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Easter revision 2018 > Neuro > Flashcards

Neuro Flashcards

1
Q

Where does cauda equina start?

A

T12/L1

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2
Q

Is the cauda equina part of SNS or PNS?

A

PNS

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3
Q

Condition where posterior neuropore of neural tube fails to close?

A

Rachischisis

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4
Q

Does spina bifida have neurological deficits?

A

Yes! But no cognitive deficit

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5
Q

Causes of hydrocephalus?

A

Spina bifida, cerebral aqueduct stenosis

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6
Q

Types of spina bifida?

A

Occulta, meningocele (arachnoid only), myelomeningocele (arachnoid and neural tissue)

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7
Q

How can we detect neural tube defects prenatally?

A

Serum alpha fetoprotein

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8
Q

What is an arnold-chiari malformation?

A

Cerebellum sits in foramen magnum, hydrocephalus results. Type II chiari malformations due to myelomeningocele.

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9
Q

Why do we have a cauda equina?

A

Because after 3mo’s the vertebral column grows faster than the cord

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10
Q

What do neural crest cells become?

A

Dorsal root ganglions, bones of face and skull, melanocytes, adrenal medulla, schwann cells

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11
Q

Why are neural crest cells so vulnerable to teratogens?

A

They have a very complex migratory pattern

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12
Q

Name two genetic diseases associated with neural crest cells?

A

Hirschprung’s disease- nerves missing from GI so constipation
DiGeorge- problem in neural crest migration e.g. leading to abnormal facies, thyroid problems, cardiac defects

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13
Q

Where do somatic reflex arcs synapse?

A

ventral horn of spinal cord

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14
Q

What is the jendrassik maneouvre?

A

clench teeth and lock hands and pull, easier to elicit reflexes

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15
Q

What do you use gadolinium for?

A

Can reveal vascular tumours or meningiomas on MRIs because it doesn’t cross the BBB normally and will reveal if the BBB has been breached

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16
Q

Name the three types of glia

A

Astrocytes, oligodendrocytes, microglia

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17
Q

What do astrocytes do?

A

Provide lactate (neurons can’t store glycogen so need lactate for citric acid cycle for ATP), re-uptake of neurotransmitters and to mop up K+

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18
Q

Astrocytes and oligodendrocytes are from ____, microglia are from ____

A

astro and oligo from ectoderm, microglia from mesoderm

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19
Q

Name layers of the BBB

A

Lumen of capillary, basement membrane and endothelial cells surround it, then pericytes are around endothelial cells and can make capillaries contract, then foot processes of astrocytes

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20
Q

Can T cells enter the CNS?

A

Yes, but then something in the brain inhibits a pro-inflam response

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21
Q

What channel opens in neurons that triggers release of presynaptic neurotransmitter?

A

Calcium channels

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22
Q

Name inhibitory neurotransmitters of CNS

A

Glycine, GABA

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23
Q

Name mixed + and - neuroTs of CNS

A

NA, 5-HT, dopamine

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24
Q

Name activatory neuroTs of CNS

A

Glutamate, ACh

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25
Q

Name amino acid neuroTs

A

GABA, glycine, glutamate

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26
Q

Name biogenic amine neuroTs

A

ACh, NA, dopamine, 5-HT

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27
Q

Location of ACh neurons

A

Basic ace- nucleus basalis & septal neurones

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28
Q

Location of dopamine neurons

A

Nigrostriatal pathway, mesolimbic, mesocortical

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29
Q

Location of NA neurons

A

Locus coeruleus of pons

Medulla

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30
Q

Location of 5-HT neurons

A

Brainstem raphe nucleus

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31
Q

Are you aroused in this locus?

A

NA!

Na is the neuroT, locus ceruleus is the place

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32
Q

What does ACh have a role in?

A

Arousal. In the nucleus basalis, arousal is basic

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33
Q

What are the dopamine pathways roles?

A

Nigrostriatal is motor control, mesolimbic/cortical are mood, arousal, reward.

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34
Q

Two neuroTs involved in patellar reflex?

A

Glutamate to activate effector quadriceps, glycine to inhibit hamstrings to relax them

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35
Q

What are the jobs of the cerebellar peduncles and the cerebral peduncles?

A

Cerebellar peduncles attach cerebellum to brainstem and cerebral peduncles (crux cerebri) attach cerebrum to brainstem

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36
Q

Where is the tectum? (and what does it consist of)

A

Dorsal part of midbrain. The superior and inferior colliculi together make the tectum

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37
Q

What do the medullary pyramids do?

A

Descending motor pathways

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38
Q

How is glycine involved in sleep?

A

Glycine in the basal ganglia paralyses LMNs in sleep

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39
Q

What do arachnoid granulations do?

A

Transfer CSF from subarachnoid space into dural venous sinuses

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40
Q

What do the neural tube and the neural canal become?

A

The neural tube becomes the tissue of the CNS and the neural canal becomes the ventricular system

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41
Q

What is white matter?

A

Axons and glial cells

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42
Q

What structures is ventricle IV associated with?

A

Pons, medulla, cerebellum

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43
Q

Where are ventral and dorsal root cell bodies found, respectively?

A

Ventral root cell bodies are in the gray matter of the spinal cord and dorsal root cell bodies are in ganglia

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44
Q

What meningeal layers cover the spinal cord?

A

Pia, arachnoid and dura, and the arachnoid and dura are very tightly connected together and CSF circulates in subarachnoid space

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45
Q

Where does C8 emerge?

A

Between vertebrae C7 and T1

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46
Q

What is the conus medullaris?

A

Terminal end of the spinal cord at L1/2. Cauda equina is below (which is dorsal and ventral roots below the conus medularis)

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47
Q

What’s a safe level for LP?

A

L3/4. Go lower in babies because their conus medullaris is at L3.

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48
Q

Which modalities travel in spinothalamic?

A

Temperature, pain, pressure (crude touch)

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49
Q

Which modalities travel in dorsal column?

A

Two-point discrimination, fine touch, vibration, propioception

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50
Q

How does the acuity of a sensory neuron relate to the size of its receptive field?

A

Big receptive field = lower acuity, small receptive field = higher acuity

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51
Q

Does the brain think in terms of dermatomes?

A

No, it converts them to the homunculus

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52
Q

What nerve symptoms can a patient with vitamin B12 deficiency (e.g. due to pernicious anemia where intrinsic factor not made)?

A

Glossitis, parasthesia, muscle weakness (due to denervation of dorsal column and sometimes lateral columns)

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53
Q

Hirschsprung’s disease?

A

Absence of ganglions in GI causing constipation and need for surgery

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54
Q

Where would vibration from the leg travel (in which side) and where would it synapse (in which nuclei)

A

Enters the dorsal column medially and synapses in the gracile nucleus of the medulla

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55
Q

Where would vibration from the arm travel (in which side) and where would it synapse (in which nuclei)

A

In the lateral side of the dorsal column, synapsing in the cuneate nucleus of the medulla

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56
Q

Where are upper and lower body in the spinothalamic tract

A

Upper is deep

Lower is superficial

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57
Q

What are c and a fibres

A

C are pain

A are mechanosensory and can activate inhibitory interneurones to inhibit pain eg if rubbing

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58
Q

Where do DC and ST fibres decussate

A

DC decussates in medulla (gracile and cuneate nuclei)

ST decussates in dorsal horn of spinal cord

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59
Q

Where do DC and ST fibres swap lower and upper fibre positions to be in the right position for the homunculus

A

DC lower fibres start medially, after the medulla they decussate and swap sides so still medial on their contralateral side
ST lower fibres synapse in dorsal horn and decussate, go to contralateral side in same positions so need a swap over in the tertiary neurones in cortex

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60
Q

Describe Brown-Sequard

A

When one half of the spinal cord is damaged, you get DC (fine touch, 2 point, vibration, propio) damage on ipsilateral side because it hasn’t decussated yet and ST damage (crude touch, pain, temp) on ipsilateral side because its already decussated

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61
Q

What nerve symptoms might vegans present with?

A

Parasthesia and muscle weakness- can cause a B12 deficiency which denervates particularly posterior and sometimes lateral columns. Might also have a smooth tongue!

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62
Q

What’s syringomyelia?

A

Cyst in the spinal cord that expands over time, may be caused by a chiari malformation

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63
Q

What is lateral inhibition and which cells are responsible for it?

A

When one neuron becomes excited it reduces the activity of its neighbours. Horizontal cells do this.

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64
Q

What cells are present at the fovea?

A

Cone cells in high amounts
No ganglions
No bipolar cells

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65
Q

Describe the pathway of light information to the optic nerve

A

Through cornea, through lens, through the neural layer of the retina (ganglions then bipolar cells then photoreceptors) then the pigmented layer of the retina and then choroid

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66
Q

Describe the impulse pathway in the eye

A

Photoreceptors –> bipolar cells –> ganglions –> optic nerve

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67
Q

What technique do you use to look at the retina e.g. for retinal detachment

A

Optical coherence tomography

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68
Q

The right visual field is received by which orbit

A

The left side of the orbit

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69
Q

A lesion in the right optic nerve produces what deficit

A

Monocular vision loss

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70
Q

A lesion in the optic chiasm produces what deficit

A

Bitemporal hemianopia

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71
Q

A lesion in the right optic tract produces what deficit

A

Contralateral homonymous hemianopia (ie right orbit of both eyes, left visual field of both eyes)

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72
Q

A lesion in the right superior/parietal fibres produces what deficit

A

Contralateral inferior quandrantonopia

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73
Q

A lesion in the inferior/temporal fibres produces what deficit

A

Contralateral superior quandrantonopia

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74
Q

A posterior cerebral artery stroke produces what deficit

A

Contralateral homonymous hemianopia with macula sparing

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75
Q

What results in macula sparing

A

Posterior cerebral artery supplies most of occipital lobe where PVC is but the MIDDLE cerebral artery supplies the occipital pole which supplies the macula

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76
Q

Describe the pathway for the pupillary reflex

A

Light enters left eye, left optic nerve, optic chiasm, optic tract, splits to enter pretectal area, projects onto both EDW nuclei for consensual, ciliary ganglion, pupil constricts via sphincter pupillae

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77
Q

Describe the accomodation reflex in terms of contracting the ciliary muscle (and when you’d do this)

A

Optic nerve, optic chiasm, optic tract, LGN, pre-tectal area, EDW, CN III to ciliary ganglion, contracts ciliary muscle
If ciliary muscle is contracted, suspensory ligaments are slack, so lens is fat and the object is near

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78
Q

What are the three Cs of accomodation

A

Pupillary constriction, convergence (medial rectus) and convexity of lens

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79
Q

Why do you get glare with cataracts

A

Because of the contrast of light levels getting through cloudy patches vs clear patches

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80
Q

What is internuclear opthalmoplegia

A

Damage to the medial fasiculus (white matter tract) that is responsible for adducting affected eye when other eye moves laterally. Communicates between CNs III, IV, and VI and coordinates eye movements: responsible for optokinetic, saccadic and vestibulocular movements

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81
Q

What are optokinetic, saccadic and vestibulocular movements

A

Optokinetic- fixation on objects moving relative to head
Saccadic- quick eye movements
Vestibulocular- movement of eyes in relation to movement of head

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82
Q

In what disease could you get internuclear opthalmoplegia

A

MS- involves demyelination of white matter structures such as the medial fasiculus

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83
Q

Considering which structures are nearby, in a patient with a tumour in the cerebral aqueduct of the midbrain what eye symptoms could result?

A

Close to EDW- this is where accomodation occurs so eyes won’t accomodate. Also where it would signal to constrict the pupil so that won’t happen in the same eye
The oculomotor nucleus is also close- down and out eye

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84
Q 
Describe functions of the midbrain "mickey mouse": 
Ears
Eyes 
Tears
Nose 
Nose hairs
Mouth 
Lips
Double chin
A

Ears- cerebral peduncles so descending motor tracts
Eyes- red nuclei, motor function
Tears- medial lemniscus. Part of DC, ascending sensory tract on its way to the thalamus
Nose- CN III and EDW
Nose hairs- CN III fibres
Mouth- cerebral aqueduct
Lips- periaqueductal grey matter
Double chin- superior colliculus. Does reflex responses of visual system eg look at lightning. Inferior colliculus at lower levels does reflexes to auditory stimuli

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85
Q

Which two paired arteries supply the brain?

A

Internal carotid and vertebral arteries

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86
Q

Name the branches of the internal carotid that form the circle of willis

A

(Opthalmic artery), posterior communicating, anterior cerebral, and then continues as the middle cerebral

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87
Q

How do the paired vertebral arteries contribute to the circle of willis?

A

Give off posterior inferior cerebellar artery, combine to form basilar artery, pontine arteries, anterior inferior cerebellar artery, superior cerebellar artery, end by birfurcating as the posterior cerebral artery

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88
Q

Where do the anterior, middle, and posterior cerebral arteries supply?

A

Anterior is misleading because its mostly medial at the front
Middle is lateral frontal and parietal, and superior temporal
Posterior is occipital and inferior temporal

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89
Q

What important branch of the middle cerebral artery is prone to emboli

A

Lenticulostriate branches- role in motor function

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90
Q

What do the pontine arteries of the basilar artery do and what condition results if there is a problem

A

Supply the pons

Locked in syndrome

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91
Q

Which vessels supply the cerebellum and where else do they help supply?

A

Superior cerebellum
Anterior inferior
Posterior inferior
Also supply the brainstem on their way down

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92
Q

Lenticulostriate vessels supply the…

A

Internal capsule

93
Q

Which neurones are involved in the motor pathway? (always descending)

A

UMN and LMN

94
Q

Where are UMNs and LMNs located

A

UMN are exclusively CNS, LMN has cell body in CNS but axon goes into PNS

95
Q

Where are the cell bodies of LMNs located

A

Either in the ventral horn of the spinal cord or the motor nuclei in the brainstem

96
Q

Describe the patellar reflex

A

Muscle spindle detects stretch in patellar tendon
Afferent fibre along L3 spinal nerve travels to ventral horn of spinal cord, where it synapses with a LMN that will send an efferent signal to contract the quads
The sensory neurone also sends a signal to an inhibitory interneurone at L5 which acts to inhibit the LMN for the hamstrings, relaxing them to allow contraction of the quads
This is called reciprocal inhibition

97
Q

What is reciprocal inhibition

A

In reflexes you inhibit one action to allow for activation of the other e.g. in patellar reflex the hamstrings are inhibited

98
Q

What is the purpose of tendon reflexes

A

Postural correction- e.g. if get blown by wind it will detect the extending and act to contract to bring you back to normal

99
Q

What is the babinski reflex

A

If stimulated on lateral border of foot this elicits plantarflexion in normal adults. In babies and people with UMN damage this causes plantarextension

100
Q

Name UMN damage signs

A

Hyperreflexia (because overall effect of UMNs on LMNs is inhbitiory)
Extensor Babinski
Hypertonia
Weakness

101
Q

Name LMN damage signs

A 
Areflexia 
Hypotonia 
Weakness 
Wasting
Fasiculation
102
Q

What is spinal shock

A

UMN signs (except weakness) take days-weeks to develop so UMN damage initially presents as LMN signs. This is because LMNs are initially depressed following UMN damage but later become excited

103
Q

Where are UMN cell bodies found

A

Precentral gyrus only

104
Q

Describe the journey from the cell body of an UMN for the lower limb to its target

A 
Starts in medial precentral gyrus 
Through corona radiata 
Internal capsule 
Enters midbrain via cerebral peduncles 
Enters medulla via medullary pyramids
Decussates in the medulla 
On other side is part of the lateral corticospinal tract in the lateral funiculus
Descends down spinal cord to synapse with LMN in ventral horn
105
Q

What is the lateral corticospinal tract

A

Part of the route of an UMN after it decussates in the medulla- it is responsible for fine, dextrous movements in the extremities e.g. hands

106
Q

How is the route of an UMN supplying the face different to other UMNs

A

It starts more laterally in the precentral gyrus, as normal descends through corona radiata and internal capsule but instead of decussating in the medulla it leaves the internal capsule to go in the corticobulbar tract

107
Q

Tell me about the facial motor nuclei and how it affects UMN lesions

A

So the facial motor nuclei to the upper face has bilateral UMN innervation but the lower face is unilateral. This means that if there is a lesion of the left UMN, this results in right lower face paralysis but not right upper face paralysis (because still receiving innervation from other side)
= UMN lesion is forehead sparing

108
Q

How will facial nerve lesions present compared to UMN lesions supplying face?

A

Facial nerve lesion = complete unilateral paralysis

UMN lesion supplying face = forehead sparing unilateral lower face paralysis

109
Q

What are the vestibulospinal and reticulospinal tracts?

A

Vestibulospinal- connects semicircular canals to spinal cord so allows postural changes with movement info
Reticulospinal- connects reticular formation to spinal cord so inhibitory pathways in sleep go through here

110
Q

How does the cerebellum connect with the brainstem and name the different parts of this structure

A

Cerebellar peduncles
Superior c.p. connects to midbrain
Middle c.p. connects to pons
Inferior c.p. connects to medulla

111
Q

Via what structure does the cerebellum communicate with the cortex

A

Thalamus

112
Q

Describe the structure of the cerebellum and what the different parts control

A

Vermis in the midline controls the trunk

The lateral hemispheres control the limbs

113
Q

Tracts in the cerebellum are ipsi/contra lateral?

A

Ipsilateral

114
Q

What is ataxia?

A

Lack of coordination

115
Q

What kind of symptoms could a vermis lesion cause

A

Pressing on 4th ventricle –> hydrocephalus
Truncal ataxia
Abnormal gait

116
Q

Describe symptoms of cerebellar disease

A 
DANISH
Dysdiadochokinesis 
Ataxia (e.g. ataxic gait)
Nystagmus 
Intention tremor 
Slurred speech
Hypotonia
117
Q

What is the basal ganglia

A 
Caudate nucleus 
Putamen 
Globus pallidus (interna and externa) 
Thalamus 
Substantia nigra (pars compacta and pars reticularis)
118
Q

What is the striatum

A

Putamen + caudate nucleus

119
Q

What is the lentiform nucleus

A

Putamen + globus pallidus

120
Q

Tell me about the substantia nigra

A

The pars compacta is more dorsal and has dopamingergic neurons- double D.
The pars reticularis is ventral

121
Q

Is dopamine excitatory or inhibitory?

A

Can be either!

122
Q

How do the direct and indirect pathways of the basal ganglia affect the thalamus with and without presence of dopamine?

A

Direct is excitatory to the thalamus and then more excitatory with dopamine
Indirect is inhibitory to the thalamus and then excitatory with dopamine

123
Q

What sort of symptoms do basal ganglia disorders cause

A

Dyskinesis, abnormal motor control, altered posture, altered muscle tone

124
Q

Define Parkinson’s disease

A

Chronic progressive movement disorder with unilateral bradykinesia, hypertonicity and resting tremor. Also micrographia, shuffling gait (risk of falls), depression, reduced facial expression, dementia, hypophonia.

125
Q

How does Parkinson’s disease affect the basal ganglia pathways

A

Direct without dopamine is overall stimulatory (but less so)

Indirect without dopamine is inhibitory

126
Q

Define Huntingdon’s disease

A

AD progressive neurodegenerative disorder, onset 30-50yrs. Chorea (abnormal jerky movements), dystonia, incoordination, cognitive decline, behavioural difficulties, abnormal gait. Occurs due to loss of GABAnergic neurones in the striatum (putamen + caudate nucleus)

127
Q

What is chorea

A

Abnormal jerky movements, occurs with Huntingdon’s disease

128
Q

How does Huntingdon’s cause its effects

A

Loss of gabanergic neurons in the striatum (caudate nucleus + putamen)

129
Q

Where is the subthalamic nucleus?

A

Just medial to the substantia nigra

130
Q

What is hemiballismus?

A

Dysfunction in contralateral subthalamic nucleus (structure just medial to substantia nigra). Causes large amplitude unilateral abnormal movement- sudden intense flailing motion. Often secondary to subcortical lacuna strokes

131
Q

What can a subcortical lacuna stroke cause?

A

Hemiballismus

132
Q

Following destruction of C3 and C4 spinal cord, at what levels would UMN and LMN signs appear?

A

C3 and C4 have had their LMNs destroyed so will have LMN signs (hyporeflexia, hypotonia) but below this LMNs are fine but have lost connections with UMNs so will have UMN signs (hyperreflexia, hypertonia), extensor plantar reflex

133
Q

How will motor signs be different if spinal cord damage is blunt or sharp?

A

If it is blunt it will destroy the LMNs in those segments so will get LMN signs there and UMN signs below
If it is sharp the LMNs themselves will be intact so just initial spinal shock (looks like LMN) and then UMN signs

134
Q

What is motor neurone disease?

A

Group of diseases with differential LMN and UMN involvement. ALS is both LMN and UMN, SMA is pure LMN

135
Q

What does this suggest: 73yo F left hand tremor, bilateral hypertonia (but more on L side), shuffling gait, paucity of movement

A

Parkinson’s- Suggests neurodegeneration in SNc (R side especially).

136
Q

Where is this lesion: 29yo F unsteady gait, vertigo, 3mo progression, impaired coordination (R side more), nystagmus, slurred speech

A

Right cerebellar hemisphere

137
Q

If having cerebellar surgery, what could you damage?

A

Brainstem, anything in jugular foramen (IX,X,XI), IAM (VII,VIII), vertebral arteries, occipital lobe

138
Q

Define dermatome and myotome

A 
Dermatome = area of skin supplied by a single spinal nerve 
Myotome = muscles supplied by a single ventral root
139
Q

What pattern is information arranged in the cord versus the brain, and where changes this organisation?

A

Spinal cord is dermatomal
Brain is homuncular
Thalamus changes the code

140
Q

What structure does the thalamus squash?

A

The third ventricle

141
Q

What colours are grey matter, white matter and CSF on a CT

A

CSF black
Grey matter white
White matter dark

142
Q

Name the parts of the internal capsule and where it runs between

A

Anterior limb, genu, posterior limb

Runs between cortex-thalamus

143
Q

Which part of brain do these go to:
Left visual fields –>
Superior visual fields –>
Inferior visual fields –>

A

Left to right hemisphere
Superior to inferior radiations
Inferior to superior radiations

144
Q

If the lateral ventricles inflated, what structures could they damage?

A

Corpus callosum, caudate nucleus, corona radiata, cortex

145
Q

If the third ventricle inflated, what could it damage?

A

Thalamus

146
Q

What is the medial lemniscus?

A

Part of the dorsal column between the medulla where the fibres decussate and the thalamus

147
Q

If the cerebral aqueduct expanded, what could it damage?

A

Passes through midbrain so could damage CN III motor nuclei, EDW, medial lemniscus, cerebral peduncles

148
Q

Which structures are immediately above and below the lateral ventricles?

A

Corpus callosum is above (with cingulate gyrus above that)

Fornix is below

149
Q

The internal capsule is between…

A

The globus pallidus interna and the thalamus

150
Q

Which structures are involved in motor planning

A

Prefrontal cortex thinks of movement it wants to do
Basal ganglia chooses a set of movements
Cerebellum looks at current position of limbs to decide which sequence the movements should be carried out in

151
Q

Where do inputs to the cortex come from?

A
  1. Other cortical neurones

2. The thalamus

152
Q

What is the major output of the cortex?

A

Pyramidal cells (excitatory neurones, particularly prominent in motor and premotor areas. UMNs are a type of pyramidal cells)

153
Q

What functions does the frontal lobe have

A

Judgment, social and sexual behaviour, personality, Broca’s area (motor component of speech), precentral gyrus so motor centre (inc. continence), memory, problem solving

154
Q

What functions does the parietal lobe have

A

Postcentral area so sensory centre, Wernicke’s area (comprehension of speech), calculation, writing, understanding body image, awareness of external environment, superior optic radiations

155
Q

Temporal lobe functions

A

Primary auditory cortex
Olfactory cortex
Inferior optic radiations pass through
Memory and emotion

156
Q

Tell me about cerebral lateralisation

A

Left hemisphere is normally language functions and calculation/logic
Right is normally body image, emotion, music, visuospatial awareness

157
Q

Why might you cut someone’s corpus callosum?

A

In epilepsy to prevent activity spreading from one hemisphere to the other

158
Q

Where are Broca’s and Wernicke’s areas located?

A

Broca lateral inferior frontal (near motor cortex)

Wernicke inferior parietal (near auditory cortex)

159
Q

How are Broca’s and Wernicke’s connected?

A

Arcuate fasciculus

160
Q

What are Broca’s and Wernicke’s aphasia?

A

Broca’s- can understand speech but has difficulty speaking

Wernicke’s- no problem speaking but problem understanding (fluent speech that doesn’t make sense)

161
Q

How do you speak a written word?

A

Visual cortex in the occipital lobe receives visual information → Wernicke’s area which converts visual signals into words → via arcuate fasiculus → Broca’s area makes motor plan → motor cortex in precentral gyrus to move the mouth

162
Q

How do you speak a thought?

A

Thoughts could come from anywhere in the cortex → Wernicke’s area comprehends these and turns into words → arcuate fasiculus → Broca’s area makes motor plan → motor cortex in precentral gyrus moves the mouth

163
Q

Name the two types of memory and where they are stored

A

Declarative (explicit facts)
Non-declarative (implicit, motor skills, emotion)
Declarative stored across cerebral cortex, non-declarative stored in cerebellum

164
Q

Name a part of the brain that’s important for consolidating declarative memories

A

Hippocampus- strengthens association between neurones by making them release more neuroTs, more post-synaptic Rs

165
Q

Define arousal

A

Being directed towards a goal or avoiding something noxious

166
Q

Define consciousness

A

Being aware of internal and external states

167
Q

What are the two ingredients for consciousness

A

Cerebral cortex and reticular formation

168
Q

What is the reticular formation

A

Important for consciousness, group of interneurones in the brainstem that communicates with the cortex and receives input from cortex and somatosensory system

169
Q

What are the three excitatory outputs of the reticular formation

A
  • -> basal forebrain nuclei –> ACh to excite cortex
  • -> hypothalamus –> histamine to excite cortex
  • -> thalamus –> glutamate to excite cortex
170
Q

Why can antihistamines and anticholinergics make you drowsy?

A

Outputs from the reticular formation:

  • basal forebrain nuclei use ACh to excite cortex
  • hypothalamus uses histamine to excite cortex
171
Q

What are the ascending fibres called that go between the reticular formation and its relay stations?

A

Reticular activating system

172
Q

What three things does the GCS assess?

A

eye opening, motor response, verbal response

173
Q

Name 2 ways to assess consciousness

A

GCS (scale)

EEG

174
Q

What do cortical neurones have a tendency to do?

A

Synchronise! This is what happens in sleep

175
Q

Describe a normal sleep

A

5-6 cycles of sleep, between REM-stage 1-stage 4- REM

176
Q

What are alpha and beta waves

A

Beta waves are eyes open or REM sleep, 50Hz frequency

Alpha waves are eyes closed- less inputs to brain so more synchrony, waves slow down 10Hz

177
Q

What is stage 1 sleep

A

Background of alpha waves (10Hz) with some theta waves (5Hz)

178
Q

What is stage 2/3 sleep

A

Background of theta waves (5Hz) with final death throws called sleep spindles and big broad K complexes

179
Q

What is stage 4 sleep

A

Dominated by K complexes which here are called delta waves (1Hz)

180
Q

What area is responsible for REM sleep?

A

Pons

181
Q

Why is it hard to wake people up in REM sleep?

A

The thalamus is strongly inhibited so its hard to get inputs up to the cortex

182
Q

Why do you get floppy limbs in sleep?

A

The RF sends glycinergic projections down to LMNs to inhibit them

183
Q

Why do you get nocturnal bruxism?

A

Teeth grinding at night even though limbs are floppy is because teeth grinding is controlled by cranial nerves which reside in the brainstem, rather than LMNs in the spinal cord (which are inhibited by glycine)

184
Q

What other things happen in REM?

A

Consolidation of knowledge and autonomic effects such as penile erection

185
Q

Compare and contrast coma and persistent vegetative state

A

Coma- widespread cortical and brainstem damage, no sleep-wake cycle, unresponsive to stimuli
Persistent vegetative state- sleep-wake cycle detectable, cortex is damaged but RF is relatively spared, can respond to stimuli via brainstem reflexes, some spontaneous eye opening

186
Q

What is locked in syndrome

A

Fully conscious but no control of body (cortex is fine but pons is not)- caused by damage to pontine artery

187
Q

Name ways in which infection could reach brain

A

In the blood e.g. meningitis
Direct spread e.g. basal skull fracture, infection in danger triangle
Iatrogenic e.g. LP

188
Q

Define meningitis

A

Inflammation of the leptomeninges (arachnoid and pia), with or without septicaemia

189
Q

Name causative organisms of meningitis at different ages

A

Babies: e.coli, listeria monocytogenes
2-5: Haemophilus influenza type B (hence vaccine happens then)
5-30: neisseria meningitidis

190
Q

Define SIRS, sepsis, severe sepsis, septic shock

A

SIRS is resp rate over 20, temp over 38 or less than 36
Sepsis is SIRS with infection confirmed
Severe sepsis is sepsis with organ failure, hypotension, hypoperfusion
Septic shock is when hypotension won’t respond to fluids

191
Q

Typically encephalitis (i.e. infecting neurones) is what type of organism? Give examples

A

Viral

e.g. rabies affects brainstem, herpes affects temporal lobe

192
Q

Viral replication within neurones (as in encephalitis) produces which microscopic pathology

A

Inclusion bodies (look like owl’s eyes)

193
Q

How does encephalitis present and how should you treat

A

Less acutely than meningitis with headaches, vomiting, photophobia. Manage supportively

194
Q

Define dementia

A

Global loss of intellect, reason and personality without damage to consciousness. Most common cause is Alzheimer’s (also Lewy body, vascular, Picks disease)

195
Q

What is Alzheimer’s disease

A

Most common cause of dementia. An exaggerated ageing process with senile atrophy (loss of cortical neurones), wider sulci and narrower gyri
Tau proteins become hyperphosphorylated and clumps –> neurofibrillary tangles
Amyloid proteins abnormal –> amyloid plaques

196
Q

Name a cause of familial Alzheimer’s disease and why it causes this

A

Down’s syndrome (30-40yo). Chromosome 21 encodes for amyloid precursor protein, presinilin genes 1 and 2 (which break amyloid down). So problems with these –> abnormal amyloid –> amyloid plaques

197
Q

What is ICP normally, on coughing/straining, and what level must it be lower than

A

Normally 10mmHg
On coughing 20mmHg
Must be lower than the systolic BP otherwise blood can’t get here

198
Q

Up to what level can vascular mechanisms keep ICP compensated? Beyond this what happened?

A

Up to 60mmHg

Above this you get hypertension so that the BP is higher than the ICP

199
Q

What is Cushing’s reflex?

A

Hypertension (need BP to be higher than ICP to maintain perfusion)
Bradykinesia (aortic arch baroreceptors trigger vagus)
Low resp rate (ischaemia to medulla respiratory centres)

200
Q

Name three types of brain herniation

A

Subfalcine- cingulate gyrus pushed under falx cerebrum (may be asymptomatic, haemorrhage, ischaemia, contralateral leg weakness)
Uncal/tentorial- uncus goes through tentorium (presses on midbrain, CN III, cerebral peduncle so contra leg weakness)
Cerebellar- “coning”, cerebellum into foramen magnum (reduced consciousness, resp and heart dysfunction)

201
Q

Name benign and malignant CNS tumours

A

Benign- meningioma

Malignant- most common is mets to the brain (lung, colon). Also astrocytomas

202
Q

Risk factors for stroke

A

HTN, hyperlipidemia, DM

203
Q

Name categories of stroke

A

Ischaemic (80%)- normally from embolism

Haemorrhagic (20%)

204
Q

What is a subarachnoid haemorrhage

A

Rupture of a berry aneurysm (abnormal outpouching of vessel). Risks are HTN, male, PCKD. Sudden thunderclap headache

205
Q

Define dementia

A

Progressive decline in cognitive function leading to global impairment of memory, intellect and personality that affects ability to cope with daily living

206
Q

Name reversible causes of dementia

A

Depression, trauma, vitamin deficiency, alcohol, thyroid disorders

207
Q

Describe possible presenting symptoms of dementia

A

altered personality, wandering, anomic aphasia (can’t retrieve word they want), dysphagia, reduction in food intake, apraxia

208
Q

What should you do if patient presents with possible dementia

A 
MMSE (mini mental state exam) to ascertain baseline 
Check for reversible causes of dementia 
Full neuro exam
CT/MRI 
Memory clinic refer
209
Q

Describe delirium

A

Acute confused state that has presented suddenly e.g. fall, severe pain, constipation, UTI. Signs are fluctuating mental status, fluctuating agitated/very quiet, inattention, disorganised thinking

210
Q

What score do you test for dementia and delirium

A 
Dementia MMSE
Delirium CAM (confusion assessment method)
211
Q

Describe the progression of dementia from AD, Lewy body, and vascular

A

AD- slope
Vascular- step wise
Lewy body- loopy up and down

212
Q

How does dementia with lewy bodies link to Parkinson’s?

A

Parkinson’s is Lewy bodies in the substantia nigra
In dementia w LB they are in the SN and the cortex, presenting with bradykinesia and resting tremor PLUS visual hallucinations, cognitive impairment, frequent falls

213
Q

Describe management of dementia

A

Meds: can give acetylcholinerase for mild/mod AD but doesn’t work in most
Family: discuss care, mental capacity to make decisions now and in the future
Memory aids and therapies (pets, babies)

214
Q

Define seizure

A

A sudden irregular discharge of electrical activity in the brain causing symptoms e.g. sensory disturbance, convulsions

215
Q

What is status epilepticus

A

Continuous epileptic seizures without recovery of consciousness in between, a medical emergency, may become cyanotic

216
Q

What are the first and second most common partial seizures and what makes them more likely to occur

A

First- temporal lobe epilepsy (often comes with auras). More common in 1st/2nd decade following fever or early brain injury
Second most common parietal lobe

217
Q

Name the five types of generalised seizures

A 
Affect whole brain 
Absence (daydreaming)
Myoclonic (break muscle jerking)
Tonic (increased tone)
Atonic (drop to floor)
Tonic-clonic (increased tone then convulsions)
218
Q

Give causes of epilepsy

A 
Vascular- stroke, TIA
Infection- TB, meningitis
Trauma- intracerebral haemorrhage
Autoimmune- SLE
Metabolic- hypoxia, hypoglycaemia, thyroid
Iatrogenic- drugs
Neoplastic
Congenital
219
Q

Describe management of epilepsy

A

Acutely ABCDE and benzos (lorazepam, diazepam- GABAa agonists)
MRI for new onset seizures, EEG can support diagnosis but not diagnose

220
Q

How does dementia most commonly result in death

A

Dysphagia and aspiration

221
Q

Diagnose: patient with one sided weakness and sensory loss in limb/genitals plus urinary incontinence

A

ACA stroke

UI from paracentral lobules in medial frontal and parietal

222
Q

Diagnose: patient with one sided weakness and sensory loss in upper limb/face plus leg, contralateral hemianopia, hemispatial neglect, global aphasia,

A

MCA stroke

Face too because its affected internal capsule (MCA branches lenticulostriate artery)

223
Q

Diagnose: patient with contralateral heminanopia with macula sparing

A

PCA stroke

224
Q

Diagnose: patient with DANISH symptoms and R sided oculomotor deficit and L sided weakness

A

Cerebellar artery stroke

Get crossed deficits (ipsilateral CN with contralateral long nerves)

225
Q

Diagnose: fully conscious but no motor control

A

Basilar artery/pontine artery stroke

226
Q

Diagnose: blindess from a stroke

A

Basilar artery stroke (bilateral loss of PVC occipital lobe supply)

227
Q

Hyperdense =, hypodense =

A

Hyperdense is white!

Hypodense is black

228
Q

Name non stroke causes of weakness/dysphagia

A

Hypoglycemia
Epilepsy
Intracranial tumours
Migraine

Easter revision 2018 (11 decks)

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