivided into motor (e.g. tonic-clonic) and non-motor (e.g. absence)
specific types include:
→ tonic-clonic (grand mal)
→ tonic
→ clonic
→ typical absence (petit mal)
→ myoclonic: brief, rapid muscle jerks
→ atonic
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156
Q

what are the features of a tonic-clonic / grand mal seizure?

A

prodrome/aura - dizziness, irritability
LOC ± epileptic cry and fall to the ground
then initial tonic phase - generalised muscle spasms for a few secs
then clonic phase - sharp, repetitive muscle jerks.
may see tongue biting, incontinence and salivation.
when jerks stop, patients usually unconscious for another half an hour or so, then are drowsy and confused for several hours (recovery)
may have headache (from fall) or back pain (from muscle spasms) in recovery period.

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157
Q

what are the features of a focal, temporal lobe epilepsy?

A

aura - psychic symptoms (e.g. deja/jamais vu), hallucinations (olfactory, gustatory, visual images), epigastric rising sensation
automatisms - chewing and lip smacking.

HEAD:
Hallucinations
Epigastric rising/emotional lability
Automatisms
Deja vu/dysphasia post-ictal
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158
Q

what are the features of a focal, frontal (motor) lobe epilepsy?

A

Head/leg movements , posturing, post-ictal weakness

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159
Q

what are the features of a focal, parietal (sensory) lobe epilepsy?

A

paraesthesiae

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160
Q

what are the features of a focal, occipital (visual) lobe epilepsy?

A

floaters/flashers

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161
Q

what are the features of a Jacksonian march seizure?

A

focal motor attack beginning in the corner of the mouth, the thumb and index finger, or the big toe
movements rapidly spread across face or ascend limb

associated with organic brain disease causing the epilepsy e.g. tumour in motor region
afterwards, affect limb may remain weak - Todd’s paralysis

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162
Q

what is Todd’s paresis/paralysis?

A

focal weakness after a partial seizure, usually resolves completely within 48h

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163
Q

describe the features of febrile convulsions

A
seizures associated with fever
child aged 6 months - 5 years
brief (< 15mins) and generalised, although some might have focal and prolonged attacks
usually isolated attack
doesn't require prophylactic AEDs
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164
Q

what is West’s syndrome (infantile spasms)?

A

triad of:

1) brief spasms beginning within first few months of life - shock-like flexion of arms, head and neck with drawing up of feet (salaam attack)
2) progressive learning difficulties
3) hypsarrhythmia on EEG

usually has an identifiable cause e.g. perinatal asphyxia, encephalitis, metabolic disorders, cerebral malformations
Rx - vigabatrin/steroids

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165
Q

what are petit mal / absence seizures?

A

generalised epilepsy, usually starts in childhood (peak onset 4-8yrs)
attacks occur without warning - child stares into space and stops talking, eyes may flutter/roll up under lids.
recovery within seconds, may have many attacks per day

EEG: 3Hz generalized, symmetrical

sodium valproate, ethosuximide
good prognosis: 90-95% become seizure free in adolescence

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166
Q

what is juvenile myoclonic epilepsy / Janz syndrome?

A

onset: teens; F:M = 2:1
1) Infrequent generalised seizures, often in morning
2) Daytime absences
3) Sudden, shock like myoclonic (involuntary jerking) seizure - usually in morning (patient inexplicably spills/throws breakfast across room)
usually good response to sodium valproate - carbamazepine can make it worse!!

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167
Q

list some causes of epilepsy in neonates

A
birth trauma
intracranial haemorrhage
hypoxia
hypoglycaemia
hypocalcaemia
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168
Q

list some causes of epilepsy in children

A

congenital anomalies

tuberous sclerosis

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169
Q

list some causes of epilepsy in young adults

A

head injuries

drugs and alcohol

170
Q

list some causes of epilepsy in middle-aged adults

A

cerebral tumour

171
Q

list some causes of epilepsy in the elderly

A

cerebrovascular disease

degenerative disorders e.g. Alzheimer’s

172
Q

list some causes of epilepsy across all age groups

A

infection - meningitis, encephalitis, abscess
inflammation - MS (rare), vasculitis
metabolic encephalopathy

NB - all the ones on cards in specific age groups can probs cross age groups
also majority of epilepsy occurs without specific cause!

173
Q

list some differentials for epilepsy

A
syncope
cardiac dysrhythmia 
pseudoseizures
hyperventilation/panic attacks
TIAs
migraine
narcolepsy
hypoglycaemia
vestibular disorders
174
Q

how is epilepsy investigated/diagnosed?

A

aim of investigation is to confirm/support clinical diagnosis, classify epileptic syndrome and establish a cause if there is one.
EEG - usually only after second seizure due to frequent false positives and negatives.
telemetry = EEG + video recording
EEG may be ambulatory/prolonged.

brain CT/MRI - especially if later onset epilepsy, partial attacks ± focal neurological signs and EEG abnormalities
realistically most adults presenting to A&E with isolated, first seizure would get scanned!

175
Q

explain basic principles of drug therapy for epilepsy

A

usually only started after a second attack

careful outpatient follow up needed - aiming for lowest effective dose of single drug

176
Q

give some reasons for refractory epilepsy

A

non-compliance with meds
pseudoseizures/non-epileptic attacks (either alone or in combo with genuine seizures)
associated structural brain disease
alcohol and lifestyle (e.g. sleep deprivation)

177
Q

when would you consider starting AEDs after only a single seizure?

A
  • the patient has a neurological deficit
  • brain imaging shows a structural abnormality
  • the EEG shows unequivocal epileptic activity
  • the patient or their family or carers consider the risk of having a further seizure unacceptable
178
Q

what is the usual drug of choice for generalised tonic-clonic seizures?

A

sodium valproate

may use - phenytoin, carbamazepine, lamotragine

179
Q

what is the usual drug of choice for partial seizures?

A

carbamazepine

also - sodium valproate, phenytoin, lamotragine

180
Q

what is the usual drug of choice for absence seizures?

A

ethosuximide

also - sodium valproate, lamotrigine

NB - carbamazepine can make them worse!

181
Q

what is the usual drug of choice for myoclonic seizures?

A

sodium valproate

also - clonazepam, lamotrigine

182
Q

when might surgery be considered for epilepsy?

A

if a defined, operable site of seizure onset is identified, particularly if intractable to drug treatment.

in some, surgery may be performed even if onset site unclear - hemispherectomy, disconnection (section of corpus callosum) - RARE

183
Q

what lifestyle/general advice should be given to someone with epilepsy?

A

avoid triggers if identified e.g. flickering lights, alcohol

driving - can only drive after seizure free interval of 6 months, must inform DVLA (for HGV/passenger carrying must be seizure free, without AED for 10 years) - unless epilepsy has only ever occurred during sleep.

employment - not allowed to work in armed or emergency services, aircraft pilot etc

leisure - NEVER swim alone, inform lifeguards, wear bike helmets etc

184
Q

what causes subarachnoid haemorrhage?

A

bleeding into subarachnoid space, commonly due to:

  • head injury / trauma
  • rupture of an aneurysm - congenital weakenings at junctions in circle of Willis
  • arteriovenous malformation (angiomas) - malformed vessels, also congenital - enlarge and present in adult life
  • pituitary apoplexy
  • arterial dissection
  • mycotic (infective) aneurysms
  • perimesencephalic (an idiopathic venous bleed)
185
Q

how does a subarachnoid haemorrhage classically present?

A
  • headache: typically sudden-onset (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’) and occipital
  • nausea and vomiting
  • meningism (photophobia, neck stiffness)
  • coma
  • seizures
  • sudden death
  • raised ICP signs on fundoscopy etc
  • focal neurology due to false localisation from raised ICP
186
Q

how would you investigate someone with a suspected SAH?

A
  • CT head - shows acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.

LP - to confirm SAH if CT is negative - performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (straw coloured CSF). xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure)

cerebral angiography (if pt stable) to look for source of bleeding and direct treatment

to look for cause - CXR/ECG for pulmonary oedema and cardiac arrhytmias, clotting for bleeding disorders

187
Q

how is an SAH managed?

A

treat according to cause:

  • most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, minority require a craniotomy and clipping by a neurosurgeon
  • patient should be kept on strict bed rest, well controlled BP and should avoid straining in order to prevent a re-bleed of the aneurysm
  • vasospasm is prevented using nimodipine and treated with hypervolaemia, induced-hypertension and haemodilution
  • hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt§
188
Q

list some possible complications of aneurysmal SAH

A

Re-bleeding (in around 30%)
Vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
Hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
Seizures
Hydrocephalus
Death

189
Q

what is hydrocephalus?

A

condition in which there is an excessive volume of cerebrospinal (CSF) fluid within the ventricular system of the brain - caused by an imbalance between CSF production and absorption, can occur in raised ICP if CSF flow obstructed

190
Q

what can cause a spontaneous intracerebral haemorrhage (haemorrhagic stroke -think they’re the same??) ?

A
  • HTN, with microaneurysm formation (Charcot-Bouchard aneurysms)
  • bleeding into tumours
  • trauma
  • blood disorders
  • blood vessel disorder - AV malformations, vasculitis, amyloid
191
Q

what is the classical clinical triad that occurs in parkinsons?

A

1) akinesia/bradykinesia - poverty of movement
2) rigidity
3) tremor - shaking back and forth, usually of upper limbs

192
Q

describe the pathophysiology of Parkinson’s

A

thought to be to do with atrophy/neuronal loss of dopaminergic neurones (the ones that produce dopamine) in the substantia nigra
remaining neurones contain intracellular inclusions called Lewy bodies.

increasingly common with age (onset usually around 60+ yo)

193
Q

what are the bradykinesic features of Parkinson’s disease?

A
  • difficulty with complex motor tasks (dressing, shaving etc)
  • handwriting becomes smaller (micrographia)
  • ‘mask-like’ face due to poverty of facial expression
  • quiet and monotonous speech
  • abnormal gait and stance
194
Q

what are the gait features of Parkinson’s disease?

A
  • flexed/stooped posture
  • unable to maintain normal stance in response to pressure (i.e. you can knock them over really easily if push gently from behind or in front - propulsion/retropulsion)
  • ‘freezing’ - difficulty initiating walking
  • small, shuffling steps (‘festinant’)
  • loss of normal arm swing
  • severe postural instability = risk of falls
195
Q

describe the rigidity seen in Parkinson’s disease

A

increase in muscle tone - relatively constant throughout range of movement of joint - ‘lead pipe’ rigidity (rather than spasticity!)

cogwheel rigidity is more due to tremor superimposed on lead pipe - repeated flexion and extension of arm or rotation at wrist.

196
Q

describe the tremor seen in Parkinson’s disease

A
  • mostly affects hands, may involve upper/lower limb or jaw - not the head or neck
  • hands = pill rolling
  • present at rest, exacerbated by anxiety or stress
  • improves/disappears on movement
  • early on - asymmetrical (true for other physical signs as well!) - then progresses to bilateral
197
Q

define tremor

A

tremor = involuntary, repetitive, rhythmic sinusoidal movement usually affecting 1+ limbs, occasionally involving the head (titubation), face, jaw or trunk

198
Q

give some more features of Parkinson’s (beyond - bradykinesia, gait, tremor, rigidity)

A
mask-like facies
flexed posture
micrographia
drooling of saliva
psychiatric features: depression is the most common feature (affects about 40%); dementia, psychosis and sleep disturbances may also occur
impaired olfaction
REM sleep behaviour disorder
fatigue
postural hypotension
199
Q

how is Parkinson’s disease diagnosed?

A

generally clinical based on the triad of features.
CT/MRI head unhelpful.
I‑FP‑CIT single photon emission computed tomography (SPECT) can be considered if struggling to differentiate from essential tremor - looks for nigrostriate dopaminergic lesion.
OR - see if they respond to drugs

200
Q

what are the features and management of essential tremor?

A

autosomal dominant condition which usually affects both upper limbs

Features -
postural tremor: worse if arms outstretched
improved by alcohol and rest
most common cause of titubation (head tremor)

Management -
propranolol is first-line
primidone is sometimes used

201
Q

what drugs are used first-line in Parkinson’s?

A

if the motor symptoms are affecting the patient’s quality of life: levodopa

if the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived), levodopa or monoamine oxidase B (MAO‑B) inhibitor

202
Q

give some info on levodopa

A

usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide - becomes co-carelodpa or co-beneldopa) to prevent peripheral metabolism of levodopa to dopamine

reduced effectiveness with time (usually by 2 years)

unwanted effects, particularly of prolonged use: dyskinesia (involuntary writhing movements), ‘on-off’ effect, dry mouth, anorexia, palpitations, postural hypotension, psychosis, drowsiness
no use in neuroleptic induced parkinsonism

203
Q

explain ‘wearing-off’ / ‘on-off’ effects regarding L dopa

A

start to occur after 2-5yrs
wearing off = when individual doses produce only short-lived effects before they wear off
on-off effects = where patient can switch from symptomatic benefit from meds (on) to akinetic-rigid state (off), often without predictable relationship to dose timings

204
Q

what are dyskinesias, in relation to L dopa?

A

involuntary movements occurring in relation with drug treatment e.g. twisting, turning movements when dopamine levels high or painful sustained muscle contractions, usually in feet, when levels low (peak dose vs wearing off dyskinesias)

205
Q

what is selegiline?

A

monoamine oxidase type B inhibitor - inhibits breakdown of dopamine secreted by what dopaminergic neurons remain
potentially useful in early Parkinson’s disease - might be neuroprotective and delay needing L-DOPA

206
Q

what are COMT inhibitors?

A

e.g. Entacapone, tolcapone
COMT is an enzyme involved in the breakdown of dopamine, and hence may be used as an adjunct to levodopa therapy
used in conjunction with levodopa in patients with established PD
tolcapone - highly restricted due to very rare occurrence of fatal liver failure

207
Q

what are dopamine agonists, what is their role in parkinson’s management?

A

e.g. bromocriptine, cabergoline, pergolie, ropinirole, pramipexole, rotigotine, apomorphine

useful in early PD for delaying need for L-DOPA
the ergot derived ones (first 3) can cause pulmonary/retroperitoneal fibrosis, so the others usually preferred.

208
Q

what is chorea/choreiform movement?

A

irregular, random, variable - flowing/dancing quality.

can affect any part of body

209
Q

give some causes of chorea

A

acquired:

  • chronic L-DOPA therapy
  • postinfectious (Sydenham’s chorea + rheumatic fever)
  • polycythaemia rubra vera
  • SLE
  • hyperthyroidism
  • pregnancy, oral contraceptives
  • phenytoin, alcohol, neuroleptics

Huntington’s chorea - associated with Huntington’s disease

210
Q

what are athetoid movements?

A

slower, more writhing quality than chorea

associated with cerebral palsy

211
Q

list some causes of tremor

A

rest tremor:
- Parkinson’s
postural tremor (worse with maintained posture):
- essential tremor
- physiological, exaggerated by anxiety, thyrotoxicosis, alcohol, drugs (salbutamol)
kinesis tremor (worse during movement/intention tremor):
- cerebellar disease - MS, hereditary ataxias
- tumours, infarct, haemorrhage of cerebellum

212
Q

what is brain herniation?

A

displacement of the brain as raised ICP hits pathological levels - where it’s displaced depends on where the lesion causing the raised ICP is.
causes compression of important structures - most dangerous is ‘coning’, the compression of the brainstem downwards - neurosurgical emergency

213
Q

what is coning?

A

aka tonsillar herniation - displacement of the cerebellar tonsils through the foramen magnum.
In raised ICP this causes compression of the cardiorespiratory centre.

Can occur in Chiari 1 malformation without raised ICP

214
Q

how is hydrocephalus classified?

A

obstructive - CSF flow blocked within ventricles
communicating - CSF flow blocked ‘beyond’ ventricular system
infantile hydrocephalus
‘normal-presssure’ hydrocephalus

215
Q

what can cause obstructive hydrocephalus? how is it managed?

A

congenital abnormalities - cerebral aqueduct stenosis, Arnold-Chiari malformation
mass lesions e.g. tumour, haematoma

requires urgent surgical management - removal of excess CSF via ventricular drain
permanent management = ventriculoperitoneal shunt insertion

216
Q

what can cause communicating hydrocephalus?

A

damage to meninges/arachnoid villi
- meningitis, SAH (both can also cause obstructive hydrocephalus)

increased CSF viscosity due to high protein conc.

217
Q

list some common causes of head injury

A
RTAs
falls
assault - blunt injuries
industrial injuries
domestic accidents
sporting accidents
missile injuries - bullets and bomb fragments
218
Q

what two mechanisms cause brain damage as a result of head injury?

A

1) damage at impact - contusion/laceration of cerebral cortex at site of impact; diffuse white matter lesions due to axonal shearing
2) secondary complications - haematoma (extra/subdural, intracerebral), cerebral oedema, cerebral ischaemia, coning, infection

219
Q

what are the clinical features of head injury?

A

remember - do ABCDE approach and treat major chest injury/abdo bleeds before focussing on head injury
consider - any LOC? lucid interval? any confusion after regain of consciousness?
- persistence of headache and vomiting - haematoma?
examine:
- external evidence of trauma
- signs of basal skull fracture e.g. bilateral periorbital haematoma, subconjunctival haematoma, CSF discharge from nose/ear, bleeding from ear
- GCS

220
Q

what investigations would you do for a patient with a head injury?

A
  • skull XR if transient/persistent impairment of consciousness, signs suggestive of skull fracture, focal neurology
  • urgent CT head if level of consciousness deteriorating or skull fracture + neuro signs/seizures/confusion
221
Q

outline management of head injury

A

admit if - reduced consciousness, skull fracture, focal neurology - neurological observation, clean and suture scalp lacerations.
if severe:
surgical - evacuation of space-occupying haematoma, urgent surgery for compound skull fraction
medical - IV mannitol bolus for raised ICP (also used before surgery for haematoma), prophylactic abx for basal skull #, manage seizures appropriately

222
Q

list some possible complications/consequences of head injury

A
  • may have residual disability/impairment
  • small number = persistent vegetative state
  • CSF leakage due to dural tear - may present late with meningism, requires surgical repair
  • post-traumatic epilepsy
  • post-conscussion syndrome - headache, depression, impaired concentration
223
Q

what is normal-pressure hydrocephalus? how is it treated?

A

unique form of non-obstructive hydrocephalus characterised by large ventricles on CT but normal intracranial pressure
classic triad = dementia, incontinence and disturbed gait.
Rx - ventriculopertioneal shunting - variable results

224
Q

outline emergency management of raised ICP

A

ABCDE
correct hypotension (MAP >90mmHg) and Rx seizures
elevate head of bed, hyperventilate if intubated, mannitol IV helps lower ICP initially but can cause rebound raised ICP.
dexamethasone only helpful if tumour (lowers oedema surrounding them).
restrict fluids, monitor closely, try and work out what’s causing it and treat it.

225
Q

what syndrome is seen in uncal/transtentorial herniation (also what is this)?

A

Displacement of the uncus of the temporal lobe under the tentorium cerebelli.
syndrome - ipsilateral fixed, dilated pupil (due to parasympathetic compression of the third cranial nerve) and contralateral paralysis (due to compression of the cerebral peduncle) - then coma

Rx as for raised ICP emergency

226
Q

what syndrome is seen in tonsillar herniation? also what is this?

A

Displacement of the cerebellar tonsils through the foramen magnum - ‘coning’.
increased pressure in posterior fossa forces cerebellar tonsils through foramen magnum.
ataxia, 6th nerve palsies, upgoing plantar reflexes –> LOC, irregular breathing, apnoea – proceed rapidly!!

227
Q

what syndrome is seen in subfalcian/cingulate herniation? also what is this?

A

Displacement of the cingulate gyrus under the falx cerebri - caused by frontal mass.
may be silent unless anterior cerebral artery compressed causing stroke.

228
Q

outline classification of brain tumours

A

benign - normally not of the brain (meninges, cranial nerves etc) - histologically benign but still a SOL in cranial cavity so can be life-threatening
malignant - often gliomas (glial cell origin - locally invasive but rarely metastasise) or secondary mets from elsewhere in body

229
Q

what are the three main ways malignant brain tumours can present? how would you investigate for them?

A
epilepsy
raised ICP (chronic cause, although may acutely detiorate and cause coning)
focal neurological deficit - depends on site of lesion e.g. dysphasia, hemiparesis, personality change etc

Ix - CT/MRI scans, screening for primary neoplasm (esp CXR).

230
Q

what are meningiomas? what are the specific ways they can present?

A

benign meningeal tumours - can present similarly to malignant brain tumours i.e. epilepsy, raised ICP, dysphasia, hemiparesis, dementia.

if in olfactory groove = uni, then bilateral anosmia, papilloedema, frontal lobe dysfunction.

in parasagittal region - spastic paraparesis mimicking spinal cord lesion, UMN signs in both legs as tumour is between cerebral hemispheres

in cavernous sinus - unilateral ophthalmoplegia (III, IV and VI palsies) and trigeminal sensory loss

optic nerve - contralateral papilloedema

231
Q

what are acoustic neuromas? how do they present?

A

benign, aka scwannoma - arises from nerve sheath cells in VIII nerve complex in internal auditory meatus.
initially - unilateral sensorineural hearing loss due to damage to nerve within meatus.
as it expands it can involve V and VII, then eventually get ipsilateral ataxia due to compression of brainstem/cerebellum and bulbar nerve palsies.
eventually - raised ICP.

232
Q

what are pituitary adenomas? how do they present?

A

neurologically - classic is bitemporal hemianopia due to compression of optic chiasm + will have endocrine disturbances

233
Q

outline management options for brain tumours

A

surgery - benign tumours usually operable and curative, malignant/secondary normally not - although operation often needed to get histological diagnosis.
radiotherapy - directed at tumour in gliomas, whole brain radiation if multiple metastases.
drugs - AEDs for epilepsy, dexamethasone for raised ICP (only works in tumours!), chemo might be indicated in gliomas.

234
Q

what are the usual causative organisms of meningitis in adults?

A
Neisseria meningitidis (meningococcus)
Streptococcus pneumoniae (pneumococcus)

rarer -
mycoplasma tuberculosis - immunocompromised
listeria monocytogenes - immunocomp, neonates, >60yos
staphylococci - pts w/ head injuries, neurosurgical shunts

235
Q

list some neurological sequelae of menignitis

A

deafness (most common)
other neurological: epilepsy, paralysis
infective: sepsis, intracerebral abscess
pressure: brain herniation, hydrocephalus

236
Q

what are the clinical features of meningitis?

A

severe headache - rapid onset (minutes to hours)
pain/stiffness in neck and back
vomiting
photophobia
might present w/ altered consciousness, seizures
O/E - fever, tachycardia, shock, petechial/purpuric rash if meningococcal

237
Q

what neurological signs would you see in meningitis?

A

‘meningism’ - neck stiffness on attempted flexion, high-pitched ‘meningeal’ cry in infants
Kernig’s positive
deteriorating level of consciousness
raised ICP - papilloedema, bulging fontanelles
CN palsies and other focal signs

238
Q

what would you see in CSF of untreated bacterial menigitis?

A

turbid CSF, raised CSF pressure
polymorph leucocytosis
raised protein, low glucose (eats sugar, sh*ts out protein)

239
Q

what would you see in CSF of viral meningitis?

A

clear or turbid CSF
glucose slightly low (60-80% of plasma glucose)
protein normal/raised
lymphocytosis

240
Q

what would you see in CSF of tuberculous meningitis?

A

slightly cloudy CSF, fibrin web
lymphocytosis
raised protein, low glucose (eats sugar, sh*ts out protein)

241
Q

give some CI’s to LP in meningitis - how else would you investigate?

A

focal neurological signs
papilloedema
deteriorating consciousness

head CT needed to excluded mass lesion mimicking meningitis before you can do LP

242
Q

what investigations would you do for meningitis, beyond head CT/LP?

A
full blood count (neutrophilia)
U&amp;Es (hyponatraemia)
CRP
coagulation screen (for DIC)
blood culture (can be +ve even with sterile CSF)
whole-blood PCR
blood glucose
blood gas
243
Q

list some possible complications of meningitis

A

acute - seizures, abscess formation, hydrocephalus, inappropriate ADH secretion, septic shock
DIC (if meningococcal)
can be left with LDs, epilepsy, hearing loss - particularly if a child!

244
Q

how do you treat bacterial meningitis in adults? give initial, empirical treatment?

A

if pre-hosp and suspecting meningococcal (e.g. rash) - IM benpen immediately then urgent transfer.

IV cefotaxime (+amoxicillin if >50yrs old)

245
Q

once CSF/blood cultures have come back, how do you treat bacterial meningitis?

A

according to local policy/guidelines BNF says:
Meningococcal meningitis = IV benpen or cefotaxime
Pneuomococcal meningitis = IV cefotaxime
Haemophilus influenzae = IV cefotaxime
Listeria = IV amoxicillin + gentamicin

246
Q

outline contact treatment for bacterial meningitis

A

give household contacts rifampicin or ciprofloxacin - if meningococcal disease.
notify local health protection agency and/or PHE.

247
Q

what can cause brain abscesses?

A

otitis media, paranasal sinuses, head injury/surgery

distant spread e.g. bronchiectasis, pelvis, bacterial endocarditis

248
Q

what are the clinical features of a brain abscess?

A

collection of pus, effectively a SOL so features depend on location:
raised ICP - common
focal signs e.g. hemiparesis, ataxia etc
seizures

can have fever, but not always
progression is over days or even a few weeks so a major differential is brain tumour

249
Q

how do you investigate a brain abscess?

A

CT or MRI

LP is CI’ed due to coning risk.
bloods - FBC (neutrophil leucocytosis) and blood cultures.

250
Q

how do you manage a brain abscess?

A

typically surgical - decompress/drain abscess, it may reform after wards.
might give broad-spec abx until cultures done e.g. cefotaxime + metronidazole
steroids may help with oedema

251
Q

list the different forms of neurosyphilis

A
  • mild, self-limitng meningitis due to secondary syphilis
  • meningovascular syphilisy
  • gumma
  • tabes dorsalis
  • “general paralysis of the insane”
  • congenital neurosyphilis
252
Q

what is meningovascular syphilis?

A

inflammation of meninges and cerebrospinal arteries in tertiary syphillis
presents as subacute meningitis w/ focal signs e.g. CN palsies, hemiparesis, wasting of intrinsic hand muscles (syphilitic amyotrophy)

253
Q

what is syphilitic amyotrophy?

A

wasting of intrinsic hand muscles seen in neurosyphilis

254
Q

what is gumma?

A

focal meningovascular disease seen in neurosyphilis - presents as intracranial mass lesion e.g. w/ epilepsy, focal deficits, raised ICP etc
also present generally in tertiary syphilis as granulomatous lesions of skin/bone

255
Q

what is tabes dorsalis? what are the features?

A

seen in neuro/ tertiary syphilis

  • optic atrophy, Argyll Robertson pupils, ptosis
  • painful abdo crises
  • truncal analgesia
  • painless urinary retention
  • lancinating pains in legs
  • absent knee and ankle reflexes
  • ataxic stomping gait
  • positive Romberg’s test (sways/falls when eyes closed)
  • downgoing plantars
  • loss of deep pain sense - can get ulcers
256
Q

what are the features of “general paralysis of the insane” as seen in neurosyphilis?

A
dementia, delusions of grandeur, frontal lobe features, epilepsy
Argyll Robertson pupils, optic atrophy
dysarthria
tremulousness
spastic paraparesis
upgoing plantars
257
Q

how is neurosyphilis diagnosed and treated?

A

syphilis serology in blood/CSF
CSF might also show lymphocytes, raised protein, oligoclonal bands
Rx - IM procaine pencillin + oral probenecid
often steroids given concurrently to prevent Jarisch-Herxheimer reaction (inflammatory response to rapid killing of spirochaetes)

258
Q

aetiology/pathogenesis of viral encephalitis

A

viral invasion of brain –> lymphocytic inflammatory reaction w/ necrosis of neurones and glia

HSV1 most common in developed world (95%)
also - herpes zoster, CMV, EBV, adenovirus, mumps

259
Q

what are the clinical features of encephalitis?

A

headache, fever, deteriorating level of consciousness over hours -> days.
focal neuro signs - HSV commonly affects temporal lobe so e.g. aphasia
seizures, vomiting, psychiatric symptoms

260
Q

how is encephalitis investigated/diagnosed?

A

CSF: lymphocytosis, elevated protein, normal glucose, raised pressure
PCR for HSV
CT: in HSV - medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients
MRI is better
EEG pattern: HSV = characteristic lateralised periodic discharges at 2 Hz

261
Q

how is encephalitis managed?

A

IV aciclovir (for HSV encephalitis)

prognosis depends on how early this is started.

ganciclovir is CMV, but prognosis a lot worse for this and other weird causes.

262
Q

give basic info on shingles vaccine

A

offered to all patients aged 70-79 years
is live-attenuated and given sub-cutaneously

main contraindications are immunosuppression.

Side-effects
injection site reactions
less than 1 in 10,000 individuals will develop chickenpox

263
Q

what is shingles?

A

acute, unilateral, vesicular, itchy/painful rash in a single dermatome - due to reactivation of dormant VZV that has sat in the nerve root.

264
Q

how is shingles treated?

A

oral aciclovir - helps initial symps and reduced risk of post-herpetic neuralgia

265
Q

what is post-herpetic neuralgia?

A

persisting pain in a dermatome following shingles - can be severely painful, can’t really treat it, lasts 1-2 yrs.

266
Q

what is herpes zoster ophthalmicus?

A

reactivation of the varicella zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve
features:
vesicular rash around the eye, which may or may not involve the actual eye itself
Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement

267
Q

how do you treat herpes zoster ophthalmicus?

A

oral antiviral treatment for 7-10 days, ideally started within 72 hours
Topical antiviral treatment is not given in HZO

oral corticosteroids may reduce the duration of pain but do not reduce the incidence of post-herpetic neuralgia

ocular involvement requires urgent ophthalmology review

complications -
ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia

268
Q

what is Ramsay Hunt syndrome? features/management?

A

(herpes zoster oticus) - reactivation of the varicella zoster virus in the geniculate ganglion of the seventh cranial nerve.

Features
auricular pain is often the first feature
facial nerve palsy
vesicular rash around the ear
other features include vertigo and tinnitus

Management
oral aciclovir and corticosteroids are usually given

269
Q

what kind of motor symptoms/signs might a patient with a spinal cord lesion present with?

A

usually UMN signs affecting both legs - spastic paraparesis
if cervical spine lesion, might affect all 4 limbs - spastic tetraparesis - may also have mixed LMN/UMN features in upper limps due to damage to cord and nerve roots in the neck

270
Q

what kind of sensory symptoms/signs might a patient with a spinal cord lesion present with?

A

they’ll have a sensory level - a threshold at which sensation below is impaired and above is normal.

in presence of a spastic paraparesis, this indicates a spinal cause - although not that useful for localisation e.g. sensory level at T10 indicates a lesion at, or above, T10 rather than just at T10

271
Q

what kind of autonomic symptoms/signs might a patient with a spinal cord lesion present with?

A

bladder involvement is an early feature - urgency/frequency and then incontinence.
bowel symps less common, poss will see constipation.
erectile dysfunction common.

general features indicating spinal disease = hx of neck/back pain or injury

272
Q

explain the difference between extrinsic and intrinsic spinal cord lesions, and how they might present?

A
extrinsic = compression by e.g. tumour, prolapsed disc - produces sensory loss including sacral dermatomes (saddle anaesthesia)
intrinsic = damage more central parts of spinothalamic tract first, producing sacral sparing - but this is not a strict rule.
273
Q

what is Brown-Sequard syndrome?

A

characteristic pattern of sensory/motor deficits occurring when lesion damages only one side of cord (complete = cord hemisection)
sensory pattern is accurately localising.
ipsilateral UMN weakness (as descending corticospinal tracts decussate in medulla)
proprioception/vibration loss is also ipsilateral (as posterior column ascending fibres don’t decussate till medulla)
BUT pain/temperature (spinothalamic) loss is contralateral (because these fibres decussate two levels above entry level)

274
Q

what are the tracts involved in Brown-Sequard syndrome and how does each one produce symptoms?

A
  1. Lateral corticospinal tract –> Ipsilateral spastic paresis below lesion
  2. Dorsal columns –> Ipsilateral loss of proprioception and vibration sensation
  3. Lateral spinothalamic tract –> Contralateral loss of pain and temperature sensation
275
Q

what is syringomyelia?

A

CSF filled cavity (syrinx) develops centrally in the spinal cord, producing characteristic deficits - usually starts in lower cervical cord but could expand
‘cape-like’ (neck and arms) loss of sensation to temperature but preservation of light touch, proprioception and vibration - classic e.g. is they’ve burned their hands without noticing.
Other sympts/signs - spastic weakness (predominantly of the upper limbs), paraesthesia, neuropathic pain, upgoing plantars and bowel and bladder dysfunction

276
Q

give some causes of syringomyelia

A

a Chiari malformation: strong association
trauma
tumours
idiopathic

277
Q

how do you investigate/manage syringomyelia?

A

Ix - full spine MRI with contrast to exclude a tumour or tethered cord. brain MRI - to exclude a Chiari malformation.

Treatment will be directed at treating the cause of the syrinx. In patients with a persistent or symptomatic syrinx, a shunt into the syrinx can be placed.

278
Q

what is cervical spondylosis?

A

most common cause of spinal cord disease >50yrs old
degenerative (osteoarthritis) disease of C spine leads to compression due to:
- calcification, degeneration, protrusion of intervertebral discs
- osteophytes
- calcification and thickening of longitudinal ligaments

279
Q

list some causes of spinal cord disease

A

MS (if <40yrs - most common)
cervical spondylosis (most common if >50yrs)
trauma - vertebral fractures, disc protrusions (although normally spontaneous rather than traumatic)
infection - epidural abscess, Pott’s disease of spine, syphilis, HIV
inflammation - MS, postviral transverse myelitis, sarcoid, SLE, ankylosing spondylitis
vascular - infarct of spinal cord, AV malformation, epidural haematoma
congenital - Arnold-Chiari malformation –> syringomyelia
inherited - hereditary spastic paraplegia
neoplasm - vertebral mets compressing cord, benign extrinsic tumours (neurofibroma, meningioma), intrinsic tumours (ependymoma, glioma, mets)
degenerative - in cord = MND, in spine = spondylosis w/ cord compression

280
Q

how do you manage a patient presenting with possible spinal cord compression?

A

MRI imaging/myelography
give high dose oral dexamethasone to reduce oedema.
treat cause.

281
Q

what is degenerative cervical myelopathy? give some symptoms

A

degenerative condition of cervical cord.
symptoms can include any of the following - keep an eye out for progressive/deteriorating symptoms:
- pain in neck, upper or lower limbs
- loss of motor function - loss of digital dexterity, preventing simple tasks such as holding a fork or doing up their shirt buttons, arm or leg weakness/stiffness leading to impaired gait and imbalance
- loss of sensory function causing numbness
- loss of autonomic function (urinary or faecal incontinence and/or impotence)

282
Q

how should degenerative cervical myelopathy be diagnosed and treated?

A

C spine MRI is gold standard - shows disc degeneration and ligament hypertrophy, with accompanying cord signal change.
early surgical decompression is key.

283
Q

what is cervical radiculopathy?

A

impingement of cervical nerve roots, often due to prolapse of degenerate cervical intervertebral disc backwards.
also caused by spondylosis or tumours (rare)

284
Q

what clinical features might you see in a cervical radiculopathy?

A

neck pain radiating down arm (often in myotome distribution rather than dermatome)
segmental muscle weakness
loss of relevant tendon reflexes
dermatomal sensory impairment

285
Q

outline the segmental innervation of upper limb muscles (ie by nerve route)

A

C5 - most shoulder movements, biceps
C6 - brachioradialis (elbow flexion), wrist extension and abduction
C7 - triceps (elbow extension), wrist extension and adduction, finger extension
C8 - wrist flexion and adduction, finger flexion
T1 - intrinsic muscles of hand

286
Q

how do you manage cervical radiculopathy?

A

if disc disease - conservative management with NSAIDs, muscle relaxants, use of collar, physiotherapy
some will need cervical MRI with view to surgery (to widen foramen/remove disc material)

287
Q

what is cauda equina syndrome?

A

damage to / compression of cauda equina (bundle of nerves at bottom of spinal cord) usually due to lumbar disc herniation

288
Q

what are the features of cauda equina syndrome?

A

severe back pain
urinary incontinence/retention
reduced sensation in the perianal area (saddle anaesthesia)
decreased anal tone

289
Q

how should you manage a patient presenting with cauda equina syndrome?

A

it can be rapidly progressive so refer for urgent MRI and surgical review - urgent surgical decompression needed (laminectomy) to prevent permanent paralysis/sphincter dysfunction.
if malignant cause - dexomethasone to reduce oedema around the tumour and minimise compression.

290
Q

what clinical features might suggest a lumbar disc prolapse?

A

low back pain and tenderness
sciatica (pain radiating down back of leg from buttock to ankle)
wasting/weakness of gastrocnemius and soleus
S1 sensory loss
depressed ankle reflex

if L5 root lesion compressed by L4/5 prolapse = sciatic pain + foot drop, + L5 sensory impairment

291
Q

how is sciatica/lumbar disc prolapse managed?

A

conservative - gentle exercise, NSAIDs, physiotherapy

root injections with local anaesthetic/steroids

292
Q

what is multiple sclerosis?

A

chronic cell-mediated autoimmune disorder characterised by demyelination in the central nervous system.
lesions disseminated in time and space!
first lesion usually optic neuritis

293
Q

briefly explain pathophysiology of MS

A

affects white matter of brain/spinal cord and optic nerves.
chronic inflammatory damage to myelin - form ‘plaques’ (areas with lots of demyelination)
reduction in conduction velocity leads to loss of signals down these pathways.

294
Q

what causes MS?

A

main theory is some kind of environmental agent triggers it in a genetically susceptible individual (major histocompatibility complex, MHC, has genetic role).
it’s 3x more common in women, typically diagnosed in a 20-40yo, and linked to latitude (how far north/south you live).

295
Q

what is optic neuritis? features?

A

inflammatory demyelination of one (less commonly = both) optic nerves - either part of MS or clinically isolated syndrome (or syphilis/diabetes can cause)
features:
unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
relative afferent pupillary defect
central scotoma

296
Q

what is anterior cord syndrome?

A

caused by ischemia of the anterior spinal artery, resulting in loss of function of the anterior two-thirds of the spinal cord
this incl descending corticospinal tract, ascending spinothalamic tract, and autonomic fibers.
characterized by a corresponding loss of motor function, loss of pain and temperature sensation, and hypotension.

symptoms come on really fast, Ix = MRI, Rx = treat cause (e.g. aortic aneurysm, vasculitis, sickle cell)

297
Q

how do you treat optic neuritis?

A

should resolve over weeks-months

sometimes give high dose oral steroids

298
Q

give some visual symptoms you might get in MS, apart from optic neuritis

A

optic atrophy
Uhthoff’s phenomenon: worsening of vision following rise in body temperature (can occur with sensory/motor features too)
internuclear ophthalmoplegia

299
Q

what sensory features are typically seen in MS?

A

pins/needles
numbness
trigeminal neuralgia
Lhermitte’s syndrome: paraesthesiae in limbs on neck flexion

300
Q

what motor features are typically seen in MS?

A

spastic weakness: most commonly seen in the legs

301
Q

what cerebrellar/other features are typically seen in MS?

A

cerebellar -
ataxia: more often seen during an acute relapse than as a presenting symptom
tremor

Others -
urinary incontinence
sexual dysfunction
intellectual deterioration

302
Q

what are the different sub-types of MS?

A
  • relapsing-remitting disease
  • secondary progressive disease
  • primary progressive disease
  • progressive-relapsing disease
303
Q

describe the course of relapsing-remitting MS

A
most common form, accounts for around 85% of patients
acute attacks (e.g. last 1-2 months) followed by periods of remission with NO neurological signs
304
Q

describe the course of secondary progressive MS

A

describes relapsing-remitting patients who have deteriorated and have developed neurological signs and symptoms between relapses
around 65% of patients with relapsing-remitting disease go on to develop secondary progressive disease within 15 years of diagnosis
gait and bladder disorders are generally seen

305
Q

describe the course of primary progressive MS

A

accounts for 10% of patients
progressive deterioration from onset
more common in older people

306
Q

describe course of progressive relapsing MS

A

patient has acute attacks, with steadily worsening/progressing features in between
rare

307
Q

how is MS diagnosed?

A

key is lesions dissemninated in time and space
brain/spine MRI can show plaques - not specific to MS so need clinical features as well.
LP - CSF shows oligoclonal bands by electrophoresis - indicates local synthesis of immunoglobulins.

308
Q

how do you manage an acute relapsed of MS?

A

high dose methylpred, IV or PO for 3-5 days - improves speed of recovery but not severity of the exacerbation

309
Q

how is modification of MS course achieved/attempted?

A

beta interferon can reduce relapse rate (certain criteria must be met before you can use it though)
other drugs:
- glatiramer acetate: immunomodulating drug - acts as an ‘immune decoy’
- natalizumab: a recombinant monoclonal antibody
- fingolimod: sphingosine 1-phosphate receptor modulator

310
Q

what are the criteria for starting an MS patient on beta interferon?

A
  • relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided
  • secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)

reduces number of relapses and MRI changes, however doesn’t reduce overall disability

311
Q

describe symptomatic management options used in MS

A

for spasticity - baclofen, gabapentin, dantrolene, tizanidine, diazepam, botox injections into specific muscles, also physio!
for cerebellar tremor - clonazepam, isoniazid, gabapentin
for fatigue - excl other causes (e.g. anaemia, depression), trial amantadine - also mindfulness/CBT
for bladder problems - oxybutynin or tolterodine, intermittent self-catheterisation
for erectile dysfunction - sildenafil

312
Q

define mononeuropahty

A

damage to a single peripheral nerve e.g. by trauma (esp. pressure) or damage to their loody supple

313
Q

what is polyneuropathy?

A

multiple peripheral nerves affected by inflammatory/metabolic/toxic processes leading to a diffuse, distal, symmetrical pattern of damage - usually affects lower limbs before upper

314
Q

what is carpal tunnel syndrome?

A

compression of median nerve at wrist, as it passes through the carpal tunnel
occurs e.g. in isolation (manual labour, typing at computers) or with causes of multiple neuropathies (e.g. diabetes) or with abnormal soft tissue ‘crowding’ the carpal tunnel

315
Q

give some medical conditions associated with carpal tunnel

A
pregnancy
diabetes mellitus
local deformity e.g. secondary to osteoarthritis, fracture
rheumatoid arthritis
myxoedema
acromegaly
amyloidosis
316
Q

what are the clinical features of carpal tunnel?

A
  • pain/parasthesiae in hand - thumb, index and middle fingers
  • wasting and weakness of thenar eminence
  • sensory loss in hand (thumb + 2.5 fingers)
  • positive Tinel’s / phalen’s tests
  • often bilateral
317
Q

what are Tinel’s / Phalen’s tests?

A
Tinel's = tapping over carpal tunnel produces tingling paraesthesiae in thumb/2.5 finger distribution
Phalen's = prayer sign (maximal wrist flexion) for 60 secs produces same tingling
318
Q

how is carpal tunnel diagnosed and treated?

A

electrophysiology shows prolonged action potential (motor and sensory)
Rx - splinting of hand, esp at night; local steroid injection; surgical decompression

319
Q

what are the clinical features of an ulnar neuropathy?

A

ulnar can be damaged anywhere on course, but commonly at elbow

  • pain/tingling paraesthesiae from elbow down to forearm, down ulnar border of hand (little finger +0.5)
  • wasting/weakness of intrinsic muscles
  • sensory loss to little + 0.5 fingers
  • characteristic claw hand deformity in chronic lesions
320
Q

how is an ulnar neuropathy diagnosed/treated?

A

nerve conduction studies might localise site of lesion
mild - splinting of arm at night with elbow extended
surgical decompression - not as successful as for carpal tunnel

321
Q

what is a radial palsy?

A

pressure on radial nerve in upper arm can lead to acute wrist drop ± sensory loss in superficial radial nerve (back of hand, not really fingers)
due to prolonged abnormal posture of arm - Saturday night palsy (arm draped awkwardly over arm chair)

322
Q

what is meralgia paraesthetica?

A

compression of lateral cutaneous nerve of the thigh as it passes under inguinal ligament
sensory loss in an oval on the front/lateral thigh
associated with change in weight

323
Q

what is a lateral popliteal palsy?

A

damage to common peroneal nerve common as it winds around fibular neck
leads to foot drop - weakness of ankle dorisflexion and eversion and of extensor hallucis longus, w/ variable sensory loss
foot drop can also be caused by an L5 lumbar root lesion.

324
Q

list some causes of multifocal neuropathy/mononeuritis multiplex

A
  • malignant infiltration
  • vasculitis/connective tissue disease - RA, SLE, polyarteritis nodosa, Wegener’s granulomatosis
  • sarcoidosis
  • diabetes mellitus
  • infection - leprosy, herpes zoster, HIV, Lyme disease
  • hereditary neuropathy with liability to pressure palsies
325
Q

list some causes of polyneuropathies

A

infection - leprosy, diphtheria, Lyme disease, HIV
inflammatory - GBS, CIDP, sarcoid, Sjogren’s, vasculitis (SLE, polyarteritis nodosa)
neoplastic - paraneoplastic, paraproteinaemia
metabolic - DM, uraemia, myxoedema, amyloid
nutrition - vit deficiency esp thiamine, B12
toxic - alcohol, lead, arsenic, gold, mercury etc
drugs - isoniazid, vincristine, cisplatinum, metronidazole, nitrofurantoin, phenytoin, amiodarone

326
Q

what is chronic inflammatory demyelinating polyneuropathy?

A
  • cause of peripheral neuropathy
  • antibody mediated inflammation results in segmental demyelination of peripheral nerves
  • males more commonly affected than females
  • features similar to GBS, with motor features predominating
  • more insidious onset, over weeks to months - often thought of as the chronic version of GBS
  • high protein content in the CSF
  • treatment with steroids and immunosuppressants may have a role (unlike in GBS)
327
Q

outline the major causes of peripheral neuropathy according to motor vs sensory loss

A

Predominately motor loss:
Guillain-Barre syndrome
porphyria
lead poisoning
hereditary sensorimotor neuropathies (HSMN) - Charcot-Marie-Tooth
chronic inflammatory demyelinating polyneuropathy (CIDP)
diphtheria

Predominately sensory loss:
diabetes
uraemia
leprosy
alcoholism
vitamin B12 deficiency
amyloidosis

Alcoholic neuropathy:
secondary to both direct toxic effects and reduced absorption of B vitamins
sensory symptoms typically present prior to motor symptoms

Vitamin B12 deficiency:
subacute combined degeneration of spinal cord
dorsal column usually affected first (joint position, vibration) prior to distal paraesthesia

328
Q

how do polyneuropathies present? treatment?

A

depends on cause, commonly distal numbness/pain (glove and stocking)
motor - distal weakness, wasting
foot/hand deformity if long standing - pes cavus/claw hand
Rx - depends on cause - CIDP/vasculitis = steroids/immunomodulation

329
Q

what is myasthenia gravis?

A

autoimmune disorder - pts have circulating antibodies to acetylcholine receptors at the neuromuscular junction

associated with thymus pathology (hyperplasia, atrophy, tumour/thymoma)

330
Q

what are the clinical features of myasthenia gravis?

A

key feature is muscle fatigability - muscles become progressively weaker during periods of activity and slowly improve after periods of rest:

  • extraocular muscle weakness: diplopia
  • proximal muscle weakness: face (myasthenic snarl), neck, limb girdle
  • ptosis
  • dysphagia, dysarthria (nasal speech) - bulbar signs
  • involvement of respiratory muscles - this makes it an emergency!
331
Q

how do you investigate myasthenia gravis?

A
  • single fibre electromyography: high sensitivity (92-100%)
  • CT thorax to exclude thymoma
  • CK normal
  • serum acetylcholine autoantibodies: around 85-90% have these - in the rest, about about 40% have anti-muscle-specific tyrosine kinase antibodies
  • Tensilon test: IV edrophonium reduces muscle weakness temporarily - not commonly used anymore due to the risk of cardiac arrhythmia
332
Q

list some exacerbating factors for myasthenia gravis

A

most common = is exertion resulting in fatigability - symptoms become more marked during the day

drugs:
penicillamine
quinidine, procainamide
beta-blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines
333
Q

what are the management options for myasthenia gravis?

A

long-acting anticholinesterase e.g. pyridostigmine - symptomatic relief, can end up needing increasing doses so get muscarinc side effects (salivation, vomiting, abdo pain, diarrhoea)
immunosuppression: prednisolone then add azathiprine if still no response
thymectomy - if there’s a thymoma
if really severe - plasma exchange/IVIG

334
Q

how does Duchenne’s muscular dystrophy present? how do you differentiate Becker’s from this?

A

progressive proximal muscle weakness from 5 years
calf pseudohypertrophy
Gower’s sign: child uses arms to stand up from a squatted position
30% of patients have intellectual impairment

Becker’s =
develops after the age of 10 years
intellectual impairment much less common

335
Q

what are the dystrophinopathies?

A
  • X-linked recessive
  • due to mutation in the gene encoding dystrophin, dystrophin gene on Xp21
  • dystrophin is part of a large membrane associated protein in muscle which connects the muscle membrane to actin, part of the muscle cytoskeleton
  • in Duchenne muscular dystrophy there is a frameshift mutation resulting in one or both of the binding sites are lost leading to a severe form
  • in Becker muscular dystrophy there is a non-frameshift insertion in the dystrophin gene resulting in both binding sites being preserved leading to a milder form
336
Q

what are the common features of the myopathies? list some causes as well

A

Features:
symmetrical muscle weakness (proximal > distal)
common problems are rising from chair or getting out of bath
sensation normal, reflexes normal, no fasciculation

Causes
inflammatory: polymyositis
inherited: Duchenne/Becker muscular dystrophy, myotonic dystrophy
endocrine: Cushing's, thyrotoxicosis
alcohol
post-polio syndrome
337
Q

what is myotonic dystrophy?

A

autosomal dominant disorder - abnormally sustained muscle contraction (myotonia) - manifests as inability to release grip.
features start age 20-30, involves cardiac, skeletal and smooth muscle.

General features:

  • myotonic facies (long, ‘haggard’ appearance)
  • frontal balding
  • bilateral ptosis
  • cataracts
  • dysarthria

Other features:

  • myotonia (tonic spasm of muscle)
  • weakness of arms and legs (distal initially)
  • mild mental impairment
  • diabetes mellitus
  • testicular atrophy
  • cardiac involvement: heart block, cardiomyopathy
  • dysphagia

diagnosis - electromyopathy
Rx - phenytoin, mexiletine

338
Q

what are the inflammatory myopathies?

A

polymyositis - can occur on its own or w/ autoimmune connective tissue disorders e.g. systemic sclerosis, fibrosing alveolitis, Sjogren’s
dermatomyositis - lilac (heliotrope) rash affecting face ± purple-red rash to knuckles and anterior chest wall, other estensor surgaces

features - proximal myopathy ± dysphagia due to pharyngeal muscle involvement, muscle pain, tenderness, arthralgia, Raynaud’s

Rx - need histological confirmation, then treat with steroids and immunosuppressants e.g. azathioprine.

339
Q

give some info on statin associated myopathy

A

myopathy: includes myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase.

Risks factors for myopathy include advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus.

Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)

340
Q

what kind of myopathy can glucocorticoid steroids cause?

A

proximal myopathy

341
Q

what is cerebral palsy?

A

range of mostly motor neurological deficits arising from pre- or perinatal insults
often in comb with LDs, behavioural problems and epilepsy

342
Q

list some risk/causative factors for cerebral palsy

A

prematurity

antenatal - foetal hypoxia or infection, developmental abnormalities, twins, maternal age
perinatal - postmaturity, traumatic delivery w/neonatal intracranial haemorrhage
postnatal, if preterm - hypoxia, hypoglycaemia, cerebral ischaemia or haemorrhage, hypothermia
postnatal, fullterm - infection, trauma, kernicterus

343
Q

explain some different patterns/manifestations of cerebral palsy

A
spastic diplegia (Little's disease) - congenital spastic parapareis, with shortening/deformity of legs --> walking difficulty. upper limbs spared.
spastic hemiplegia - w/ hemianopic and hemisensory deficits, epilepsy, LDs
athetoid - choreoathetiod movements developing in early childhood, usually normal cognitive function although dysarthria can make communication difficult
344
Q

how is cerebral palsy managed?

A
  • multidisciplinary approach is needed
  • treatments for spasticity include oral diazepam, oral and intrathecal baclofen, botulinum toxin type A, orthopaedic surgery and selective dorsal rhizotomy
  • anticonvulsants, analgesia as required
345
Q

give some info on spina bifida

A
  • Non fusion of the vertebral arches during embryonic development
  • Three categories; myelomeningocele, spina bifida occulta and meningocele
  • Myelomeningocele is the most severe type with associated neurological defects that may persist in spite of anatomical closure of the defect

spina bifida occulta - skin and tissues (but not not bones) may develop over the distal cord, site may be identifiable by a birth mark or hair patch

management is surgical.
prevent with folic acid supplements in pregnancy

346
Q

what is an Arnold-Chiari malformation?

A

herniation of cerebellar tissue, and sometimes lower part of brainstem through foramen magnum - congenital.

347
Q

what is Huntington’s disease? outline the genetics

A

inherited neurodegenerative condition, progressive and incurable condition resulting in death 20 years after the initial symptoms develop.

Genetics:
autosomal dominant
trinucleotide repeat disorder: repeat expansion of CAG
results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia
due to defect in huntingtin gene on chromosome 4
MRI - caudate atrophy, enlarged frontal horns

348
Q

what clinical features are typical of Huntington’s disease?

A

presents at age 35-40ish (although genetic anticipation = might present earlier and earlier down the generations)
progressive chorea and dementia/personality changes
also - dystonia, saccadic eye moveemnts

349
Q

how do you manage Huntington’s disease?

A

no treatment slows progression.

counselling and genetic testing for relatives.

350
Q

what is Wilson’s disease?

A

autosomal recessive disorder characterised by excessive copper deposition in the tissues - esp liver and basal ganglia
Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion.
caused by a defect in the ATP7B gene located on chromosome 13.

351
Q

how does Wilson’s disease present? how is it treated?

A

in childhood - cirrhosis
in adolescence - neuro features - akinetic rigid syndrome, dystonia, cerebellar signs, psychiatric signs
Kayser-Fleischer rings on slit lamp
Ix - serum copper and caeruloplasmin, urinary copper excretion
Rx - copper chelation with penicillamine

352
Q

what is Friedrich’s ataxia?

A

an early-onset hereditary ataxias - autosomal recessive, trinucleotide repeat disorder characterised by a GAA repeat in the X25 gene on chromosome 9 (frataxin).

The typical age of onset is 10-15 years old.
Gait ataxia and kyphoscoliosis are the most common presenting features.

353
Q

what are the features of Friedrich’s ataxia?

A
Neurological features:
absent ankle jerks/extensor plantars
cerebellar ataxia
optic atrophy
spinocerebellar tract degeneration

Other features:
hypertrophic obstructive cardiomyopathy (90%, most common cause of death)
diabetes mellitus (10-20%)
high-arched palate

354
Q

what is Charcot-Marie-Tooth disease?

A

most common hereditary peripheral neuropathy
results in a predominantly motor loss
no cure, and management is focused on physical and occupational therapy.

Features:

  • Frequently sprained ankles
  • Distal muscle weakness
  • Distal muscle atrophy
  • Hyporeflexia
  • Stork leg deformity
  • Pes cavus
  • Hammer toes
355
Q

describe the genetics of Alzheimer’s disease

A
  • most cases are sporadic
  • 5% of cases = autosomal dominant trait
  • mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
  • apoprotein E allele E4 - encodes a cholesterol transport protein
356
Q

describe the underlying pathology of alzheimer’s diease

A
  • macroscopic: widespread cerebral atrophy, particularly involving the cortex and hippocampus
  • microscopic: cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
  • biochemical: there is a deficit of acetylcholine from damage to an ascending forebrain projection

Neurofibrillary tangles = paired helical filaments are partly made from a protein called tau
in AD tau proteins are excessively phosphorylated

357
Q

describe the non-pharmacological management of Alzheimer’s disease

A

NICE recommend offering:

  • ‘a range of activities to promote wellbeing that are tailored to the person’s preference’
  • group cognitive stimulation therapy for patients with mild and moderate dementia

other options to consider include group reminiscence therapy and cognitive rehabilitation

358
Q

describe the pharmacological management of Alzheimer’s disease

A

NICE updated it’s dementia guidelines in 2018:

  • three acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease
  • memantine (an NMDA receptor antagonist) is in simple terms the ‘second-line’ treatment for Alzheimer’s, NICE recommend it is used in the following situations:
    → moderate Alzheimer’s in patient intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
    → as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
    → monotherapy in severe Alzheimer’s
359
Q

what are the characteristic pathological features of Lewy body dementia?

A

alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas

360
Q

what are the features of Lewy body dementia? how is it diagnosed?

A

Features:

  • progressive cognitive impairment
  • parkinsonism
  • visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)

Diagnosis:

  • usually clinical
  • single-photon emission computed tomography (SPECT) can be used (commercially known as a DaTscan)
361
Q

how is Lewy body dementia managed?

A
  • both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.
  • AVOID antipsychotics/antiparkinsonian drugs - will make them worse!
362
Q

describe the underlying pathology of frontotemporal dementia (in Pick’s disease)

A

Focal gyral atrophy with a knife-blade appearance is characteristic of Pick’s disease.

Macroscopic - Atrophy of the frontal and temporal lobes

Microscopic -
Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques
363
Q

what clinical features suggest a vascular dementia?

A
  • abrupt onset and stepwise progression rather than smooth or gradual
  • presence of vascular disease
  • nocturnal confusion, fluctuating cognition
  • emotional lability

it’s due to multiple small infarcts in the brain

364
Q

what is a chronic subdural haemtoma?

A

mostly occurs in elderly/alcoholic, can follow minor head injury - pay not be able to identify history of trauma!

Rupture of the small bridging veins within the subdural space rupture and cause slow bleeding - common in elderly/alcoholic because they have brain atrophy so bridging veins are held taught

365
Q

how does a chronic subdural haematoma present? what would you see on CT? management?

A

several week to month progressive history of either confusion, reduced consciousness or neurological deficit.
On CT - crescentic in shape, not restricted by suture lines and compress the brain (‘mass effect’). chronic subdurals are hypodense (dark) compared to the substance of the brain (acute subdurals are hyperdense and appear bright)

If incidental finding / no associated neurological deficit then manage conservatively
If pt confused, has an associated neurological deficit or has severe imaging findings = surgical decompression with burr holes is required.

366
Q

what is motor neurone disease?

A
neurological condition of unknown cause which can present with both UMN + LMN signs.
rarely presents before 40 years
various patterns of disease:
  - amyotrophic lateral sclerosis
  - primary lateral sclerosis
  - progressive muscular atrophy
  - progressive bulbar palsy. 

combination of clinical patterns seen in some

367
Q

give some info on amyotrophic lateral sclerosis MND

A

typically LMN signs in arms and UMN signs in legs

in familial cases the gene responsible lies on chromosome 21 and codes for superoxide dismutase

368
Q

what type of signs would you see in primary lateral sclerosis MND?

A

UMN signs only

369
Q

what type of signs would you see in progressive muscular atrophy MND?

A

LMN signs only
affects distal muscles before proximal
carries best prognosis

370
Q

what type of signs would you see in progressive bulbar palsy MND?

A

palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
signs of mixed bulbar and psuedobulbar palsy e.g. wasted, fasciculating tongue but brisk jaw reflex
carries worst prognosis

371
Q

what clinical features suggest MND?

A
  • fasciculation
  • the absence of sensory signs/symptoms
  • the mixture of LMN and UMN signs
  • wasting of the small hand muscles/tibialis anterior is common

Other features:

  • doesn’t affect external ocular muscles
  • no cerebellar signs
  • abdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature
372
Q

how do you investigate MND?

A

diagnosis is usually clinical, but:

  • nerve conduction studies show normal motor conduction and can help exclude a neuropathy
  • Electromyography (EMG) shows a reduced number of action potentials with an increased amplitude
  • MRI is usually performed to exclude the differential diagnosis of cervical cord compression and myelopathy
373
Q

MND management/prognosis?

A

Riluzole:

  • prevents stimulation of glutamate receptors
  • used mainly in amyotrophic lateral sclerosis
  • prolongs life by about 3 months

Respiratory care:
- non-invasive ventilation (usually BIPAP) is used at night

Symptomatic:

  • anticholinergics for reducing saliva secretion when swallowing difficult
  • baclofen/dantrolene/diazepam for spasticity
  • antidepressants
  • quinine for cramp
  • laxative for constipation
  • phyiotherapy
  • home adaptations

Prognosis:
poor: 50% of patients die within 3 years

374
Q

list some metabolic causes of an acquired acute ecephalopathy (presenting with confusion/coma/seizures)

A

hypoxia
hypoglycaemia
respiratory/renal/hepatic failure
electrolytes - sodium (high/low), calcium/magneisum high/low
vitamin deficiencies
endocrine disorders - hypopituitarism, thyroid up/down, myxoedema, insulinoma
toxins - CO, lead, alcohol

375
Q

what deficiency causes Wernicke-Korsakoff syndrome?

A
vitamin B1 (thiamine) deficiency - urgent IV pabrinex (contains vitamins B and C - thiamine, riboflavin, pyridoxine, nicotinamide and ascorbic acid)
usually occurs in chronic alcoholism, can also get in hyperemesis gravidarum!
376
Q

how does Wernicke’s encephalopathy present? how does this link to Korsakoff’s?

A

triad of:
ophthalmoplegia - nystagmus, third/sixth nerve palsies
ataxia
confusion

when this goes untreated, pt ends up with antero and retrograde amnesia + confabulation = Korsakoff’s - can’t really treat this!

377
Q

what is Lambert-Eaton myasthenic syndrome?

A

seen in association with small cell lung cancer, and to a lesser extent breast and ovarian cancer
caused by an antibody directed against pre-synaptic voltage gated calcium channel in the peripheral nervous system.
Features:
- repeated muscle contractions lead to increased muscle strength
- limb girdle weakness (affects lower limbs first)
- hyporeflexia
- autonomic symptoms: dry mouth, impotence, difficultly micturating
- ophthalmoplegia and ptosis not commonly a feature (unlike in myasthenia gravis)

EMG - incremental response to repetitive electrical stimulation

Management - treatment of underlying cancer
immunosuppression, for example with prednisolone and/or azathioprine
intravenous immunoglobulin therapy and plasma exchange may be beneficial

378
Q

what is status epilepticus?

A

recurring seizures, patient doesn’t regain consciousness between attacks, for 30 mins or more - though cut off to being treating usually 5 mins.

risky because if untreated –> anoxia –> brain damage/death

379
Q

give some possible causes of status epilepticus

A
if existing seizure disorder - non-compliance, alcohol, sleep withdrawal
no previous seizures:
 - trauma
 - infection - meningitis, encephalitis, abscess
 - tumour
 - stroke
 - metabolic, hypoxia
 - drug OD, alcohol
380
Q

describe management of status epilepticus

A

ABCDE !!!!
in community - buccal midazolam or rectal diazepam, unless they have IV access in which case IV lorazepam - call ambulance
in hospital:
1) IV lorazepam, if unavailable give IV diazepam, if can’t get IV access - buccal midazolam
2) give two doses of first-line treatment
3) still no luck - IV phenobarbital or phenytoin

if still nothing = ‘refractory status epilepticus’:
adults - IV midazolam, propofol or thiopental sodium
children/young people - IV midazolam or thiopental sodium

381
Q

what is Guillain-Barre syndrome?

A

acute inflammatory demyelinating polyneuropathy, often triggered by an infection (classically Campylobacter jejuni).
mostly motor involvement, often including respiratory nd bulbar muscles making it an emergency

382
Q

describe the pathogenesis of Guillain-Barre syndrome?

A
  • cross reaction of antibodies with gangliosides in the peripheral nervous system
  • correlation between anti-ganglioside antibody (e.g. anti-GM1) and clinical features has been demonstrated
    anti-GM1 antibodies in 25% of patients
383
Q

describe the features of Guillain-Barre

A

characteristic features = progressive weakness of all four limbs - maximum deficit reached within hours - days.

  • classically ascending weakness i.e. the lower extremities are affected first, however it tends to affect proximal (within the limb i.e. proximal lower limb, then rest of lower limb, then proximal upper limb etc) muscles earlier than the distal ones
  • sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs. Some patients experience back pain in the initial stages of the illness

Other features:

  • areflexia
  • cranial nerve involvement e.g. diplopia
  • autonomic involvement: e.g. urinary retention

Less common findings
- papilloedema: thought to be secondary to reduced CSF resorption

384
Q

how do you investigate/diagnose GBS?

A
  • LP = raised CSF protein w/ normal cell count
  • EMG + nerve conduction may confirm demyelinating neuropathy
    (all of these can be normal early in disease)
  • 25% of pts will have circulating ganglioside abs
385
Q

how do you manage a patient with GBS?

A
  • regular vital capacity measurements to monitor for involvement of respiratory muscles
  • ECG montoring also
  • admit to ICU if VC deteriorating or swallow problems - can need artificial ventilation and NG feeding etc
  • LMWH for DVT prophylaxis
  • mouth and eye care

immunological treatment - plasma exchange or high dose IVIG - speeds rate of recovery, reduces complications

c. 80% will make complete recovery, but this can take months

386
Q

give some indicators for poor prognosis in Guillain-Barre syndrome

A
  • increasing patient age
  • rapid onset of weakness
  • need for ventilation
  • antiganglioside abs
  • preceding diarrhoeal illnes
  • electrophysiology showing signif. axonal degeneration
387
Q

what is a myasthenic crisis?

A

acute myasthenia gravis symptoms affecting bulbar muscles, diaphragm, intercostal muscles
can occur at any point in someone with severe MG.
Rx - airway/ventilation support, plasma exchange/IVIG.

388
Q

what are the NICE criteria indicating a head injury patient requires immediate CT?

A

GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
suspected open or depressed skull fracture.
any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
post-traumatic seizure.
focal neurological deficit.
more than 1 episode of vomiting

389
Q

what are the NICE criteria indicating a head injury patient requires CT within 8 hours?

A

adults with any of the following risk factors who have experienced some LOC or amnesia since the injury:
age 65 years or older
any history of bleeding or clotting disorders
dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
more than 30 minutes’ retrograde amnesia of events immediately before the head injury
any patient on warfarin

390
Q

give some basic info on how head injury damages the brain

A
  • primary brain injury may be focal (contusion/haematoma) or diffuse (diffuse axonal injury)
  • diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons
  • intra-cranial haematomas can be extradural, subdural or intracerebral, while contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact
  • secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury. The normal cerebral auto regulatory processes are disrupted following trauma rendering the brain more susceptible to blood flow changes and hypoxia
  • the Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre terminal event
391
Q

what are the features of an extradural (epidural) haematoma?

A

Bleeding into the space between the dura mater and the skull.
Often results from acceleration-deceleration trauma or a blow to the side of the head.
majority of epidural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery.

Features:

  • raised intracranial pressure
  • some patients may exhibit a lucid interval
392
Q

what are the features of a subdural haematoma?

A

Bleeding into the outermost meningeal layer.
Most commonly occur around the frontal and parietal lobes.

Risk factors include old age, alcoholism and anticoagulation.

Slower onset of symptoms than a epidural haematoma.

393
Q

what are the features of a subarachnoid haemorrhage?

A

Classically causes a sudden occipital headache.
Usually occurs spontaneously in the context of a ruptured cerebral aneurysm but may be seen in association with other injuries when a patient has sustained a traumatic brain injury.

394
Q

describe the CT findings of an extradural haematoma

A

hyperdense (bright), biconvex (or lentiform) collection around the surface of the brain.

395
Q

describe the CT findings of an acute subdural haematoma

A

hyperdense (bright), crescenteric collection surrounding the brain that is not limited by suture lines

396
Q

describe the CT findings of a chronic subdural haematoma

A

hypodense (dark), crescenteric collection around the surface of the brain that is not limited by suture lines

397
Q

describe the CT findings of an intracerebral haemorrhage

A

hyperdensity (bright lesion) within the substance of the brain.

398
Q

describe the CT findings of a SAH

A

hyperdensity within the cisterns or the brain and the sulci

399
Q

describe the CT findings of an intraventricular haemorrhage

A

hyperdensity within the dark CSF spaces within the ventricles.

400
Q

what are the clinical features of an extradural haematoma?

A

loss of consciousness, a lucid interval and then a rapid decline in consciousness. Mass effect on the brain will cause uncal herniation and a fixed, dilated pupil due to third cranial nerve compression.

401
Q

what are the clinical features of an acute subdural haematoma?

A

caused by high-speed injuries or acceleration-deceleration injuries and is therefore commonly associated with other brain injuries.
spectrum of severity of clinical presentation from an asymptomatic patient to those who are severely comatose.

402
Q

what are the clinical features of a chronic subdural haematoma?

A

typically present several weeks after a mild head injury with progressive confusion, loss of consciousness, weakness or higher cortical function

403
Q

what is the definitive management of an extradural haematoma?

A

craniotomy and evacuation of the haematoma.

404
Q

what is the definitive management of an acute subdural haematoma?

A

decompressive craniectomy.

405
Q

what is the definitive management of a chronic subdural haematoma

A

definitive treatment is burr hole drainage - if symptomatic, if not just leave to resolve

406
Q

what is squint? how can it be divided?

A

Squint (strabismus) is characterised by misalignment of the visual axes.
concomitant = due to imbalance in extraocular muscles, convergent is more common than divergent
paralytic = due to paralysis of extra-ocular muscles
can be examined using corneal light reflection test

prefixes ‘eso’ = inward deviation
‘exo’ = outward

407
Q

what causes concomitant squint? management?

A

usually congenital
if tested separately, they have full movement of both eyes
extraocular muscles and nerves grossly normal
no diplopia

Rx - refer - correct refractory error, glasses with prisms, maybe surgery - needs correcting to avoid amblyopia

408
Q

what causes paralytic squint? management?

A

usually acquired damage to extraocular muscles or nerves
third/fourth/sixth nerve palsies etc

Rx - refer, treat cause if poss, prisms on glasses if not

409
Q

what is amblyopia?

A
lazy eye
usually caused by:
 - constant strabismus.
 - asymmetric refractive errors.
 - any orbital pathology affecting ocular growth or clarity e.g. early onset cataract

presents either with visible strabismus, or unilateral deterioration in acuity

410
Q

list some treatment options for amblyopia

A
  • correct refractory errors
  • treat any treatable cause
  • patch to occlude the healthy eye
411
Q

list some features of a seizure that might indicate NEAD

A
  • tend to last longer than epileptic - e.g. up to and over 25 mins
  • might go in and out of episodes
  • atypical episodes - eyes screwed shut (you can’t open them), thrashing about or stiff as a board, move (slowly) away when you approach, back arching, thrusting of hips
  • might still see tongue biting/incontinence
  • more aware of surroundings - can remember conversations occurring during episode
  • won’t drop their O2 sats like in epilepsy
  • if they’re getting loads, they tend to only come on in stressful situations/when people will definitely be around
  • no post-ictal confusion, recovery ‘instant’ (<1 min)
  • don’t tend to injure themselves like epileptic seizures do, because they don’t happen when driving/cooking etc
412
Q

list some vascular causes of unilateral visual loss

A
  • amaurosis fugax/central retinal artery occlusion
  • central retinal vein occlusion
  • anterior ischaemic optic neuropathy - GCA
413
Q

list some non-vascular causes of unilateral visual loss

A
  • optic neuritis
  • retinal detachment - floaters with reduced acuity
  • vitreous haemorrhage - also floaters
  • acute angle-closure glaucoma
414
Q

give some features suggestive of optic neuritis

A
  • reduced acuity over a few days
  • pain on moving eye
  • exacerbated by heat/exercise
  • afferent pupillary defect
  • dyschromatopsia (reduced colour vision, especially loss of red)
415
Q

what is ‘pinhole correction’?

A

used when test visual acuity - corrects refractive error to see if it’s a neuro problem or if the patient just needs glasses;

416
Q

what is a Marcus Gunn pupil?

A

reduced afferent pupillary reflex, sign of past optic neuritis

417
Q

what features suggest acute angle-closure glaucoma?

A

painful red eye, nausea/vomiting, cloudy elliptical pupil, can be triggered by ipatropium bromide - suspect it if they were fine till they used their inhalers!

418
Q

list the DANISH cerebellar signs

A
Dysdiadochokinesis
Ataxia
Nystagmus
Intention tremor
Slurred, staccato speech
Hypotonia
419
Q

what is syncope?

A

abrupt and transient LOC with loss of postural tone that follows a sudden fall in cerebral perfusion

420
Q

what is a seizure?

A

clinical manifestation of disordered electrical activity in the brain