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Year 2 > NEURO: Part 3 > Flashcards

NEURO: Part 3 Flashcards

1
Q

At what level does the spinal cord finish at

A

L1

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2
Q

Where does the caudal equine start at

A

L1 and continues into lumbar vertebra

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3
Q

Where are sensory neurone ganglion found

A

Dorsal root ganglion

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4
Q

Why is analgesia aimed at sensory neurone cell bodies

A

Have a higher SA

Take up anaesthetics better

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5
Q

What neurones do Epidural anaesthetics give

A

Sensory block than motor

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6
Q

At what level is an epidural given

A

Below L1

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7
Q

Why is an epidural given below L1

A

Allows us to anaesthetise the lower body but maintains brain function (need to keep breathing lol)

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8
Q

Where is the tube for epidural delivery inserted

A

BELOW L1 outside the dura mater - local anaesthetic is then put into epidural space

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9
Q

Where will the epidural then diffuse to after delivery

A

To dorsal root ganglion - will stop cell bodies from functioning so no pain felt

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10
Q

Why do we use a blunt needle when delivering an epidural

A

Do not want it to go into the CSF

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11
Q

What happens if the epidural ends up in the CSF

A

Will travel up the spine to the brain - respiratory failure

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12
Q

What is the best way to sample CSF

A

LUMBAR PUNCTURE

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13
Q

At what vertebral levels is lumbar puncture done

A

L3/4

L4/5

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14
Q

Why is a sharp needle done for a lumbar puncture

A

Since we want to penetrate the dura and extract CSF plunger to aspirate

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15
Q

What is the role of Nerve conduction Studies

A

Looks at peripheral nervous system; motor neurone -> root -> nerve -> NMJ -> muscle

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16
Q

Describe the nerve conduction study in sensory function assessment

A
  1. AP triggered by electrical stimulation

2. Potential is recorded using sticky electrodes to measure size of response and its speed

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17
Q

Describe the nerve conduction study seen in motor function assessment

A
  1. AP triggered causing ACh to be released at the NMJ
  2. ACh activates ACh receptors on muscle and causes muscle contraction - visible twitch
  3. Measure size of response and speed
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18
Q

What damage is indicated in small response of nerve conduction

A

Axon loss

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19
Q

What damage is indicated in slow response of nerve conduction

A

Demyelination

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20
Q

Role of Electromyography

A

EMG detects myopathies (pathology of muscle),

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21
Q

Why is an EMG more accurate than NCS in myopathies

A

NCS will be normal but EMG won’t be

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22
Q

Describe how EMG works

A
  1. Uses needle to detect electrical activity of muscle

2. Records activity of individual motor units

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23
Q

Why would we use EMG to look at big motor units

A

For nerve/motor neurone pathology

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24
Q

Why would we use EMG to look at small motor units

A

Muscle pathology - myopathy

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25
Q

Can axonal neuropathies be treated

A

No

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26
Q

Can demyelinating neuropathy be treated

A

Yes

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27
Q

When can NCS AND EMG be used

A 
Investigate:
Focal nerve entrapment
Generalised neuropathy 
Myopathy
Motor Neurone disease
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28
Q

When is Electroencephalography used

A

When looking at brain pathologies (e..g seizures)

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29
Q

What is EEG

A

Electrodes are placed in specific locations on the scalp

Patient asked to do various things during recording (close eyes, hyperventilate)

Epilepsy

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30
Q

Describe the anatomical location of the brainstem

A

Posterior fossa with the cerebellum

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31
Q

What separates the cerebrum from the cerebellum

A

Tentorium

so cerebrum sometimes called superiortentorium and cerebellum inferiortentorium

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32
Q

What structures does the brainstem have to go through to meet the spinal cord

A

Tectorial hiatus

Foramen magnum

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33
Q

What parts of the skull does the oculomotor nerve run over

A

Petrous apex of the temporal bone

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34
Q

Under what condition can we get a CN3 palsy

A

When the CN3 is fractures or inflamed, CN3 can push against the bone

FIXED DILATED PUPIL

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35
Q

Signs of cerebellar syndrome

A

Ataxia = loss of full control of body movements (limbs not steady)

Nystagmus = rapid eye movements (Ipsilateral)

Deficit is ON SAME SIDE AS CEREBELLAR LESION

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36
Q

Where is the periaqueductal grey located

A

Floor of the 4th ventricle

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37
Q

What is the role of the brainstem

A
  1. Alertness
  2. Sleep/Wake
  3. REM + Non-rem sleep
  4. Resp centre
  5. CV centre
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38
Q

How many cerebellar peduncles are there

A

3

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39
Q

Where are the cavernous sinuses located

A
  1. Lateral aspect of the body of the sphenoid bone
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40
Q

Blood supply of the cavernous sinus

A

Superior and inferior ophthalmic veins
Superior cerebral vein
Dural venous sinus

41
Q

What structures pass through the cavernous sinus

A

O TOM CAT

O - Oculomotor nerve
T - Trochlear
O - Ophthalmic trigeminal
M - Maxillary trigeminal
C - Carotid (internal)
A - Abducens
T - Trochlear nerve
42
Q

On an MRI what colour is bone

A

BLACK

43
Q

Criteria for brainstem death

A
  1. Pupils do not change
  2. Cornea reflex
  3. Caloric vestibular reflex
  4. Cough reflex
  5. Gag reflex
  6. Respirations
  7. Response to pain
44
Q

What is the caloric vestibular reflex

A

Placing cold or warm water into the external auditory canal producing currents in opposite direction:

If water is 44 degrees or above: Both eyes will turn towards the contralateral ear

If water is cold: Eyes will turn to ipsilateral ear

45
Q

What are the three main examinations done during a head injury

A
  1. Glasgow coma scale - measure level of consciousness
  2. Look at materialising signs: Identify which hemisphere issue is with
  3. Look at pupils for signs of raised ICP

ALSO MONITOR VITAL SIGNS

46
Q

Max score you can get in the glasgow coma scale

A

14

47
Q

3 categories of Glasgow coma scale

A
  1. Motor response
  2. Verbal response
  3. Eye opening response
48
Q

When and why can’t the GCS be used

A

Within one hour of the event - inaccurate

49
Q

How do we check for lateralising signs

A

Check painful stimuli response: Pinch behind the ear and will see what side has issue (R hand may come up but not L)

Thus Right hemisphere issue

50
Q

What features of the eye are going to indicate increased ICP

A
  1. Fixed dilated pupil (CN3 palsy)

2. Papilloedema

51
Q

How is head injury managed

A
  1. IV MANNITOL
  2. Diazepam
    3, Intubation - IF GCS is less than 8
  3. Neurosurgery
52
Q

What is MANNITOL

A

A diuretic - reduces oedema and thus ICP

53
Q

Why is Diazepam used in head injuries

A

Stops seizures

54
Q

Describe the neurosurgeon procedures done for head injuries

A
  1. ICP monitor insertion

2. Burrholes or carniectomy to relieve ICP

55
Q

What is BUrrholes

A

Small holes made in the skull to reduce pressure

56
Q

What is Craniectomy

A

Part of the skull is removed to relief pressure

57
Q

What check should we always do for people with head injury

A

Shave the head to check for lacerations as these may result in fatal bleeding

Suture lacerations and then do a CT

58
Q

Define TIA

A

A brief episode of neurological dysfunction due to temporary local ischaemia without infarction

59
Q

Define infarction

A

Tissue death due to poor oxygen supply

60
Q

How long does it take for TIA symptoms to resolve

A

24 hours

61
Q

What condition do TIAs foreshadow

A

MI and strokes

62
Q

In what gender is TIA common in

A

Black Males

63
Q

Why are blacks at a greater risk of TIA

A

Greater genetic risks of hypertension and atherosclerosis predisposition

64
Q

What is the main cause of a TIA

A

Atherothromboembolism from carotid artery (internal??)

Cardioembolism from: Mural thrombus post-MI or AF
Valve disease
Prosthetic valve

Hyperviscoity: Olycythaemia, SCA, Raised WCC or myeloma

Hypo perfusion in younger people

65
Q

What conditions can cause hypo perfusion

A

Cardiac dysrhythmia

  1. Postural hypotension
  2. Decreased flow through atheromatous arteries
66
Q

Risk factors for TIA

A
  1. Age
  2. Hypertension
  3. Smoking
  4. Diabetes
  5. Heart Disease: Valvular, ischaemic or AF
  6. Past TIA
  7. PAD
  8. Raised PCV
  9. Polycythaemia Vera
  10. Combined oral contraceptive pill
  11. Hyperlipidaemia
  12. Excess alcohol
  13. Clotting disorder
  14. Vasculitis (SLE, giant cell arteritis)

A Hat Prayed Readily Al lDay Hoping Sidrah’s Cat Presents Happiness Very Rapidly, Poor Cat

67
Q

What is the most common cause of a TIA

A

Cerebral ischaemia

68
Q

How long does a TIA last for

A

5-15 mins (resolves before cell death can occur)

69
Q

Differential diagnosis of TIA

A

Same symptoms but if they gradually progress:
Demyelination
Tumour
Migraine

70
Q

Clinical Presentation of all TIAs

A
  1. SUDDEN loss of function, usually lasting for minutes, with complete recovery and NO infarction
71
Q

Clinical presentation of carotid artery anterior circulation TIA

A

SUPPLIES frontal and medial part of cerebrum:

  1. Weak, numb CONTRALATERAL leg and milder arm symptoms
  2. Hemiparesis: Weakness on entire side of th body
  3. Hemi sensory disturbances
  4. Dysphagia (language impairment)
  5. Amaurosis fugax
72
Q

What is Amaurosis fugax

A
  1. Sudden transient loss of vision in one eye (‘curtains coming down vertically into field of vision)
73
Q

What causes Amaurosis fugal

A
  1. Temporary reduction in retinal and ophthalmic ciliary blood flow = temporary retinal hypoxia
74
Q

Clinical presentation of Vertebrobasilar artery TIA

A
  1. Diplopia (double vision)
  2. Vertigo
  3. Vomiting
  4. Choking and dysarthria (unclear articulation of speech but understandable)
  5. Ataxia
  6. Hemisensory loss
  7. Hemianopia vision loss
  8. Loss of consciousness
  9. Transient global amnesia (episode of confusion/amnesia lasting several hours before complete recovery)
  10. Tetra paresis (muscle weakness affecting all 4 extremities)
75
Q

Differential diagnosis of a TIA

A
  1. STROKE (can’t be distinguished until full recovery)
  2. Hypoglycaemia (symptoms spread and intensify over few mins with visual scintillations - blinking)
  3. Migraine aura
  4. Focal epilepsy
  5. Intracranial lesion (tumour or subdural haemotoma)
  6. Syncope due to arrhythmia
  7. Todd’s paralysis (transient weakness of arm, hand or leg after seizure)
  8. Retinal or vitreous haemorrhage
  9. Giant cell arteritis

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76
Q

Why is Giant cell arteritis mistaken for TIA

A
  1. Raised ESR
  2. Thickening and tenderness of temporal artery
  3. Monocular, temporary visual impairment
77
Q

How is TIA diagnosed

A
  1. FBC
  2. Carotid artery doppler ultrasound
  3. MR/CT angiography
  4. ECG
  5. CT or diffusion weighted MRI
  6. ECHO monitoring
78
Q

What are we looking for in FBA for TIA

A
  1. Polycythaemia
  2. ESR (raised in vasculitis)
  3. Hypoglycaemia
  4. Creatinine, electrolytes
  5. Cholesterol
79
Q

Why is a carotid artery doppler ultrasound done

A

Lok for stenosis/artheroma

80
Q

Role of MR/CT angiography for TIA

A

Extent of stenosis

81
Q

Role of ECG in TIA

A

Lok for AF or evidence of MI

82
Q

How is TIA managed

A
  1. ABCD2 score risk
  2. ASPIRIN + DIPYRIDAMOLE
  3. CLOPIDOGREL in long-term
  4. Anticoagulant (WARFARIN)
  5. Simvastatin
  6. Ramipril or Candesartan
  7. Improve diet, stop smoking

DO NOT DRIVE FOR AT LEAST 4 week following TIA

83
Q

What is the ABCD2 score risk assessment

A
  1. Age > 60 = 1
  2. Blood pressure >140/90 = 1
  3. Clinical features:
    Unilateral weakness = 2
    Speech disturbance without weakness = 1
  4. Duration of symptoms:
    Symptoms lasting more than 1 hour = 2
    Symptoms lasting 10-59 mins = 1
  5. Diabetes = 1
84
Q

What does an ABCD2 score of 6 or more mean

A
  1. Predicts a stroke and referred to specialist immediately

ALL PATIENTS WITH SUSPECTED TIA should be seen within 7 days

85
Q

Consequence of a score greater than 4

A

Specialist referral within 24 hours

86
Q

What conditions can increase risk of stroke

A
  1. AF
  2. More than 1 TIA in on week
  3. TIA on anticoagulant
87
Q

Role of purkyne cells in the cerebellum

A
  1. Receive synaptic inputs from the cerebellar nuclei
88
Q

What neurotransmitter is used by purkinje cells

A

GABA (they had inhibitory effects)

89
Q

What are the role of the granular cells

A

These are thin, unmyelinated axons that transmit into the purkyne layer

90
Q

What do granule cells use as a neurotransmitter

A

Glutamate (excitatory effect on purkyne cells)

91
Q

Where do mossy fibres originate from

A

Pontine nucleus

92
Q

Role of mossy fibres

A

Excitatory synapses with granule cells

93
Q

Where do climbing fibres originate from

A

Inferior olivary nucleus on contralateral side of brainstem

94
Q

Name the four nuclei of the cerebellum

A

Dentate
Globose
Emboli form
Fastigial

95
Q

Modalities of the dentate nucleus

A

Proprioception
nociception
Somatic input

Responsible for execution and planning of fine movement

96
Q

Describe the direct pathway

A

Check book

97
Q

Describe indirect pathway

A

Check book

98
Q

What forms the ventral striatum

A

Olfactory tubercle and Nucleus accumbens

99
Q

What forms the dorsal striatum

A

Caudate nucleus

Putamen

Year 2 (155 decks)

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