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Neurology Flashcards

1
Q

What is epilepsy? What are some causes of epilepsy?

A

Chronic neurological disorder w recurrent unprovoked seizures.
Genetic, neuro abnormalities, metabolic/immune disorder, chronic infection

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2
Q

What are the motor clinical features of epilepsy seizures?

A

Tonic (stiff muscles)
Clonic (rhythmic muscle jerk),
Myoclonic (shock jerks)
Atonic (loss of motor tone)
Spasms

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3
Q

Gabanergic vs glutamatergic

A

Gabanergic - GABA = main inhib neurotransmitter
Glutamatergic - glutamate = excitatory neurotransmitter

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4
Q

What is the pathophysiology behind a seizure?

A

Bursts of excitatory action potentials in neurons = synchronous hyperexcitable activity

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5
Q

What are the different types of seizures and how are they defined?

A

Focal - electrical activity is confined to one part of the brain, symptoms depend on the part of brain affected
Generalised - electrical activity affects all/most of brain, symptoms are more general and involve more of the body

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6
Q

What are the different types of focal seizures?

A
  1. Complex = focal impaired awareness, loss of consciousness after aura or at start of seizure, often come from temporal lobe, get post ictal sx
  2. Simple = focal aware, no loss of consciousness, get focal sx, no post ictal sx
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7
Q

What are the sx of seizure when the frontal lobe is involved?

A

Jacksonian features - progresses from eg. twitching in finger to twitch/tingle/weak entire hand
Dysphasia - lang disorder
Todds palsy - weakness/paralysis in body after seizure

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8
Q

What are the sx of seizure when occipital and parietal lobes is involved?

A

Parietal - tingling/numbness and motor sx
Occipital - visual sx eg. spots/lines in visual field

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9
Q

What does each lobe of the brain do?

A

Parietal - sensory, vision, comprehension of speech (Wernicke’s area), calculation and writing
Temporal - vision, hearing, olfaction, memory and emotion (amygdala) (hippocampus)
Frontal - motor, expression of speech (Broca’s area), behaviour, continence, eye movements, olfaction
Occipital - vision

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10
Q

What are the types of generalised seizures?

A
  • Absence - brief loss of consciousness/awareness, no convulsion, mainly in children and last for a few seconds
  • Tonic clonic - whole body stiff and loss of consciousness w convulsions
  • Myoclonic - sudden jerk of limb, trunk or face
  • Atonic - loss of muscle tone = pt falls, still conscious
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11
Q

What is the treatment for absence seizures?

A

Sodium valproate or ethosuximide
Carbamazepine worsens seizures

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12
Q

What is the treatment for tonic clonic and atonic seizures?

A

Sodium valproate or lamotrigine

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13
Q

What is the treatment for myoclonic seizures?

A

Sodium valproate or levetiracetam/topiramate if pt of childbearing age
Carbamazepine worsens seizures

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14
Q

What is the treatment of focal seizures?

A

Carbamazepine or lamotrigine

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15
Q

What are the reg regarding epilepsy and driving?

A

Car/motorbike:
- One off seizure = reapply in 6 months
- >1 seizure = reapply in 1 year
- Seizure after change in antiepilpetic meds = reapply to drive if seizure >6 months ago
Big vehicles:
- One off seizure = reapply in 5 years
- >1 seizure = reapply when seizure free for 10 years

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16
Q

What are some of the triggers of a seizure?

A
  • Stress/anxiety
  • Antidepressants and antipsychotics
  • Lack of sleep/tired
  • Hypoglycaemia
  • Heavy alcohol
  • Flashing lights
  • Periods
  • Fever illnesses
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17
Q

What are the ix into seizures?

A
  • EEG, measures electrical activity of brain, supports diagnosis but can’t be used to exclude
  • ECG - rule out arrhyhthmia
  • Bloods = FBC, U&E, LFT, glucose
  • MRI/CT to look for structural abnorm
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18
Q

What are some epilepsy mimics?

A
  • Syncope and anoxic seizures due to loss of cerebral blood flow
  • Pseudoseizures - behavioural, psychological, psychiatric
  • Sleep related conditions
  • Paraoxysmal movement disorders
  • Migraines
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19
Q

What anti epileptics can you not use in child bearing aged females?

A

Sodium valproate
Carbamazepine to be avoided
Lamotrigine and levetiracetam safe in pregnancy

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20
Q

What anti epileptics interact w the pill?

A

Topiramate and oxcarbazepine

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21
Q

Levatiracetam:
- Use
- SE and contraindications
- Interactions
- Bloods needed

A

U - is an add on therapy, good for all seizures
SE - dizziness, headache, irritability, loss of strength and energy, behaviour changes, suicidal thoughts, drowsiness
I - doesn’t seem to have any
B - not needed ?

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22
Q

Lamotrigine:
- Use
- SE and contraindications
- Interactions
- Bloods needed

A

U - good for all seizures
SE - rash, diplopia, tremor
I - carbamazepine and phenytoin
B - not needed ?

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23
Q

Sodium valproate:
- Use
- SE and contraindications
- Interactions
- Bloods needed

A

U - good for all seizures but not in women of child bearing age
SE - weight gain, hair loss comes back curly, oedema, ataxia, tremor, teratogenicity
I - lamotrigine = extreme tiredness and slurred speech
B - LFTS and FBC 6 months after start and then every 12 months

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24
Q

Topiramate:
- Use
- SE and contraindications
- Interactions
- Bloods needed

A

U - for all types of seizures?
SE - drowsiness, diarrhoea, dizzy, nausea, weight loss, depression, don’t take if hx of glaucoma or renal stones
I - metformin, venlafaxine, diltiazem
B -

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25
Q

Carbameazepine:
- Use
- SE and contraindications
- Interactions
- Bloods needed

A

U - focal seizures, worsens myoclonic seizures
SE - SIADH, drowsiness, diplopia, ataxia, don’t use in pregnancy, blood disorders
I - anticoagulants, clarithromycin, antidepressants
B - FBC

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26
Q

Phenytoin:
- Use
- SE and contraindications
- Interactions
- Bloods needed

A

U - focal seizures, status epilepticus
SE - peripheral neuropathy, lymphadenopathy, sore/swollen gums, hirsuitism
I - other antiepilpetics
B -

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27
Q

What is status epilpeticus?

A

Seizure >30 mins or multiple seizures over 30 mins w/o complete resolution. Should be assumed at 5 mins.
Is an emergency as risk of brain damage increases as the condition persists.

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28
Q

What is the acute management of status epilepticus?

A
  1. Immediate management - AtoE, IV access and bloods, check BM, give O2
  2. 1st dose benzo - 4mg IV lorazepam or 10mg PR diazepam
  3. 2nd dose benzo
  4. IV phenytoin w ECG monitoring
  5. ITU - general anaesthesia and intubation w IV thiopentone
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29
Q

What are the Ix into status epilepticus?

A

Initial - O2 sats, BM
Bloods - ABG, FBC, U+E, LFT, CRP, Ca, Mg, clotting
If giving glucose in hx of alcohol abuse pt = IV pabrinex to avoid Wenicke’s encephalopathy

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30
Q

What qs do you need to ask in a headache hx?

A

Onset and duration
Nature of headache
Site of headache
Pattern and timing
Exacerbating and releiving factors
Associated sx
DH - esp analgesia use

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31
Q

What drugs can cause medication over use headache?

A
  • Paracetamol, aspirin, NSAIDs if used >15 days a month
  • Triptans, opioids >10 days a month
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32
Q

What are the red flags associated w headache?

A
  • Thunderclap headache
  • Associated fever
  • Meningism
  • Raised ICP = headache worse in morn, lying down and cough
  • New neuro deficit or cog dysfunc
  • Personality change
  • Deteroriating conscious level
  • Recent head injury
  • New onset headache >50
  • Hx of malaignancy
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33
Q

What are the CF of tension headache?

A

Tight band headache, worse at end of day, responds to simple analgesics.
Triggers - stress, poor posture, lack of sleep

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34
Q

What are the CF of migraine?

A

Throbbing, unilateral, often disabling and need to lie down
Photophobia and phonophobia
Aura

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35
Q

What is the management of migraine?

A
  • Simple analgesics
  • Sumatriptan (cause throat and chest tightness)
  • Anti emetic eg. metoclopramide/prochlorperazine
  • Amitryptylline/propanolol prophylaxis
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36
Q

What are the CF of med overuse headache?

A

Headache for 15 days or more a month, pt has existing headache disorder and reg analgesics aren’t working.

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37
Q

How do you manage med overuse headache?

A

Stop all analgesics, headaches will get worse before they get better

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38
Q

What are the CF of cluster headaches?

A

Severe unilateral stabbing pain behind eyeball, wakes you up at night. Affects men.
Runny nose, ptosis and teary eyes.
Triggers - alcohol, cigs, volatile smells, change in temp.
Normally a life long disease

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39
Q

What is the management of cluster headaches?

A
  • Avoid triggers
  • Verapamil prophylaxis
  • Acute attack = 100% O2 and subcut/nasal triptan
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40
Q

What are the CF of subarachnoid haemorrhage?

A
  • Thunderclap headache, maximal pain
  • Can also have neck stiffness
  • Then seizures, neurological deficits, decreased consciousness and death
  • Sentinel headaches in months proceeding
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41
Q

How do you ix subarachnoid haemorrhage?

A

CT, MRI
Lumbar punc - look for xanthochromia
Cerebral angiography is gold standard

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42
Q

What is the prognosis of subarachnoid haemorrhage?

A

1/3 die
1/3 recover
1/3 disability

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43
Q

What is the management of subarachnoid haemorrhage?

A
  • Surgery = clipping and coiling, thrombosis of blood in aneurysm
  • CCB eg. nimodipine to prevent ischaemia
  • Control raised ICP - mannitol, loop diuretics
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44
Q

What are the complications of subarachnoid haemorrhage?

A
  • Vasospasm
  • Hydrocephalus
  • Seizures
  • Rebleeding
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45
Q

What are the CF of a SOL?

A
  • Headache worse on waking, lying down, coughing
  • Vomiting and morning headache
  • CN palsies esp abducens
  • Drowsiness, seizure, pupil abnormalities, papilloedema
  • Cushing’s reflex = widened pulse pressure not HTN eg. 120/80 - 120/30, brady, abnormal breathing
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46
Q

What are the IX into SOL?

A
  • CT/MRI - decide if is primary or met tumour
  • Biopsy if needed
  • Bloods - FBC, U+E, LFTS (Na+ low in SIADH)
  • CXR/mammography to find primary tumour
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47
Q

What are the differentials for SOL?

A
  • Metastatic - breast, lung or melanoma
  • Primary CNS tumour - meningioma (benign) or glioblastoma (malignant)
  • Cerebral abscesses, more common in those who are immunosuppressed
  • Haematoma
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48
Q

What is the management of SOL?

A
  • Treat underlying cause
  • Manage raised ICP
  • Treat complications eg. anticonvulsants
  • Sx treatment eg. headache, N+V
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49
Q

What is idiopathic intracranial HTN?

A

Raised ICP, mostly in young and obese women. Opening pressure >25 cmH2O

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50
Q

What are the clinical features of idiopathic intracranial HTN?

A
  • Headache, features described already
  • Visual disturb = visual darkening or loss, due to optic nerve ischaemia
  • Drug associations - OCP, steroids, tetracycline, Vit A, lithium
  • Abducens palsy
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51
Q

What are the ix into idiopathic intracranial HTN?

A
  • Fundoscopy = bilat papilloedema
  • BP measurement
  • Urinalysis to exclude pregnancy (preeclampsia) and look for renal disease
  • MRI to exclude other causes of raised ICP
  • LP to measure opening pressure
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52
Q

What is the management of IIH?

A
  • Weight loss, best evidence
  • Carbonic anhydrase inhib (reduced CSF production), have huge list of SEs
  • Therapeutic LPs
  • Surgical CSF shunting in resistant cases
  • Optic nerve sheath fenestration to protect against visual loss
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53
Q

What is the prognosis of IIH and what are the complications?

A

Permanent visual loss.
Recurrence can occur in 1/3rd of pt.

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54
Q

What are the CF of temporal arteritis?

A
  • Jaw claudication
  • Pain brushing hair
  • New onset headache >50
  • Decreased pulsation in temporal artery
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55
Q

What is the management of temporal arteritis?

A

Pred 60-100mg OD 2 weeks and then consider reducing.
IV methylpred for 1-3 days if acute visual sx.
Baby aspirin to avoid thrombotic events

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56
Q

What are the CF of intracranial venous thrombosis?

A
  • Headache, confusion, drowsiness
  • N+V
  • Impaired vision
  • Seizures, reduced consciousness, focal neuro deficits, CN palsies, papilloedema
  • Presence of RF associated w VTE
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57
Q

What are the ix into intracranial venous thrombosis?

A
  • Non contrast CT = hyperdensity in affected sinus
  • CT venogram to look for filling defect - empty delta sign
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58
Q

What is the management of intracranial venous thrombosis?

A

LMWH and address RF

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59
Q

What are the CSF findings in different types of meningitis?

A

Bacterial - reduced glucose, increased protein, gram stain positive, raised WBC >1000
Viral - normal glucose, normal protein protein, WBC <300
TB - normal protein, slightly reduced glucose, WBC - 100-500

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60
Q

What are the CSF findings in SAH and Guillan Barre Syndrome?

A

SAH = xanthochromia - yellow tinge due to bilirubin from RBC breakdown
Guillan Barre = increased protein w/o increased WBC

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61
Q

What is normal WBC in the CSF?

A

< 3

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62
Q

What is Parkinson’s disease?

A

Progressive degenerative disorder due to loss of neurones in the brainstem and basal ganglia.
Dopaminergic neurone loss in the substantia nigra = inadequate dopamine transmission.
There is often Lewy Body formation in affected neurones.

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63
Q

What is the normal dopaminergic stimulation of the motor cortex?

A

Substantia nigra produces dopamine, this activates the direct pathway which inhibits the globus pallidus interna.
The inhibited globus pallidus interna can no longer inhibit the thalamus.
The thalamus therefore is able to excite the motor cortex w glutamate = movement.

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64
Q

What are the changes in the stimulation of the motor cortex in Parkinson’s disease?

A

Parkinson’s = loss of dopaminergic neurones = less dopamine. Dopamine is no longer activating the direct pathway so the globus pallidus interna is no longer inhibited.
GPi then inhibits the thalamus, reducing excitation of the cortex = reduced movement.

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65
Q

What are the motor features of Parkinson’s?

A
  • Bradykinesia
  • Lead pipe rigidity (resistance to passive movement)
  • Asymmetric tremor eg. 4-6Hz rest tremor or pill rolling tremor
  • Parkinsonian gate = small shuffling steps
  • Hypomimic facies
  • Micrographia
  • Glabellar tap
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66
Q

What are the non motor features of Parkinson’s?

A
  • Autonomic involvement - constipation, posturalhypotension, erectile dysfunc
  • Olfactory loss
  • REM behavioural disorder = re enacts dreams
  • Depression and anxiety (reduced dopamine)
  • Hallucinations
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67
Q

How do you distinguish IPD from other causes of Parkinsoniasm?

A

A significant improvement w treatment (levodopa)

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68
Q

What are other causes of Parkinsoniasm?

A
  • Parkinson plus syndromes = feature motor features of Parkinson’s disease w additional features to distinguish them for IPD
  • Drug induced = anti psychotics, anti emetics, lithium, methyldopa
  • Post encephalitis, tremor, vascular
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69
Q

What drugs can be used in the management of IPD?

A
  • Levodopa, give w carbidopa (co-careldopa) to prevent peripheral breakdown
  • Dopamine agonists eg. ropinirole
  • MAO-B inhibitors eg. rasagiline
  • COMT inhibitors
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70
Q

Co-careldopa:
- MOA
- SEs

A

MOA - levodopa is converted into dopamine by DOPA decarboxylase once it crosses the blood brain barrier, carbidopa is a carboxylase inhib and prevents peripheral conversion
SE - N+V, dizziness

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71
Q

Dopamine agonists:
- MOA
- SEs

A

MOA - bind to dopamine receptors
SEs - sedation, hallucinations, impulse control disorders, psychiatric SE

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72
Q

MAO-B inhibitors:
- MOA
- SEs

A

MOA - prevent the breakdown of dopamine
SE - dry mouth, N+V, dizziness

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73
Q

What are some impulse control disorders?

A
  • Gambling
  • Hypersexuality
  • Compulsive shopping
  • Desire to increase dose
  • Punding - repetitive motor behaviour
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74
Q

What are some non oral treatments used in IPD and why are they needed?

A
  • Apomorphine injections = injectable dopamine agonist, often by infusion pump
  • Deep brain stimulation = surgically inserted device that sends constant electrical signals via wires helping to manage IPD sx - akinesia, rigidity and tremor
  • Duodopa = gel form of levodopa, administered via PEJ tube

Needed if patients stop becoming responsive to treatment and SEs of drugs are outweighing benefits.

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75
Q

What are the 4 phases of IPD?

A
  1. Early stage = sx mild and normal life is possible
  2. Maintenance stage - good response to treatment
  3. Advanced stage - poor response to drugs and there are motor SEs
  4. Palliative stage - unable to live independently and need MDT support
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76
Q

What are COMT inhibitors?

A

Inhibit peripheral breakdown of levodopa = more levodopa crosses blood brain barrier. Only works if use w levodopa
Eg. entacapone

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77
Q

What are some complications of deep brain stimulation?

A

Intracerebral haemorrhage and confusion

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78
Q

What are some motor complications of advancing IPD?

A
  • On-off fluctuations = dyskinesia to immobility
  • Dyskinesia = hyperkinetic movement eg. jerking, twitch, writhing
  • Freezing of gait
  • Wearing off phenomenon towards the end of dose
  • Falls
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79
Q

What are some non motor complications of advancing IPD?

A
  • Aspiration pneumonia
  • Nutritional def, dysphagia and weight loss
  • Bladder, bowel and sex dysfunc
  • Pressure sores
  • Sleep disorders
  • Dementia and depression
  • Postural hypotension
  • Impulse control disorders and psychosis
  • Olfactory loss but not often tested
80
Q

What is Parkinsonism?

A

Any clinical syndrome involving bradykinesia w at least one of either rigidity, tremor or postural instability. For example IPD is a type of Parkinsonism.

81
Q

What are some other Parkinsonism conditions that can be mistaken for IPD?

A
  • Vascular pseudoparkinsonism
  • Drug induced Parkinsonism
  • Benign essential tremor
  • Demential w Lewy bodies
82
Q

What are the CF of vascular pesudoparkinsonism?

A

Normally caused by ischaemic brain lesions or strokes.
- Lower body parkinsonism - probs w walking and balance
- Less likely to have a tremor

83
Q

What are the CF of drug induced parkinsonism?

A

Caused by dopamine antagonists - anti psychotics, anti emetics, lithium
- More likely to be symmetrical
- Less likely to have a tremor
- Akinesia w loss of arm swing
- Orofacial dyskinesia
- Remains static
Treat by removing drug

84
Q

What are the CF of dementia w Lewy bodies?

A
  • Fluctuating cognition
  • Parkinsonism
  • Visual hallucinations
  • Progressive cognitive impairment
  • Dementia first then movement disorder follows
85
Q

What are the clinical features of benign essential tremor?

A
  • Tremor w movement, less noticeable at rest
  • Most obvious in the hands
  • Tremor can affect the voice but doesn’t in IPD
  • IPD tremor felt more at rest
86
Q

What is motor neurone disease? What are the different types?

A

Progressive degenerative disease effect the upper and lower motor neurones, 90% of cases are sporadic.
- Spinal ALS
- Bulbar ALS
- Progressive muscular atrophy - LMN only
- Primary lateral sclerosis - only UMN

87
Q

How is MND diagnosed?

A

Electromyograph = measures the electrical activity in the muscles and nerves
- Asymmetrical distal weakness
- Brisk reflexes
- Absence of major sensory sx and pain
- Progressive

88
Q

What is the pattern of muscle groups being affected in MND?

A
  • Limb onset - most common
  • Bulbar onset
  • Respiratory onset
89
Q

What are the clinical features of ALS?

A

Amyotrophic lateral sclerosis
- Limb weakness - wasting and fasciculation, dropping objects
- Foot drop, heaviness in legs, tripping, gait disorder, difficulty rising from low chairs, fatgiue

90
Q

What are UMN signs in ALS?

A
  • Hypertonia
  • Hyperreflexia
  • Upgoing plantars
  • Spastic gait
  • Jaw clenching
91
Q

What are LMN signs in ALS?

A
  • Weakness
  • Muscle atrophy
  • Fasiculations
  • Hyporeflexia
  • Muscle cramps
92
Q

What are the clinical features of progressive bulbar palsy?

A
  • Dysarthria - unclear speech
  • Dysphagia
  • Absent jaw jerk reflex and absent gag reflex
  • Flaccid tongue
93
Q

What type of respiratory failure is caused by neuromuscular weakness?

A

Type 2 resp failure

94
Q

What is multiple sclerosis?

A

Acquired immune mediated inflam, demyelinating condition affecting the brain and spinal cord (CNS), doesn’t affect peripheral nervous system.

95
Q

What is the clinical course of MS?

A

Women > men
Sx start 20-30s as visual/sensory disturb - optic neuritis
Early sx relapse and remit but over time progressive disability will occur:
1. Relapse remit (most common, can become secondary progressive)
2. Secondary progressive
3. Primary progressive

96
Q

What are some RF of MS?

A
  • Viral infections - EBV
  • Greater north or south of the equator = greater risk
  • Sunlight exposure
97
Q

What cells are destroyed in MS?

A

Oligodendrocytes - make myelin normally
Demyelination of white matter = reduced conduction

98
Q

What are the visual manifestations of MS?

A
  • Visual loss
  • Blurred vision
  • Optic neuritis - loss of central vision and painful eye movements
  • Poor colour differentiation
  • Relative afferent pupillary defect
  • Optic nerve swelling
  • Abducens palsy
99
Q

What are the motor and coordination manifestations of MS?

A
  • Weakness and ataxia
  • Progressive paraparesis
  • UMN signs
  • Transverse myelitis - focal inflam w/i the spin = sensory and motor sx below level of lesion
  • Cerebellar syndrome
100
Q

What are the sx associated w cerebellar lesions?

A

DANISH
Dysdiadochokinesia - prob w rapidly alt movements
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia

101
Q

What are the sensory manifestations of MS?

A
  • Paraesthesia
  • Pain (neuropathic eg. trigeminal neuralgia)
  • Heat sensitivity
  • Sexual, bladder and bowel dysfunc
102
Q

What are the cognitive and psychological manifestations of MS?

A
  • Cognitive impairment
  • Depression
  • Fatigue
103
Q

What is Lhermitte’s sign?

A

Electric shock sensation w flexion of the neck, associated w MS

104
Q

What are the ix into MS?

A
  • LP = oligoclonal bands in CSF when immunoelectrophoresis, v sensitive for MS
  • MRI = periventricular white matter lesions
105
Q

What is the McDonald criteria?

A

> 2 attacks w evidence of >2 lesion = diagnose
2 attacks w 1 lesion = diagnose if dissemination of space
1 attack w 1 lesion = diagnose once proof of dissemination in space and time
1 attack w >2 lesions = diagnose once proof of dissemination in time

106
Q

What does dissemination in space and time mean?

A

Dissemination in space = 2 or more lesions, affect 2 different parts of brain
Dissemination in time = 2 or more attacks

107
Q

What is the acute management of MS?

A
  • Glucocorticoids = 1g IV methylprednisolone every 24hrs for 3 days
  • Severe attacks unresponsive to steroids = plasma exchange
    Need to rule out infection
108
Q

What is the chronic management of MS?

A

DMTs:
1st line injectables = beta interferon and glatiramer
Oral = dimethyl fumarate, fingolimod
Biologics = natalizumab

109
Q

What is the sx management of MS?

A
  • Physio
  • Spasticity = baclogen
  • Fatigue = modafinil
  • Bladder dysfunc = anticholinergics
  • Depression = SSRIs
  • Erectile dysfunc = sildanafil
  • Tremor = clonazepam
110
Q

What is the link between MS and pregnancy?

A

MS less likely to be active when pregnant but there is the risk of relapse in postpartum period

111
Q

What is Bell’s palsy?

A

Idiopathic unilateral facial nerve palsy

112
Q

What are the CF of Bell’s palsy?

A
  • Acute but not sudden onset unilateral LMN facial weakness
  • Postauricular otalgia
  • Hyperacusis
  • Alt taste and dry mouth/eye
  • Incomplete eye closure
  • Drooling
113
Q

What are the signs of Bell’s palsy?

A
  • Loss of nasolabial fold
  • Drooping eyebrow and corner of mouth
  • Asymmetrical smile
  • Bell’s sign = upward movement of the eye on attempt to close eye
114
Q

What is the management of Bell’s palsy?

A
  • 50mg pred 10 days then taper down
  • Artificial tears and ocular lubricants
  • Can take several months to recover
115
Q

What is myasthenia gravis?

A

Auto immune disease w Ab against acetylcholine receptors on muscle fibres = reduced muscle contraction

116
Q

What are the CF of MG?

A
  • Fatiguable muscle weakness
  • Bilat ptosis, worse on sustained upgaze
  • Myasthenia snarl
  • Head droop
  • Bulbar features
  • Weak breathing and resp failure
117
Q

What are the ix into MG?

A
  • Serology = acteylcholine receptor ab
  • CT chest ?not sure why
  • Nerve stimulation test
118
Q

What is the management of MG?

A

Conservative = review
Meds = immunosuppression acutely and AChE inhib, increased Ach in synaptic cleft eg. neostigamine
- Plasmapheresis
- Thymectomy

119
Q

What are the SEs of AchE inhib?

A
  • Diarrhoea
  • Salivation
  • Lacrimation
  • Urinary freq
120
Q

What are the CF of Guillain Barre?

A
  • Progressive ascending symmetrical limb weakness
  • Paraesthesia
  • Resp muscles affected in severe cases
  • LMN signs
121
Q

What is the management of Guillain Barre?

A
  • Ventilation monitored = ABG
  • IV immunoglobulin or plasmapharesis
122
Q

What infections cause Guillain Barre?

A

Campylobacter, EBV normally 1-3 weeks after

123
Q

What are some different causes of polyneuropathy?

A
  • Diabetes
  • Idiopathic
  • Systemic - hypothyroid, CKD, CLD, amyloidosis
  • Autoimmune - Guillain Barre
  • Toxic - alcohol, chemo
  • Neoplastic - paraneoplastic syndrome
  • Hereditary - Charcot Marie Tooth
  • Nutritional - Vit b12, folate def
  • Meds - isoniazid, vincristine
124
Q

What is the most worrying presentation of polyneuropathy and why?

A

Acute onset, the worry that is may ascend affecting nerves more proximally and cause respiratory dysfunction.

125
Q

What is the pathophysiology of polyneuropathy?

A
  • Demyelination
  • Axonal degen
126
Q

What are the CF of polyneuropathy?

A
  • Motor = weakness and atrophy, reduced reflexes, hypotonia, fasciculations
  • Negative sensory sx - loss of touch, proprioception and vibration
  • Positive sensory sx - pain, paresthesia, burning
127
Q

What are the ix into polyneuropathy?

A
  • Electromyography
  • Nerve conduction studies, can determine the type of injury
  • Full bloods and serology
  • Biopsy of nerve is suspect vasculitis or amyloid
128
Q

What is the management of polyneuropathy?

A
  • Treat underlying cause - replace vit def, good glucose control, levothyroxine
  • Manage sx - gabapentin to control neuropathic pain, physical therapy and rehab
129
Q

What is muscular dystrophy?

A

Muscles break down and become weaker. Caused by reduced dystrophin which is needed for muscle contraction due to genetic mutation.
X linked recessive so most cases are males and females are carriers.

130
Q

What is the presentation of Duchenne’s muscular dystrophy?

A
  • Muscle wasting and weakness in early childhood (age 2-3)
  • Wheelchair bound before puberty
  • Will die of resp failure in early twenties
  • Child slips through parents hands when they pick them up
  • Gower’s manoeuvre
131
Q

What is Becker’s muscular dystrophy?

A
  • Muscle wasting and weakness presents in late childhood
  • Wheelchair bound in teens
  • Commonly survive into thirties
132
Q

What are the ix into muscular dystrophy?

A
  • Genetic testing is the gold standard
  • Muscle biopsies sometimes
  • Creatinine kinase first line
133
Q

What is the management of muscular dystrophy?

A
  • Physio
  • Occupational therapy
  • Physical aids
  • Steroids = improves strength and function and slows muscle weakening but for 2 years max
  • Ataluren = restore dystrophin synthesis
  • Creatine supplements
  • Treating swallowing probs
134
Q

What are the abx for meningitis?

A

Ceftriaxone and vancomycin

135
Q

Meningitis vs encephalitis

A
  • Parenchyma inflam not meninges
  • Encephalitis often viral instead of bacterial - may only need to admit and observe
  • Seizure common in encephalitis and almost always mental status alt
136
Q

What are the CF of Alzheimer’s disease?

A
  • Cognitive impairment - poor mem, disorientation, lang probs
  • Agitation, depression, sleep cycle disturb, motor disturb
  • Early impairment of memory = short term mem loss and difficulty learning new info
  • Activities of daily living problems
137
Q

What are the RF of dementia?

A
  • Age
  • Genetics
  • Cardiovascular disease
  • Depression
  • Low education attainment
  • Low social engagement and support
  • Head trauma
  • Learning difficulties
138
Q

What are the pathological changes in alzheimer’s?

A
  • Senile plaques - b-amyloid deposits outside neurons
  • Neurofibriliary tangles - hyperphosphorylated tau proteins in ares involved in memory = promote neuronal cell death
139
Q

What is the management of Alzheimer’s?

A
  • Don’t use drugs in pt w mild cognitive impairment
  • Mild to mod AD - acetylcholinesterase inhib eg. donepezil
  • Mod to severe AD - NMDA antagonist eg. memantine, helps to slow progression
  • End of life care and cae plans
140
Q

What is the pathophysiology of Lewy body dementia?

A

Accumulation of abnormal protein deposits (Lewy bodies) cause cognitive decline associated w parkinsonism.

141
Q

What are the CF of Lewy body dementia?

A
  • Fluctuating cognition
  • Visual hallucinations
  • Parkinsonism
  • REM sleep disorder
142
Q

What is the management of Lewy body dementia?

A
  • Cholinesterase inhib for pt w DLB and cognitive sx
  • Antipsychotics may worsen parkinsonism sx
  • Melatonin in REM sleep disorders
  • Levodopa
143
Q

What is the presentation of vascular dementia?

A

Multiple infarcts in the brain = sudden onset cognitive decline, step wise decline in function

144
Q

What are the CFs of vascular dementia?

A
  • Cognitive impairment
  • Agitation, depression, sleep cycle disturb, motor disturb
  • Gait abnormalities, attention and personality changes = specific
  • ADL reduce
145
Q

What are the cognitive domains assessed in a cognitive assessment?

A
  • Attention and conc
  • Recent and remote memory
  • Language
  • Praxis - planned movement
  • Executive func
  • Visuospatial func
146
Q

What are the ix into vascular dementia?

A

Used to exclude an alt diagnosis:
- Bloods - FBC, U+Es, ESR, HbA1c, LFTs, TFTs, B12
- ECG
- HIV and syphilis test
- CXR
- MRI

147
Q

What is the management of vascular dementia?

A
  • Care plans and end of life care
  • Reduce CVS RFs - modifiable and preventable
  • Memantine doesn’t work in VD
  • Donepezil only if mixed w Alzheimer’s
148
Q

What is fronto temporal dementia?

A

Atrophy of the frontal and temporal lobes causing social behaviour, personality and language.

149
Q

What are the CFs of frontotemporal dementia?

A
  • Presents at a younger age than other dementias, often misdiagnosed and needs neuroimaging
  • Early personality change, disinhibition, loss of empathy, hyperorality
  • Aphasia early on
  • Strong FH
150
Q

What are the features of FTD on neuroimaging?

A

Use MRI:
- behavioural variantFTD - atrophy
- Non fluent PPA - early atrophy and hypoperfusion
- Semantic PPA - significant ant temporal atrophy

151
Q

What is the management of FTD?

A
  • Supervision - financially and to watch if problematic behaviour
  • SALT assessment
  • SSRIs
  • Atypical antipsychotics - eg. clozapine
152
Q

What is light near dissociation?

A

Pupil constricts on convergence and focusing on near object but not in response to bright light -
Argyll Robertson pupil is an example, specific for neurosyphilis.

153
Q

What are senses make up the spinothalamic pathway?

A
  • Temperature
  • Pain
  • Crude touch
154
Q

What senses make up the dorsal column pathway?

A
  • Vibration
  • Fine touch
  • Proprioception
  • 2 point discrimination
155
Q

Where do the dorsal columns run?

A

Lower regions of the body are represented more medially in the sensory cortex, closer to the middle
Neurones corresponding to lower regions of the body run more medially and as u ascend the tracts are added laterally.
Dorsal column is in the post cord
Rarely affected w ant spinal artery lesion

156
Q

What is the spinal nerve made up of?

A

Ventral root - motor
Dorsal root and dorsal root ganglion - sensory

157
Q

Where does the dorsal column dessucate?

A

Medulla:
- Gracile nucleus = lumbar
- Cuneate nucleus = cervical

158
Q

Where do the spinothalamic tracts run?

A

Neurones corresponding to lower regions of the body run more laterally and as you ascend the upper regions of the body run more medially.
Is in the post spinal cord.

159
Q

Where does the spinothalamic tract dessucate?

A

At the level of entering the cord. Dessucates straight away.

160
Q

What is syringomyelia?

A

Cyst forming within the spinal cord, medially expands out damaging the spinothalamic and dorsal column tracts. Bilateral signs, spinothalamic signs in the cervical aspect first and dorsal column signs in the lumbar aspect first.
Greater bilateral motor impairment in upper extremities than in lower.

161
Q

Where are the locations of UMN and LMN and their cell bodies?

A

UMN reside completely in the CNS. Their cell bodies are within the primary motor cortex of the frontal lobe.
LMN = partially CNS, partially PNS. Their cell bodies are within the ventral horn and the brainstem motor nuclei (those to CNs).

162
Q

What is the pathway of an UMN?

A
  1. Originates in from the precentral gyrus of the primary motor cotex
  2. Passes into the int capsule that runs between thalamus and lentiform nucleus
  3. Then through the cerebral peduncles into the midbrain
  4. Then into the pyramids of the medulla, decussates at the ends of the pyramids
  5. Synapses w the LMN at the level of the spinal cord it supplies
163
Q

What are the cerebral peduncles?

A

Connect the cerebral hemisphere to the brainstem, CST runs through them

164
Q

How are UMN and LMN arranged in the spinal cord?

A

UMN that supply the upper limb = more laterally in the cortex, supply the lower limb = more medially in cortex.
UMN that supply the lower limb run more laterally in the spinal cord, supply the upper limb = more medially in the spinal cord.

165
Q

Do all UMN decussate at the medulla?

A

85% do but 15% don’t decussate until they synapse with their LMN.
Medulla decussate = finer movements, more distal muscles eg. hands, feet, arms, legs
Synapse decussate = cruder movements, proximal muscles eg. shoulders and hips

166
Q

Which UMN synapse in the midbrain?

A

Those that make up the corticonuclear pathway and supply the CN LMN.

167
Q

What does the int capsule contain?

A

Corticospinal tract - motor fibres to face, arms, legs

168
Q

What are the CF of UMN lesions and why?

A

UMN lesion = loss of inhibition of LMN:
- Reduced power
- Hyporeflexia first then hyperreflexia due to spinal shock
- Hypotonia first then hypertonia due to spinal shock
- Rigid paralysis
- Atrophy

169
Q

What are the CF of LMN lesions and why?

A

Loss of excitation of the muscles:
- Reduced power
- Hyporeflexia
- Hypotonia
- Flaccid paralysis
- Fasciculations
- Atrophy

170
Q

What is cervical spondylosis?

A

Osteo degenerative disease of the cervical spine, most commonly diagnosed in your 50s.

171
Q

What are the CFs of cervical spondylosis?

A
  • Neck pain
  • Radiculopathy due to nerve root compression
  • Myelopathy = injury to spinal cord due to severe compression
172
Q

What are the signs of cervical spondylosis on examination?

A
  • Neck pain accompanied by flaccid upper limb paresis
  • Variable sensory changes
  • Spastic paraparesis
173
Q

Paresis vs paraparesis

A

Paresis - partial loss of voluntary motor func of all limbs
Paraparesis - partial loss of voluntary motor func of lower limbs
Maybe the same thing ??

174
Q

What are some features of myelopathy?

A
  • Insidious progression
  • Gait disturb and clumsy hands
  • Loss of sexual, bladder, bowel func
  • Lhermitte’s sign
  • Sensory changes variable
175
Q

What are the ix into cervical spondylosis?

A
  • Diagnosis clinical
  • XR = osteophytes and narrowing of disc space but not diagnostic, common in normal middle aged pt
  • MRI if have myelopathy
176
Q

What is the management of cervical spondylosis?

A
  • Physio, pilates and neck posture imporvement
  • Analgesia and amitriptylline
  • Decompressive surgery
  • Wait and see
177
Q

What are the signs and symptoms of cauda equina syndrome?

A
  • New onset lower back pain
  • Bilateral sciatica
  • Saddle anaesthesia
  • Incontinence/retention
  • Loss of anal tone
  • Impotence
178
Q

Where does the spinal cord end and the cauda equina starts?

A

L2 and below is cauda equina

179
Q

What is the management of cauda equina syndrome?

A

Full spine MRI
Surgical decompression w/i 48 hours
If malignancy - dex 16mg daily

180
Q

What is acute respiratory distress syndrome?

A

Pulm oedema, bilat alveolar injry, hypoxaemia.
Not due to cardiogenic pulm oedema, pleural effusion or atelectasis.

181
Q

What are some causes of ARDS?

A
  • Pneumonia
  • Sepsis
  • Aspiration
  • Pancreastitis
  • Transfusion reactions
  • Trauma and fractures
  • Fat embolism
182
Q

What is the presentation of ARDS and what are the Ix?

A

Sx - severe SOB, tachypnoea, confusion, presyncope, no improvement w O2
O/E - bibasal crackles
Ix - CXR = bilat alveolar infiltrates w/o other features of HF

183
Q

What is the management of ARDS?

A
  • Ventilation
  • Haemodynamic support
  • DVT prophylaxis
  • Nutritional support
  • Repositioning of pt
  • Abx if infectious cause
184
Q

What is associated with a worse outcome of MS?

A
  • Increasing age
  • Male
  • Motor sx on onset
  • Early relapses
  • Many MRI lesions
  • Axonal loss
185
Q

What drugs can you not use in MG?

A
  • Beta blockers
  • Some antibiotics
  • Lithium
186
Q

What is Huntington’s disease and what are the CF?

A

Autosomal dominant disorder caused by repeats of the CAG trinucleotide. CF:
- Dominant inheritance
- Choreoathetosis - unwanted uncontrollable movements
- Dementia

187
Q

What are the ix into Huntington’s?

A

CT and MRI - atrophy of caudate nucleus and putamen

188
Q

How is Huntington’s managed?

A

There is no cure or way to prevent progression.
Need extensive emotional support from MDT and genetic counselling. Can use medications to control chorea eg. tetrabenzine. Death normally caused by problems associated w physical decline.

189
Q

What is the treatment of trigeminal neuralgia?

A

Carbamezapine

190
Q

What are the clinical features of multiple system atrophy?

A

Parkinsonian type - braykinesia, soft voice, tremor, stiff limb
Cerebellar type - ataxic gait, dysarthria, dysphagia, visual disturb

191
Q

MSA vs Parkinson’s

A

Parkinson’s - tremor more common in Parkinson’s, loss of smell, dementia, mask face
MSA - balance problems first and get worse faster, erectyle dysfunc, sweating probs, emotional outbursts, slightly earlier presentation and slightly faster progression

192
Q

PSP vs Parkinson’s

A

PSP - does’t respond to levodopa, eye related sx !! difficulty moving eyes up and down, blurry vision, sudden changes in vision, problem focusing and following, innappropriate outbursts (more early on than Parkinson’s)

193
Q

What is DANISH?

A

Dysdiadiodyskinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
HypOtonia

194
Q

Drug induced vs idiopathic Parkinson’s

A

Drug induced - symmetrical tremor
IPD - unilat

195
Q

What is the cause of oculomotor palsy?

A

Posterior communicating artery aneurysm until proven otherwise

Neuro and special senses block (4 decks)

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