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Y2S1- Neuro, GI, Liver > Neuroscience > Flashcards

Neuroscience Flashcards

1
Q

what does a Lower motor neurone control

A

A lower motor neurone typically controls a focal anatomically adjacent group of muscle fibres. These systems are typically concerned with individual muscle movements.

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2
Q

what does a upper motor neurone control

A

Upper motor neurones control lower motor neurones. Upper motor neurone systems are generally more concerned with actions involving groups of muscles.

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3
Q

motor end plates

A

Axons of LMNs terminate in the muscles to control the muscles.
Motor end plates (myoneural junctions) consist of the motor nerve fibre ending and the sub adjacent part of muscle fibres.

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4
Q

NMJ constituents

A

The nerve enters the muscles, the motor axon runs in the nerve, the motor axon controls the muscles: axon + muscle= NMJ

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5
Q

process of contraction at NMJ

A

Electrical impulse goes down from the nerve and causes release of ACh which activates it’s receptor. There is an ongoing electrical impulse that causes contraction in the skeletal muscle.
Skeletal muscle= ACh

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6
Q

motor unit

A

A motor unit is a motor neurone and the muscle fibres supplied by that neurone. The number of muscle fibres in a motor unit depends on the need for precision in movement.

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7
Q

cell body locations of limb, truncal and bulbar muscles

A

Limb muscles: cell bodies in spinal cord grey matter axons travel in roots/peripheral nerves
Truncal muscles: cell bodies in spinal cord grey matter axons travel in roots/thoracic nerves
Bulbar muscles: cell bodies in brain stem motor nuclei axons travel in cranial nerves

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8
Q

upper limb nerve roots

A

C5 C6 C7

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9
Q

lower limb nerve root

A

L5

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10
Q

corticospinal system

A
  • Motor control of trunk & limb musculature
  • UMN control of LMNs in the spinal cord
  • Cell bodies in the cerebral cortex and axons run through the internal capsule down to the medulla
  • Most axons cross sides in the medulla in the pyramids: decussation of the pyramidal tracts in the medulla, some remain ipsilateral but most cross lower down
  • Axons continue down the spinal cord in lateral and ventral cortico-spinal tracts
  • Lateral is the bigger tract containing more descending fibres
  • Most cerebrospinal axons run down the contralateral side in lateral cortico-spinal tracts
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11
Q

ventral and lateral portico-spinal tracts

A

The ventral cortico-spinal tract fibres terminate in the ventral grey matter of the cervical & upper thoracic cord.
The lateral cortico-spinal tract fibres run down the whole cord with fibres terminating in the ventral grey matter of all the cord.

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12
Q

control in cortico-spinal system

A
  • Most control is contralateral as most axons cross sides during descent
  • Some control can be ipsilateral or bilateral, this is particularly related to neck & trunk muscles
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13
Q

trigeminal nerve control and clinical implication

A

• UMN control of LMNs supplying jaw musculature is ipsilateral & contralateral on a 50/50 basis so jaw muscle innervation is bilateral
Clinical Implication: a stroke in one hemisphere rarely results in significant weakness of jaw muscles

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14
Q

facial nerve control and clinical implication

A

• UMN fibres that control LMNs supplying forehead & eye closure terminate ipsilaterally & contralaterally so forehead & eye closure is bilateral
• UMN fibres that control LMNs supplying mouth muscles terminate on a strongly contralateral basis so mouth muscles have unilateral innervation
Clinical Implication:
• lesion of VII nerve nucleus or VII nerve leads to weakness of all ipsilateral face and affects the contralateral
• unilateral UMN lesion affects contralateral lower face only

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15
Q

XI: Accessory Nerve & Sternocleidomastoid Muscle control

A

Motor fibres originate in either the nucleus ambiguus as the cranial root of the accessory nerve or the cervical cord grey matter. These exit the cord as rootlets forming the spinal root of the accessory nerve. This ascends upwards alongside the spinal cord, through the foramen magnum to unite with the cranial root of the accessory nerve.
One of the muscles supplied is the sternocleidomastoid. It is attached to the head and the trunk, because it is attached anteriorly on the trunk and posteriorly behind the ear

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16
Q

left and right sided control of the sternocleidomastoid muscle

A

RIGHT MUSCLE TURNS HEAD TO LEFT and LEFT MUSCLE TURNS HEAD TO RIGHT
The right side of brain controls left trunk and limbs
The left side of brain controls left SCM muscle
L hemisphere UMN control of R limbs and L SCL

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17
Q

clinical implication of left and right sided control of the sternocleidomastoid muscle

A

Clinical Implications:
• In focal epileptic seizures originating in the left frontal region, right limbs are left SCL is stimulated= The right limbs jerk and the head jerks to the right
• In a left hemisphere stroke= loss of control of R limbs and L SCM so the head is turn to left as unopposed right SCM

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18
Q

UMNs effect on LMNs clinical notes

A

UMNs have an excitatory effect on the LMNs → UMN lesions produce weakness
UMNs have an inhibitory effect on the LMNs → UMN lesions produce hypertonia ‘spasticity’

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19
Q

what determines the distribution of weakness in UMN lesion?

A

the level at which the pyramidal system is affected eg. the cervical spinal cord contains the LMN cell bodies that supply the upper limb muscles

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20
Q

middle cerebral artery occlusion stroke

A

• This artery supplies middle part of the brain so the whole part of the primary motor cortex may be wiped out so you may have contralateral hemiplegia (leads to paralysis on one side of the body)

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21
Q

internal capsule lesion stroke

A

If a small artery supplying the internal capsule is occluded and the internal capsule is damaged this can produce major contralateral hemiparesis

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22
Q

extrapyramidal system function

A
  • Critical role in the organisation of individual movements into whole actions eg. walking
  • Modifies and organises the movements that are controlled by the cortico-spinal & cortico-bulbar systems
    In order to achieve its function it facilitates movements that are required & appropriate and inhibits unwanted movements.
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23
Q

basal ganglia structures

A

the corpus striatum, substantia nigra, subthalamic nucleus

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24
Q

corpus striatum

A

complex of nuclei in the brain (gives it the striated appearance), the 2 main components are the caudate nucleus and the lenticular nucleus which is divided into the globus pallidus and the putamen.

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25
Q

neostriatum

A

consists of the caudate nucleus and putamen being talked about as a functional group.

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26
Q

substantia nigra

A

distinct pigmented nucleus in the midbrain.

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27
Q

sub thalamic nucleus

A

The subthalamus nucleus is a distinct nucleus beneath the thalamus.

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28
Q

descending tracts of EPS

A

Rubrospinal coming from the red nucleus
Vestibulospinal coming from the vestibular nuclei
Reticulospinal from the reticular formation
Tectospinal from the superior colliculus

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29
Q

connections of the EPS

A

The striatum is the input area where information goes in the extrapyramidal system for processing. The cerebral cortex, thalamus and are when input information is received.
The substantia nigra and globus pallidus are the output areas. The subthalamic nucleus and thalamus (& then motor cortex) are the areas that then receive the output information.
The substantia nigra is one of the key input and also output circuits.

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30
Q

what degenerates in idiopathic Parkinson’s?

A

the striatum-substantia nigra-striatum loops

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31
Q

clinical implications in walking

A

Muscle disease= weakness
LMN disease= weakness
CSp (corticospinal) disease= weakness & spasticity
Extrapyramidal disease= disruption of coordinated acts, not due to weakness

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32
Q

UMN signs in disease: within CNS

A
  • weakness of voluntary movement of affected msucle
  • no profound muscle atrophy but wasting over months
  • spasticity- increased muscle tone due to continuous stretch reflex
  • positive Babinski reflex- dorsiflexion of big toe when stroking lateral side of sole of foot
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33
Q

LMN signs in disease: peripheral

A
  • weakness or paralysis of affected muscle
  • profound muscle atrophy- flaccid paralysis
  • tendon reflexes weak or absent
  • fasticulations (irregular muscle twitching)
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34
Q

Parkinsonism

A
  • Bradykinesia
  • Rigidity
  • Tremor
  • Postural instability
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35
Q

CSF production

A

CSF is made in the choroid plexus, most production is in the lateral ventricle.

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36
Q

CSF movement in the brain

A

CSF is made in the choroid plexus, most production is in the lateral ventricle. It then travels to the 3rd ventricle through the interventricular foramina (foramina of Munro). Then it travels to the 4th ventricle to the cerebral aqueduct. There are 4 routes it can take to the sub-arachnoid space:
• Central canal of spinal cord
• Median aperture (foramen of Magendie)
• 2 x Lateral apertures (foramina of Luschka)
It is then absorbed in cerebral veins (dural venous sinuses) via arachnoid granulations.

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37
Q

functions of CSF

A
  • Buoyancy- important as the brain is fairly heavy and it prevents stoppage of blood flow to the brain
  • Protection from physical injury- shock absorber
  • Maintenance of brain perfusion- reduction in CSF production drops the ICP, encouraging cerebral perfusion
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38
Q

munro-kelle doctrine

A
  • The skull is a “bony box”
  • There are 3 non-compressible components (brain tissue , blood, CSF)
  • Increasing volume of one component requires a reduction in one or both others to maintain the same ICP
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39
Q

tests of CSF

A
  • Gram stain & culture- looking for microbacteria
  • Oxyhaemoglobin & bilirubin
  • Oligoclonal bands- evidence of immune system activity
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40
Q

features of high ICP

A

Headache= worse when lying down, coughing, sneezing, stooping, straining
Visual obscuration= grey/black out with ICP spikes

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41
Q

causes of high ICP

A
  • Intracranial expanding lesions- tumour, haematoma, abscess
  • Hydrocephalus- accumulation of CSF
  • Cerebral oedema – an increase in the water content of the brain, due to dysfunction of the blood-brain barrier. This can be localised (eg. around tumours) or generalised (eg following severe head injury or in hypoxic brain damage)
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42
Q

features of low ICP

A

Headache= worse when sitting down or standing up

Blurred vision, dizziness

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43
Q

causes of low ICP

A

Underproduction= dehydration, drugs

CSF leak- iatrogenic (post-LP), spontaneous

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44
Q

T1 weighted MRI

A

good for anatomy, CSF (cerebrospinal fluid) is shown as black

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45
Q

T2 weighted MRI

A

good for pathology, CSF is white, advantage is most pathology is brain has increased water so tends to stand out brighter than background brain tissue in these scans

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46
Q

Flair MRI

A

T2 with suppressed CSF, leaves pathology areas with more water to stand out eg. lesions in multiple sclerosis

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47
Q

advantages of brain CT

A
  • Fast, well tolerated, good for patients requiring ventilatory support or have metal work inside
  • Good at detecting blood (sub-arachnoid haemorrhage, intracerebral haemorrhage, subdural/ extradural haematoma) which is helpful in hemiparesis or coma presentations
  • substantial haematoma
  • blood shows up as white in the CT imaging
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48
Q

There are 3 main divisions in the cerebellum:

A
  • Vestibulocerebellum- vestibular function, middle, fastigial nucleus is connected tot eh vestibular nucleus
  • Spinocerebellum- spinal cord, interposed nucleus, spinocerebellar connections important in posture & gait
  • Pontocerebellum- communicates with brain stem- pons and neocortex, dentate nucleus, uniquely large in humans
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49
Q

THE CEREBELLAR PENDUCLES

A
  • Superior cerebellar peduncle- communicate with midbrain
  • Middle cerebellar peduncle- communicate with pons
  • Inferior cerebellar peduncle- communicate with medulla
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50
Q

Layers of the cerebellum (outer to inner)

A
  • Molecular layer- stellate cells, basket cells
  • Granule cell layer
  • Purkinje cell layer
  • White matter
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51
Q

Purkinje cells

A

fan-shaped dendritic trees, largest dendritic trees in the whole nervous system. These fibres are so large that they extend from the piriform layer into the outer molecular layer.

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52
Q

loop of information in the cerebellum

A

Information comes into the molecular layer through climbing fibres and into the granular layer through mossy fibres. It also goes to the central nuclei from both fibres. The Purkinje cells themselves sends out information to the central nuclei.

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53
Q

Ataxic Syndrome

A

loss of coordination of voluntary muscle movements

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54
Q

types of ataxic syndromes

A
  • Ataxia of upper limbs
  • Ataxia of lower limbs
  • Truncal ataxia- postural uncoordinated, unsteadiness and falls
  • Gait ataxia- gait is uncoordinates
  • Dysarthria- speech
  • Nystagmus- eyes
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55
Q

diseases of input and output tracts in the cerebellum

A
  • Neoplasia
  • Multiple sclerosis
  • Trauma
  • Drugs & toxins
  • Neurodegenerations
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56
Q

neurotransmitter process

A
  • Action Potential arrives at terminal
  • Opening of Ca2+ channels
  • Fusion of vesicles with pre-synaptic membrane
  • Transmitter release into synaptic cleft
  • Binding to postsynaptic receptors
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57
Q

structure of synapse

A

a synapse has a pre-synaptic and post-synaptic complex and in these region we find multiple proteins involved in neurotransmitter release, activation of a receptor and AP propagation.

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58
Q

Ionotropic Neurotransmitter Receptors

A
  • Ligand gated ion channels
  • Fast neurotransmission
    Inhibitory: neurotransmitter causes chloride influx and hyperpolarisation (membrane becomes more negative)
    Excitatory: neurotransmitter causes sodium influx and depolarisation (membrane potential more positive)
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59
Q

Metabotropic Neurotransmitter Receptors

A
  • Induction of second messenger systems
    • Receptor coupled to G-protein  activates intracellular enzyme systems to produce an intracellular signal using a second messenger (usually a distant ion channel allowing ion flow)
  • Slow neurotransmission neuromodulation
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60
Q

Ways drugs can act on neurotransmitters

A
  • Enhance synthesis
  • Increase release
  • Block reuptake
  • Reduce metabolism
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61
Q

glutamate synthesis and removal from synapse

A

It is synthesised from glutamine in astrocytes and it is removed from the synapse by glutamate transporters.

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62
Q

effect of high levels of glutamate, NDMA, AMPA

A

High levels of glutamate, NMDA or AMPA kill neurons. Glutamate levels rise following stroke and glutamate receptor antagonists reduce brain damage following experimental stroke.

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63
Q

Subtypes of the glutamate receptor

A

NDMA, AMPA & Kainite (ionotropic), metabotropic

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64
Q

glutamate, NDMA, AMPA and learning & memory

A

Glutamate is also important for learning and memory, there are high densities of NMDA and AMPA receptors in the hippocampus. The activation of glutamate receptors is important in long term potentiation (LTP). Glutamate receptor antagonists inhibit LTP and negatively impact learning and memory while AMPA receptor potentiators enhance LTP which positively impacts learning and memory.

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65
Q

GABA receptors

A
  • Acts via ionotropic (GABAA) and metabotropic (GABAB) receptors, and modulates flow of Cl- ions across the membrane
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66
Q

GABA

A
  • Main inhibitory neurotransmitter of the CNS (some setting can be excitatory)
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67
Q

what drugs mimic effects of GABA

A
  • Some anti-epileptic drugs mimic effects of GABA or increase bioavailability of GABA (eg gabapentin, vigabatrin)
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68
Q

benzodiazepines

A

enhance the effects of the GABA inhibitory channel which can be sedative, anxiolytic, anti-convulsant.

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69
Q

serotonin originates in

A

Serotonin originates in the raphe nucleus in the brain stem and projects throughout the cerebral cortex

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70
Q

serotonin controls

A

sleep wake cycles and mood/ emotional behaviour

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71
Q

antidepressants that utilise serotonin

A
  • Tricyclic compounds like imipramine block uptake of serotonin which increases its bioavailability.
  • Selective Uptake Inhibitors like fluoxetine (Prozac).
  • Monoamine Oxidase Inhibitors like phenelzine reduce enzymatic degradation of serotonin so there is prolonged activation of 5-HT receptors
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72
Q

ACh synthesis

A
  1. Acetylcholine is made from choline and Acetyl CoA
  2. In synaptic cleft Ach is rapidly broken down by the enzyme acetylcholinesterase
  3. Choline is transported back into the axon terminal and used to make more Ach
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73
Q

major nuclei that contain ACh

A

Major nuclei that contain Ach are the nucleus of meynert and the amygdala along with some brain stem nuclei. These project to the thalamus and the cerebral cortex.

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74
Q

pathological features of Alzheimers

A
  • Alzheimer’s can lead to frontal and temporal atrophy but in advanced cases, it can lead to global
  • Features include neurofibrillary tangles and amyloid plaques- deposited in brain parenchyma and also in blood vessels, this protein causes cerebral amyloidopathy which can lead to bleeding in the brain
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75
Q

amyloid component of the amyloid precursor protein

A
  • Integral transmembrane protein
  • Axonally transported
  • Function in synaptic transmission, neuroprotectant
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76
Q

amyloid pathway in AD

A

The enzyme alpha-secretase cleaves APP into 2 fragments neither of which are non-amyloidogenic  non-pathogenic, beta secretase cleaves APP and gamma secretase cleaves one of the APP fragments into a amyloidogenic fragment called Abeta and this is what accumulates in brain parenchyma in AD.

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77
Q

Bapineuzumab

A

an antibody targeted against amyloid β, is a passive immunotherapy that might bind to amyloid β and facilitate its clearance.

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78
Q

mutations in amyloid precursor protein cause

A

familial AD

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79
Q

Parkinson’s disease

A

degeneration of dopamine pathways in the basal ganglia. Can be treated by enhancing dopamine levels- L-DOPA but adverse effects of this include psychosis.

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80
Q

schizophrenia and dopamine

A

Increased dopamine function in the frontal cortex is associated with schizophrenia.

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81
Q

Neuroleptics

A

drugs used to schizophrenia, these are dopamine receptor anatagonists/ blockers and examples include chlorpromazine and related antipsychotics. Adverse effects of this is development of a parkinsonian syndrome.

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82
Q

blood brain barrier

A
  • separates the brain from the circulatory system
  • protects the central nervous system from toxins
  • regulates synaptic transmission and maintains a stable microenvironment
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83
Q

Cellular components of the BBB:

A
  • Physical barrier- tight junctions on endothelial cells: seal aqueous paracellular diffusion between cells
  • Pericytes
  • Astrocyte end foot processes
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84
Q

What can cross the blood brain barrier?

A
  • Lipid soluble agents
  • Transport carriers- glucose, amino acids
  • Receptor medicated endocytosis and transcytosis- insulin
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85
Q

drug criteria for crossing the BBB

A

molecular weight <400Da threshold and high lipid solubility ie. Low hydrogen bonding (≤7 hydrogen bonds).

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86
Q

can dopamine cross BBB?

A

Dopamine is too large to cross the BBB

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87
Q

Parkinson’s Carbidopa-Levadopa combination therapy

A

– L-dopa crosses BBB
– Carbidopa doesn’t cross BBB but helps prevent L-dopa breakdown in periphery
– Carbidopa inhibits DOPA-decarboxylase (DDC in brain and periphery)

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88
Q

ways for drugs to cross BBB

A

Intrathecal drug administration
– Ie. Baclofen for spasticity in multiple sclerosis
• Only a small proportion of oral baclofen penetrates brain/spinal cord
– Intrathecal pump administers drug directly into CSF
– Experimental BBB opening
– Opening of the BBB using intracarotid infusion of hyperosmolar solutions
• Effective delivery of chemotherapy drugs for brain tumours

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89
Q

cutaneous mechanoreceptors

A
  • Meissner corpuscle- lies in epidermal/dermal junction
  • Pacinian corpuscle
  • Ruffini’s corpuscles
  • Merkel’s discs
  • Free nerve endings- responsible for pain sensation scattered across dermis and epidermis
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90
Q

Dorsal column/ medial lemniscal pathway is responsible for transmitting

A

proprioception, fine touch and vibration

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91
Q

Spinothalamic pathway is responsible for transmitting

A

pain, temperature sensation and light touch & pressure

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92
Q

The Dorsal Column System

A
  • Pass through the dorsal spinal nerve root into spinal cord
  • Travel up to second order neurone in the spinal root
  • The second order neurone in the nucleus cuneatus/ nucleus grateus in the medulla
  • Dorsal columns become larger as sensory information move up the spinal cord
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93
Q

Types of pain (nociceptors)- travel up spinothalamic pathway

A
  • Thermal- stimulated by extreme temperature
  • Mechanical- mechanical damage
  • Chemical- stimulated by dissolved chemicals
    Stimulation activates the AP travelling up the ascending pain pathway.
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94
Q

neurotransmitters that activate chemical nociceptors

A

K¬¬+, 5-HT and bradykinin

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95
Q

neurotransmitters that sensitise chemical nociceptors

A

prostaglandins and leukotrienes and release of histamine and Substance P can further antagonise these nociceptors.

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96
Q

Spinothalamic Pathway

A
  • Pass through the dorsal spinal nerve root into spinal cord
  • Synapses with the second order neuron very soon after entering the spinal cord in substantia gelatinosa
  • Decussation in central white commisure
  • Travels to the VPL nucleus in thalamus before passing to primary cortex

The grey matter of the has been spilt into different types of cell type and the substansia gelatinosa makes up type 2 and 3 of the grey matter in the spinal cord.

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97
Q

The primary somatosensory cortex

A

post-central gyrus in the parietal lobe

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98
Q

generalsomatic pain from the head is conveyed by the

A

trigeminal nerve (V) From here axons pass into the pons and terminate in trigeminal sensory nuclei (second order neurones). The trigeminothalamic pathway ascends mostly with the medial lemniscal pathway.

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99
Q

Causes of headaches:

A
  • Direct stimulation of nociceptors via tirgemical nerve- sinuses, toothache, ocular, skin
  • Stimulation of periostium, arteries, venous sinuses, areas of the dura, muscle
  • Unknown causes- migraine
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100
Q

Subacute combined degeneration (spinal cord)

A
  • due to Vit B12 deficiency
  • low copper levels can also cause a similar syndrome
  • chronic alcoholism is a risk factor
  • degeneration of dorsal column leading to reduced proprioception back to CNS
  • wide gait and slapping their feet down while they walk to try and increase proprioception
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101
Q

Tabes dorsalis

A

late consequence of neurosyphilis, characterized by the slow degeneration (specifically, demyelination) of the neural tracts primarily in the dorsal root ganglia of the spinal cord.

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102
Q

Syringomyelia

A
  • cerebellum and spinal cord going down, as you pass down a large black space is seen
  • fluid filled cavity is seen called syringomyelia
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103
Q

analgesic ladder

A

Paracetamol > codeine containing drugs eg. coproxamol > morphine
(all of these steps can be with or without NSAID eg. aspirin, ibuprofen)

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104
Q

The gate theory of pain

A

nociceptive fibre coming into the CNS, it then activates the 2nd order neuron which will pass up towards the thalamic nuclei in the spinothalamic pathway ultimately to be perceived as a painful stimulus in the cortex

  • this nociceptive fibre also inhibits the inhibitory interneuron so that the 2nd order neuron can be switched on however the switching off of the inhabitants
  • an innocuous stimulus activates the large myelinated afferents fibre in this image (highlighted as blue) which will come in switch on the interneuron the inhibitory interneurons and therefore stop the 2nd order neuron being activated stopping the perception of pain
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105
Q

what is a stroke

A

rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin

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106
Q

TIA

A

Transient ischemic attacks are brief episodes of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction

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107
Q

Causes of Ischaemic Stroke

A

atherothromboembolism (atherosclerosis develops and either blocks the vessel or forms an embolus), intracerebral small artery disease (lacunar stroke), cardiac source of embolism (air, fat emboli), rare causes

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108
Q

Vascular Injuries of the Brain

A
  • Complete occlusion of a vessel  infarction
  • Hypoperfusion  watershed infarct
  • Cardiac arrest  selective vulnerability and global ischaemic injury
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109
Q

Focal ischaemic injury can be due to

A

emboli (atheromatous material, injury

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110
Q

Global ischemic injury can be due to

A

cardiac arrest and hypotensive brain injury.
develops in the setting of complete cessation of cerebral blood flow, such as may be seen in cardiac arrest. A period of selective vulnerability is then followed by more extensive neuronal loss until all grey matter is affected. The macroscopic changes require resuscitation and a period of several weeks survival.

111
Q

Fat Embolus Syndrome

A
  • Especially seen in trauma patients with fractures in long bones like femur as fat from within narrow space in femur can be released into bloodstream causing blockage of small vessels in both lungs and brain
  • In severe- can see multiple haemorrhages throughout the brain, in microscopy can see a small red globule in vascular system
112
Q

Macroscopic appearance of acute infarct

A
  • Discolouration of tissue
  • Over time, tissue undergoes liquefactive necrosis
  • Gliotic scarred brain tissue with extensive white matter and grey matter damage
113
Q

Brain injury in hypoperfusion

A
  • Water shed infarcts are seen when the systemic blood pressure falls to such a level that cerebral blood flow cannot be maintained.
114
Q

Border zone infarcts

A

occur at the boundary between two arterial territories and they are usually caused by a drop in blood pressure.

115
Q

Causes of brain haemorrhage:

A
  • Hypertension
  • Vascular malformation
  • Neoplasia
  • Trauma
  • Cerebral amyloid angiopathy
  • Iatrogenic, other blood dyscrasias
116
Q

Lipohyalinosis

A

degenerative process initiated by fibrinoid necrosis which can rupture and cause haemorrhage

117
Q

Arteriolosclerosis

A

concentric hyaline wall thickening of small arteries and arterioles. There is significant occlusion of lumens of these vessels.

118
Q

Stroke caused by cerebral venous thrombosis

A

infarction or hemorrhage in the brain, spinal cord, or retina because of thrombosis of a cerebral venous structure. Symptoms or signs caused by reversible edema without infarction or hemorrhage do not qualify as stroke.

119
Q

Lobar haematoma

A

where blood clot is predominantly in one lobe of the brain

120
Q

most common cause of lobar haematoma

A

cerebral amyloid angiopathy. This refers to process where abnormal proteins (usually associated with Alzheimer’s Disease) accumulate in blood vessels and predispose blood vessels to rupture.

121
Q

Subarachnoid haemorrhage location and stroke caused by subarachnoid haemorrhage

A

bleeding into the subarachnoid space (the space between the arachnoid membrane and the pia mater of the brain or spinal cord)
rapidly developing signs of neurological dysfunction and/or headache because of bleeding into the subarachnoid space which is not caused by trauma.

122
Q

Cerebral aneurysms:

A

swelling of artery at a junction. Can rupture and cause subarachnoid (+/- intracerebral) haemorrhage
Rarely, aneurysm may rupture into the brain parenchyma instead causing a intracerebral haemorrhage instead.

123
Q

Sagittal sinus thrombosis and causes

A

venous infarction with associated brain swelling

can be due to oral contraceptive, dehydration and meningitis

124
Q

Cortical vein thrombosis

A

may be due to meningitis.

125
Q

Regulation of cerebral blood flow (CBF)

A
  • Within limits, as blood pressure rises, cerebral vessels constrict  resistance increases, maintains flow constant, to try and maintain constant blood flow
  • As pressure falls, vessels dilate  resistance falls, flow is constant
  • 60-160 mmHg= autoregulation range
126
Q

If persistent high blood pressure in the brain:

A

• Autoregulatory range reset at a higher level
• Curve shifts to right
• Unwise to rapidly lower high blood pressure to ‘normal’,
• When BP falls below 90 mm Hg:
– autoregulation fails
– CBF drops
– ischaemic brain damage can occur

127
Q

Functions of the autonomic nervous system:

A
  • Controls the internal environment- works with endocrine system, homeostasis
  • Controls important functions not under voluntary control ie. autonomous
128
Q

Enteric nervous system

A

intrinsic collections of neurones within the wall of the digestive tract and can function independently of the CNS and PNS

129
Q

Sympathetic trunk ganglia are:

A
  • Located on both sides of the vertebral column
  • Linked by short nerves called into sympathetic trunks
  • Joined to ventral rami by white and grey rami communicantes
  • Fusion of ganglia  fewer ganglia than spinal nerves
  • The sympathetic trunk runs from the neck to lower than L2 (only receive fibres from T1 -L2)
130
Q

prevertebral ganglia

A

Not all sympathetic fibres coming from the spinal cord (T1-L2) will synapse with second neurone in sympathetic chain. Some will run through sympathetic chain without synapsing, to the prevertebral ganglia where they can synapse with the second order neurones which will send its fibers out to the appropriate viscera.

  • Prevertebral ganglia occur only in abdomen and pelvis
  • They lie anterior to the vertebral column
131
Q

sympthetic fibres passing out of the spinal cord to visceral organs

A
  • Sympathetic fibre arising in grey matter in lateral horn
  • Passes out ventral root of spinal nerve and passes into the sympathetic ganglion through a white ramus communicans
  • Some synapse with second order neurone and pass back into the spinal nerve via the grey ramus communicans
  • Others pass through without synapsing to a prevertebral ganglia
132
Q

parasympathetic nervous system cranial-sacral outflow

A
  • Cranial outflow comes from the brain and innervates organs of the head, neck, thorax, and abdomen.
  • Sacral outflow supplies the remaining abdominal and pelvic organs.
133
Q

cranial outflow of parasympathetic preganglionic fibres

A 
Preganglionic fibres run via the:
Oculomotor nerve (III)
Facial nerve (VII)
Glossopharyngeal nerve (IX)
Vagus nerve (X)
Cell bodies are located in cranial nerve nuclei in the brain stem.
134
Q

Parasympathetic Outflow via the Vagus Nerve:

A

Vagus nerve fibres innervate visceral organs of the thorax and abdomen. It stimulates digestion, reduction in heart rate and blood pressure.
Its preganglionic cell bodies are located in dorsal motor nucleus in the medulla and its ganglionic neurones are confined within the walls of the organs being innervates.

135
Q

Parasympathetic Sacral Outflow

A
  • Emerges from S2-S4
  • Innervates organs of the pelvis and lower abdomen
  • Preganglionic cell bodies are located in visceral motor region of spinal grey matter
  • Form splanchnic nerves
136
Q

motor neurones in somatic motor system

A

one motor neuron extends from the CNS to skeletal muscle and axons are well myelinated to allow rapid conduction.

137
Q

motor neurones in autonomic system

A

there is a chain of 2 motor neurones: preganglionic neuron and postganglionic neuron. Conduction of these is slower due to thinly or unmyelinated axons.
Generally, the autonomic ganglion will be very close to the viscera being innervated.

138
Q

Length of Postganglionic fibres in SS and PS

A
  • Sympathetic: long postganglionic fibres

- Parasympathetic- short postganglionic fibres

139
Q

Branching of axons in SS and PS

A
  • Sympathetic: highly branched and influences many axons

- Parasympathetic- localised effects

140
Q

Neurotransmitters released by preganglionic axons in SS and PS

A
  • Acetylcholine for both branches (cholinergic – nicotinic receptors)
141
Q

Neurotransmitter released by postganglionic axons in SS and PS

A
  • Sympathetic – most release noradrenaline (adrenergic)

- Parasympathetic – release acetylcholine

142
Q

The adrenal medulla

A

secretes large quantities of adrenaline (some NA), it is stimulated by pre-ganglionic sympathetic fibres.

143
Q

control of the ANS in the brain

A
  • Reticular formation in the brain stem exerts the most direct influence from the medulla oblongata and periaqueductal grey matter
  • Hypothalamus= main integration centre of the ANS
  • Amygdala= main limbic region for emotions
  • Control by the cerebral cortex
144
Q

horner’s syndrome: symptoms and causes

A

Symptoms:

  • Miosis (small pupil)
  • Ptosis (drooping eyelid)
  • Loss of sweating same side of face
  • Redness of conjunctiva

It may result from interruption of sympathetic fibres centrally (anywhere between the hypothalamus and upper thoracic level of the spine) or peripherally (cervical sympathetic chain).
Other causes: carotid artery dissection, brainstem stroke, syringomyelia

145
Q

Vasovagal syncope:

A

simple faint, seen commonly in young people with no underlying illness.
Sudden vasodilation occurs often caused by strong emotion  peripheral resistance decreases in arterioles and blood pressure falls, cardiac rate fails to increase  vagal stimulation may then occur leading to further bradycardia and to perspiration, increased peristalsis, yawning, nausea, pallor and salivation

146
Q

Orthostatic Hypotension

A
  • Like vasovagal syncope but brought on by getting up from reclined position or standing still for long period
  • Often person stands up and then has steady fall in blood pressure but without compensatory rise in HR
  • Mild staggering or falling may precede loss of consciousness
147
Q

autonomic dysfunction- problems with bladder controls

A

This is a common symptom of multiple sclerosis (75% of patients). Major symptoms are urgency, frequency and urge incontinence. The main cause of this is overactivity of the detrusor muscle. Involuntary bladder contraction gives rise to feeling of need to void immediately despite bladder volume being low.

148
Q

Tests for Abnormality of ANS

A
  • Pupil reactions
  • Postural blood pressure response, by bedside= a fall >30mmhg systolic and >15mmhg diastolic is abnormal
  • Variation of HR with deep breathing (sinus arrhythmia)
  • Lacrimal function
149
Q

treatment of depressive disorders

A 
Treated with:
•	Diet, exercise
•	Drugs: SSRI, SNRI, TCA, MAOI, ‘Atypical antidepressants’ 
•	Psychotherapy
•	ECT (rarely)
150
Q

treatment of anxiety disorders

A

Treated with

  • Psychotherapy
  • Drugs: SSRI, SNRI, TCA, Others
151
Q

dorsal stream in perception

A

The dorsal stream connects occipital and parietal: where?

  • Fast processing system
  • 3D idea of where objects are
152
Q

ventral stream in perception

A

The ventral stream connects occipital and temporal: what?

  • Energy intense part
  • Building up complex features to understand what the object is
153
Q

Types of attention

A
  • Focused attention: The ability to respond discretely to specific visual, auditory or tactile stimuli.
  • Sustained attention (vigilance and concentration): The ability to maintain a consistent behavioral response during continuous and repetitive activity.
  • Selective attention: The ability to maintain a behavioral or cognitive set in the face of distracting or competing stimuli. Therefore, it incorporates the notion of “freedom from distractibility.”
  • Alternating attention: The ability of mental flexibility that allows individuals to shift their focus of attention and move between tasks having different cognitive requirements.
  • Divided attention: This is the highest level of attention and it refers to the ability to respond simultaneously to multiple tasks or multiple task demands.
154
Q

prefrontal cortex and memory

A

formation of short term memories

155
Q

basal ganglia and memory

A

formation of motor and implicit memory and procedural memory, associated with habit forming

156
Q

hippocampus and memory

A

encoding short term memory into long term memory particularly episodic or autobiographical, Engrams from hippocampus transferred to neocortex esp during sleep

157
Q

the anterior stream and attention

A
  • Assesses whether it is deserving of attention
158
Q

Broca area- location and function

A

(frontal)= production of speech

159
Q

Wernicke area- location and function

A

(PTO junction) = comprehension of speech

160
Q

Arcuate fasiculus=

A

connect Broca and Wernicke

161
Q

what hemisphere is language on

A

Language is typically left hemisphere- in about 10% they are on the right and in 5% they are on both sides.

162
Q

tests for cognition

A
  1. MMSE- very limited value, poorly responsive other than in advanced dementia
  2. Addenbrooke’s Cognitive Examination III- useful, takes 20 minutes
    - Useful to chart total score to look at decline over time
    - Pattern of impairments can be useful to make diagnosis of dementia subtypes
    - Can be a very useful starting point to recognise the need for specialist neuropsychology assessment
163
Q

non-modifiable risk factors for stroke

A

age, sex, low birth weight, family history, genetic predisposition

164
Q

Apraxia

A

inability to perform purposeful movement despite motivation and preserved overall neurological function
(typically left hemisphere localisation, split between frontal and parietal lobes)

165
Q

Executive apraxia

A

deficit in sequencing complex movement SMA & PMA

166
Q

Posterior apraxia

A

deficit in the special construction of complex movements posterior parietal cortex

167
Q

Dysfunction of the corticospinal tracts leads to

A

weakness and spasticity.

168
Q

Dysfunction of the basal ganglia loops leads to

A

movement disorders- tone, posture, patterned behaviour.

169
Q

Dysfunction of the cerebellar loop leads to

A

coordination disorders.

170
Q

Paratonia/Gegenhalten:

A
  • Voluntary resistance
  • Executive system pathology
  • Typically seen in delirium/dementia
171
Q 
•	Akinesia 
•	Hypokinesia 
•	Bradykinesia 
•	Rigidity- change in tone
DEFINITIONS
A
  • Akinesia (lack of movement)
  • Hypokinesia (reduced amplitude of movements)
  • Bradykinesia (slow movement)
  • Rigidity- change in tone
172
Q

spasticity of muscles

A
  • ‘Clasp knife’
  • CST pathology
  • Pyramidal tract disorder (UMN) sign
173
Q

rigidity of muscles

A

‘lead pipe’ - BG pathology

- Extrapyramidal disorder

174
Q

UMN and EP signs of tone in muscles

A

UMN signs: spasticity, brisk reflexes, pyramidal pattern weakness
EP signs: rigidity, tremor (normal reflexes, no weakness)

175
Q

Idiopathic Parkinson’s Disease

A
  • A lack of dopamine supply (formed in the substantia nigra) to the basal ganglia
  • Alpha-synucleinopathy (cells in the substantia nigra degenerate due to an accumulation of the protein alpha synuclein)
  • Symptoms: bradykinesia, rigidity, tremor, postural instability + ‘non-motor’
  • F:M= 1:2
  • Peak incidence in 80s
176
Q

The basal ganglia structure receives signals from and project to the motor cortex.
There are 2 pathways:

A

Direct Pathway: accelerator, pro-movement D1 receptors

Indirect pathway: brake, anti-movement D2 receptors

177
Q

development of hypokinesia in Parkinsons

A

Normally there is a balance between the accelerant D1 receptors and brake D2 receptors. In Parkinson’s, there’s a reduction in activity in the direct pathway and an increase in indirect pathway activity hypokinesia

178
Q

Jerky movements examples

A

tremor (rhythmic movement between antagonist and agonists muscle pairs), chorea (dance like), tics (brief contractions

179
Q

Non jerky movements examples

A

dystonia (writers cramp), myoclonus (brief muscle twitches), stereotypies (patterned behaviour)

180
Q

Global dysfunction of cerebellum (intoxication) can have

A

slurred speech

181
Q

Patchy pathology of cerebellum (may be due to MS or mini strokes) can have

A

staccato speech- inable to monitor volume and timing.

182
Q

Upper spinal cord lesion can lead to:

A
  • Spastic tetraplegia
  • Hyperreflexia
  • Extensive plantar reponses
  • Incontinence
  • Sensory loss below level of lesion
  • Associated proprioceptive problems
183
Q

Lower spinal cord lesion can lead to:

A
  • LMN type lesion affecting upper limbs
  • UMN type lesion affecting lower limbs
  • Sensory loss below level of lesion
184
Q

Hemisection of the cord (Brown-Sequard)

A
  • Ipsilateral loss of proprioception
  • UMN sign
  • Contralateral loss of pain and temperature sensation
185
Q

Patellar tendon reflex

A

When we tap on the Patella tendon causing stretch in the tendon itself changes to intrafusal muscle fibres resulting in sensory inputs back through the spinal cord causing alpha motor neuron activation and muscle contraction at the same time in activation of the opposing muscle group

186
Q

blood supply of spinal cord

A
  • Spinal cord is supplied by a single anterior spinal artery and paired posterior spinal artery
  • Many anterior spinal artery supplies come directly from the aorta
187
Q

Anterior spinal artery thrombosis

A
  • Supplies 2/3 of spinal cord so occlusion can cause damage within this area
  • Causes LMN signs progressing to UMN signs
  • Loss of pain and temperature sensation and autonomic function
  • There is preservation of proprioception through posterior columns
188
Q

Radial Nerve (C6-C8) lesions

A
  • Damaged by fractures to the mid-shaft of the humerus
  • Compression at the same site leading to ‘Saturday night palsy’  loss of extension of wrist and fingers (wrist drop)
  • Can also have problems in dorsal aspect of hand
189
Q

Median Nerve (C5-T1, predominately C6) lesions

A
  • Carpal tunnel syndrome: predominantly sensory but may be associated with wasting of thenar muscles
190
Q

Ulnar Nerve (C7, C8, T1) lesions

A
  • May be damaged by injury at the medial epicondyle of the elbow, or at the medial aspect of the wrist.
  • Characteristic “claw hand” deformity.
191
Q

Femoral Nerve (L2-L4) lesion

A
  • May be damaged by hip dislocation, pelvic fracture, and tumors in the pelvis
  • Leads to weakness of knee extension (results in inability to lock knee while walking) and some wasting of quadriceps
192
Q

Sciatic Nerve (L4- S3) lesion

A
  • Damage to the sciatic nerve can be due to trauma to pelvic region, neoplastic compression/infiltration, or operative complication.
  • Results in foot drop and unstable ankle
193
Q

compression or irritation of a spinal root which comprises the sciatic nerve (sciatica) symptoms

A

Common:
– L5; sensory- pain in posterolateral thigh and leg, numb inner foot
• motor- weakness of dorsiflexing foot and toes
– S1; sensory- pain in posterolateral thigh and leg, numb lateral foot
• motor- weakness of foot dorsiflexion and loss of ankle jerk
Rare:
– L3+L4- diminished knee jerk, pain in anterior thigh

194
Q

Prolapsed Intervertebral Disc

A
  • The annulus fibrosis can deteriorate leading to prolapse of the nucleus pulposus putting pressure on the spinal nerve root lying behind this
195
Q

treatment of prolapsed disc

A

Prolapsed discs can heal on their own if left for long enough, it can also be treated by a microdiscectomy where the prolapsed disc is accessed posteriorly and the prolapsed material is removed, relieving pressure on the spinal nerve root.

196
Q

Common Peroneal Nerve (L4-S2) lesion

A
  • This can be damaged as it winds round the head of the fibula. This can be by fracture or compression (e.g. tight cast).
  • Results in weakness of foot dorsiflexion and eversion
197
Q

Uhthoff’s phenomenon

A

decompensation of the damaged nervous system when the patient experiences a fever, can be seen in any chronic pathology
Eg. in optimal conditions, patients with scarring in the nervous system may be fine but if they are heated up then may be decompensated and their symptoms will worsen.

198
Q

MS pathology

A
  • Inflammation
  • Demyelination ± variable extent of remyelination
  • Neuroaxonal injury/loss
  • Astrogliosis
199
Q

risk factors for MS

A

genetics, environment- Vitamin D, smoking, EBV, obesity

200
Q

investigations for MS

A
  • History/ Examination- dissemination in body and over time (space & time)
  • lumbar puncture
  • MRI
    T2 scans show areas of gliosis (scarring) in white matter

With contrast gadolinium, acute lesions will shown leaky BBB so the contrast will leak into the BBB (can show how old the lesions are)

201
Q

Ig oligoclonal bands

A

inflammatory antibodies that have leaked down from the brain. These must be compared to the serum and if these bands are seen then you know that the immune system is active.
It is seen in early relapsing remitting MS but not always seen at other times.

202
Q

Relapse and Remission Stage of MS

A

Lapses are being driven by focal areas of BBB leakage where the immune system causes local tissue damage to myelin and axons. The inflammation settles down and then the tissue is repaired and may have a degree of scarring that results in a focal area in the central nervous system, best seen in the white matter and scans but also present the grey matter. If it is in a part of the brain that we call clinically eloquent that results in symptoms and a clinical relapse

203
Q

Progressive Stage of MS

A

isn’t typified by those knew focal areas of the immune system, there’s a more diffuse activation of microglia and critically a diffuse loss of nerve cell tissue called neurodegeneration. When were look at brain scans of people with them as we see that the normal shrinkage of the brain that happens as we reach 1/4 decade and beyond as accelerated > neurodegeneration.

204
Q

tuberomammillary nucleus

A

switches on histamine which wakes up the cortex of the brain (anti-histamine makes you tired)

205
Q

VLPO nucleus

A

important in going to sleep, it is mainly inhibitory GABAergic neurons that project to centres involved in arousal including the reticular activating brain stem in brain

206
Q

the posterior lateral hypothalamus and waking up

A

the posterior lateral hypothalamus secretes orexin which switches on the reticular activating system which activates dopamine, acetylcholine, nicotinic receptors. This wakes up more and more of the brain.

207
Q

there are low levels of __ in narcolepsy

A

CSF orexin

208
Q

parainsomnias in REM

A
  1. REM sleep behavioural disorder- patients act out dreams, strongly predictive of alpha-synonucleinopathies
  2. Isolated sleep paralysis- failure to move limbs when you wake up because of failure of CST inhibition to be switched off
209
Q

parainsomnias in NREM (stage 3& 4)

A
  • Sleep walking
  • Confusional arousals
  • Night terrors
210
Q

GCS scale

A

EVM: 4, 5, 6

211
Q

process of hearing

A
  1. Sound waves enter the auditory canal, pressure differences move along the auditory canal towards the tympanic membrane
  2. The tympanic membrane receives the pressure waves and vibrates
  3. Vibration is transmitted to the ossicles in the middle ear
  4. The ossicles transmit vibrations to the oval window of the vestibule into the fluid inside
  5. Vibrations are then transmitted to the fluid around the cochlea
  6. Cells in the cochlea convert vibrations to electrical signals
  7. The electrical signals from the cochlea transmit along axons of the VIIICN
  8. The vestibulocochlear nerve goes to the brain stem effectively at the medulla/pons junction
    - The cochlear nerve and vestibular nerve join.
  9. Electrical signals in the VIII nerve arrive at the cochlear nuclei in the brain stem
212
Q

Dorsal cochlear nucleus (posterior):

A

Concerned with the quality of sound, picking apart the tiny frequency differences which allow differentiation of similar sounds
In the dorsal cochlear, axons go directly inferior colliculus  medial geniculate body  cerebral cortex

213
Q

Ventral cochlear nucleus (anterior):

A

Concerned with minute differences in the timing and loudness of the sound in each ear in order to localize sound
In the ventral cochlear nerve, axons go to the superior olive  inferior colliculus  medial geniculate body  cerebral cortex

214
Q

As the fibres go up to the primary auditory cortex, they

A

form a reticular tract in the lateral lemniscus.

215
Q

Primary Auditory Cortex

A

Situated in the temporal region

216
Q

Gliosis

A
  • Astrocyte hypertrophy and increase GFAP immunoreactivity in response to both acute and chronic insults eg. infiltrating neoplasm, infection
  • Gliotic tissue is firm and appears grey
217
Q

Vulnerable areas in the hippocampus, cerebral cortex, basal ganglia, cerebellum nd brain stem

A
  • Hippocampus: sector CA1 is most vulnerable, sector CA2 least vulnerable
  • Cerebral cortex- neurones of layers 3, 5, 6 are most vulnerable, damage is most pronounced within depths of sulci and posteriorly within the cerebral hemispheres (triple watershed zone)
  • Basal ganglia (including thalamus)- variable
  • Cerebellum- Purkinje cells
  • Brain stem- brainstem nuclei tend to be relatively preserved in adults but when they are affected, sensory nuclei are more susceptible than motor nuclei
218
Q

Rabies

A

Negri body in a neuron
Enters the body through typical bite wound, virus goes up PNS to CNS, fatal in CNS
Treatment possible while virus in PNS

219
Q

why don’t viruses form abscesses?

A

Viruses are non-purulent so don’t form abscesses (bacterial) , when virus gets into brain are encephalitis.

220
Q

Fetal Infections of the CNS:

A
  • Rubella (deafness, blindness, microcephaly)
  • CMV (microcephaly)
  • Toxoplasma (microcephaly)
  • Syphilis (tertiary forms include GPI, tabes dorsalis and meningovascular syphilis)
  • (HIV)
221
Q

Fungal Infection of the CNS•

A

rare, can cause meningitis or abscess

  • Candida
  • Aspergillus
  • Cryptococcus
222
Q

Perineurium

A

flattened perineurial cells connected by tight junctions and forming concentric layers separated by collagen

223
Q

Epineurium

A

collagenous tissue with some adipose and elastic tissue. Larger vessels found in the epineurium

224
Q

Muscular dystrophies

A

These are genetically determined destructive myopathies and they are usually progressive. This can be due to a detective protein, abnormalities of the protein dystrophin cause dystrophinopathies.

225
Q

The normal structure of the PNS is:

A
  • Mixed, sensory or motor
  • Nerve trunks composed of a variable number of nerve fascicles surrounded by the epineurium
  • Individual fascicles surrounded by perineurium
  • Connective tissue within fascicles is the endoneurium
226
Q

The outer ear consists of

A

the pinna, auditory canal (leads into middle & inner ear) and tympanic membrane (sits at auditory canal apex).

227
Q

major components of the inner ear.

A
  • Vestibule- large central area
  • Utricle & saccule- adjacent to the vestibule
  • Cochlea- on one side (receptors in the cochlear duct)
    a spiral shape and it is divided into 3 chambers – scalae. These are part of the bony labrynth and contain perilymph.
  • Semi-circular canals- on other side
228
Q

organ of corti

A

within the scala media: cochlear duct. It had a sensory epithelium, a cellular layer on basilar membrane hair cells and it is topped with hair like structures which then fit into the tectorial membrane above. The cells give rise to sensory axons.
Waves in the scala fluid cause movement of basilar membrane hair cells to produce electrical responses and their axons form part of VIII nerve.

229
Q

basilar membrane stiffness and width

A

The stiffness & width of the basilar membrane varies along the cochlea.
It is stiffest near start at oval window and gets thinner along the rest.
This allows different parts of bm to respond to different frequencies.
Coiling also enhances low frequency waves as they travel along cochlea.
Highest frequency near oval window. Lowest frequency near other end.

230
Q

Each semi circular canal has:

A
  • a continuous endolymph filled hoop
  • special hair cells that sit in a small swelling called the ampula
  • the hair cells project into a gelatinous mass called the cupula
    The semi-circular canals are paired (R&L). Movement one way causes inhibition on one side and excitation on the other.
231
Q

motion of semicircular canal

A

Motion in plane of the canal > movement of the fluid (intertia) > movement of the hairs > change in hair cell activity

232
Q

Vertigo

A

Defined as one or more of the following:

  • A distortion of static gravitational orientation- feel like you are tilted to one side
  • An erroneous perception of movement of the sufferer- feel like you are bobbing up and down, spinning
  • An erroneous perception of movement of the environment- feel like everything around you is spinning
233
Q

Benign Paroxysmal Postional Vertigo (BPPV)

A
  • Commonest cause of vertigo in general practive
  • Attacks of rotational vertigo
  • Provoked by positional change: lying down or sitting up, turning over in bed, looking up or bending forward
    Causes:
  • Parts of the otoliths break off and get lodged in the ear- degernartive otolithic debris in cupola or semicircular canal
    40% are due to antecedent event and 60% have no obvious trauma (age is a factor)
234
Q

BPPV testing and treatment

A

Testing: positional testing, carried out in 30 degrees as the semi-circular canals are in 30 degrees

Treatment: particle repositioning manoeuvres to try to move the fluid to wash out the debris

235
Q

anatomy of retina

A

The retina in the eye consists of layers of neuronal cells that are connected by synapses. Photoreceptor cells in the eye are directly light sensitive: rods, cones, photosensitive ganglion cells. These cells are low down in the retina and underneath them is a pigmented layer.

236
Q

rod and cone cells

A

Rods- function mainly in dim light, black & white vision

Cones- function in bright light, perception of colour

237
Q

Photosensitive ganglion cells

A

important for reflexive responses to light, more rare than rods and cones

238
Q

Features in the retina:

A
  • Macula: yellow oval spot near retina centre, specialised for high acuity vision, ~6mm diameter
  • Fovea: pit in the macula centre, area of greatest visual acuity and best colour vision, ~1.5mm
239
Q

why is the optic nerve slightly offset?

A

Optic nerve is slightly offset to the temporal side and this is important as you want the light to hit the fovea as it has best visual acuity, the optic nerve has no photosensitive cells and causes the blind spot.

240
Q

visual pathways

A

Axons that go down the optic nerve cross over in the optic chiasm and form the optic tract on each side and visit the lateral geniculate nucleus and then continue via optic radiation to the visual occipital cortex.

241
Q

chiasm data

A

Pre-chiasm: all data from one eye
Chiasm: half the data cross
Post-chiasm: all left visual space data on right, all right visual space data on left

242
Q

blind spot and enlarged?

A
  • BS reflects the optic nerve and the size of BS reflects optic nerve size
  • Enlarged BS= enlarged optic nerve
    > could be due to papilloedema, optic neuritis
243
Q

visual field defects- pre-chiasmal, chiasmal, post chiasmal

A

Pre-chiasmal- uniocular visual loss so only one eye/optic nerve is affected
Chiasmal- bitemporal hemianopia, in relation to pituitary gland which sits underneath (tumours), affects crossing fibres
Post chiasmal- homonymous hemianopia

244
Q

Altitudinal VFDs

A

upper half of visual field is lost in both eyes

245
Q

Muscles that control eye movements:

A
  • Superior and inferior rectus
  • Lateral and medial rectus
  • Superior and inferior obliques
246
Q

cranial nerves 3, 4, 7

A

CNIII: Oculomotor nerve controls the inferior oblique and all the recti apart from lateral rectus, control of the eyelid and pupil
CNIV: Trochlear nerve controls the superior oblique
CNVI: Abducens nerve controls the lateral rectus and abducts the eye

247
Q

recti muscles

A
  • Superior rectus moves eye up
  • Inferior rectus moves eye down
  • Medial rectus moves eye in
  • Lateral rectus moves eye out
248
Q

oblique muscles

A
  • Superior oblique moves eye down

* Inferior oblique moves eye up

249
Q

Ocular palsies

A

eye takes on abnormal position because of unopposed action of remaining intact muscles

250
Q

IV nerve palsy

A

leaves eye abnormally up

251
Q

VI nerve palsy:

A

leaves eye fails to move to the left

252
Q

III nerve palsy:

A

can’t open the eye and eye is abnormally deviated down and out

253
Q

Diplopia

A

results from failure to align eyes

254
Q

Acute Contusions

A

bruises on the surface of brain
Mostly seen in frontal and temporal regions
Can see small areas of bleeding in cortical areas

255
Q

Extradural intracranial haemmorhage

A

usually association with squamous temporal bone fractures damaging the underlying middle meningeal artery, cause deformation of the brain as it is a space occupying lesion and raises ICP, localised as the dura is tightly bound to the bone (more general in subdural haemorrhage)§

256
Q

Subdural intracranial haemmorhage

A

extensive, associated with cortical contusions and torn bridging veins (take blood from surface of brain to venous sinuses), gelatinous haematoma

257
Q

Intracerebral intracranial haemmorhage

A

superficial, associated with contusions, deeply seated often within the basal ganglia

258
Q

CNS tumours:

A
  • Anatomical location- can’t surgically remove tumour in the pons or thalamus
  • Local invasion- brain tumours show extensive local invasion, frontal lobectomy can be done to do a macroscopic resection (glioma cells infiltrate further so it is impossible to get a complete resection of even low grade tumours)
  • Angiogenesis
259
Q

Common tumour types in Brain

A
  • Metastatic tumours
  • Gliomas (astrocytomas including glioblastoma, oligodendrogliomas etc)- main group of intrinsic tumours
  • Meningiomas- generally low grade
  • In children, medulloblastoma- aggressive tumor of the posterior fossa
260
Q

Diffuse Traumatic Axonal Injury (pathological substrate of DAI)

A

widespread axonal damage caused by rotational injury of the brain – non impact.
DAI results in unconsciousness and coma.

261
Q

AD spread in brain

A

AD spreads throughout the brain, it begins in the inter rhinal cortex in the hippocampus and moves through the temporal and frontal cortex moving throughout.

262
Q

Vascular dementia cause

A

multiple infarcts- small lacunar type infarcts are seen as holes and this is caused by blockage to the penetrating reticular striate arteries (multi-infarct dementia).

263
Q

Binswanger’s disease (BD)/subcortical vascular dementia

A

type of dementia caused by widespread, microscopic areas of damage to the deep layers of white matter in the brain

264
Q

Lewy bodies made of

A

alpha synuclein protein

in PD

265
Q

common sites for MS plaques

A

Common sites for plaques include periventricular region and optic tracts.

266
Q

seizure and epilepsy definitions

A

Seizure- the manifestation of abnormal paroxysmal neuronal discharge in part(s) of the brain > failure of brain function
Epilepsy- the tendency for recurrent spontaneous seizures, a single seizure is not epilepsy

267
Q

Provoking factors of epilepsy:

A
  • Hypoglycaemia
  • Electrolyte imbalance
  • Acute head injury
  • Drug abuse
  • Alcohol withdrawal
268
Q

Risk factors for epilepsy

A
  • FHx
  • Birth- brain injury in perinatal, umbilical cord around neck
  • Febrile convulsions
  • Significant head injury
  • Encephalitis/meningitis
269
Q

tests for vibration, proprioception, light touch and pain

A
  • Vibration is tested with a tuning fork
  • Proprioception is tested with joint position sense
  • Light touch is sensed with cotton wool
  • Pain is touched with neurotips- stimulate pain and pressure pathways
270
Q

Reduction of Pain by serotonin release periaqueductal gray in midbrain

A
  • 5HT release
  • 5HT travels in CSF downwards and triggers endogenous opioid release in dorsal horn spinal cord interneurones
  • Endogenous opioids reduce incoming pain pathway activity via opioid receptors (mu, kappa, delta)
271
Q

cushing’s triad

A

hypertension and bradycardia and respiratory depression

272
Q

when should you avoid giving an LP

A

If you suspect mass lesion avoid lumbar tap → Removal of fluid creates a pressure difference, which can cause brain to move due to higher pressure induced by mass lesion at the top

273
Q

spinocerebellar pathway transmits information about

A

proprioception

274
Q

define

  • ballismus
  • chorea
  • athetosis
  • dysonia
  • myoclonus
A

Ballismus- restlessness in upper body
• Chorea- rapid, jerky involuntary body movements
• Athetosis- writhing movements of fingers
• Dystonia- muscle spasms
• Myoclonus- sudden jerking movements

Y2S1- Neuro, GI, Liver (2 decks)

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