Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2A > Neuro > Flashcards

Neuro Flashcards

1
Q

function of the frontal lobe

A 
voluntary movement on the contralateral side of the body 
dominant hemisphere (left) controls speech and writing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

function of the parietal lobe

A

language control and maths
primary sensory area
proprioception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

function of the temporal lobe

A

primary auditory cortex

understanding spoken word and sounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

function of the occipital lobe

A

primary visual and visual association cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where is Broca’s area located

A

inferior frontal gyrus in the frontal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the function of Broca’s area

A

motor production of speech

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what artery is Broca’s area supplied by

A

middle cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where is Wernicke’s area located

A

posterior temporal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the function of Wernicke’s area

A

understanding the spoken word

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the blood supply to Wernicke’s area

A

middle cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the primary motor cortex

A

region in the cerebral cortex involved in planning, control and execution of voluntary movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

where is the primary motor cortex located

A

precentral gyrus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the primary somatosensory cortex

A

region of the cerebral cortex involved in touch and sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

where is the primary somatosensory cortex located

A

postcentral gyrus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

where is CSF produced

A

lateral ventricles by the choroid plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

outline the flow of CSF

A

lateral ventricle –> 3rd ventricle via the interventricular foramen
3rd ventricle –> 4th ventricle via the cerebral aqueduct
4th ventricle –> subarachnoid space medially via the foramen of Magendie and laterally via the foramen of Luschka
returns to the venous system via arachnoid villi into the superior sagittal sinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the corpus callosum

A

commissural fibres of white matter that connect the right and left hemispheres together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the function of the corpus callosum

A

links functionally similar areas of the 2 hemispheres together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the components of the brain stem

A

midbrain
pons
medulla oblongata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the three divisions of the midbrain

A

tectum
tegmentum
cerebral peduncles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the tectum composed of

A

superior and inferior colliculi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the function of the superior colliculi

A

sensitive to visual changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the function of the inferior colliculi

A

sensitive to auditory events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the tegmentum composed of

A

periaqueductal gray, red nucleus and substantia nigra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the blood supply to the midbrain

A

basilar artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

which cranial nerves originate from the pons

A

trigeminal (V)
abducens (VI)
facial (VII)
vestibulocochlear (VIII)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

blood supply of the pons

A

pontine branches of the basilar artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the role of the medulla oblongata

A
  1. houses the ascending and descending nerve tracts along with brainstem nuclei and is the place where decussation of most nerve fibres occurs
  2. contains the autonomic cardiovascular and respiratory centres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

blood supply to the medulla

A

posterior inferior cerebellar artery
anterior spinal artery
branches of the distal vertebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

contents of the olfactory foramen

A

olfactory nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

contents of optic canal

A

optic nerve and opthalmic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

contents of superior orbital fissure

A

CN3, 4, V1 (opthalmic branch), 6 and superior opthalmic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

contents of the foramen rotundum

A

V2 (maxillary branch)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

contents of the foramen ovale

A

V3 (mandibular branch)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

contents of the foramen spinosum

A

middle meningeal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

contents of the internal acoustic meatus

A

CN7, CN8, labrinthyne arteries and vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

contents of the jugular foramen

A

jugular vein, CN9, 10, 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

contents of the hypoglossal canal

A

hypoglossal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

contents of foramen magnum

A

spinal cord and vertebral arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are the three layers of the meninges

A

dura mater
arachnoid mater
pia mater

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

function of the meninges

A

provide a supportive framework for the cerebral and cranial vasculature and with CSF protect the CNS from mechanical damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what does the dura mater consist of

A

outer endosteal layer

inner meningeal layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what does the arachnoid mater consist of

A

subarachnoid cisterns full of CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what does the pia mater form

A

the blood brain barrier and is closely adherent to the underlying nervous tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the function of the blood brain barrier

A

prevents unwanted molecules getting out of the blood and into the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

arterial blood to the brain arrives within the skull via two pairs of vessels…

A

internal carotid arteries

vertebral arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

how do the internal carotid arteries enter the skull

A

through the carotid canal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

how do the internal carotid arteries interact

A

they interconnect to the form the circle of willis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how much of the brain’s blood supply is supplied by the internal carotid arteries

A

80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

how much of the brain’s blood supply is supplied by the vertebral arteries

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

how to the vertebral arteries interact

A

fuse to form the basilar artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what does the anterior cerebral arteries supply

A

anteromedial aspect of the cerebrum back to the parietal lobe
olfactory cortex
corpus callosum
internal capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what does the middle cerebral arteries supply

A

most of the lateral portions of the cerebrum
part of the internal capsule
basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what does the posterior cerebral arteries supply

A

medial and lateral sides of the cerebrum posteriorly
occipital lobe
posteromedial aspect of the parietal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is the venous drainage of the brain

A

cerebral veins first drain into dural venous sinuses and then into the internal jugular vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how many cervical, thoracic, lumbar and sacrum vertebrae

A

7, 12, 5, 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

name of cervical vertebrae C1 and C2

A

C1 : atlas

C2 : axis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is the nucleus pulposus

A

soft, semi-fluid core of the intervertebral disc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is the annulus fibrosus

A

outer later of the intervertebral disc

10-12 concentric layers of collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is the conus medullaris

A

spinal cord tapers to a cone towards the end

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is the cauda equina

A

nerves from the lower part of the cord, lumbar and sacral nerves hang obliquely downwards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what is the filum terminale

A

fibrous strands extending from the conus medullaris to the coccyx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what part of the spinal tract contains the ascending and descending nerve fibres

A

outer part of the spinal cord in the white matter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what does the inner part of the spinal tract contain

A

grey matter than contains nerve cell bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

name the two ascending spinal tracts

A
  1. spinothalamic

2. dorsal column-medial lemniscus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what is an upper motor neurone

A

neurons of the motor cortex and descending pathways involved
synapse of neurons not muscle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what is a lower motor neurone

A

neurons that synapse directly onto muscle cells and stimulate their movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what sensation does the spinothalamic tract convey

A

pain
temperature
crude touch + pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

outline the spinothalamic tract

A
  1. nerve endings (from nociceptors and mechanoreceptors) in the body send info down axon
  2. spinothalamic tract enters the spinal cord at Lissauer’s fasciculus and ascends 1-2 layers within
  3. synapses onto cell body in dorsal horn of grey matter
  4. axon from this neurone crosses over in ventral white commissure
  5. axon ascends via spinothalamic fasciculus
  6. axon ascends through brain stem and synapses onto the thalamus
  7. thalamus sends projections to the post central gyrus of the cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what sensations does the dorsal medial lemniscal column carry

A

proprioception
fine touch
vibration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

outline the DCML

A
  1. first order neurone periphery enters the spinal column
    - upper limb (T6 and above) ascends up the lateral fasciculus cuneatus
    - lower limb (below T6) ascends up the medial fasciculus gracilis
  2. fibres ascend up the dorsal column in respective fasciculi to either the cuneate or gracilis nuclei at the medulla
  3. fibres synapse with second order neurons
  4. second order neurons decussate at internal arcuate fibres to travel in the medial lemniscus and ascend to the ventral posterolateral nucleus in the thalamus
  5. synapse with third order neurons at the thalamus and travel to the sensory cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

function of the corticospinal tract

A

a motor tract that conveys axial and limb voluntary motor control to generate muscle movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

outline the corticospinal tract

A
  1. upper motor neurons begin in the pre-central gyrus (primary motor cortex) and run as separate neurons (corona radiate)
  2. neurons converge and leave the cortex, descending through the internal capsule
  3. neurons pass through the midbrain, Pons and peduncles into the medulla
  4. 75% of fibres decussate at the level of the pyramids and descend down the lateral corticospinal tract –> synapse with a LMN –> innervate the limbs
  5. Remaining 25% of fibres descend down the anterior corticospinal tract and decussate as they leave the anterior white commissure –> synapse with a LMN –> innervate axial muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what is significant about the area postrema

A

only area that lacks a blood brain barrier. toxins enter here to alert the brain of a presence and induce vomiting to remove toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

two types of summation

A

temporal and spatial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

types of synapse

A

electrical and chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

function of the somatic nervous system

A

innervates skeletal muscle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

neurotransmitter in somatic nervous system

A

acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what does the autonomic nervous system innervate

A

smooth muscle, cardiac muscle, glands, GI neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

how many neurons is the autonomic nervous system made up of

A

2 neurons in series (pre and post ganglionic)
1st neuron has cell body in the CNS
this synapses with a neuron outside CNS in an autonomic ganglion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

describe the sympathetic nervous system including neurons and neurotransmitters

A
  • fight or flight response
  • neurons leave CNS from thoracic and lumbar regions
  • sympathetic ganglia
  • preganglionic fibre (myelinated)–> acetylcholine – nictonic receptor –> postganglionic fibre (non-myelinated) –> noradrenaline –> adrenergic receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

which cranial nevers are parasympathetic

A

CN3, 7, 9, 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

describe the parasympathetic nervous system including neurons and neurotransmitters

A
  • neurones leave brainstem and sacral portion of spinal cord
  • rest or digest
  • single myelinated preganglionic fibre –> acetylcholine –> nicotinic receptor –> non-myelinated postganglionic fibre –> acetyl choline –> muscarinic receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what is substance P

A

peptide neurotransmitter involved in pain transmission and is a vasodilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what is a stroke

A

rapid onset of neurological deficit caused by a vascular lesion and is associated with infarction of the central nervous tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what are the two types of stroke

A

ischaemic and haemorrhagic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what is an ischaemic stroke

A

ischaemia of brain tissue caused by a lack of blood supply which leads to infarction and death of neural tissue resulting in loss of functionality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what is a haemorrhagic stroke

A

primary intracerebral haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

aetiology of an ischaemic stroke

A

cerebral infarction due to am embolism or thrombosis
cardiac emboli (AF, endocarditis)
atherothromboembolism (e.g from carotids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

aetiology of a haemorrhagic stroke

A

intracerebral or sub-arachnoid haemorrhage
primary : hypertensive, lobar haemorrhages due to amyloid deposition
secondary : anticoagulants, mets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

name 5 risk factors for stroke

A 
hypertension 
diabetes 
smoking and alcohol 
hyperlipidaemia
obesity 
heart disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

signs of an ACA territory stroke

A

main symptoms are focused around the leg because of the homonculus

  • leg weakness
  • sensory disturbance in the legs
  • gait apraxia
  • incontinence
  • drowsiness
  • akinetic mutism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

signs of a MCA territory stroke

A
  • contralateral arm and leg weakness
  • contralateral sensory loss
  • hemianopia (caused by damage to the optic radiations)
  • aphasia
  • dysphagia
  • facial droop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

signs of a PCA territory stoke

A

patients mainly experience visual problems

  • contralateral homonymous hemianopia
  • prosopagnosia
  • only time a headache is associated with a stroke!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what are the signs that would point to a posterior circulation stroke?

A
  • motor deficits - hemiparesis, tetraparesis and facial paresis
  • dysarthia and speech impairment
  • visual disturbances
  • vertigo, nausea and vomiting
  • locked in syndrome - aware but cannot respond
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what is the management plan in ischaemic strokes?

A
  1. FAST - important to recognise quickly!
  2. diagnose a stroke clinically
  3. CT head (ensure that it is ischaemic not haemorrhagic)
  4. thrombolytic treatment
  5. risk management treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what is the thrombolytic treatment used in acute stroke management

A

IV alteplase

must give within 4 1/2 hours!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what are 3 contraindications for giving thrombolytic treatment in the acute management of stroke?

A 
haemorrhage 
active bleeding
warfarin or heparin 
aneurysm 
pregnant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what is an alternative therapy for ischaemic stroke and when would you use this?

A

clot retrieval

use if the clot is in one of the large arteries of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what is the treatment for haemorrhagic stroke?

A

stop anticoagulants if on any
control BP with beta blocker
surgical - clipping or coiling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what are the 4 risk management treatments used in acute stroke?

A
  1. antiplatelets - 300mg aspirin for 2 weeks then lifelong clopidogrel
  2. statin
  3. AF treatments if found to have AF (NOACs, warfarin)
  4. antihypertensives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

name three primary preventative measures used to stop a stroke ever happening

A
  1. treat hypertension
  2. treat diabetes
  3. treat hyperlipidemia
  4. quit smoking
  5. exercise
  6. treat cardiac disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what treatment is used post-stroke for re-enablement?

A

physiotherapy
speech and language therapists (swallowing and speech)
occupational therapists for home modification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what complications can arise after a stroke related to immobility?

A
  • pressure sores
  • aspiration pneumonia
  • constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

what is the definition of a transient ischaemic attack?

A

an ischaemic (usually embolic) neurological event with symptoms lasting less than 24 hours (but they are often much less than this e.g 30 mins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

what is the pathophysiology behind TIAs

A

inadequate cerebral blood supply leading to ischaemia –> hypoxia of brain tissue –> transient loss of function with resolution but possible remittance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

aetiology of TIAs (name three causes)

A

atherothromboembolism
cardioembolism (mural thrombosis post MI or in AF)
hyperviscosity (polycythaemia, sickle cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

clinical presentation of a TIA depends on what?

A

depends on which area of the brain has become ischaemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

clinical presentation of a TIA affecting the anterior circulation

A
  • amaurosis fugax (fleeting loss of vision in one eye) if the retinal artery is occluded
  • hemiparesis
  • hemisensory loss
  • aphasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

clinical presentation of a TIA affecting the posterior circulation

A
  • diplopia, vertigo, vomiting
  • hemianopic visual loss
  • hemisensory
  • ataxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

what tests would you do to investigate a TIA

A 
bloods 
- FBC for polycythaemia
- glucose for hypoglycaemia 
Carotid doppler +/- angiography 
CT head 
ABCD2 score to assess their risk of having another stroke in the next two days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

what are the categories in an ABCD2 score and what points to a patient to be at a particularly high risk for a stoke?

A 
Age > 60 = 1 point 
Blood pressure > 140/90 = 1 point 
Clinical features 
- unilateral weakness = 2 points 
- speech disturbance w/o weakness = 1 point
Duration of symptoms 
- symptoms lasting > 1hr = 2 points 
- symptoms lasting < 1hr = 1 point 
Diabetes = 1 point

A score over 6 strongly predicts a stroke within the next week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What is the treatment for a TIA?

A
  1. antiplatelet medication : aspirin 300mg for 2 weeks then 75mg clopidogreal lifelong
  2. cardiovascular risk factors controlled
  3. statin if high cholesterol
  4. carotid endarterectomy (recommended in patients where their internal carotid artery is > 70% and operative risk is acceptable).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

what can you not do if you have had a TIA?

A

drive for 1 month

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What is the pathophysiology behind a subarachnoid haemorrhage

A

spontaneous rupture causes a rapid release of arterial blood into the subarachnoid space causing an increased intracranial pressure and possibly a cerebrovascular accident

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

aetiology of subarachnoid haemorrhage

A

Most commonly caused by a berry aneurysm rupture
common sites are at bifurcations like:
- posterior communicating and internal carotid
- anterior communicating and ACA/MCA

congenital arteriovenous malformations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What are 4 risk factors for developing a subarachnoid haemorrhage?

A

hypertension
smoking
alcohol misuse
polycystic kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

symptoms of a subarachnoid haemorrhage

A
  • THUNDERCLAP HEADACHE –> sudden onset very severe
  • nausea
  • loss of consciousness/collapse
  • seizures
  • coma may follow
  • may be a preceding sentinel headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Signs of a subarachnoid haemorrhage

A
  • neck stiffness
  • kernig’s sign (unable to extend patient’s leg at the knee when thigh is flexed - takes 6 hours to develop)
  • retinal bleeds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

what investigations would you do in a suspected subarachnoid haemorrhage ?

A
  • CT HEAD - seen as a star shaped lesion due to blood filling in gyro patterns around the brain and ventricles
  • Lumbar puncture if the CT is negative but the history is very suggestive of a SAH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

If you need to do a lumbar puncture for a SAH what is very important to consider when taking it and why?

A

Must make sure that it is done over 12 hours after the headache onset to allow the breakdown of RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

what does a positive sample from a lumbar puncture show when investigating subarachnoid haemorrhage?

A 
Xanthochromic sample (yellow due to bilirubin) confirms diagnosis. 
As this differentiates between old blood from SAH vs a bloody tap.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What is the treatment of a subarachnoid haemorrhage?

A
  • resuscitation if needed
  • refer to neurosurgery immediately (endovascular coiling (preferred where possible) or surgical clipping)
  • IV fluids
  • Nimodipine is a Ca2+ antagonist that reduces vasospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

what is the pathphysiology of a subdural haematoma?

A

rupture of bridging veins between the cortex and venous sinuses that causes an accumulating haematoma between the dura and arachnoid space. Causes a rise in intracranial pressure and can shift midline structures away from the clot.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

consequence of a subdural haematoma if left untreated?

A

eventual tentorial herniation and coning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

aetiology of a subdural haematoma

A
  • Majority from head injury (can be minor and up to 9 months previous)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

what group of people are most susceptible to subdural haematomas

A

elderly as brain atrophy makes bridging veins vulnerable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

risk factors for subdural haematomas

A

falls (epileptics, alcoholics)

anticoagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

symptoms of a subdural haematoma

A
  • fluctuating level of consciousness +/- insidious physical/intellectual slowing
  • sleepiness
  • headache
  • personality change
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

signs of a subdural haematoma

A
  • increased ICP (headache, reduced GCS, papilloedema)
  • localizing neurological symptoms
  • seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What investigations would you do in a suspected subdural haematoma?

A

CT head

  • shows clot +/- midline shift of structures
  • crescent shaped collection of blood over 1 hemisphere
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

what is the treatment of subdural haematomas?

A
  • reverse clotting abnormalities
  • surgical removal of clot - emergency craniotomy and clot evacuation
  • IV mannitol if increased ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

what is the pathophysiology of an extradural haematoma?

A

traumatic skull fracture (usually temporal/parietal bone) leads to a rupture, typically in the middle meningeal artery and vein, causing blood to accumulate between the bone and the dura.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

aetiology of an extradural haematoma

A

traumatic skull fracture, usually to the temporal and parietal bones
trauma to the temple

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

what are the clinical features of an extradural haematoma?

A
  • beware the lucid interval pattern. this may last a few hours to days. progressive deteriorating consciousness after any head injury that initially produced no loss of consciousness. This is caused by a raising ICP.
  • increasingly severe headache
  • vomiting, confusion, seizures
  • +/- hemiparesis with brisk reflexes and an upgoing plantar
  • if bleeding continues the ipsilateral pupil dilates, coma deepens and bilateral limb weakness develops
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

complications from an extradural haematoma?

A
  • brainstem compression causing deep and irregular breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

what are the late signs in an extradural haematoma

A

bradycardia

increased blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

what investigations would you do in a suspected extradural haematoma?

A

CT head
- shows a biconvex/lens-shaped haematoma because the tough dural attachments keep the bleed more localised
Skull Xray
- may be normal or may show fracture lines crossing the course of the middle meningeal vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

what is the treatment for an extradural haematoma?

A
  • surgery for clot evacuation +/- ligation of the bleeding vessel
  • IV mannitol if increased ICP + intubation and ventilation if patient unconscious
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

define epilepsy

A

condition that is defined by recurrent, unprovoked, epileptic seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

what is the difference between epilepsy and epileptic seizures?

A

epilepsy is a chronic condition

an epileptic seizure is one event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

what is the definition of an epileptic seizure?

A

paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excessive hypersynchronous ( groups of brain cells depolarizing at exactly the same time) neuronal discharges in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

what is the definition of a non epileptic seizure?

A

paroxysmal event in which changes in behaviour, sensation and cognitive function caused by mental processes associated with psychosocial distress (situational)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

what are 5 characteristics of an epileptic seizure

A
  1. stereotypical seizures (they are the same in each patient)
  2. positive ictal symptoms (seeing /hearing / feeling something that isn’t there)
  3. may occur from sleep
  4. typical seizure phenomena (lateral tongue bite, head turning)
  5. lasting for a relatively short amount of time (30-120 seconds)
  6. negative postictal symptoms (weakness)
  7. cyanosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

what are 3 characteristics of a non-epileptic seizure?

A
  1. rapid or slow postictal recovery
  2. prolonged duration (1-20 minutes)
  3. dramatic motor phenomena or prolonged atonia (loss of muscle strength)
  4. eyes/mouth closed
  5. ictal crying
  6. shaking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

what is syncope?

A

paroxysmal event in which changes in the behaviour, sensation and cognitive processes are caused by an insufficient blood or oxygen supply to the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

3 causes of syncope

A

low blood pressure
arrhythmia
blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

what are 5 features of syncope ?

A
  1. more likely to occur from standing
  2. rarely from sleep
  3. situational
  4. presyncopal symptoms (dizzy + lightheaded, seeing stars over visual field, washy noises - associated with the posterior aspects of the brain)
  5. Duration 5-30 seconds
  6. recovery within 30 seconds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

what are the steps in diagnosing epilepsy (investigating transient loss of consciousness)

A
  1. is it a primary brain problem (disturbance of brain function) or a secondary brain problem (problem with blood circulation i.e syncope)?
  2. if a primary brain problem - is it an epileptic seizure of a non epileptic seizure? (injury during seizures and tongue biting are more suggestive of epilepsy) HISTORY - appreciate that this is difficult if you are going off of recollection and have no video.
  3. if deemed to be epilepsy what type of epilepsy is it?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

what are the two main types of epilepsy?

A
  1. structural/metabolic epilepsy (focal epilepsy)

2. generalised (idiopathic) epilepsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

what is a focal seizure?

A

a seizure that originates from one part of the brain (they can gradually spread causing a secondary generalised seizure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

what are the three types of focal seizure

A
  1. partial seizures without impairment of consciousness (e.g Jacksonian seizures)
  2. partial seizures with impairment of consciousness (e.g psychomotor seizures)
  3. secondary generalised seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

what features would you see in focal temporal lobe seizure?

A
  • autonomic features (lip smacking, swallowing)
  • manual movements (fumbling and fiddling)
  • dysphagia
  • Deja vu / jamais vu
  • hallucinations of smell, taste or sound
  • emotional disturbance
    They are unconscious!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

what features would you see in a focal frontal lobe seizure?

A
  • awareness will be fully retained but they cannot control movement
  • motor features: posturing or peddling movements
  • Jacksonian march : spreading focal motor seizure with retained awareness
  • usually from sleep
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

what features would you see in a focal parietal lobe seizure?

A

sensory disturbances - tingling, numbness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

what is the first line treatment for focal seizures?

A
  • carbamazepine

- lamotrigine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

what is a common cause of focal epilepsy

A

hippocampal sclerosis - caused by prolonged febrile seizure in early life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

aetiology of epilepsy

A

2/3 are idiopathic

structural : cortical scarring (head injury), developmental , hippocampal sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

what investigations would you do in a presenting apparent seizure?

A
  • thorough history, look for provoking causes
  • consider an EEG - cannot exclude epilepsy and can give a false positive
  • MRI : investigated for a structural lesion
  • drug levels
  • lumbar puncture if an infection was suspected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

what is a generalised (idiopathic) seizure?

A

originates at some point within the brain but rapidly engaging bilaterally distributed networks leading to simultaneous onset of widespread electrical discharge with no localizing features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

what are three types of generalised (idiopathic) seizure

A
  • absences seizures
  • myoclonic
  • primary generalised tonic-clonic seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

what is an absence seizure

A
  • generalised seizure
  • brief blank spells where consciousness is lost but no movement
  • e.g may stop in middle of a sentence, when seizure has stopped may be able to re pick up the sentence
  • presents in childhood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

what are the features of myoclonic seizure?

A
  • brief, quick, sudden jerk of a limb, face or trunk
164
Q

what are the features of a tonic-clonic seizure ?

A
  • loss of consciousness
  • tonic phase - limbs stiffen, mouth and eyes open, limited movement
  • clonic phase -individual spikes of electrical activity hitting the muscle so there are fast big jerky movements.
  • negative post-ictal symptoms
165
Q

what is the first line treatment for generalised (idiopathic) epilepsy?

A
  • valproate

- lamotrigine

166
Q

name three side effects of carbamazepine

A 
dizziness
drowsiness
dry mouth
nausea 
vomiting 
vision disorders
167
Q

what is the mechanism of action of carbamazepine and lamotrigine?

A
  • work on pre-synaptic excitability
  • sodium channel blockers
  • stop depolarization and stop the release of excitory neurotransmitters
168
Q

what is the mechanism of action of pregabalin and gabapentin (two medications which can also be used to treat focal seizures)

A
  • calcium channel blockers

- directly inhibit the presynaptic neurone

169
Q

what is the mechanism of action of valproate ?

A
  • targets and inhibits GABA transaminase (which normally degrades GABA)
  • if this is inhibited GABA metabolism is reduced and GABAergic neurotransmission is increased
  • inhibits presynaptic neurone
170
Q

how do we use epileptic treatment and what is the potential progression?

A
  1. try to use as a monotherapy (try the lowest possible effective dose)
  2. if that doesn’t work consider alternative monotherapy or combinations of drugs that have different modes of action
  3. surgery
  4. electrostimulation
171
Q

what are the surgical treatment options for epilepsy

A
  1. resective surgery - only for focal epilepsy - try to cut out the area of the brain where the seizure originates
  2. tractotomy - surgical severing of nerve tracts
172
Q

what is electrostimulation (a potential treatment option for epilepsy)?

A
  • vagal nerve stimulation
  • sends electrical impulses to the brain through the vagus nerve which stops synchronization in the brain
  • usually can just help reduce frequency
173
Q

What is the pathology of Parkinson’s disease?

A
  • loss of domaminergic neurons in the substantia nigra causing an alteration in neural circuits within the basal ganglia which regulates movement
  • Lewy bodies in neurons (abnormal intracellular aggreagtes of protein)
  • pale substantia nigra
174
Q

aetiology of Parkinson’s ?

A 
unknown 
often sporadic
thought to have a genetic susceptibility which is triggered by the environment
oxidative stress
mitochondrial dysfunction
175
Q

what are the three cardinal features of Parkinson’s disease?

A
  1. Bradykinesia - slowness or absence of movement
  2. Tremor - at rest, unilateral
  3. Rigidity - causing pain
176
Q

What is the clinical presentation of Parkinson’s Disease?

A

ALWAYS ASYMMETRICAL. SLOW GRADUAL PROGRESSION OVER TIME.

  1. Bradykinesia - slowness or absence of movement (e.g problems doing up buttons, smaller writing etc.)
  2. Tremor - at rest, unilateral
  3. Rigidity - caused by increased tone
    • if you ask the patient to make repetitive movements over time there will be a decrease in amplitude and decrease in accuracy of the movement over time (usually starts off better)
  4. Small stepped wide gait with a stooped posture (shuffling)
  5. Problems initiating movement e.g walking
  6. Reduced arm swinging on one side
  7. Reduced facial expression
177
Q

how do you diagnose Parkinson’s disease?

A
  • Diagnosis is clinical

- can do a DaTSCAN which images the dopanergic terminals or the nigrostriatal neurons in the putamen

178
Q

what are the three pharmacological supportive treatments used in managing Parkinson’s?

A
  1. L-Dopa (levodopa) (first line treatment!)
  2. Dopamine agonists (first line treatment in younger patients) e.g ropinirole
  3. Enzyme inhibitors
    - catechol-o-methyl-transferase inhibitors (tolcapone)
    - monoamino-oxidase-B inhibitors (selegiline)

usually a combination of these treatments

179
Q

pharmacological mechanism of L-Dopa

A
  • L-Dopa is the naturally occurring pre-cursor substance of dopamine
  • tyrosine –> L-Dopa –> Dopamine
  • acts at dopamine receptor to increase the amount in the brain
  • must be given with a peripheral dopa-decarboxylase inhibitor like carbidopa so that the levodopa can cross into the brain

this combination drug : co-careldopa

180
Q

what is the pharmacological mechanism of dopamine agonists

A

e. g ropinirole
- supports the action of L-Dopa
- works at the post synaptic dopamine receptors

181
Q

what is the pharmacological mechanism of the enzyme inhibitors used in treatment of Parkinson’s?

A
  • they decrease the naturally occurring breakdown of dopamine to increase the dopamine levels in the brain
182
Q

what are the three preparations of L-Dopa and when are they used?

A
  • dispersible L-Dopa : rapid acting can be used 1st thing in morning
  • standard release - day time
  • slow release - night
183
Q

what motor complications can patients develop in late stage Parkinson’s?

A
  • on-dyskinesias : hyperkinetic movements when drugs work
  • off-dyskinesias : fixed, usually painful muscle
  • freezing : unpredictable loss of mobility
184
Q

along with pharmacological interventions what other management should be involved in Parkinson’s disease?

A
  • MDT approach!
  • physiotherapist and occupational therapist

monitor mood as depression is very common in Parkinson’s

185
Q

how are headaches classified? Give some examples for each classification

A

primary (no underlying cause for the headache) and secondary headaches
painful cranial neuropathies and other face pains e.g trigeminal neuralgia

primary : migraine, cluster, tension type
secondary : meningitis, SAH, GCA, medication overuse

186
Q

what is the difference between primary and secondary headaches regarding diagnosis?

A

primary headaches are syndromes diagnosed by the history and examination
in secondary headaches there will be an abnormal result i.e on a brain scan or blood test

187
Q

red flags in a patient presenting with headache that need an urgent referral

A
  • thunderclap headache - SAH
  • seizure + new headache
  • suspected meningitis or encephalitis
188
Q

what is the clinical presentation of a tension type headache

  • how many to diagnose
  • time course
  • characteristics
A
  • 10 or more attacks occurring for less than 1 day a month
  • headache lasts 30mins-7 days
  • bilateral
  • pressing/squeezing/tightening quality
  • mild to moderate intensity
  • not aggravated by routine physical activity
  • NEED TO HAVE : no nausea or vomiting, only one of : photophobia and phonophobia
189
Q

treatment of tension type headaches

A
  • reassurance
  • lifestyle advice : exercise, avoid triggers
  • symptomatic treatment for episodes : aspirin, paracetamol
190
Q

investigations for a suspected tension type headache

A

clinical diagnosis

191
Q

what is the clinical presentation of a cluster headache?

A
  • rapid onset of severe unilateral orbital/supraorbital and/or temporal pain lasting 15-180 minutes if untreated
  • ipsilateral cranial autonomic features (red, swollen eye, lacrimation)
  • unilateral pain
  • sense of restlessness/agitation
  • attacks have a frequency from 1 every other day to 8 a day
  • often nocturnal
192
Q

how do you diagnose cluster headaches?

A

at least 5 headaches fulfilling the clinical presentation

193
Q

what is the treatment for cluster headache?

A
  • 100% Oxygen for 15 minutes
    Preventives
  • avoid triggers (e.g alcohol)
  • corticosteroids e.g verapamil for short term
194
Q

what is the clinical symptom of a medication overuse headache and what drugs can cause these?

A
  • regular headache for more than 15 days of the month

- combination analgesics

195
Q

treatment for medication overuse headache?

A
  • withdraw the analgesic

- give aspirin / naproxen to help with the rebound headache

196
Q

what is the clinical presentation of a migraine without aura?

A
  • moderate - severe headache
  • attacks last between 4 and 72 hours
  • can be aggravated by routine physical activity
  • pulsating
  • unilateral
    during the headache at least one of the following:
  • nausea and/or vomiting
  • photophobia and phonophobia
197
Q

list some potential triggers for migraines

A 
CHOCOLATE 
Chocolate 
Hangovers
Orgasms
Cheese/caffeine 
Oral contraceptives
Lie-ins
Alcohol 
Travel
Exercise
198
Q

what is an aura, experienced in 20% of migraine patients

A

patients can see flashing lights / zig-zag lines

feel that part of their vision is blurry or lost part of their vision

199
Q

what are the clinical presentations of migraines with auras?

A

aura has only of the following:
- fully reversible visual symptoms including positive and negative features
- fully reversible dysphasic speech disturbance
at least two of the following
- homonymous visual symptoms and/or unilateral sensory symptoms
- at least 1 aura symptom develops gradually over 5 mins or more
- each symptom lasts more than 5 and less than 60 minutes

200
Q

how do you diagnose a migraine with aura ?

A

2 attacks fulfilling the clinical presentation

201
Q

what investigations would you do in a suspected migraine?

A
  • diagnosis is clinical

- can exclude other causes by doing CRP, ESR, CT/MRI /lumbar puncture if there are red flags present

202
Q

pharmacological treatment of migraines to stop an attack

A 
combination therapy 
- oral triptan + NSAIDs
- oral triptan + paracetamol 
monotherapy 
- oral triptan
- NSAID
- aspirin
- paracetamol

consider adding an anti-emetic

203
Q

pharmacological and non-pharmacological preventative treatment of migraines

A

topiramate / propranolol (stay on for a few months and can titrate dose up, use if having attacks more than 5 days a month)

acupuncture 10 sessions (2nd line)

Amitriptyline (3rd line)

Botulinum toxin type A injections

  • prophylaxis of chronic migraine
  • need to have tried several oral drugs first
204
Q

list some potential triggers for migraines

A 
CHOCOLATE 
Chocolate 
Hangovers
Orgasms
Cheese/caffeine 
Oral contraceptives
Lie-ins
Alcohol 
Travel
Exercise
205
Q

what is an aura, experienced in 20% of migraine patients

A

patients can see flashing lights / zig-zag lines

feel that part of their vision is blurry or lost part of their vision

206
Q

what are the clinical presentations of migraines with auras?

A

aura has only of the following:
- fully reversible visual symptoms including positive and negative features
- fully reversible dysphasic speech disturbance
at least two of the following
- homonymous visual symptoms and/or unilateral sensory symptoms
- at least 1 aura symptom develops gradually over 5 mins or more
- each symptom lasts more than 5 and less than 60 minutes

207
Q

how do you diagnose a migraine with aura ?

A

2 attacks fulfilling the clinical presentation

208
Q

what investigations would you do in a suspected migraine?

A
  • diagnosis is clinical

- can exclude other causes by doing CRP, ESR, CT/MRI /lumbar puncture if there are red flags present

209
Q

pharmacological treatment of migraines to stop an attack

A 
combination therapy 
- oral triptan + NSAIDs
- oral triptan + paracetamol 
monotherapy 
- oral triptan
- NSAID
- aspirin
- paracetamol

consider adding an anti-emetic

210
Q

pharmacological and non-pharmacological preventative treatment of migraines

A

topiramate / propranolol (stay on for a few months and can titrate dose up, use if having attacks more than 5 days a month)

acupuncture 10 sessions (2nd line)

Amitriptyline (3rd line)

Botulinum toxin type A injections

  • prophylaxis of chronic migraine
  • need to have tried several oral drugs first
211
Q

what is the pathophysiology of trigeminal neuralgia

A

compression of the trigeminal nerve resulting in demyelination and excitation of the nerve resulting in erratic pain signalling

212
Q

what are potential triggers for trigeminal neuralgia?

A

washing the affected area
shaving
eating
talking

213
Q

name two potential causes of trigeminal neuralgia?

A
  • idiopathic

- secondary to a tumour

214
Q

what is the clinical presentation of trigeminal neuralgia?

A
  • pain occurring in one or more distributions of the trigeminal nerve with no radiation beyond the trigeminal distribution
  • reoccurring in paroxysmal attacks from a fraction of a second to 2 mins
  • electric shock like, stabbing, shooting or sharp
  • severe intensity
  • precipitated by innoculous (talking or chewing) stimuli to the affected side of the face
215
Q

investigations in suspected trigeminal neuralgia

A
  • MRI head to rule out any secondary cause e.g tumour

- diagnosis is clinical : at least three attacks unilateral face pain fulfilling the clinical presentation

216
Q

what is the treatment for trigeminal neuralgia?

A

carbamazepine (anticonvulsant)

217
Q

aetiology of multiple sclerosis?

A

unknown
believe that individual has to be genetically susceptible and be exposed to an environmental factor that triggers the illness (e.g EBV infection is shown to be associated)

218
Q

2 facts about the epidemiology of multiple sclerosis?

A
  • more prevalent in caucasians
  • women > men
  • peaks between 20-30 years old
  • less likely the closer you live to the equator (vitamin D levels)
219
Q

what is the pathophysiology of multiple sclerosis?

A
  • chronic autoimmune inflammatory disorder of the CNS
  • autoreactive T lymphocytes are activated
  • can cross the BBB
  • cause a cascade immune response
  • results in damage to myelin
  • myelin heals poorly with thinner, inefficient myelin and eventually causes axonal loss of oligodendrocytes
220
Q

what are the pathological features of an active lesion in multiple sclerosis?

A
  • hypercellular plaque edge due to infiltration of tissue with inflammatory cells
  • demyelination breakdown products present
  • extensive BBB disruption
221
Q

what are the pathological features of a chronic, inactive lesion in MS?

A
  • hypocellular plaque
  • loss of axons and demyelination (no breakdown products)
  • atrophy
222
Q

what are the two types of demyelination seen in multiple sclerosis?

A
  1. macrophage mediated demyelination

2. antibody mediated demyelination

223
Q

is myelin able to regenerate in multiple sclerosis?

A

some of the cells will survive
body is able to remyelinate but this myelin is thin and ineffective
these patients may recover fully but if you stress that axon by exposing it to heat you get impaired conduction (i.e in a hot shower or hot environment) (UHTOFF’S PHENOMENON)

224
Q

what is the clinical presentation of multiple sclerosis?

A

DEMYELINATION
Diplopia
Eye movements are painful (optic neuritis)
Motor weakness (spastic and progressive)
nYstagmus
Elevated temperature worsens symotoms (uhtoff’s phenomenon)
Lhermitte’s sign (sudden sensation, like an electric shock, that passes down the back of the neck when flexed)
Intention tremor
Neuropathic pain (e.g trigeminal neuralgia, pins and needles)
Ataxia (trunk and limb)
Talking slurred (dysarthria)
Impotence
Overactive bladder (incontinence)
Numbness (decreased vibration sensation)

225
Q

what are the symptoms of MS associated with?

A

the site where the CNS is affected e.g spinal cord - spastic weakness, optic nerves - optic neurtitis

226
Q

what are the three clinical courses that MS can run?

A
  1. relapsing/remitting course
  2. secondary progressive
  3. primary progressive

can also have lesions in a preclinical setting - asymptomatic patients but have lesions which can be picked up on MRI

227
Q

what is the most common type of MS?

A

relapsing / remitting

228
Q

what is relapsing / remitting MS

A

clearly defined disease relapses with full recovery OR with sequelae and residual deficit (partial recovery). Periods between disease relapses are characterised by a lack of disease progression (they are stable between relapses).

229
Q

what is secondary progressive MS

A

initial relapsing / remitting disease course followed by progression with or without occasional relapses, minor remissions or plateaus

230
Q

what is primary progressive MS

A

disease progression from onset with occasional plateaus and temporary minor improvements allowed

231
Q

what is the diagnostic criteria for MS?

A

clinical diagnosis
two or more CNS lesions disseminated in time and space (attacks occur at multiple sites with 30 or more days in between attacks)

232
Q

investigations in suspected MS?

A
  • MRI with contrast - active lesions are white
  • CSF - Lumbar puncture (electrophoresis shows IgG bands - inflammatory proteins only seen in CSF not in serum)
  • evoked responses - delayed response in visual, auditory , somatosensory and brainstem potentials
233
Q

two differential diagnoses when investigating MS?

A

autoimmune : SLE

infectious : lyme disease, syphillis, AIDs

234
Q

what is the treatment for an acute relapse/attack in MS?

A

Oral or IV methylprednisolone can speed up recovery from an acute exacerbation of MS
Does not alter overall prognosis

235
Q

what are the disease modifying treatments used in MS?

A

treated aggressively in the relapse/remitting phase

  • dimethyl fumerate oral BO
  • monoclonal antibodies
    - alemtuzumab (acts against T cells) IV
    - natalizumab (acts against VLA-4 receptors that allow immune cells to cross the BBB) (this is treatment for highly active relapsing MS)
236
Q

what can be used to manage symptoms in MS?

A
  • spasticity : baclofen or gabapentin
  • tremor : botulinum toxin type A injections
  • urgency/frequency : intermittent self-catheterization
237
Q

lifestyle advice for MS?

A
  • regular exercise
  • stop smoking
  • avoiding stress
238
Q

what is the definition of motor neuron disease?

A

a cluster of neurodegenerative diseases, characterized by a selective loss of neurons in the motor cortex, cranial nerve nuclei and anterior horn cells.
Upper and lower motor neurons can be affected

239
Q

what is the main difference between MND and MS?

A

In MND there is no sensory loss or sphincter disturbance

240
Q

what is the most typical type/clinical pattern of MND?

A

Amyotrophic lateral sclerosis (ALS)

- loss of motor neurons in motor cortex AND anterior horn of the cord so there are combine UMN and LMN signs

241
Q

what is the aetiology of MND?

A

unknown

242
Q

what differentiates MND from myasthenia gravis?

A

MND never affects eye movements

243
Q

what is the second most common clinical pattern of MND, affected 10-20% of all MND?

A

Progressive Bulbar Palsy

- only affects cranial nerves IX-XII

244
Q

what are the signs of LMN pathology?

A

EVERYTHING LOWERS

  • reduced muscle tone
  • muscle atrophy
  • fasciculations
  • depressed reflexes
245
Q

what are the signs of muscle atrophy in MND affecting the following regions:

  • bulbar
  • upper and lower limbs
  • resp muscles
A
  • furrowing of tongue and fasciculations.
  • upper and lower limb weakness. May have bilateral footdrop from wasing and weakness
  • weak breathing muscles. diaphragm may be higher up in chest than it should be
246
Q

Investigations in suspected motor neuron disease

A
  • Neurophysiology : nerve conduction studies, electromyography (shows that problem is with LMN and not the muscles)
  • MRI head and spine (looking for structural pathology)
  • Blood tests (muscle enzymes - increasing creatinine kinase due to atrophy)
  • Lumbar puncture (to exclude inflammatory causes)
247
Q

what are the signs of UMN pathology?

A

EVERYTHING GOES UP

  • increased muscle tone (affected limb is spastic)
  • tendon reflexes go up (pathologically brisk)
  • positive Babinski sign (plantar responses extensor)
  • characteristic pattern of limb weakness
    • upper limb : flexor muscles > extensor
    • lower limb : flexor muscles < extensor
248
Q

what may you observe if the patient has bilateral lesions of the UMN system?

A

pseudobulbar palsy emotional lability

- laugh longer/louder than normally would and may cry much more easily than normally would

249
Q

clinical presentation of ALS?

A
  • stumbling spastic gait
  • foot drop +/- proximal myopathy
  • weak grip (door handles don’t turn)
  • weak shoulder abduction (hair washing is hard)
  • UMN signs
  • LMN signs
250
Q

what is the diagnostic criteria for ALS / MND

A
  • no diagnostic test

- definite MND : lower and upper motor neuron signs in 3 regions

251
Q

what is the treatment for MND? What is its mechanism of action

A

Riluzole

inhibitor of glutamate release and NMDA receptor antagonist

252
Q

what is meningitis?

A

inflammation of the meninges

253
Q

what are the non-infective causes of meningitis?

A
  • paraneoplastic
  • drug side effects
  • autoimmune (vasculitis/SLE can cause sterile meningitis)
254
Q

how can infection enter the CSF and brain?

A
  • via blood stream –> if bacteraemic can get seeding of infection into CSF
  • extracranial infection –> colonisation in nasopharynx of causative bacteria / otitis media / sinusitis
  • neurosurgical or trauma
255
Q

what is the pathophysiology of meningitis?

A
  1. bacteria in CSF
  2. because CSF is sterile there are no WBC and the bacteria can replicate freely and rapidly
  3. Inflammation
  4. Blood brain barrier breaksdown
  5. neutrophils/lymphocytes enter the CSF
  6. more inflammation
  7. can cause brain swelling
256
Q

what are the symptoms of meningitis?

A

Fever
headache
neck stiffness (may not be able to touch chin to chest)

Later:

  • decreasing GCS
  • petechial rash (non-blanching) if bacterial
257
Q

what is meningism

A
  • neck stiffness
  • photophobia
  • Kernig’s sign (pain and resistance on passive knee extension with hip fully flexed)
258
Q

If a suspected meningitis patient arrived at a GP surgery what would be the management the GP should give?

A

IM Benzylpenicillin

Admit the patient

259
Q

What is the immediate management steps for a patient in hospital with meningitis

A
  1. Assess GCS
  2. Blood culture
    + FBC, U&E, CRP, serum glucose + lactate
  3. Broad spectrum antibiotics
  4. Lumbar puncture
  5. Steroids
260
Q

what first line broad spectrum antibiotics would you give a patient with suspected meningitis innitially?
What type of antibiotics are these?
Why do we use these?

A

Ceftriaxone or cefotaxime
3rd generation cephalosporins
They are able to cross the blood brain barrier

261
Q

what patients should you not give cephalosporins to ?

A
  • if they are penicillin allergic leading to anaphylaxis)
  • immunocompromised
  • recent travel
262
Q

what steroids should you give a patient with meningitis ?what does it do?

A

IV dexamethasone

helps to reduce brain swelling and reduce neurological sequele

263
Q

what is the definitive investigation to diagnose meningitis

A

Lumbar puncture

264
Q

when investigating meningitis what do you test the CSF for?

A
  1. microscopy : look for white or red blood cells
  2. gram stain : look for organisms
  3. culture : blood and chocolate agar plates
  4. protein
  5. glucose
  6. Viral PCR : looking for certain viruses
265
Q

when is a lumbar puncture contraindicated in a patient with suspected meningitis ?

A
  1. abnormal clotting (platelets/coagulation)
  2. petechial rash
  3. raised ICP - look for papilloedema
266
Q

what is the most common causative organism of meningitis?
And what type of bacteria is it?
What colour on staining would it be ?
is it an acute or chronic cause for meningitis?

A

Gram negative diplococci : Neisseria meningitidis
pink
acute

267
Q

what group of people usually present with Neisseria meningitidis ? Why?

A

university students
5-10% of adults are carriers of the bacteria without symptoms
when go to uni and large groups of adults mix then some can become infected

268
Q

what are three bacterial causes of acute meningitis?
what type of bacteria are they?
what colour would they be on staining?

A
  1. Neisseria meningitidis (gram negative diplococci ; pink)
  2. Streptococcal pneumoniae (gram positive diplococci ; purple)
  3. Listeria (gram positive rod ; purple)
  4. Group B streptococci (gram positive cocci ; purple)
269
Q

Listeria can be a bacterial cause of acute meningitis, what group of people are more likely to present with this as the cause?

A

immunosuppressed
elderly
neonates

270
Q

name three viral causes of acute meningitis ?

A
  • enterovirus
  • herpes simplex virus
  • varicella zoster virus
271
Q

bacterial causes of chronic meningitis ?

how would one of them stain?

A
  • mycobacterium tuberculosis (green on phenol-auramine staining)
  • syphillis
272
Q

how does the CSF appear in bacterial meningitis?

A

cloudy (pus cells)

273
Q

how does the CSF appear in viral meningitis ?

A

clear

274
Q

how does the CSF appear in TB meningitis?

A

clear with a fibrin web

275
Q

what are the risk factors for developing bacterial meningitis?

A
  • student
  • recent travel (e.g to Sub Saharan Africa)
  • Immunosuppressed
276
Q

what are the risk factors for developing viral meningitis

A
  • near small children / a small child
277
Q

what would you see in CSF microscopy for bacterial meningitis?

A

polymorph neutrophils

278
Q

what would you see in CSF microscopy for viral and TB meningitis?

A

lymphocytes

279
Q

what would protein level in CSF be like in a patient with meningitis?

A

High

280
Q

what would the glucose level in CSF be like in a patient with bacterial meningitis

A

Low (use the glucose to reproduce)

281
Q

What would the glucose level in CSF be like in a patient with viral meningitis?

A

Normal (virus does not need glucose to replicate)

282
Q

what is a clinical presentation of viral meningitis?

A
  • had a recent viral infection
  • less severe
  • no rash
283
Q

what other step do you need to do if the patient has Neisseria Meningitidis?

A
  • inform public health england
  • identify close contacts (partners, sharing kitchen and household contacts in droplet range)
  • give ciprofloxacin prophylaxis
284
Q

what is encephalitis?

A

inflammation of the brain

285
Q

aetiology of encephalitis

A

usually always viral

  • herpes simplex
  • varicella zoster
  • other viral : measles, mumps, rubella, EBV
  • other : rabies
  • non-infective : autoimmmune, paraneoplastic

more common in the immunocompromised

286
Q

clinical presentation of encephalitis?

A
  • preceding flu-like illness (hours -days)
  • altered GCS (confusion, drowsiness, coma)
  • odd behaviour
  • fever
  • seizures
  • memory loss
  • focal neurological signs
  • history of travel

as viral meningitis can progress to encephalitis the patient may have a history of meningism

287
Q

what is the management of encephalitis?

A
  • Bloods cultures, serum for viral PCR
  • MRI of the head +/- EEG
    (white areas = inflammation)
  • Lumbar puncture
    • lymphocytic CSF
    • high protein and normal glucose
    • viral PCR
  • HIV test
288
Q

treatment of encephalitis?

A 
mainly supportive 
- pain killers
- fluids
- nutritional support 
physio and neuro rehab
289
Q

what pharmacological treatment can you give to patients with encephalitis where the cause is HSV or ZVZ

A

Aciclovir

290
Q

what is the definition of dementia?

A

a set of symptoms including memory loss and a decline in the previous level of normal cognitive functioning including abilities problem solving or language. It is a gradual and progressive onset.

291
Q

what are the 4 subtypes of dementia?

A
  1. Alzheimer’s disease
  2. Vascular dementia
  3. Lewy body dementia
  4. Fronto-temporal dementia
292
Q

What is the clinical presentation of frontotemporal dementia?

A
  • behavioural / personality change
  • disinhibition
  • emotional unconcern
293
Q

what is the most common cause of dementia?

A

Alzheimer’s disease

294
Q

what is the pathophysiology of Alzheimer’s disease?

A
  • accumulation of beta amyloid peptide results in progressive neuronal damage
  • cerebral cortex atrophy
  • intracellular neurofibrillary tangles
  • increase in number of extracellular amyloid plaques
  • loss of neurotransmitter acetylcholine
  • enlarged ventricles
295
Q

name 2 areas of the brain that are most susceptible to neuronal loss in Alzheimer’s disease?

A
  • hippocampus
  • amygdala
  • temporal neocortex
  • subcortical nuclei
296
Q

what is the aetiology of vascular dementia?

A

cumulative effect of many small strokes

297
Q

what is the aetiology of Lewy body dementia?

A

Lewy bodies in the brainstem and neocortex

298
Q

what is the aetiology of fronto-temporal dementia?

A

frontal and temporal atrophy with loss of over 70% of spindle neurons

299
Q

name 3 risk factors for developing Alzheimer’s disease?

A
  • 1st degree relative with AD
  • Down’s syndrome
  • depression
  • loneliness
  • smoking
300
Q

what features differentiate depression from dementia?

A

Depression

  • onset and decline often rapid with a trigger/life event
  • subjective complaints of memory loss (obvious early on)
  • patients are distressed / unhappy variability in cognitive performance - they ‘don’t know’ answers

Dementia

  • vague, insidious onset
  • unaware / attempt to hide problems
  • mood may be labile, cognitive performance is consistent and answer all questions
301
Q

what is the clinical presentation of Alzheimer’s disease?

A
  • suspect in adults > 40 years old with:
  • persistent, progressive and global cognitive impairment
  • short term memory loss
  • semantically empty speech (lacking detail)
  • selective amnesia
  • visuo-spatial skill affected
  • anosognosia - a lack of insight into the problems endangered by the disease e.g missed appointments, mishandling of money

Later :

  • irritability
  • mood disturbance
  • behavioural change (aggression)
302
Q

clinical presentation of vascular dementia?

A

stepwise deterioration with short periods of stability, sudden onset

303
Q

clinical presentation of Lewy body dementia?

A
  • fluctuating cognitive impairment

- detailed visual hallucinations

304
Q

clinical presentation of fronto-temporal dementia

A
  • executive impairment
  • behavioural/personality changes
  • disinhibition
  • episodic memory and spatial orientation are preserved until later stages
305
Q

what are the investigations involved in diagnosing someone with Alzheimer’s disease

A
  1. take a history from the patient
  2. assess cognitive function 6CIT
    - year? month? address? count 20-1?months of the year in reverse?repeat that address?
  3. MMSE <17/30 = serious cognitive impairment
  4. blood tests - vitamin deficiencies, thyroid dysfunction
    Specialised diagnostic tests
  5. Structural MRI
    - can see atrophy / shrinking of the hippocampal region
  6. Amyloid imaging
    - PET scan or CSF
  7. FDG PET
    - looks at glucose metabolism, in AD there is a loss of uptake of glucose
306
Q

name three preventative measures for developing AD?

A
  • healthy body weight
  • healthy diet
  • decrease alcohol consumption
  • no smoking
  • regular exercise
  • engage in leisure activity (socially active)
  • higher occupation (cognitively active)
  • control vascular risk factors (e.g blood pressure control)
307
Q

what pharmacological management can be used in treatment of AD?

A
  • acetylcholinesterase inhibitors e.g donepezil or rivastigmine (they increase the amount of ACh in the synapse)
  • antiglutamatergic treatment e.g memantine
    (recommended in patients with severe disease)
308
Q

name three features which differentiate dementia from delirium?

A
  • dementia is insidious and progressive, delirium is acute and fluctuating
  • dementia lasts months-years, delirium lasts hours - weeks
  • dementia has normal consciousness and is a disorder, delirium has altered consciousness and can be due to stroke, metabolic or infective causes
309
Q

name three types of primary brain tumour

A
  • meningiomas (benign)
  • germ cell tumours
  • sellar region tumours
  • gliomas
  • schwannoma (tumour of cranial nerve roots - benign)
  • Primary CNS lymphoma
310
Q

what is the most common primary brain tumour

A

gliomas including astrocytomas (most common) and oligodendroglioma

311
Q

what are more common primary or secondary brain tumours?

A

secondary metastatic brain tumours

312
Q

what are the top 2 cancers than cause brain mets?

A

lung and brain

313
Q

what gives a clue that the brain tumour is secondary not primary?

A

there are usually multiple mets and they have a rounded appearance with oedema surrounding them

314
Q

how are brain tumours classified ?

A

1 by cell type (histological features) + molecular genetic features
2 grade using morphology into 4 grades of malignancy. to do this we look for mitotic activity, vascular proliferation and necrosis

315
Q

what are gliomas?

A

tumours of the neuroepithelial cells

astrocytomas are the most common

316
Q

what is the risk for grade II gliomas?

A

that they will go on and undergo anaplastic transformation into high grade malignant tumours

317
Q

what are the 4 grades of malignancy as defined by the WHO classification of gliomas

A

I : benign paediatric tumour; pilocytic astrocytoma (characterised by rosenthal fibres present in children, cerebellum and are cystic)

II : premalignant tumour; diffuse astrocytoma (hypercellularity pleomorphism)

III ; anaplastic astrocytoma (proliferation, mitotic activity)

IV; glioblastoma (cellular necrosis, hypoxia within tumour. microvascular proliferation)

318
Q

what are diffuse astrocytomas? and what is the difficulting with them when it comes to treatment?

A

tumour cells infiltrate diffusely into the brain so it is difficult to tell where the tumour ends
it is not curable by surgical resection

319
Q

what is a medulloblastoma

A

cerebellum tumour

320
Q

what is the aetiology of brain tumours?

A
  • majority of causes are unknown
  • childhood exposure to ionising radiation (more predisposed to developing a tumour)
  • family history
  • immunosuppression - more susceptible to CNS lymphoma
321
Q

what are the symptoms of a brain tumour?

what features of each of these symptoms suggests a history more likely of a brain tumour

A
  1. headaches
    - caused by raised ICP
    - woken up by headache
    - worse in the morning and when lying down
    - associated with nausea and vomiting
    - worse by coughing/sneezing
  2. Seizures
    - lower grade tumours more likely to present
    - type and characteristics of the seizure depend on where the tumour is
  3. Focal symptoms
    - where in the lobes would give rise to the focal symptoms seen i.e loss of function of that area
322
Q

what genetic factors are oligodendrogliomas associated with

A

1p19q co-deletion

IDH1 mutation

323
Q

what are 3 features of an oligodendroglioma?

A
  • calcification of tumour
  • round uniform nuclei with cytoplasmic clearing
  • in grade III can have vascular proliferation
324
Q

what are the signs suggestive of a brain tumour

A 
papilloedema 
Focal neurological deficit (rapidly progressing is a red flag!) 
- hemiparesis
- hemisensory loss
- visual field defect 
- dysphagia
325
Q

what investigations would you do in a suspected brain tumour?

A 
MRI head 
MR angiography sometimes necessary to define site or blood supply of the mass 
Brain biopsy (histology and molecular markers)
326
Q

what tests are included in low grade protocol scanning or brain tumours?

A
  • blood flow through mass
  • MR spectroscopy - chemical composition of mass (do not want there to be high lactate peaks)
  • serial scans to measure the rate of growth
  • contrast dye to see if the tumour enhances
327
Q

what is the treatment for a high grade glioma?

A
  • treat the oedema surrounding the tumour with corticosteroids
  • surgery : ideally resection - as much of the mass as possible
  • radical radiotherapy
  • chemotherapy
328
Q

what is the treatment for a low grade glioma?

A
  • surgery : early resection

- radiotherapy and chemotherapy

329
Q

what is the pathophysiology of raised intracranial pressure?

A
  1. as volume of the lesion begins to increase initially there is a compensatory phase caused by a reduction in CSF volume so there is no rise in pressure
  2. then there is an exponential increase in pressure and lesion starts to press on adjacent structures
330
Q

what are the three layers of the cerebellum?

A
  1. molecular layer - gray matter
  2. purkinje layer - single layer with large purkinje cells
  3. granular layer - white matter
331
Q

what is cerebellar dysfunction usually caused by

A

loss of the purkinje cells

332
Q

what are the signs of cerebellar ataxia?

A 
DANISH
Dysdiadochokinaesia 
Ataxia (limb, gait, truncal)
Nystagmus 
Intention tremor
Slurred speech (can be staccato speech) 
Hypotonia
333
Q

what are the 4 main classifications of cerebellar ataxia?

A
  1. congenital
  2. diseases where ataxia is only one of the many features and may not be the main one
  3. familial ataxias (1/3)
  4. sporadic (acquired) ataxia
334
Q

what are 4 subtypes of sporadic (acquired) ataxias?

A
  • toxic : alcohol
  • immune mediated ; gluten ataxia
  • neurodegenerative ; multi-system atrophy
  • idiopathic sporadic
  • vascular
335
Q

investigations in cerebellar ataxia?

what is pathognomonic sign of multi system atrophy?

A

MRI brain scan

  • can exclude obvious structural problems
  • hot cross bun sign
336
Q

investigations in secondary brain tumours?

A
  • MRI head

- CT/MRI abdomen and chest

337
Q

aetiology of spinal cord compression

A
  • disc prolapse

- secondary malignancy, spinal metastases (most commonly associated with lung, prostate, breast)

338
Q

what is the clinical presentation of spinal cord compression

A
  • progressive bilateral weakness of legs
  • UMN signs below the level of the lesion
  • LMN signs at the level of the lesion
  • back pain
  • sensory loss below the level of the lesion
339
Q

investigations in suspected spinal cord compression

A

MRI spine
CXR of chest - primary lung malignancy
Bloods

340
Q

Treatment for spinal cord compression

A
  • dexamethasone

- surgical decompression

341
Q

what is the pathophysiology of cauda equina syndrome

A

nerve root compression caudal to the termination of the spinal cord at L1/2

342
Q

aetiology of cauda equina syndrome

A

herniation of lumbar disc (most commonly L4/5 + L5/S1)
tumour
trauma

343
Q

Clinical presentation of cauda equina syndrome

A

major difference is that leg weakness is flaccid and areflexic

  • bilateral sciatica - sensory loss/pain in the back of thigh/leg + lateral aspect of little toe
  • bladder/bowel dysfunction (decreased sphincter tone)
  • back pain
  • saddle anaesthesia
344
Q

investigations of cauda equina syndrome

A

MRI of spinal cord

345
Q

Treatment of cauda equina syndrome

A

surgery for emergency pressure relief + conservative treatment

346
Q

what is the pathophysiology of carpal tunnel syndrome?

A

inflammation of the carpal tunnel leads to entrapment of the median nerve at the wrist causing pain and loss of sensation

347
Q

aetiology of carpal tunnel syndrome?

A
  • anything causing swelling/compression of the tunnel
  • rheumatoid arthritis
  • local tumours (lipomas)
  • myxoedema
348
Q

clinical presentation of carpal tunnel syndrome

A
  • aching pain in the hand and arm (especially at night)
  • paraesthesia in thumb, index and middle fingers relieved by dangling hand over the edge of the bed and shaking (wake and shake)
  • sensory loss
  • weakness of abductor pollicis brevis +/- wasting of thenar eminence
349
Q

investigations in carpal tunnel

A
  • neurophysiological examination (nerve conduction studies)
  • Phalen’s test - patient can only maximally flex wrist for 1 minute
  • Tinel’s test - tapping on nerve at wrist induces tingling
350
Q

what is the treatment for carpal tunnel

A
  • splinting

- local steroid injections +/- decompression surgery

351
Q

what muscles does the median nerve innervate

A

LLOAF

  • 2x lumbricals
  • opponens policis
  • abductor pollicis brevis
  • flexor pollicis brevis
352
Q

what is a mononeuropathy

A

1 nerve involved

353
Q

what are the 4 types of nerve fibre ? and are they myelination or not? are they large or small? what do they transmit?

A

large myelinated
A-alpha : proprioception
A-beta : light touch, pressure, vibration

small
A-gamma (myelinated) - pain and cold
C (unmyelinated) - pain and hot

354
Q

how are polyneuropathies classified?

A

large fibre vs small fibre
chronic vs acute
axonal vs demyelinating

355
Q

what are the three patterns of clinical presentation of chronic axonal polyneuropathies

A
  1. symmetrical sensorimotor
  2. asymmetrical sensory
  3. asymmetrical sensorimotor.
356
Q

clinical presentation of a symmetrical sensorimotor polyneuropathy?

A
  • long fibres are affected first
  • tingling/pain in soles / fingertips
  • if untreated becomes more proximal
  • eventually motor symptoms develop after sensory to become sensorimotor
357
Q

clinical presentation of an asymmetrical sensory polyneuropathy ?

A
  • only sensory

- patchy distribution of symptoms, do not follow a specific nerve/root distribution

358
Q

name 1 cause for an asymmetrical sensory polyneuropathy

A
  • paraneoplastic

- gluten sensitivity or coeliac disease

359
Q

what is the clinical presentation of asymmetrical sensorimotor polyneuropathy?

A 
multiple mononeuropathies (mononeuritis multiplex)
not specific pattern as multiple nerves are affected, not all at the same time
360
Q

one cause of asymmetrical sensorimotor polyneuropathy?

A

vasculitis

361
Q

aetiology of peripheral neuropathies ?

A 
DAVID
Diabetes 
Alcohol 
Vitamin deficiency (B12) 
Infective (HIV, hepatitis)
Drugs
362
Q

investigations in suspected peripheral neuropathies?

what does the neurophysiological examination show / identify?

A
  • history
  • clinical examination (reduced or absent tendon reflexes, sensory deficit, weakness and muscle atrophies)
  • neurophysiological examination (nerve conduction studies identify the extent/severity of the peripheral neuropathy and type)
363
Q

what difference would a nerve conduction study show between an axonal neuropathy and a demyelinating neuropathy?

A

axonal - reduced responses (amplitude decreased) of the potentials because of loss of axons

demyelinating - slow conduction velocities

364
Q

what would be lost in a median nerve lesion at the wrist?

A
  • precision grip (LLOAF muscles)

- sensory loss of radial 3.5 fingers and palm

365
Q

what are the signs of an ulnar nerve lesion? (C7-T1)

When would the ulnar nerve be susceptible to damage

A

weakness/wasting of:
- interossei (cannot cross fingers in good luck sign)
- medial lumbricals (ulnar claw)
-hypothenar eminence
sensory loss over medial 1.5 fingers and the ulnar side of the hand

elbow trauma

366
Q

what are the signs of radial nerve lesion ? (C5-T1)

what could cause damage to the radial nerve?

A
  • wrist and finger drop
    muscles involved: BEAST : brachioradialis, extensors, abductor pollicis longus, supinator, triceps

compression against the humerus

367
Q

aetiology of brachial plexus mononeuropathy?

signs of brachial plexus mononeuropathy?

A
  • trauma, radiotherapy, prolonged heavy rucksack

- pain/paraesthesia and weakness in affected arm in variable distribution

368
Q

aetiology of phrenic nerve mononeuropathy?

signs of phrenic nerve mononeuropathy?

A
  • lung cancer, myeloma, TB

- orthopnoea (shortness of breath) with raised hemidiaphragm on CXR

369
Q

signs of lateral cutaneous nerve of the thigh mononeuropathy? (L2-L3)

A

meralgia paraesthetica - antero-lateral burning thigh pain from entrapment under the inguinal ligament

370
Q

aetiology of sciatic nerve neuropathy? (L4-S3)

signs of sciatic nerve neuropathy?

A
  • damaged by pelvic tumours or fractures to the pelvis/femur
  • sensory loss below the knee laterally
  • foot drop
371
Q

aetiology of common peroneal nerve (L4-S1) neuropathy?

signs of common peroneal nerve neuropathy?

A
  • often damaged as it winds round the fibular head from trauma or sitting cross legged
  • foot drop
  • weak ankle dorsiflexion
  • sensory loss over dorsal foot
372
Q

signs of tibial nerve (L4-S3) neuropathy?

A

inability to tiptoe (plantarflexion), invert foot or flex toes
sensory loss over sole

373
Q

what does a left optic nerve lesion cause

A

left anopia (blindness in left eye)

374
Q

what does an optic chiasm lesion cause

A

bitemporal hemianopia

375
Q

what does a L optic tract lesion cause

A

contralateral (right) homonymous hemianopia

376
Q

what does a lesion in the L Baum’s (parietal) loop cause

A

inferior right homonymous quadrantanopia

377
Q

what does a lesion in the L Meyer’s (temporal) loop cause ?

A

superior right homonymous quadrantanopia

378
Q

what are the signs of a third cranial nerve palsy?

A

ptosis
fixed dilated pupil (caused by the parasympathetic fibres of III damaged)
eye looks down and out

379
Q

what are the signs of a IVth nerve palsy?

A

diplopia on looking down and in

380
Q

signs of VIth nerve palsy?

A

horizontal diplopia on looking out

381
Q

signs of Vth nerve palsy?

A

when open mouth the jaw deviates to the side of lesion
muscles of mastication affected
corneal reflex lost

382
Q

signs of VIIth lesion

A

Bell’s palsy
face droop and weakness
forehead sparing (only bottom 2/3 are affected in UMN lesions)

383
Q

signs of IX and Xth lesion?

A

when saying ah, uvula deviates away from the side of the lesion
gag reflex lost

384
Q

sign of XIIth lesion?

A

tongue deviates to the side of the lesion

385
Q

what are the three ‘clusters’ of cranial nerves?

A
  1. 3,4,5,6 all run in cavernous sinus
  2. 7,8 run through petrous part of the temporal bone through the internal acoustic meatus
  3. 9,10,11,12 all exit through jugular foramen
386
Q

what is cavernous sinus syndrome?

A

combination of facial numbness and the eye on that side not moving +/- dilated pupil

387
Q

what is the pathophysiology of myasthenia gravis?

A

autoimmune disorder
antibodies to nicotinic acetylcholine receptors on the post synaptic side of the NMJ
leads to less working post synaptic receptor sites leading to fewer action potentials firing, blocking the excitatory effect of ACh on the nicotinic receptors

both B and T cells are implicated

388
Q

aetiology of myasthenia gravis?

A 
associated with autoimmune disease (esp rheumatoid arthritis and SLE) 
thymic hyperplasia (under 50 + female)
thymic atrophy/tumour (over 50 + male)
389
Q

symptoms of myasthenia gravis?

A

slowly increasing or relapsing muscular fatigue
order that muscles are affected:
extra-ocular > bulbar > face > neck > limb girdle > trunk

390
Q

name three things that can exacerbate myasthenia gravis?

A 
pregnancy
infection
emotion
exercise 
hypokalemia
391
Q

signs of myasthenia gravis

A 
ptosis 
diplopia 
dysphasia
dysarthria 
myasthenic snarl on smiling
392
Q

investigations in suspected myasthenia gravis

A
  1. serum antibodies : increased anti-ACh antibodies, muscle specific tyrosine kinase
  2. electromyogram : decremental muscle response to repetitive nerve stimulation
  3. ask patient to count to 50 - voice fades
  4. CT to exclude thymoma
393
Q

treatment in myasthenia gravis?

A
  1. symptom control : anticholinesterase (pyridostigmine)
  2. immunosuppression : treat relapses with prednisolone
  3. thymectomy may be needed (esp in younger patients)
394
Q

pathophysiology of Huntington’s disease ?

A

presence of mutant protein which causes loss of neurones in the striatum (caudate nucleus and putamen) of the basal ganglia, causing depletion of the GABA (inhibitory) and acetylcholine neurotransmitters
Less regulation of dopamine to the striatum causes increased movement

395
Q

aetiology of Huntington’s disease?

A
  • autosomal dominant inheritance
  • CAG repear in the Huntington protein gene (HTT) on chromosome 4
  • more than 35 CAG repeats = HD
  • number of repeats can be indicative of age of onset and severity
  • usually presents in middle age (30-40s)
396
Q

what is the clinical presentation of HD?

A 
Early
- irritability and depression
- personality change 
Later
- chorea (jerky/twitching movements that become more pronounced as disease progresses) 
- dementia +/- fits 
- psychiatric problems
397
Q

investigations into suspected Huntington’s?

A

Genetic diagnosis

MRI head shows striatum atrophy in moderate - severe disease

398
Q

Treatment of Huntington’s disease?

A
  • no cure
  • counselling for patient and family
  • treat chorea symptoms with benzodiazepines, sodium valproate
  • treat depression with SSRIs like citalopram
  • treat aggressive behaviour with antipsychotics like risperidone
  • genetic counselling
399
Q

what is the treatment for chronic peripheral polyneuropathies

A

always symptomatic - usually the damage that has been done to the nerve is not reversible

pain relief : amitryptilline, gabapentin, pregablin
cramps : quinine
balance : physiotherapy / walking aids

400
Q

what is the pathophysiology of Guillain-Barre Syndrome?

A

acute inflammatory demyelinating polyneuropathy

demyelination and axonal degeneration due to a trigger causing antibodies to attack nerves

401
Q

aetiology of GBS?

A
  • presents a few weeks later post infection

- this trigger causes antibodies which attack the nerves

402
Q

what are the common infections that can trigger GBS?

A

usually resp or GI tract

  • campylobacter jejuni
  • Cytomegalovirus
  • Epstein Barr Virus
403
Q

clinical presentation of GBS?

A
  • rapid progressive symmetrical ascending (starts in toes) muscle weakness a few weeks post infection
  • pain in back and limbs
  • proximal muscles are more affected like the trunk, respiratory and cranial nerves (VII)
  • sweating, increased pulse and BP changes
404
Q

investigations into GBS?

A

nerve conduction studies - slow conduction
lumbar puncture - CSF has raised protein with normal WCC
monitor FVC for resp involvement

405
Q

treatment of GBS?

A

IV immunoglobulin or plasma exchange

ventilation if resp muscles involved

406
Q

major side effect of sodium valproate ?

A

teratogenic (disturbs development of fetus)

Phase 2A (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions