NEURO: Part 3 Flashcards
1
Q
At what level does the spinal cord finish at
A
L1
2
Q
Where does the caudal equine start at
A
L1 and continues into lumbar vertebra
3
Q
Where are sensory neurone ganglion found
A
Dorsal root ganglion
4
Q
Why is analgesia aimed at sensory neurone cell bodies
A
Have a higher SA
Take up anaesthetics better
5
Q
What neurones do Epidural anaesthetics give
A
Sensory block than motor
6
Q
At what level is an epidural given
A
Below L1
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)
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
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
10
Q
Why do we use a blunt needle when delivering an epidural
A
Do not want it to go into the CSF
11
Q
What happens if the epidural ends up in the CSF
A
Will travel up the spine to the brain - respiratory failure
12
Q
What is the best way to sample CSF
A
LUMBAR PUNCTURE
13
Q
At what vertebral levels is lumbar puncture done
A
L3/4
L4/5
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
15
Q
What is the role of Nerve conduction Studies
A
Looks at peripheral nervous system; motor neurone -> root -> nerve -> NMJ -> muscle
16
Q
Describe the nerve conduction study in sensory function assessment
A
- AP triggered by electrical stimulation
2. Potential is recorded using sticky electrodes to measure size of response and its speed
17
Q
Describe the nerve conduction study seen in motor function assessment
A
- AP triggered causing ACh to be released at the NMJ
- ACh activates ACh receptors on muscle and causes muscle contraction - visible twitch
- Measure size of response and speed
18
Q
What damage is indicated in small response of nerve conduction
A
Axon loss
19
Q
What damage is indicated in slow response of nerve conduction
A
Demyelination
20
Q
Role of Electromyography
A
EMG detects myopathies (pathology of muscle),
21
Q
Why is an EMG more accurate than NCS in myopathies
A
NCS will be normal but EMG won’t be
22
Q
Describe how EMG works
A
- Uses needle to detect electrical activity of muscle
2. Records activity of individual motor units
23
Q
Why would we use EMG to look at big motor units
A
For nerve/motor neurone pathology
24
Q
Why would we use EMG to look at small motor units
A
Muscle pathology - myopathy
25
Can axonal neuropathies be treated
No
26
Can demyelinating neuropathy be treated
Yes
27
When can NCS AND EMG be used
```
Investigate:
Focal nerve entrapment
Generalised neuropathy
Myopathy
Motor Neurone disease
```
28
When is Electroencephalography used
When looking at brain pathologies (e..g seizures)
29
What is EEG
Electrodes are placed in specific locations on the scalp
Patient asked to do various things during recording (close eyes, hyperventilate)
Epilepsy
30
Describe the anatomical location of the brainstem
Posterior fossa with the cerebellum
31
What separates the cerebrum from the cerebellum
Tentorium
| so cerebrum sometimes called superiortentorium and cerebellum inferiortentorium
32
What structures does the brainstem have to go through to meet the spinal cord
Tectorial hiatus
| Foramen magnum
33
What parts of the skull does the oculomotor nerve run over
Petrous apex of the temporal bone
34
Under what condition can we get a CN3 palsy
When the CN3 is fractures or inflamed, CN3 can push against the bone
FIXED DILATED PUPIL
35
Signs of cerebellar syndrome
Ataxia = loss of full control of body movements (limbs not steady)
Nystagmus = rapid eye movements (Ipsilateral)
Deficit is ON SAME SIDE AS CEREBELLAR LESION
36
Where is the periaqueductal grey located
Floor of the 4th ventricle
37
What is the role of the brainstem
1. Alertness
2. Sleep/Wake
3. REM + Non-rem sleep
4. Resp centre
5. CV centre
38
How many cerebellar peduncles are there
3
39
Where are the cavernous sinuses located
1. Lateral aspect of the body of the sphenoid bone
40
Blood supply of the cavernous sinus
Superior and inferior ophthalmic veins
Superior cerebral vein
Dural venous sinus
41
What structures pass through the cavernous sinus
O TOM CAT
```
O - Oculomotor nerve
T - Trochlear
O - Ophthalmic trigeminal
M - Maxillary trigeminal
C - Carotid (internal)
A - Abducens
T - Trochlear nerve
```
42
On an MRI what colour is bone
BLACK
43
Criteria for brainstem death
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
What is the caloric vestibular reflex
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
What are the three main examinations done during a head injury
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
Max score you can get in the glasgow coma scale
14
47
3 categories of Glasgow coma scale
1. Motor response
2. Verbal response
3. Eye opening response
48
When and why can't the GCS be used
Within one hour of the event - inaccurate
49
How do we check for lateralising signs
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
What features of the eye are going to indicate increased ICP
1. Fixed dilated pupil (CN3 palsy)
| 2. Papilloedema
51
How is head injury managed
1. IV MANNITOL
2. Diazepam
3, Intubation - IF GCS is less than 8
4. Neurosurgery
52
What is MANNITOL
A diuretic - reduces oedema and thus ICP
53
Why is Diazepam used in head injuries
Stops seizures
54
Describe the neurosurgeon procedures done for head injuries
1. ICP monitor insertion
| 2. Burrholes or carniectomy to relieve ICP
55
What is BUrrholes
Small holes made in the skull to reduce pressure
56
What is Craniectomy
Part of the skull is removed to relief pressure
57
What check should we always do for people with head injury
Shave the head to check for lacerations as these may result in fatal bleeding
Suture lacerations and then do a CT
58
Define TIA
A brief episode of neurological dysfunction due to temporary local ischaemia without infarction
59
Define infarction
Tissue death due to poor oxygen supply
60
How long does it take for TIA symptoms to resolve
24 hours
61
What condition do TIAs foreshadow
MI and strokes
62
In what gender is TIA common in
Black Males
63
Why are blacks at a greater risk of TIA
Greater genetic risks of hypertension and atherosclerosis predisposition
64
What is the main cause of a TIA
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
What conditions can cause hypo perfusion
Cardiac dysrhythmia
2. Postural hypotension
3. Decreased flow through atheromatous arteries
66
Risk factors for TIA
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
What is the most common cause of a TIA
Cerebral ischaemia
68
How long does a TIA last for
5-15 mins (resolves before cell death can occur)
69
Differential diagnosis of TIA
Same symptoms but if they gradually progress:
Demyelination
Tumour
Migraine
70
Clinical Presentation of all TIAs
1. SUDDEN loss of function, usually lasting for minutes, with complete recovery and NO infarction
71
Clinical presentation of carotid artery anterior circulation TIA
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
What is Amaurosis fugax
1. Sudden transient loss of vision in one eye ('curtains coming down vertically into field of vision)
73
What causes Amaurosis fugal
1. Temporary reduction in retinal and ophthalmic ciliary blood flow = temporary retinal hypoxia
74
Clinical presentation of Vertebrobasilar artery TIA
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
Differential diagnosis of a TIA
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
Sam's Heart Failure Might Stress Tom's Grandma's Intimate Relationship
76
Why is Giant cell arteritis mistaken for TIA
1. Raised ESR
2. Thickening and tenderness of temporal artery
3. Monocular, temporary visual impairment
77
How is TIA diagnosed
1. FBC
2. Carotid artery doppler ultrasound
3. MR/CT angiography
4. ECG
5. CT or diffusion weighted MRI
6. ECHO monitoring
78
What are we looking for in FBA for TIA
1. Polycythaemia
2. ESR (raised in vasculitis)
3. Hypoglycaemia
4. Creatinine, electrolytes
5. Cholesterol
79
Why is a carotid artery doppler ultrasound done
Lok for stenosis/artheroma
80
Role of MR/CT angiography for TIA
Extent of stenosis
81
Role of ECG in TIA
Lok for AF or evidence of MI
82
How is TIA managed
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
What is the ABCD2 score risk assessment
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
What does an ABCD2 score of 6 or more mean
1. Predicts a stroke and referred to specialist immediately
| ALL PATIENTS WITH SUSPECTED TIA should be seen within 7 days
85
Consequence of a score greater than 4
Specialist referral within 24 hours
86
What conditions can increase risk of stroke
1. AF
2. More than 1 TIA in on week
3. TIA on anticoagulant
87
Role of purkyne cells in the cerebellum
1. Receive synaptic inputs from the cerebellar nuclei
88
What neurotransmitter is used by purkinje cells
GABA (they had inhibitory effects)
89
What are the role of the granular cells
These are thin, unmyelinated axons that transmit into the purkyne layer
90
What do granule cells use as a neurotransmitter
Glutamate (excitatory effect on purkyne cells)
91
Where do mossy fibres originate from
Pontine nucleus
92
Role of mossy fibres
Excitatory synapses with granule cells
93
Where do climbing fibres originate from
Inferior olivary nucleus on contralateral side of brainstem
94
Name the four nuclei of the cerebellum
Dentate
Globose
Emboli form
Fastigial
95
Modalities of the dentate nucleus
Proprioception
nociception
Somatic input
Responsible for execution and planning of fine movement
96
Describe the direct pathway
Check book
97
Describe indirect pathway
Check book
98
What forms the ventral striatum
Olfactory tubercle and Nucleus accumbens
99
What forms the dorsal striatum
Caudate nucleus
| Putamen
