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ΩΩ 2a Bateman - Systems Based > Neurology > Flashcards

Neurology Flashcards

1
Q

WHAT IS A TRANSIENT ISCHAEMIC ATTACK?

A

Blood flow to part of the brain TEMPORARILY stops

Lasts for less than 24 HOURS

NO lasting damage

Usually caused by emboli

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2
Q

What are the risk factors for TIAs?

A

Non-modifiable risk factors
Age
Sex
Family history
Race/ethnicity

Modifiable risk factors
Smoking
Hypertension
Diabetes
Hyperlipidemia
Activity level

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3
Q

What are the causes of TIAS?

A

Thromboembolism
From carotid

Cardioembolism
Post-MI or AF

Hyperviscosity
Polycythaemia,

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4
Q

What are the signs and symptoms of a TIA?

A

Mimic a stroke in the same vessel

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5
Q

What are the tests for TIAs?

A

Carotid Doppler

Angiography

Fundoscopy (amaurosis fugax)

Listen for carotid bruits because of atherosclerosis

Aim to find the cause and define vascular risk
FBC + prothromibin (test for bleeding/hypercoaguable conditions)
ESR
U&Es
Glucose (if low could cause altered mental state)
lipids (risk for atherosclerotic disease)

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6
Q

What is the treatment for TIAs?

A
  • Reduce risk factors
    Blood pressure/diabetes/cholesterol
  • Antiplatelet drugs
    Clopidogrel or aspirin
  • Warfarin/DOAC (if cardiac emboli)
  • Carotid endarterectomy (if >70% stenosis)
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7
Q

What is the ABCD2 scale?

What are the values?

A

Scale to determine risk of having a future stroke. 2/7 days

Age ≥60 yrs old 1 point

Blood pressure ≥140/90 1 point

Clinical features
Unilateral weakness 2 points
Speech disturbance without weakness 1 point

Duration of symptoms
Symptoms lasting ≥1h 2 points
Symptoms lasting 10–59min 1 point

Diabetes 1 point

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8
Q

What does the scores indicate in ABCD2?

A

More than 6 strongly predicts a stroke

More than 4 should be seen by a specialist in 24 hours

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9
Q

WHAT IS AMAUROSIS FUGAX?

A

Painless progressive loss of vision in one or two eyes

“like a curtain descending over my field of view”

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10
Q

What causes amaurosis fugax?

A

Emboli passing into the retinal artery

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11
Q

What are the tests for amaurosis fugax?

A

Ultrasound

MRI and CT

Fundoscopy

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12
Q

What is the treatment for amaurosis fugax?

A
  • Atherscleoric lesion = ASPIRIN or CLOPIDOGREL
  • Cartoid atherscleosis = Carotid endarterectomy
  • Cadiac cause = warfarin/correct AF
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13
Q

WHICH IS THE MORE COMMON STROKE?

A

ischamemic

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14
Q

WHAT IS AN ISCHAEMIC STROKE?

A

Interupption of the blood supply to the brain

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15
Q

What causes ischaemic stroke?

A
  • Thromobsis
  • Embolism
  • Systemic hypoperfusion
  • Cerebral venous sinus thrombosis
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16
Q

What are the signs and symptoms of a stroke?

A

Depends on location of the stroke

Symptoms affected the contralateral side of the brain area

Cerebral (contralateral sensory loss or hemiplegia—initially flaccid)

Brainstem (quadriplegia, dis- turbances of gaze and vision, locked-in syndrome)

Lacunar (ataxic hemiparesis, pure motor, pure sensory, sensorimotor, and dysarthria/clumsy hand)

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17
Q

What are the investigations for a stroke?

A

Clinical examination - NIHSS (national institues of health stroke scale)

  • Risk factors
    Hypertension
  • Cardiac cause
    Echo/ECG
  • Carotid
    Ultrasound/bruits

CT/MRI/Angiography

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18
Q

What is the treatment for an ischaemic stroke?

A

1st line: Thrombolysis
IV alteplase

2nd line: Antiplatelets
Clopidogrel 75mg OD

Stroke therapy long term
S+L
Physio
OT

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19
Q

When must thombolysis be given in an ischaemic stoke and what are the contraindications?

A

Less than 4.5 hours

  1. Surgery in last 3 months
  2. Patient on warfarin
  3. Hx of active malignancy
  4. Platelets <100,000/mm3
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20
Q

WHAT IS A HEMORRHAGIC STROKE?

A

Rupture of a blood vessel or abnormal vascular structure

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21
Q

What are the different types of hemorrhagic strokes?

A

Intracerebral hemorrhage

Subarachnoid hemorrhage

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22
Q

What are the causes of haemorrhagic strokes?

A
  • Hypertensive haemorrhage
  • Ruptured aneurysm
  • Ruptured AV fistula
  • Drug induced bleeding
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23
Q

What are the signs and symptoms of a stroke?

A

Depends on location of the stroke
Symptoms affected the contralateral side of the brain area

  1. Cerebral (contralateral sensory loss or hemiplegia—initially flaccid)
  2. Brainstem (quadriplegia, disturbances of gaze and vision, locked-in syndrome)
  3. Lacunar (ataxic hemiparesis, pure motor, pure sensory, sensorimotor, and dysarthria/clumsy hand)
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24
Q

What are the investigations for a stroke?

A

Clinical examination - NIHSS (national institues of health stroke scale)

  • Risk factors
    Hypertension
  • Cardiac cause
    Echo/ECG
  • Carotid
    Ultrasound/bruits

CT/MRI/Angiography

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25
Q

What is the treatment for a haemorrhagic stroke?

A
  • Control BP
    B-blocker
  • Beriplex if warfarin-related bleed
  • Clot evacuation
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26
Q

How do you distinguish between a haemorrhagic and ischaemic stroke?

A

CT head

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27
Q

WHAT ARE THE DIFFERENT INTER-CRANIAL HAEMORRHAGE?

A

Extradural haemorrhage

Subdural haemorrhage

Subarachnoid haemorrhage

Intracerebral haemorrhage

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28
Q

WHAT ARE SOME EXAMPLES OF INTRACEREBRAL HAEMORRHAGE?

A

Lobar haemorrhage

Thalamic haemorrhage

Pontine haemorrhage

Cerebellar haemorrhage

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29
Q

What are the different layers of the meninges?

A

—Dura, usually firmly adherent to the inside of the skull

—Arachnoid, more adherent to the brain

——Pia, on the surface of the brain and cannot be separated from the brain

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30
Q

Where are the meningeal vessels? What veins cross the subdural space?

A

—Meningeal vessels are in the Extradural space

—Bridging veins cross the subdural space

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31
Q

In which space does the circle of willis lie?

A

—The circle of Willis lies in the subarachnoid space

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32
Q

Are there any blood vessels below the pia?

A

—There are no vessels deep to the Pia, the Pia forms part of the blood brain barrier

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33
Q

WHAT IS A SUBARACHNOID HAEMORRHAGE?

A

—Rupture of the arteries forming the circle of Willis

—Often because of ‘Berry aneurysms’

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34
Q

What are the causes of subarachnoid haemorrhages?

A

Trauma

Berry aneurysm

Arteriovenous malformations

Idiopathic

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35
Q

What are the signs and symptoms of a subarchanoid haemorrhage?

What is the headache called which they call a warning sign of a leaky vessel?

A

Symptoms
—Sudden onset severe headache (—‘Thunderclap headache’)
Photophobia
Reduced consciousness
Vomiting
Collapse
Seizures

Sign
Kernig’s sign
Terson syndrome (retinal, subhyaloid and vitreous bleeds)
3rd oculomotor palsy (posterior communicating artery)

Sentinel headache

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36
Q

What are the investigations for a subarchanoid haemorrhage?

A

CT
Spider sign

LP
CSF bloody early
Becomes xanthochromic (yellow), breakdown of haem to bilibrubin

Angio
To determine location

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37
Q

What is the treatment for subarchanoid haemorrhage?

A

Neurosurgery!!!!

Keep blood pressure low

Keep hydrated and nutrition

Nimodipine (recued vasospasm)

If anneurysm deteced either coil or clipping.

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38
Q

WHAT IS A SUBDURAL HAEMORRHAGE?

A

Bleeding between the dura on the skull and the arachnoid layer

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39
Q

What is the cause of subdural haemorrhages?

Where is the bleeding from? Who is it most common in?

A

Trauma

Bleeding from bridging veins

—Commonest where the patient has a small brain (alcoholics, dementia)

Occurs in ‘shaken babies’

GRADUAL

Gradual rise in ICP over many weeks

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40
Q

What are the symptoms of a subdural haemorrhage?

A

Fluctuating level of consciousness

Slow physical or intellectual slowing
Sleepiness
Headache
Personality change, and unsteadiness.

Neurological symptoms happen later

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41
Q

What investigations can you do for a subdural haemorrhage?

A

CT/MRI shows clot ± midline shift

Look for crescent-shaped collection of blood over 1 hemisphere.

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42
Q

What is the treatment for a subdural haemorrhage?

A
  1. Evacuation 1st-line
  2. Craniotomy is 2nd-line
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43
Q

Where does bleeding occur in subdural haemorrhage?

A

Between arachnoid and dura

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44
Q

WHAT IS AN EXTRADURAL HAEMORRHAGE?

A

Bleed between skull and dura membrane

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45
Q

How is an extradural haemorrhage caused? What artery bleeds in extradural?

A

—Traumatic

—Fractured skull

—Bleeding from Middle Meningeal Artery and vein
Also dural venous sinus

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46
Q

What normally happens to the pressure during an extradural bleed?

What period is seen?

A

——Rapid rise in inter-cranial pressure (ICP)

Conscious level falls or is slow to improve

Lucid period

—Coning and death if not treated

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47
Q

What symptoms does an extradural haemorrhage show?

A

Increasingly severe headache

Vomiting

Confusion, and fits follow

Brainstem compression later on

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48
Q

What investigations for an extradural haemorrhage can you do?

A

CT
Haematoma
Often biconvex/lens-shaped

X-ray
Fractures

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49
Q

How can you treat a extradural haemorrhage?

A

Clot evacuation ± ligation of the bleeding vessel.

Care of the airway in an unconscious patient

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50
Q

What is the difference in CT shape for extradural and subdural haemorrhage?

A

Biconvex/lens-shaped in extradural
the blood forms a more rounded shape

Compared with the sickle-shaped
Subdural haematoma as the tough dural attachments to the skull keep it more localized

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51
Q

WHAT IS EPILEPSY?

https://www.youtube.com/watch?v=L0XqL2I35n8

A

Seizure diorder

Recurrent and unpredictable seizures

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52
Q

What is the definition of an epileptic seizure?

A

Paroxysmal event

Caused by excessive, hypersynchronous neuronal discharges

Behaviour, sensation or cognitive processes change

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53
Q

What is the treatment of focal epilepsy?

How do they work?

A

Carbamazepine (inhibits Na+ channels)

Lamotrigine (inhibits glutamate release)

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54
Q

What is the first line of therapy for generalised epilepsy?

A

Sodium Valproate

Lamotrigine

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55
Q

What is the main excitatory transmittor in the brain? What is the receptor for it?

A

Glutamate

NMDA

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56
Q

What are the patinet only signs of a seizure?

A

Fear

Certain smells

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57
Q

What is the main inhibitory transmittor in the brain? What is the receptor?

A

GABA

GABA receptors

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58
Q

What are the outward signs of a seizure?

A

Jerking

Moving

Losing consciousness

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59
Q

What is it called when a seizure starts focal and becomes generalised?

A

Focal onset bilateral tonic-clonic

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60
Q

What is it called when both hemispheres of the brain are affected?

A

Generalised
Can start as focal and become generalised

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61
Q

What is a jacksonian march?

Which lobe is this most common in?

A

When jerky movements affect one area then move to other areas

Most common in frontal lobe

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62
Q

What are the focal seizures divided into?

A

_Simple partial
Without impaired awareness_
Small area
Strange sensation - hearing or tasting
Jerky movements
Awake and alert

_Complex partial
With impaired awareness_
Loss of awareness
May not remember

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63
Q

What is it called when the effect of a seizure is limited to one hemisphere or single lobe

A

Focal or partial seizure

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64
Q

What is the treatment of a staticus epilepticus?

A

Open + maintain airway

Community - Diazepam

Hospital - Lorazepam

Give phenytoin if seizures continue

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65
Q

What is a seizure called if it lasts longer than 5 minutes ongoing or without returning to normal?

What type of seizure is it normally?

A

Status epilepticus

Usually tonic-clonic

MEDICAL EMERGENCY

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66
Q

What are generalised seizures divided into?

A

Tonic
Muscles stiff and flexed
Fall backward

Atonic
Suddenly relaxed muscles
Fall forward

Clonic
Violent muscle contractions
Convulsions

Tonic-Clonic

Myoclonic
Short muscle twitches

Absence
Spaced out, unresponsive

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67
Q

What are the different parts of seizure?

Prodrome

Aura

Ictal symptoms

Post-ictal symptoms

A

Prodrome= mood/behaviour change

Aura = part of seizure patient is aware of

Ictal symptoms = dependent on part of brain affected

Post-ictal symptoms = headache, confusion, amnesia, etc.

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68
Q

Where do complex partial seizures always start?

A

Temporal lobe

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69
Q

WHAT IS PARKINSON’S?

A

Movement disorder where the dopamine producing neurons in the substantia nigra of the brain die

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70
Q

What is the cause of parkinson’s?

A

Usually no known cause

Sometimes
Genetic with environment

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71
Q

What are the direct and indirect pathways?

A

Control movement
Direct = movement
Indirect = no movement

Direct
Striatum
Global pallidus interna
Substantia nigra pars reticularis
Thalamus

Indirect
Striatum
Global pallidus externa
Subthalamic nucleus

https://www.youtube.com/watch?v=NcIWYCkKwVA

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72
Q

What happens in parkinson’s to the substantia nigra?

What do the remaining neurons contain?

A

Blackened areas gradually disappear

These form
Lewy bodies containing alpha-synuclein protein

Present in the dopamine neurons before they die

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73
Q

What are the signs and symptoms of parkinsons?

A

Resting tremor (Pill roll)

Rigidity (cog-wheel)

Bradykinesia

Postural instability

Also non motor symptoms (dementia)

NO WEAKNESS

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74
Q

What are the investigations for parkinsons?

A

Medical history and examination

Give levodopa and improvement in symptoms helps with diagnosis

MRI and CT to rule out other causes

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75
Q

What is the management for Parkinson’s?

A

Increase dopamine
Co-careldopa
L-DOPA (levodopa) + carbidopa
Dopamine receptor agonists
Ropinirole

Decrease dopamine breakdown
MAO-B inhibitor
Selegiline
COMT inhibitor
Entacapone

Motor symptom treatment
Amantadine and anticholingergics

Surgery
Deep brain stimulation

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76
Q

How does levodopa work?

A

Levodopa crosses blood brain barrier

Converted to dopamine

By dopa decarboxylase

Within nigrostriatal neurons

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77
Q

What does the no weakness of parkinson’s tell you?

A

Not a disease of motor cortex or corticospinal pathway diseases

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78
Q

What does the resting tremor of parkinson’s tell you?

A

Not a cerebellar disase

As would be action or intention tremor

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79
Q

WHAT IS HUNTINGTON’S DISEASE?

A

Cell loss within a specific set of neurons in the basal ganglia and cortex

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80
Q

What is the cause of huntingtons disease?

What does it cause the death of and where?

A
  1. Autosomal dominant
  2. CAG repeated sequece of DNA
  3. Abnormal protein produced
  4. Death of GABA (inhibitory) neurons particularly
  5. Striatum
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81
Q

What gene is involved with what is the code?

How many is need for huntingtons disease?

A

Huntingtin gene

Contains triplet repeat CAG

Normal person has 10-35
HD has >36

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82
Q

What is anticipation?

What does more repeats mean?

When is anticipation more likely?

A

CAG repeats increase with generations.

More repeats means an earlier onset.

Anticipation more likely if parent affected is the father.

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83
Q

What are the symptoms of huntingtons disease?

When is the normal onset?

A

Chorea

Psychiatric/behavioural changes

Cognitive decline and dementia

30-50

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84
Q

What are the investigations forhuntingtons disease?

A

History
Confirm chorea

Imaging
Bicaudate diameter

Exclude differentials

Genetic testing

Histology
Identify huntington

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85
Q

How can you treat huntingtons disease?

A

Chorea
Tetrabenazine

Agression
Risperidone

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86
Q

WHAT ARE THE DIFFERENT TYPES OF HEADACHES?

And give some examples for each?

A

Primary
Tension, cluster, migraine, sins

Secondary
Meningitis, encephalitis, GCA, medication overuse, venous thrombosis, tumour, SAH

Other
Trigeminal neuralgia

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87
Q

What are secondary headaches?

A

Red flag headaches

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88
Q

WHAT IS A MIGRAINE?

A

Recurrent headache associated

Visual & GI disturbance

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89
Q

What is the location of a migraine?

A

Unilateral

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90
Q

What are the features of a migraine?

How long does it last?

A

Gradual onset

Crescendo pattern

Moderate-severe intensity

Duration 4-72 hours

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91
Q

What are migraine’s associated symptoms?

A

Nausea

Vomiting

Photophobia

Phonophobia

Aura - feeling something about to happen

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92
Q

What is the treatment for migraines?

Acute and prophylaxis?

A

Acute
Oraltriptan e.g. Sumatriptan
+ NSAID e.g. Ketoprofen

Prophylaxis
B-blocker e.g. Propanolol

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93
Q

What are the triggers of migraines?

A

Chocolate

Hangobers

Orgasms

Cheese

Oral contraceptives

Lie-ins

Alcohol

Travel

Exercise

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94
Q

WHAT IS A TENSION HEADACHE?

A

More muscular

Most common reason why over the counter analgesics are bought

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95
Q

What is the location of a tension headache?

A

Bilateral eyebrow region

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96
Q

What is the character of tension headaches?

A

Pressure or tightness which waxes and wanes

Duration is variable

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97
Q

What are the associated symptoms which a tension headache?

A

None

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98
Q

WHAT ARE CLUSTER HEADACHES?

A

Hyperactivity to 5HT

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99
Q

Where is the pain in a cluster headache?

A

Rapid onset severe unilateral, orbital, supraorbital or temporal pain

100
Q

What is the character of cluster headaches?

How long do they last?

A

Pain begins quickly, deep, continuous pain, excrusiating and explosive in quality

Duration 30 mins to 3 hours

101
Q

What are the associated symptoms of cluster headaches?

A

Pain

Hornems

Ptosis
Drooping of eyelid

Miosis
Unable to dilate pupils

Lacrimation

Nasal discharge

102
Q

What is the treatment for a cluster headache?

How can you prevent them?

A

100% oxygen

Sumatriptan

Verapimil

Lithium

103
Q

WHAT IS GIANT CELLS VASCULITS?

A

Vascultis that affect the carotid artery

When they affect the temporal artery

They cause headaches

104
Q

Who does giant cell arteries affect?

A

Older than 50 year olds

Women more than men

105
Q

What does giant cell arteritis cause?

What does it lead to high amount in, in the blood?

A

Lots of inflammation

Leading to high ESR and CRP

106
Q

What does a biopsy look like of an affected giant cell arteritis artery?

A

Giant cell infiltration of elastic lamina between tunica intima and media

107
Q

What does segmental giant cell mean?

A

Only sections of the artery are affected

Could take out unaffected part of vessel

108
Q

What are the treatments for giant cell arteritis?

A

Corticosteroids

109
Q

What condition is GCA associated with?

A

POLYMYALGIA RHEUMATICA

110
Q

What are the symptoms for GCA?

A

Headache

Scalp tenderness (egon combing hair)

Jaw claudication

Amaurosis fundax

111
Q

What drugs do you need to prescribed with steroids?

A

PPI (gastric protection) & bisphosphonate(bone protection)

112
Q

What does the trigeminal nerve do?

What are the branches called?

A

Sensation to the face

Three branches

  1. Opthalmic
  2. Maxillary
  3. Mandibular
113
Q

What are sinus headaches?

A

Associated with sinusitis

114
Q

WHAT IS TRIGEMINAL NEURALGIA?

(this quesiton inside headaches)

115
Q

What is the epidemology of trigeminal neuralgia?

116
Q

What is the treatment for trigeminal neuralgia?

A

1st line Carbamazapine

2nd line Lamotrigine, phenytoin or gabapentin

Surgery

117
Q

What is the diagnosis of trigeminal neuralgia?

A
  1. ≥3 attacks of unilateral facial pain
  2. Pain in ≥1 division of trigeminal nerve with no radiation

3.Pain must have 3 of the following:
Paroxysmal attacks lasting from 1-180 seconds
Severe intensity
Electric shock-like/shooting/stabbing/sharp
Precipitated by innocuous stimuli to the affected side of the face (vibration, washing/shaving, brushing teeth, etc.)

  1. No neurological deficit
118
Q

What are the symptoms of trigeminal neuralgia?

A

Sudden severe pain

Sharp, stabbing, piercing

Comes and goes
More when chewing or mouth movemnts

119
Q

What side of the face will be affected?

A

Only one side

120
Q

WHAT IS CAUDA EQUINA SYNDROME?

Where is the damage?

A

Compression of nerve roots

Spinal damage distal to L1

121
Q

What vertebrae are involved with cauda equina?

122
Q

What are the symptoms of cauda equina?

A

Foot drop

Numbness

Saddle anesthesia

Bladder and Bowel incontinence

123
Q

What are the tests for cauda equina syndrome?

124
Q

What is the treatment for cauda equina?

A
  1. Surgical decompression by full laminectomy
125
Q

What is the anatomy of the spine?

What happens in cauda equina?

A

Nucelus pulposus surrounded by annulus fibrosis

Herniates out and compresses spine

126
Q

What is the difference between cauda equina and sciatica?

A

In cauda equina you get

  1. Saddle anaesthesia
  2. Bladder dysfunction
  3. Sexual dysfunction
  4. Decreased anal tone

Sciatica is just

  1. Back pain
127
Q

WHAT IS SCIATICA?

A

Pain in the distribution of the sciatic nerve, ie felt in the thigh and, MOST IMPORTANTLY, below the knee

A pain that is not felt below the knee is not sciatica

128
Q

What are the risk factors for sciatica?

A

Personal factors including:

  1. Age (peak 45-64 years)
  2. Increasing risk with height
  3. Smoking
  4. Psychological stress

Occupational factors include:

  1. Strenuous physical activity - for example, frequent lifting, especially while bending and twisting
  2. Driving
  3. Vibration of the whole body
129
Q

What are the cuases of sciatica?

A
  1. Disc herniation:
    Common sites of herniation are L4-L5 and L5-S1
  2. Malignancy
  3. Infection
  4. Vascular compression
130
Q

What are the investigations for sciatica?

A
  1. MRI
  2. Check for red flags
    e. g. malignancy, fractures, cauda equina syndrome
131
Q

What is the treatment for sciatica?

A
  1. Conservative treatment for 6-8 weeks.
    Keep active
    Provide - paracetamol, NSAIDs, codiene, morphine
  2. Steroid injections

If pain doesn’t improve after 6-8 weeks then you should refer to MSK

  1. Surgery
    Laminectomy
    Discetomy
132
Q

What is a radiculopathy and what causes it?

What is the treatment?

A

Radiculopathy= NERVE ROOT gives LMN

Disc prolapse

Osetoarthrits

Conservative

133
Q

What is a myelopathy and what causes it?

What is the treatment?

A

Myelopathy= CORD gives UMN

Oseophytes

Disc prolapse (slower onset)

Tumour (slow onset)

Surgical decompression

134
Q

WHAT IS MULTIPLE SCLEROSIS?

https://www.youtube.com/watch?v=yzH8ul5PSZ8

A

Inflammatory, demyelinating disease.

Specific to the central nervous system.

Has relapsing and remitting symtptoms.

135
Q

When does MS begin?

A

Between the ages of 20-40

136
Q

What is the cause of MS?

A

Vit D deficiency

Genetics
Female
HLA DR2

Environment
Infections

137
Q

What are the symptoms of MS?

What is the sign seen in MS?

A

Optic neuritis (impaired vision and eye pain)

Nystagmus, double vision and vertigo

Bladder and sexual dysfunction

Spasticity and other pyramidal signs

Sensory symptoms and signs

Lhermitte’s sign (electric shock-like sensation that occurs on flexion of the neck.)

138
Q

What is the diagnostic criteria for MS?

A

Two or more CNS lesions disseminated in time and space

Exclusion of conditions giving a similar clinical picture

139
Q

What are the investigations for MS?

A

History
E.g. brief unexplained visual loss.

CSF
Oligoclonal bands of IgG

MRI
Plaques

Visual evoked potential
Measures nervous system response to visual stimuli

140
Q

What is the treatment for MS?

How would you treat the symptoms?
E.g. tremor and spasticity?

What do you give for an acute relapse?

A

Chronic - reduce relpase rate

  1. 1st line = Beta Interferon
  2. 2nd line = Glatiramer acetate
  3. 2nd line = Natalizumab

Symptom management

  1. Tremor = Beta blocker
  2. Spasticity = Baclofen

Acute relapse

  1. Steroids = IV Methylprednisolone 5 days
141
Q

What are the differential diagnosis of MS?

A

SLE

Lyme disase

AIDS

142
Q

What is the criteria for MS?

143
Q

What are the characterisitcs of fatigue specific to MS?

What is this phenomenom called?

A

Exacerbated by heat

Improved by cool temperatures

Called Uthoff’s

144
Q

What does all this destruction of nerves leave behind in MS?

A

Fibrosis

Plaques or sclera

145
Q

What happens in MS?

Pathology (Start with T cell)

What does this lead to?

A

T cell ligand on BBB wall

It then gets activated by myelin

Causes more expression of surface ligands on BBB

Also releases cytokines, vasodilation and damage to oligodendrocytes

B cells mark myelin, macrophages eat it

Regulatory T cells stop this eventually

Sensory, motor and cognitive problems

146
Q

What type of hypersensitivity reaction is MS?

A

Type 4 (cell mediated)

147
Q

What are the different types of MS?

A

Relapsing remmiting MS

Secondary progressive MS

Primary progressive MS

Progressive relapsing MS

148
Q

What is charcot’s neurological triad?

What is it described in?

A

Dysarthria

Nystagmus

Intention tremor

MS

149
Q

WHAT IS MYASTHENIA GRAVIS?

https://www.youtube.com/watch?v=bYGxGdu9MsQ

A

Autoimmune disease of acetylcholine receptors

150
Q

What type of sensitivity reaction is myasthenia gravis?

A
  1. Type 2
  2. IgG Cytotoxic injury
  3. Damage or lysis to host cells medaited by autoantibodies
151
Q

What do the B cells release?

(Two antibodies)

A

Release IgG antibodies
Bind to the nicotinic receptors
Unable to bind acetylcholine
No contractions
Antibodies can also affect complement pathway

Muscle receptor specific tyrosine kinase antibodies
Attack inside cells

CAUSE INFLAMMATION

152
Q

What is the epidemology of myasthenia gravis?

A

BIMODAL!!!!!

Women in 20-30s

Older men 60-70s

153
Q

What are the symptoms of myasthenia gravis?

When do the symptoms get worse?

A

Muscle weakness

Ptosis
Drooping eyelid

Diplopia
Double vision

Towards the end of the day

154
Q

How is myasthenia gravis diagnosed?

A

Bedside test
Arm outstretched, count to 50

Antibodies
Anti-AChR antibodies increase in 90%
MuSK antibodies (muscle specific tyrosine kinase)

Neurophysiology
Decremental muscle response

Imaging
CT of thymus

155
Q

What is the treatment for myasthenia gravis?

A

Acetylcholinesterase inhibitors
Pyridostigmine

Immunosupressive drugs
Prednisone

Surgical removal of thymus
Reduce helper T cells

156
Q

What is a myesthemic crisis?

A

Life threatening part of the disease

Affect muscles of breathing

157
Q

What is associated with myasthenia gravis in 10% of cases?

A

Thymic neoplasm

158
Q

WHAT IS MOTOR NEURON DISEASE?

A

Cluster of major degenerative diseases

Selective loss of neurons in motor cortex

Cranial nerve nuclei, and anterior horn cells

159
Q

What are the lower motor neuron symptoms?

A
  1. Hypo-reflexia
  2. Hypo-tonia
  3. Denervation atrophy
  4. Babinski -ve
  5. FASCICULATIONS
160
Q

What are the upper motor neuron symptoms?

A
  1. Hyper-reflexia
  2. Hyper-tonia
  3. Spasticity
  4. Babinski +ve
  5. NO fasiculations
161
Q

What does ALS result loss of?

A

Motor neurons in motor cortex and the anterior horn of the cord

162
Q

What is the most common type of MND?

What gene is affected?

A

ALS/amyotrophic lateral sclerosis

SOD-1 gene

163
Q

How is MD different from myasthenia?

A

MND never affects eye movements

164
Q

How is motor neuron different to MS and polyneuropathies?

A

No sensory loss or sphincter disturbance

165
Q

What are the investigations for motor neuron?

A

Neurophysiology nerve conduction studies
Electromyography

Blood tests
Creatine Kinase

MRI head/spine
Lumbar puncture
Exclude differentials

166
Q

What is the treatment of motor neuron disease?

A

Antiglutamatergic drugs
Riluzole
Slows progression

Baclofen, diazepam
Spasicity

Amitriptyline
Drooling

Pallative
Tracheostomy

167
Q

What are the different onset of symptoms of ALS?

A

Limb onset
Dropped foot, awkwardness running

Bulbar onset - worse prognosis
Dysphagia
Slurred speech
Difficulty speaking

Progress to same symptoms

168
Q

What are characteristic of motor neurons?

A

Fasciculations

169
Q

What are the different types of motor neuron disease?

Do they do upper or motor neuron damage?

A

ALS (Amyotropic Lateral sclerosis) (Both)

Progressive bulbar Palsy

Progressive muscular atrophy (Only LMN)

Primary lateral sclerosis (Only UMN)

170
Q

WHAT IS GUILLAIN-BARRE SYNDROME?

A

Acute neuropathy

171
Q

What are the symptoms of guillain-barre syndrome?

A

Symmetrical

Rapid ascending paralysis and sensory deficits

Absent reflexes

NO WASTING

172
Q

What type of neuropathy is it?

A

Demyelinating

Two types
Axonal motor
Axonal sensorimotor

173
Q

What is the most likely cause of guillain-barre syndrome?

A

Infection
Campylobacter jejuni

2-4 weeks following GI or resp infection

174
Q

What is the treatment of guillain-barre?

A
  1. Plasmaphoresis (plasma exchange)
  2. IV - Ig
    Clear debris
  3. IV antibiotics
175
Q

What are the tests for guillain-Barre syndrome?

A

LP
High protein and low WBC in CSF

Nerve conduction studies
Slower conduction

Electromyography
Decreased muscle involvement

176
Q

WHAT ARE PERIPHERAL NEUROPATHIES?

A

Any disorder of the peripheral nervous system

177
Q

Where can a peripheral neuropathy affect?

A

The receptors at the skin, to the peripheral nerve, to the spinal nerve or selectively affects the dorsal root ganglia where the cell bodies of the first sensory neuron are.

178
Q

What are the demyelinating neuropathies normally?

A

Genetic or inflammatory

179
Q

What is an example of an acute neuropathy?

A

Guillain-Barre syndrome

180
Q

How can peripheral neuropathies be calssified?

A

Acute and chronic

181
Q

What is the pattern of nerve involvement called for symetical sensorimotor neuropathy? What nerves are involved first?

A

Length-dependent

Initially sensory, but eventually sensorimotor

(longer fibers are affected first)

182
Q

What are the common causes of polyneuropothies?

A

DAVID

Diabetes

Alcohol

Vitamin deficiency (B12)

Infective (GB)

Drugs (isoniazid)

183
Q

What are the common mononeuropathies?

A

Carpal tunnel syndrome (median nerve)

Ulnar neuropathy (entrapment at thecubitaltunnel)

Peronealneuropathy (entrapment at the fibular head)

Cranial mononeuropathies(III or VII cranial nerve palsy)
idiopathic
immune mediated
ischemic

184
Q

How can you distinguish axonal neuropathies, what groups?

A

Symmetrical Sensorimotor

Asymmetrical Sensory

Asymmetrical Sensorimotor

185
Q

What are the two different types of neuropathy in terms of number of nerves?

A

Mononeuropathy: problem with one nerve

Polyneuropathy : problem with many nerves

186
Q

What is affected first in symetrical senori-motor neuropathies?

A

Initially with sensory symptoms affecting the
Toes and fingers

187
Q

What are the motor symptoms of neuropathies?

A
  1. Muscle cramps
  2. Weakness
  3. Fasciculations–muscle twitches
  4. Atrophy

High arched feet (pes cavus)

188
Q

What is ataxia?

A

Poor balance

Sensory (loss of proprioception) or cerebellar

189
Q

What is asymetical sensorimotor also called?

A

Mononeuritis multiplex

190
Q

What nerves are affected in asymetical sensory neuropathy?

A

Dorsal root ganglon exclusively

191
Q

What is the most common neuropathy?

A

Symetrical sensorimotor

192
Q

What would each type of neuropathy tell you in nerve conduction studies?

A

Demyelinating –> slow conduction velocities

Axonal –> reduced amplitudes of the potentials

193
Q

What are nerve conduction tests useful for?

A

Telling the type of neuropathy

194
Q

What are the first steps in diagnostic approach for peripheral neuropathies?

A

History

Clinical examination
Reduced or absent tendon reflexes
Sensory deficit
Weakness –muscle atrophies

Neurophysiological examination (i.e. NCS/QST)

195
Q

What are the causes of axonal peripheral neuropathies?

A

Associated with systemic diseases

Inflammatory–immune mediated (mainly acute)

Infectious (i.e. hepatitis, HIV, Lyme)

Ischemic (i.e. vasculitis)

Metabolic (i.e. Fabry’s, porphyria)

Hereditary (CMT, HLPP)

Toxins (pharmaceuticals, environmental toxins, B6)

196
Q

WHAT IS CARPAL TUNNEL SYNDROME?

A

Compression of the median nerve in the carpal tunnel in wrist

197
Q

What is the treatment for carpal tunnel?

A
  1. Splinting
  2. Corticosteroids injections
  3. Surgery of ligament
198
Q

What are the tests for carpal tunnel?

A

Electrophysiological testing

Description of symptoms

Phalen’s moneuver
Flex wrist down for 1 min - tingling

Tinel’s sign
Tap nerve

199
Q

What are the risk factors for capal tunnel?

A

Typing

Obesity

Pregnancy

Rheumatoid

200
Q

What causes carpal tunnel syndrome?

A

Inflammation of nearby tendons and tissues

Causing oedema

Causing compression

201
Q

What are the symptoms of carpal tunnel syndrome?

A

Pain, numbness and tingling

Thumb
Index
Middle
RIng finger(thumb side)

Wasing of abductor policisbrevis and thenar eminence

202
Q

WHAT ARE THE COMMON PRESENTATIONS OF A BRAIN TUMOUR?

Why do these occur?

A

Headache, worse in morning

N+V

Seizures, focal neurological deficits

Papiloedema

Symptoms of a raised ICP

203
Q

What is the treatment of a brain tumour?

A

Oral steroids (dex) can help to relieve symptoms

Surgery

204
Q

When are the features of raised ICP worse and better?

A

Worst on waking from sleep in the morning.

Increased by coughing, straining, and bending forwards

Sometimes relieved by vomiting

205
Q

Where are the sites that cancers to the brain metastisise from?

A

Lung (most common)

Breast

Bowel

206
Q

What are the investigations for a brain tumour?

A

CT with contrast/MRI.

Brain biopsy

207
Q

WHAT IS MENINGITIS?

https://www.youtube.com/watch?v=gIHUJs2eTHA

A

Inflammation of the meninges (membrane covering the brain)

Leptomeninges

208
Q

What are most types of primary brain tumours?

A

The majority are glial cell in origin:

Astrocytoma (85-90%)

Oligodendroglioma’ (~5%)

209
Q

What are the grades of brain tumours?

A

Grade 1 resectable

Grade 2 10 years

Grade 3 and 4 12 months

210
Q

What are the red flag symptoms of a brain tumour?

A

Headache with history of malignancy

New onset focal seizure

Cluster headache

Rapidly progressing focal neurology

Papilloedema

211
Q

What are the leptomeninges?

A

Inner two layers

212
Q

What are the clinical signs of meningitis?

What signs are associated with meningitis?

What is the rash from?

A

Fever
Headache
Neck stiffness
Photophobia
Phonophobia

Kernig’s sign
Brudzinski’s sign

Petechial rash (non-blanching)
Meningococcal septicaemia

213
Q

What are the differential diagnosis of meningitis?

A

Malaria

Encephalitis

Septicaemia

Subarachnoid

214
Q

What are the main investigations for bacterial meningitis?

A

Blood cultures
FBC, U&E, CRP, serum Glucose, lactate

Lumbar puncture
Glucose decrease, protein increase, WBC

CT Head

Throat swabs
Pneumococcal and Meningococcal serum PCR

215
Q

What is the management of bacterial meningitis?

A

IM benzylpenicillin

<3 months
Cefotaxime + Amoxocillin

>3 months
Ceftriaxone

Sometimes dexamethosome added to help inflammatory response

216
Q

What meningitis prophylaxis do you give to people who were in contanct with a patient with meningitis??

A

Rifampicin

217
Q

What are the viral causes of meningitis?

A

Herpes

HIV

EBV

Mumps

218
Q

What are the bacteria causing meningitis?

A

0 - 3 months

  1. Group B Streptococcus (most common cause in neonates)
  2. E. coli
  3. Listeria monocytogenes

3 months - 6 years

  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
  3. Haemophilus influenzae

6 years - 60 years

  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
219
Q

WHAT IS ENCEPHALITIS?

A

Swelling of the brain

220
Q

What causes encephalitis?

A

Herpes simplex virus - 1 - in 95% of cases

Virus

Autoimmune

221
Q

What are the signs and symptoms of encephalitis?

A

Bizarre encephalopathic behaviour or confusion

Decreased GCS or coma
Fever
Headache

Focal neurological signs
Seizures
History of travel or animal bite.

222
Q

What are the investigations for encephalitis?

A

LP - CSF
Increased CSF protein and lymphocytes, and decreased glucose. PCR for HCV

Bloods
Cultures

Contrast-enhanced CT
Focal bilateral temporal lobe involvement is suggestive of HSV encephalitis.

EEG
lateralised periodic discharges at 2 Hz

223
Q

What is the management of encephalitis?

What would you give for seizures?

A

IV Acyclovir

Phenytoin
Seizures

224
Q

What happens to the brain in encephalitis?

A

Brain swells causing oedema and may destroy the nerve cells

May cause bleeing and brain damage

225
Q

WHAT IS HERPES ZOSTER?

226
Q

What is the treatment for shingles?

What is the treatment for post-herpetic neuralgia?

A

Acyclovir

Amitriptyline
Post-herpetic neuralgia

227
Q

What is the diagnosis of shingles?

A

The rash

Quality of pain

Location

228
Q

What are the symptoms of shingles?

A

Rash across a dermatome that doesn’t cross the midline

Stabbing, piercing pain

229
Q

How is herpes zoster caused?

A

Varicella zoster virus reactivates

It lays dormant in dorsal root ganglion

230
Q

WHAT IS DEMENTIA?

A

A clinical syndrome with many underlying causes

231
Q

What is dementia characterised by?

A

Decline in memory, intellect or personality severe enough to intere with daily life

232
Q

What are the clinical features of Alzheimer’s?

A

Memory Loss

Visuospatial problems

Reasoning and language problems

Psychiatric features

Death

233
Q

What are the risk factors for Alzheimer’s?

A

Increased Age

Female

Poor socioeconomic status

ph of head injury

Down syndrome

234
Q

What is the pathophysiology of Alzheimer’s?

A

Presence of extracellular plaques in the cortex composed of
beta amyloid peptide

Intracellular
neurofibrillary tangles composed of tau.

235
Q

What is the treatment for Alzheimer’s?

A

Acetylcholinesterase inhibitors
(Donepezil, rivastigmine) can give modest benefit

NMDA-Receptor antagonist
(Memantine) may also help

236
Q

What is dementia with lewy bodies?

A
  1. A type of dementia with characteristic
  2. Alpha-synuclein cytoplasmic inclusions (Lewy bodies)
  3. In the substantia nigra, paralimbic and neocortical areas
237
Q

What are the clinical features of Lewy body dementia?

A
  1. Progressive cognitive impairment
    In contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
    Cognition may be fluctuating, in contrast to other forms of dementia
    Usually develops before parkinsonism
  2. Parkinsonism
  3. Visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
238
Q

What are the investigations for Lewy body dementia?

A
  1. Usually clinical
  2. Single-photon emission computed tomography (SPECT) is increasingly used
239
Q

What is the management for Lewy body dementia?

A
  1. Both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s
  2. Neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism.
240
Q

What is FTD dementia?

A

Selective degeneration of the frontal and temporal lobes

Onset typically in middle age

FH present in 40%

241
Q

What are the clinical features of FTD dementia

A
  1. Progressive deterioration in behaviour, personality and language
  2. Disinhibition
  3. Increased appetite
242
Q

What are the investigations for FTD?

A

SPECT Scan

  1. Atrophy of the frontal and temporal lobes
  2. Pick bodies - spherical aggregations of tau protein (silver-staining)
  3. Gliosis
  4. Neurofibrillary tangles
  5. Senile plaques
243
Q

What is the management for FTD?

A
  1. No helpful drugs

Focus on managing symptoms

  1. SSRI for aggitation and disinhibition
  2. Antipsychotics for behaviour
244
Q

How much of dementia does vascular make up?

What its risk factors

A

10% dementia

RFs: Increased BP, Smoking, PH of stroke/IHD, obesity, diabetes, cholesterol

245
Q

How can you distinguish vascular dementia from alzeihmers?

A
  1. Mood changes more prominent
  2. Degree of memory loss less obvious
  3. Focal neurological symptoms
  4. Imaging: patches rather than overall

ΩΩ 2a Bateman - Systems Based (11 decks)

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