Neuro

Question 1

What are proprioceptors?

Answer 1

the type of sensor receptors that monitor the movements of our own bodies. They allow you to know where your body is and provide vital feedback information for the control of motor systems.

Question 2

What do muscle spindles detect?

Answer 2

the stretch of muscle

Question 3

What is the very basis of neurones and muscle fibres in motor control?

Answer 3

there is a single synapse to each of the muscle fibres. Each action potential in the motor neurone will produce one in each of the four muscle fibres, and they will then twitch.

Question 4

Twitches are all or nothing events - how can the force of contraction be modified?

Answer 4

1. change the frequency of action potential firing in the active motor units
2. change the number of active motor units
3. change the type of active motor units

This is how movements are ‘graded’.

Question 5

What aspects may affect how much excitatory input needs to go to a cell to reach its action potential?

Answer 5

• bigger cell body = bigger input

- small ‘red’ motor units are more easily excited, so they are recruited first

Question 6

How do muscle spindles control posture?

Answer 6

1. muscle contracting too little to overcome gravity
2. spindle stretched, increasing afferent activity
3. increased excitation of the motor neurone pool
4. increased force of contraction

Question 7

What is the structure surrounding gamma motor control?

Answer 7

• fusiform capsule
• intrafusal fibres inside the capsule
• only have actin myosin contractile machinery at the ends
• the afferents associated with the muscle spindle are associated with the stretchy middle bit and are only affected when it stretches

Question 8

What happens in gamma motor control?

Answer 8

1. muscle stretches as part of a voluntary movement
2. intrafusal centres do not stretch, so afferent activity unchanged
3. no excitation of motor neurone pool
4. muscle doesn’t resist stretching

Muscle spindles also ensure accuracy of movement.

Question 9

What happens in gamma motor control when you pick up something which is heavier than you expected?

Answer 9

1. muscle shortens too slowly, but intrafusal ‘poles’ are not loaded so they shorten as intended
2. intrafusal centres stretch, increasing afferent activity
3. increased excitation of the motor neurone pool
4. increased force of contraction ‘corrects’ the movement

Contraction can also be influenced by inhibition

Question 10

What happens in inhibition of gamma motor control?

Answer 10

1. muscle stretches as part of a voluntary movement
2. descending control systems activate inhibitory interneurones
3. reduced activity in the motor neurone pool
4. muscle doesn’t resist stretching

Question 11

What is reciprocal inhibition?

Answer 11

• Ia afferents excite interneurons that directly inhibit antagonist motor neurones
• these interneurones are glycinergic
• they act through ligand-gated receptors on the motor neurone itself

Question 12

What is presynaptic inhibition?

Answer 12

• Ia afferents excite interneurones that inhibit release of neurotransmitter from antagonist Ia afferents
• these interneurones are GABAergic
• they act through metabotropic receptors (GABAb) on the axon terminals

Question 13

What are lower motor neurone lesions?

Answer 13

In skeletal muscle, ‘lower motor neurone’ = alpha motor neurone

Lower motor neurone lesions denervate the muscle, causing FLACCID WEAKNESS

• weakness
• wasting
• loss of reflexes
• fasciculations and fibrillations

Question 14

What are upper motor neurones?

Answer 14

An upper motor neurone carries signals from the brain to the spinal motor circuits.

Question 15

How do upper motor neurones initiate and control movement?

Answer 15

• controlling alpha motor neurones
• controlling gamma motor neurones
• controlling inhibitory interneurones

Motor neurones in the brain have axons which descend through the spinal cord which terminate where they can activate the inhibitory control.

Question 16

What does loss of upper motor neurones result in?

Answer 16

• weakness (brain can’t tell muscles to contracT)
• increased muscle tone and reflects (brain can’t control reflex arcs)
• no wasting (muscles remain active due to reflex input)

Question 17

Where is an upper motor neurone lesion?

Answer 17

Upper motor neurones are in the brain, but an upper motor neurone LESION can be anywhere between the cell body and the LMN.

Question 18

What two classes can the intrafusal muscle fibres be divided into?

Answer 18

• ‘nuclear bag’ fibres are associated with ‘type Ia afferents’
• ‘nuclear chain’ fibres are associated with ‘type II’ afferents (and type Ia to some extent)
• group II afferents encode length of muscle

Question 19

About group II afferents…

Answer 19

• thinner, slower axons
• mainly indirect connection to alpha motor neurones
• response in proportion to length of muscle
• important for maintaining limb position and posture, and for resting muscle tone

Loss of upper motor neurone input to group II reflexes causes hypertonia

Question 20

How can hypertonia (from UMN lesions) be treated?

Answer 20

• by suppressing the group II reflex

- boosting noradrenergic transmission helps (mechanisms uncertain): alpha 2 agonists (e.g. tizanidine) and L-DOPA

Question 21

About group Ia afferents…

Answer 21

• thicker, faster axons
• monosynaptic connection to alpha motor neurones
• responds to the rate of change in length (e.g. velocity of movement)
• important for correcting rapid unintended movements e.g. perturbations of gait

loss of upper motor neurone input to group Ia reflexes causes a velocity-dependent increase in tone (spasticity)

Question 22

How can spasticity (from UMN lesions) be treated?

Answer 22

• need to damp down the group Ia reflex
• this can be done by a non-specific increase in spinal inhibition: boost the effectiveness of GABAa receptors - benzodiazepines
• or more specifically by mimicking the effect of presynaptic inhibition: activate GABAb receptors (baclofen)

Question 23

In what circumstances are stretch receptors not always suppressed during voluntary movements?

Answer 23

• they are ‘switched on’ at key moments during some stereotyped movements…
• including a burst of activity in the afferents
• which boosts muscle excitation when needed

e.g. adds force to the contraction of the flexor muscles as they life the foot off he ground during walking

Question 24

What do golgi tendon organs do?

Answer 24

measure tension generated by active muscle contraction

Question 25

How do golgi tendon organ (GTO) afferents control the strength of muscle contraction?

Answer 25

GTO afferents activate two pathways that control the strength of muscle contraction. Upper motor neurones control which is active at any moment. The two pathways are GTO driven INHIBITION and EXCITATION

Question 26

How is the boosting of excitation done in relation to GTO?

Answer 26

in dynamic situations (e.g. walking) a pathway via an excitatory interneurone is enabled. This is used to boost muscle contraction at key points in the gait cycle.

Question 27

What are the two ways that the gold tendon organ can work?

Answer 27

- loss of GTO driven inhibition will cause hypertonia in static situations (e.g. standing) - loss of GTO driven excitation will cause weakness in dynamic situations (e.g. gait)

Question 28

What is the very basics of local anaesthetics?

Answer 28

- act locally, as they are applied to discrete areas of the body - prevent perception of pain by CNS - block generation/conduction of action potentials (APs) by inhibiting voltage-gating Na+ channels

Question 29

What is the importance of the pH of local anaesthetics?

Answer 29

local anaesthetics are weak bases (pKa of 7-9) - they act as proton acceptors at physiological pH (7.2) - more LA is in ionised/membrane impermeable form - act as proton donors in alkaline conditions (pH>7-9) - more in in non-ionised/membrane permeable form

Question 30

Why does LA procaine have a shorter half life than than LA lignocaine?

Answer 30

Because ester bones are susceptible to hydrolysis, and procaine has an ester bond where lignocaine has an amide bond

Question 31

How does the generation and conduction of action potentials occur?

Answer 31

1. Resting membrane potential is ~ -75mV - high K+ inside cell ~140mM/low K+ outside cell ~6mM - due to Na+/K+ ATPase - membrane selectively permeable to K+ ions (so negative inside cell) 2. during stimulation membrane depolarises to ~ -50mV - membrane depolarisation - reaches threshold of Na+ channels - opens channels and depolarisation (downstroke of APs)

Question 32

What is the mechanism of action of local anaesthetics?

Answer 32

LAs block Na+ channels: - block generation and conduction of APs - no APs, no information sent to CNS, no perception of pain - local anaesthetics will block any voltage-dependent Na+ channel irrespective of the tissue - hence these drugs are given locally to reduce systemic effects

Question 33

What is the effect of pH on local anaesthetics?

Answer 33

There is an interesting point with local anaesthetics: - action of LAs are increased in alkaline pH - but ionised LAs more effective at blocking Na+ channels

Question 34

Why does pH have an effect on local anaesthetics?

Answer 34

- LAs act on the part of the Na+ channel structure that is accessed from the inside of the cell - alkaline pH makes more drug into non-ionised form (LA), which can cross the 'fatty' myelin sheath and axonal membrane - inside the cell (pH 7.2), more drug becomes ionised into the LAH+ form, which blocks the Na+ channel - remember 'ion trapping'

Question 35

How do LAs block Na+ channels?

Answer 35

Mechanisms of blocking Na+ channels by LAs: - some block of closed state: unionised state - some block of open state: ionised state - substantial block of channels in inactivated state - ionised state

Question 36

What are 'use-dependent' drugs?

Answer 36

- LAs that only block Na+ channels in the inactivated state - only work when there is high activity - less side effects, low activity neurones not affected - principle of other drugs; anti-epileptic, class I cardiac anti-arrhythmic

Question 37

Why are pain fibres blocked before other sensory or motor neurones, when all fibres use Na+ channels to generate and conduct APs?

Answer 37

- LAs block small diameter axons before large ones - LAs usually block unmyelinated before myelinated fibres - nociceptive impulses are conducted in Adelta fibres (small diameter myelinated axons) and C fibres (unmyelinated axons) - pain sensation is lost first - increasing concentration/time LAs block all axonal conduction causing local paralysis (remember loss of movement after injection of LA at dentist)

Question 38

What are some unwanted effects of LAs on the CNS?

Answer 38

- if LAs enter the brain, this leads initially to stimulations (tremor, agitation and may produce convulsions) - subsequent CNS depression, respiratory problems

Question 39

What are some unwanted effects of LAs on the CVS?

Answer 39

- decreased cardiac output due to LAs blocking cardiac Na+ channels which leads to decreased Ca2+ influx and decreased force of contraction - increased vasodilation, due to inhibition of sympathetic nerve activity innervating blood vessels - decreases vascular tone - both these actions will cause a decrease in blood pressure --> potentially effect blood flow to vital organs

Question 40

What are possible bought of administration of LAs?

Answer 40

- SURFACE ANAESTHESIA: applied to mucosal surface e.g. bronchial (bronchoscopy), nose, cornea - LAs do not cross skin very well - NERVE BLOCK: LA injected close to sensory nerve e.g. dentistry - SPINAL ANAESTHESIA: LA injected into subarachnoid space between second and fifth lumbar vertebrae enters straight into CSF, e.g. surgery when inappropriate to use general anaesthetic, hip replacement in elderly - EPIDURAL: LA injected into epidural space, outside meninges, where it diffuses to and blocks nerve roots e.g. childbirth

Question 41

What happens when LAs are administered with adrenaline?

Answer 41

LAs can be administered with adrenaline. Adrenaline produces vasoconstriction by acting on alpha1 adrenoceptors on vascular smooth muscle cells within the walls of blood vessels. Vasoconstriction keeps the LA localised to the area of injection. Vasoconstriction inhibits absorption of the LA from the extracellular spaces into the blood - reduces possibility of systemic toxicity. It also prolongs the LA action.

Question 42

What do you need to beware of when administering adrenaline with LAs?

Answer 42

- local hypoxia | - absorption of adrenaline --> arrhythmia

Question 43

Where is the primary motor cortex?

Answer 43

The pre central gyrus of the frontal lobe, just anterior to the central sulcus.

Question 44

What does the primary motor cortex control?

Answer 44

voluntary movement of the opposite half of the body. Also called the motor strip, or M1.

Question 45

Where is the premotor cortex and what does it do?

Answer 45

Immediately infront of the motor strip and it is involved in movement planning and preparation.

Question 46

Where is the primary somatosensory cortex?

Answer 46

Just behind the motor strip, in the post central gyrus of the parietal lobe.

Question 47

What does the primary somatosensory cortex do?

Answer 47

received ascending (sensory) projections for all sensory modalities including light touch, joint position sense, pain, temperature etc. It is also called the sensory strip, S1

Question 48

What is the homunculus?

Answer 48

Motor cortex: size of cortical representation of each body part in proportion to precision of motor control Sensory: amount of cortex devoted to each body part is proportional to tactile sensitivity In both areas the hands, face and tongue have disproportionately large representations.

Question 49

What parts do the upper/lower body occupy in the primary motor and sensory areas?

Answer 49

In primary motor and sensory areas there is an orderly point-to-point representation of the opposite half of the body. The lower part of the body including the lower limbs occupies the medial surface of the hemisphere. On the convexity, the upper limb and hand areas are superior and the face/tongue areas or inferior.

Question 50

What are the two parts of the primary motor pathway?

Answer 50

1. the corticospinal tract 2. the corticobulbar pathway sometimes referred to collectively as the pyramidal tract or pyramidal motor system as the corticospinal component passes through the pyramids of the medulla.

Question 51

What does the corticospinal tract do?

Answer 51

projects from the motor and premotor areas of the frontal love to all levels of the spinal cord. It controls voluntary movements of the contralateral (opposite) limbs/trubnk and consists of approximately one million axons each side.

Question 52

What does the corticobulbar pathways do?

Answer 52

It is the voluntary motor supply to the brain stem (the motor cranial nerve nuclei) and therefore controls movements of the jaw, face tongue, larynx and pharynx. The word 'bulb' is an old fashioned term for the lower brain stem.

Question 53

Where do the fibres of the corticospinal tract originate?

Answer 53

- About 2/3 of the fibres originate from the motor and premotor areas of the frontal lobe - axons project to anterior horn of spinal cord grey matter (influence spinal motor neurones) - the remaining 1/3 arise from parietal lobe - project to dorsal horn of spinal cord, helping to 'filter out' sensations generated by movement

Question 54

What is the pathway of the fibres of the corticospinal tract?

Answer 54

- leave the cerebral cortex to enter subcortical white matter - pass through corona radiate first before entering the posterior limb of the internal capsule - internal capsule is an anatomical bottleneck so the arrangement of motor fibres is contact so even tiny amount of damage can lead to paralysis - continues to descend through anterior part of brain stem - pass in turn through CRUS CEREBRA, BASILAR PONS and then the PYRAMIDS OF THE MEDULLA - crosses the midline at the lowermost border of the medulla (approx at foramen magnum) - 90% of fibres cross posteriorly and laterally to enter lateral column of spinal cord as the lateral corticospinal tract - remaining 10% continue in the anterior part of the cord on either sid elf the midline and become the anterior (uncrossed) corticospinal tract.

Question 55

What is involved in voluntary movement?

Answer 55

involves a two-neutron cain between the motor cortex and skeletal muscle. The first neurone has its cell body in the motor/premotor cortex of the frontal lobe and an axon that contributes to the corticospinal tract. These cells are referred to as UMN. upper motor neurones which make up the corticospinal tract extend the full length of the spinal cord and synapse on LMNs.

Question 56

What is the difference in the symptoms of damage to the corticospinal tract in the brain or brain stem and in the spinal cord?

Answer 56

in brain/brain stem: weakness on opposite side of body spinal cord: weakness is ipsilateral

Question 57

What are the two most important somatosensory pathways?

Answer 57

- dorsal column pathway | - spinothalamic tract

Question 58

What are the similarities between the dorsal column pathway and spinothalamic tract?

Answer 58

- first neuron lies within the dorsal root ganglion - the second neurone crosses the midline and ascends to the thalamus - the third neurone lies in the ventral posterior nucleus of the thalamus and project to the primary somatosensory cortex. The main different is the position of the second neurone and therefore the point of crossing.

Question 59

What is the dorsal column pathway to do with?

Answer 59

fine, precisely located (or discriminative) touch, joint position sense, proprioception and vibration sense.

Question 60

Where does the dorsal column pathway originate form?

Answer 60

from low threshold mechanoreceptors and nerve impulses are transmitted to the brain via large diameter fibres that are thickly-myelinated and have high conduction velocities of up to 120m/s

Question 61

How is the dorsal column pathway best tested?

Answer 61

using a high amplitude, low frequency thing fork applied to bony prominences

Question 62

What is the spinothalamic tract to do with?

Answer 62

- pain and temperature sensation | - usually tested using sterile neurological examination pins or volatile spray producing a cold sensation

Question 63

Where does the spinothalamic tract originate?

Answer 63

from nociceptors and thermoreceptros. Pain and temperature impulses are transmitted to the brain via thinly-myelinated A-delta fibres and unmyelinated c-fibres, both of which are of comparatively small diameter and have relatively slow conduction velocities.

Question 64

What is neurylation?

Answer 64

The folding of the neural plate into neural tube. This process is triggered by growth factors released from notochord.

Question 65

How does the neural tube begin?

Answer 65

Begins as a single layer of neuroepithelial cells which divide symmetrically to increase in number, and then asymmetrically forming neuroblasts which can migrate. This is triggered by MCPH1

Question 66

What is the growth of the neural tube dependent on?

Answer 66

The type of growth is dependent on the morphogen gradient: BMP, wnt - dorsal aspect of developing brain Sonic hedgehog - ventral brain Where they are in the neural tube triggers the chemical signals around and determines what they will become eventually. This is all dependent on chemical guidance signals.

Question 67

What are example of chemical guidance signals in the neural tube?

Answer 67

Reelin: outwards - produced in marginal zone Neuregulins: dorsally Semaphorin slits: ventrally

Question 68

How are the cells laid down in the neural tube?

Answer 68

in an inside out fashion - the layer build up from the inside out. This is controlled by changing chemical signals.

Question 69

what determines the way that axons grow?

Answer 69

Our neuritis need to fid connection. The growth cone consists of lamellopodia and filopodia. These grow in relation to positive/negative (attractive/repulsive) signals. The axons travel according to signalling proteins via way points.

Question 70

What happen in synaptogenesis?

Answer 70

- axons look for potentially useful cells - relies on complementary adhesion molecules - this triggers the formation of pre- and post-synaptic structures --> IMMATURE SYNAPSE (e.g. neurexin and neuroligin)

Question 71

what happens if surface molecules in synaptogenesis are not complementary?

Answer 71

When the surface molecules are not complementary, the connection fails. The filopodia retract as a result - e.g. alpha motor neurones and antagonist muscles

Question 72

What is the function of specific pathways (as opposed to modulatory pathways)?

Answer 72

sensory, motor, cognitive 'processing'

Question 73

What is the function of modulatory pathways?

Answer 73

controls the state of the system

Question 74

What are the types of neural responses in specific pathways (as opposed to modulatory pathways)?

Answer 74

highly specific, event-related, information rich

Question 75

What are the types of neural responses in modulatory pathways?

Answer 75

non-specific, linked to sleep-wake cycle, behavioural state

Question 76

What is the synaptic transmission like in specific pathways?

Answer 76

fast, time dependent

Question 77

What is the synaptic transmission like in modulatory pathways?

Answer 77

slow, imprecisely timed

Question 78

What is the primary receptor type in specific pathways?

Answer 78

ionotropic

Question 79

What is the primary receptor type in modulatory pathways?

Answer 79

metabotropic

Question 80

What is the anatomy of specific pathways like?

Answer 80

precisely located (e.g. topographic)

Question 81

What is the anatomy of modulatory pathways like?

Answer 81

diffuse

Question 82

What happens in sleep-wake cycles?

Answer 82

- the thalamus relays information to the cortex - when we are awake, sensory information is relayed to the cortex, via the thalamus. - inputs are ignored when we are asleep - due to the inhibitory interneurone --> the cortex instead received synchronised information - regular impulses are put into it.

Question 83

What happens during REM?

Answer 83

during REM, the thalamus doesn't follow a typical sleep pattern. the brain changes a bit so an EEG becomes more random - the brain is making up its own sensory inputs. During REM sleep the muscles become paralysed and this is when you dream.

Question 84

What happens when someone has an REM disorder?

Answer 84

Their muscles don't become paralysed and so they enact their dreams.

Question 85

About Acetylcholine?

Answer 85

- one of the first NTs described - roles in ANS and PNS - in CNS; 2 long axon projections: - -> pontomesencephalic tegmenjtum: thalamus - -> Basal forebrain: neocortex and hippocampus

Question 86

About serotonin?

Answer 86

aka 5-HT - indolamine - appetite, mood, sleep, aggression - 2 pathways: rostral group-away from brain, caudal group-towards brain

Question 87

About norepherine?

Answer 87

- attention and arousal - ANS - fight/flight - multiple systems - be aware of the locus coeruleus system - projects diffusely - alertness, increased responsiveness, memory - defects can cause anxiety

Question 88

About dopamine?

Answer 88

2 pathways: NIGROSTRIATAL PATHWAY: projection to the basal ganglia, initiation of voluntary movement MESOLIMBIC PATHWAY: ventral tegmentum, projects to amygdala and ventral striatum - wakefulness, reward and reinforcement

Question 89

What can happen as a result of defective mesolimbic pathway?

Answer 89

schizophrenia

Question 90

About histamine?

Answer 90

- projects to thalamus and cortex | - excites wake promoting cycles

Question 91

What is falling asleep associated with?

Answer 91

Increased GABAergic activity

Question 92

What happens as a result of suppression of the modulatory systems?

Answer 92

circadian rhythm, tiredness --> adenosine build up, illness

Question 93

What increased during REM sleep?

Answer 93

There is an increase in activity from the pontomesencephalic tegmentum - desynchronising thalamic cells

Question 94

About the frontal lobe...

Answer 94

- primary motor cortex - contains BROCAS AREA - production of speech - PREFRONTAL REGION: dorsolateral-executive function, orbitofrontal-personality, social behaviour

Question 95

What is Broca's aphasia?

Answer 95

- reduced verbal output | - difficulty in speech

Question 96

About the parietal lobe...

Answer 96

- the post central gyrus contains the primary somatosensory cortex - DOMINANT: goal directed movement - NON-DOMINANT: understand special relations

Question 97

About the occipital lobe...

Answer 97

- primary visual cortex - V1: hemianopia - V2, V3: akinetopsia, achromatopsia

Question 98

About the temporal lobe...

Answer 98

- primary auditory cortex: hearing | - contains Wernicke's area: language comprehension

Question 99

What is Wernicke's aphasia?

Answer 99

fluent, non-sensical, meaningless speech

Question 100

What is included in the limbic system?

Answer 100

hippocampus amygdala anterior thalamic nuclei limbic cortex

Question 101

About the hippocampus...

Answer 101

- knowing where you are/navigations (taxi driver) | - bilateral damage causes profound anterograde amnesia - can't form new memories

Question 102

About the amygdala...

Answer 102

- evaluates significance of events - detects anger - facilitates social interactions - learning and memory Input: cortical inputs, olfactory inputs Output: toward hypothalamus (efferent) initiates response in ANS 'FFF'

Question 103

What can defects in the amygdala cause?

Answer 103

- anxiety - phobias - depression - autism - epilepsy - schizophrenia

Question 104

What is the limbic lobe concerned with?

Answer 104

motivation, mood and memory

Question 105

What does the limbic lobe include?

Answer 105

cingulate and parahippocampal gyri

Question 106

Lesions of what can impair memory formation?

Answer 106

cingulate gyrus

Question 107

What are the responses to stimulation of the limbic lobe?

Answer 107

stimulation of the anterior aspect: painful response, pupils dilate, CV changes stimulation of posterior: emotional content of visual and tactile sensations

Question 108

What is controlled by the corticospinal system?

Answer 108

trunk and limb muscles

Question 109

What is controlled by the corticobulbar system?

Answer 109

head and neck (mouth and throat) - speaking and swallowing

Question 110

What are the corticospinal and corticobulbar tracts known as collectively and where do they originate?

Answer 110

pyramidal tracts they originate in the cerebral cortex and carry motor signals to the spinal cord and brain stem

Question 111

What does the corticospinal tract control?

Answer 111

skilled, voluntary movements

Question 112

What does damage to the corticospinal tract cause?

Answer 112

contralateral paralysis or weakness (contralateral because it crosses over)

Question 113

Where does the corticospinal tract originate?

Answer 113

the primary motor cortex, infront of the central sulcus

Question 114

What is the pathways of the corticospinal tract?

Answer 114

pre central gyrus corona radiate internal capsule (posterior limb) enters the crus cerebra of midbrain and passes through ventral portion of pons subtotal decussation to caudal medulla and oblongata lateral and anterior corticospinal tracts

Question 115

Which sides of the body to upper motor neurone lesions affect?

Answer 115

Above the motor decussation: opposite side affected Below the motor decussation: same side affected

Question 116

What is the cerebellum responsible for?

Answer 116

planning movements as well as execution compares the movements planned with those actually carried out

Question 117

What are the motor advisors?

Answer 117

The basal ganglia and the cerebellum

Question 118

What is the comparison done in the cerebellum known as?

Answer 118

feed forward comparator

Question 119

Where does feedback come from to the cerebellum?

Answer 119

ear, eyes, vestibular nuclei, proprioceptors

Question 120

What is the feed forward comparator?

Answer 120

cerebellum takes in all the feedback and modifies the action the second time

Question 121

What is the spinocerebellum responsible for?

Answer 121

regulating muscle tone and posture

Question 122

What is the cerebrocerebellum responsible for?

Answer 122

high level planning movements, cognitive functions - pontine nuclei afferents and BL thalamus efferents

Question 123

What is the vestibulocerebellum responsible for?

Answer 123

maintaining balance and eye movements

Question 124

What kind of neurones are lower motor neurones?

Answer 124

second order neurones

Question 125

What are symptoms of UMN lesions?

Answer 125

- pyramidal weakness - no wasting of muscles - spasticity, clasp knife response, clonus - hyperreflexia - positive Babinski reflex, extensor planter response - absent abdominal relfexes

Question 126

What are the symptoms of LMN lesions?

Answer 126

- weakness (paralysis or paresis) - wasting of individual muscles - hyporeflexia - hypotonic or flaccidity - fasciculations

Question 127

What is proprioception?

Answer 127

the sense of the relative position of neighbouring parts of the body - including rate and trajectory of body movements

Question 128

What are the two types of muscle spindle fibres?

Answer 128

Type Ia afferents associated with nuclear bag fibres --> encode velocity of stretch Type 2 afferents - associated with nuclear chain fibres --> encode length of muscle

Question 129

What is the difference in contractility of extrafusal and intrafusal muscle fibres?

Answer 129

extrafusal muscles contract intrafusal muscles have contractile edges innervated by gamma motor neurones, but the middle portion is elastic not contractile. The afferents fire when they are stretched in the middle.

Question 130

What happens in the muscle fibres during voluntary movement?

Answer 130

- alpha motor neurones fire when voluntary movements occur - gamma motor neurones simultaneously fire keeping the middle bit taught and unchanged as both contract a corresponding amount

Question 131

What happens in the muscle fibres in involuntary movement?

Answer 131

afferent firing activating alpha motor neurones so contracts more and get more stretch - e.g. muscle more stretched than expected when something is heavier than you thought this is the stretch reflex

Question 132

What is the role of muscle spindles?

Answer 132

if the muscle is voluntarily stretched - central portion unchanged = no excitatory activity. Descending control systems also inhibit contraction so that the muscle doesn't resist stretching. Posture - if the muscle contracts too little to overcome gravity - central portion is stretched and the muscle contracts more. if an unexpected load causes a movement to be inaccurate, same process as above takes place

Question 133

What are the two types of inhibition (proprioceptors)?

Answer 133

- reciprocal inhibition | - presynaptic inhibition

Question 134

What is reciprocal inhibition (proprioceptors)?

Answer 134

antagonist motor neurone inhibited by Ia afferent of contracting muscle

Question 135

What is presynaptic inhibition (proprioceptors)>

Answer 135

contracting Ia afferent inhibits release of NT from antagonist Ia afferent (so there is no stretch in the antagonist muscle) eg as soon as afferent fires saying bicep is contracting, inhibitory efferent will stop the triceps contracting at the same time

Question 136

What is an UMN lesion?

Answer 136

anywhere between cell body and LMN causing loss of regulation of reflexes and conscious control

Question 137

What is an LMN lesion?

Answer 137

the alpha motor neurone lesion causes loss of innervation to muscle

Question 138

What is the role of golgi tendon organs?

Answer 138

measure tension generated by contraction (stretching doesn't usually cause much tension) they are within the tendon

Question 139

What states does the UMN control whether the muscle is in?

Answer 139

inhibited: static situations excited: dynamic situations

Question 140

When do afferents fire in relation to golgi tendon organs?

Answer 140

when the tendon squeezes - when these fire there are UMN and upper control systems that decide what happens - they can either activate an excitatory pathway or an inhibitory pathway

Question 141

What is an example of a dynamic situation (golgi tendon organs)?

Answer 141

Walking

Question 142

What is an example of a static situation (golgi tendon organs)?

Answer 142

standing still

Question 143

what might the loss of the golgi tendon organ pathway cause?

Answer 143

weakness in gait, or hypotonia - can't stand still

Question 144

What are possible types of injury in the CNS?

Answer 144

- developmental - trauma - ischaemic - hypoxic - inflammatory - neurodegenerative - infection - tumours

Question 145

What is a direct response to brain injury?

Answer 145

inflammation and oedema

Question 146

About stroke...

Answer 146

- acute loss of blood supply damages the region supplied by the blocked artery - it takes 6-8 minutes of blood supply interruption (ischaemia) to cause neuronal cell death (infarction) - most cerebral vascular occlusions will reopen spontaneously within 24 hours, but for the neurones this is too late - during this time it has been calculated you lose 2 million neurones per minute

Question 147

What is hypoxic brain injury?

Answer 147

reduction of whole brain oxygenation - preferentially affects the most metabolically active parts of the brain --> grey matter: cerebral cortex, basal ganglia

Question 148

What is the series of events in multiple sclerosis?

Answer 148

inflammation demyelination neuronal dysfunction

Question 149

What happens as a consequence of axon death?

Answer 149

- upstream: the cell body may die via apoptosis (retrograde degeneration) - downstream: the distal axon dies via Wallerian degeneration (anterograde degeneration)

Question 150

What are the consequences of denervation for the target neurone?

Answer 150

- from subtle changes e.g. transmitter hypersensitities in spinal cord injury resulting in spasticity - to transneuronal atrophy or degeneration eg visual and auditory systems

Question 151

What is meant by anterograde?

Answer 151

directed forwards in time

Question 152

What is the definition of retrograde?

Answer 152

Directed or moving backwards

Question 153

What is retrograde degeneration?

Answer 153

- depending on site there may be rapid degeneration of the projecting neurone - eg cortical stroke leads to rapid degeneration of thalamic neurone that project to the cortex

Question 154

What are mechanisms of spontaneous recovery in the CS?

Answer 154

- glial scarring - neurogenesis - regeneration

Question 155

What is glial scarring?

Answer 155

- glial scar formation (gliosis) is a reactive cellular process involving proliferation of astrocytes and microglia after injury to the CNS - this is a mechanism to protect any part of the healing process - in the context of neuronal injury however, formation of a glial scar has been shown to have both beneficial and detrimental effects - regenerates a tissue barrier after blood-brain barrier compromise and promotes revascularisation of injured brain - in particular, neuro-developmental inhibitors are secreted by astrocytes that prevent axon regrowth and regeneration

Question 156

What is neurogenesis?

Answer 156

- the birth of new neurones - nervous system could repair itself if it could grow new neurones - occurs in many non-mammalian vertebrates e.g. amphibians, songbirds

Question 157

Where is there evidence for significant neurogenesis?

Answer 157

- hippocampus (dentate gyrus) near the lateral ventricles (subventricular zone), supplying the olfactory bulb - both important for memory, so perhaps memory does' grow'

Question 158

What happens in regeneration?

Answer 158

- regrowth of severed axons - occurs in non-mammalian vertebrates - occurs effectively in mammals peripheral nervous system only

Question 159

Why is myelin critically important (and in regeneration)?

Answer 159

- provides a guide tube for the sprouting end of a severed neurone to grow through - extending axon guided to its destination during development

Question 160

What happens with regeneration in the human CNS?

Answer 160

- true regeneration of axonal projections rare - developmental loss of regenerative ability --> down regulation of growth related genes - due to micro environment --> trophic factors vs inhibitory factors --> glial scars - chemical/physical barrier

Question 161

What are treatments that can modulate recovery of incurable neurological diseases?

Answer 161

Neurorehabilitation: the clinical specialty that is devoted to the restoration and maximisation of functions that has been lost due to nervous system injury from whatever cause capitalises the way the brain normally learns to relearn lost function

Question 162

What is neural plasticity?

Answer 162

the ability of the brain to change structurally and functionally as a result of input from the environment - this is a normal phenomenon underlying brain function - reorganisation of neuronal processes resulting in functional and structural rearrangement - widespread: sensory, motor, visual, language systems at all levels of neuroaxis - plasticity occurs on a variety of levels, ranging from cellular changes due to learning, to large scale changes involved in cortical remapping in response to injury

Question 163

What is somatotopy?

Answer 163

point-for-point correspondence of an area of the body to a specific point in the CNS.

Question 164

What do discrete areas of the cortex do?

Answer 164

- control motion of specific small groups of muscles - receive sensation from specific areas of the body - subserve vision from specific areas of the visual field - subserve audition for specific pitches of sound

Question 165

Are specific area son the brain specific to certain functions?

Answer 165

- functions are also shared and to an extent degenerate - flexible and subject to neural plasticity - can be changed by: peripheral and central injury electrical stimulation learning and experience - eg cortical representation of left hand finger movements is expanded in violinists --> the homunculus is not fixed

Question 166

How do you fix the brain is you can't grow new neurones?

Answer 166

- COMPENSATION: having one brain area take over the functions damaged in another area, simple neural recovery: uninjured tissue takes over functions of lost neurones - presynaptic neurons sprout more terminals: form additional synapses with their targets and postsynaptic neurones, also add more receptor cells - REORGANISATION: a more dramatic form of neural recovery, can involve major brain areas

Question 167

What is reorganisation of neurones?

Answer 167

stimulation continues to shape synaptic construction and reconstruction throughout the individuals life --> experience is critical - a shift in connections that changes the function of an area of the brain - much of the change resulting from experience in the mature brain involves reorganisation - in some cases (not all) can lead to cortical remapping

Question 168

What are examples of neural plasticity after brain injury?

Answer 168

- hemispherectomy in young children: outcome can be surprisingly good, language reorganisation and relative intellectual preservation - in deaf people portions of visual cortex may be used for reading braille and other non-visual function - recovery of function after stroke

Question 169

What are putative mechanisms?

Answer 169

Neural plasticity can be expressed as activity dependent modifications int eh efficacy of existing synapses: - unmasking (removal) of inhibitory pathways - long term potentiation - synaptogenesis

Question 170

Briefly about adult stem cells?

Answer 170

- pluripotent - limited tissues (bone marrow, muscle, brain) - -> discrete populations of adult stem cells generate replacements for cells that are lost through normal wear and tear, injury or disease - umbilical cord/placenta

Question 171

What are the 'bystander' effects of stem cell transplantation?

Answer 171

- intrinsically neuroprotective - anti-inflammatory - delivery of trophic factors - overcome natural inhibitors

Question 172

What is the CPG?

Answer 172

responsible for the collection of neurones which makes movements happy. This is all controlled by the spinal cord and doesn't require the brain.

Question 173

What happens if you lose the anterior horn cell?

Answer 173

you are paralysed as it is the final connection to the muscle

Question 174

About the phrenic nucleus...

Answer 174

supplied phrenic nerve - C3, C4, C5 - supplies diaphragm - breathing

Question 175

About the spinal accessory nucleus...

Answer 175

up into skull and back down - C5, C6 - supplies sternocleidomastoid, trapezius - head turning, shoulder shrugging

Question 176

About Onus's nucleus...

Answer 176

sacral canal, where parasympathetic fibres come out - S2, S3, S4 - supplied external urethral and anal sphincters - continence

Question 177

What does the amount of grey matter in the spinal cord depend on?

Answer 177

muscle bulk at that level i.e. there is lots at the locations of the arms and legs, less as you go down

Question 178

What types of movements are there?

Answer 178

- reflexes: stereotypes (automatic, simple reflex arcs, triggered by proprioceptors) - rhythmic movements: breathing, walking, sometimes automatic sometimes voluntary (semi-automatic, involving brain stem and spinal cord. Do not necessarily require attention, can be controlled voluntarily) - voluntary actions: motor neurone direct connection form spinal cord, corticospinal tract (least automatic, e.g. writing, playing piano, speaking, goal-directed, dependent upon cerebral cortex)

Question 179

What is the flexor/withdrawal reflex?

Answer 179

- polysynaptic (several segments) - cutaneous reflex - elicits limb withdrawal - triggered by nociceptors - leads to limb flexion

Question 180

What is the crossed extensor reflex?

Answer 180

- triggered at the same time - causes contralateral limb extension - supports body weight eg stand on a pin and pull one leg away but straighten the other to support weight

Question 181

How is an action potential reached in the sensory system?

Answer 181

- external event/stimulus - sensory receptor cell detects and converts the energy in the stimulus into an electrical potential (transduce) - depolarisation of membrane - if gets afferent up to threshold - action potential

Question 182

What are possible answers to damaged/lost receptors (e.g. hearing)?

Answer 182

- transplantation of surviving receptors - production of new receptors from stem cells - gene therapy to make other retinal cells photosensitive

Question 183

What allows for one detail/discriminative touch?

Answer 183

receptive fields which are very small and close together, allowing the brain to reconstruct the afferent of the singles sent on the brain pad. if you have a small receptive field then you need lots of afferents to innervate that field - small receptive field require high innervation density

Question 184

Why is temporal resolution limited?

Answer 184

spatial resolution is limited, temporal resolution is limited. the two signals produce tapping in one little area right on top of each other and will probably feel like a single tap.

Question 185

what is the action potential threshold?

Answer 185

the membrane potential at which action potentials are triggered. this is a function of the vgNa+ channel and can be treated as a constant

Question 186

What is the 'activation' threshold?

Answer 186

the minimum stimulus strength that will depolarise a receptor enough to generate action potentials. sensory systems use receptors with a range of different activation thresholds.

Question 187

What is 'perceptual' threshold?

Answer 187

the minimum stimulus strength that will generate enough action potentials to be detected. perceptual threshold is the bit we can most easily test in a clinical environment this is the limit that someone can reliably detect the stimulus - this will change depending on how long the subject is attending to the stimulus - if they get bored it will shrink

Question 188

What is activation a measure of?

Answer 188

the sensitivity of the axon.

Question 189

How do sensory systems adapt to constant stimuli?

Answer 189

in the periphery the signals get stripped of a lot of redundant information. pressing against receptive ending gently, more strongly ad then more strongly again (more and more lines firing) gently there is a bit of depolarisation and low frequency action potentials firing, and this gets more as you press harder. this only works over a short period of time and is varied form receptor to receptor. virtually every receptor in every pathways adapt. this means that when you have a stimulus lasting longer than a few ms the initial response is to how hard you press, but if you maintain this pressure then the receptor will reset itself to its original, so now it can respond equally strongly to a new change, avoiding the receptor reaching its maximum frequency of firing and can't respond anymore. otherwise the system would saturate.

Question 190

Why do receptors adapt?

Answer 190

- different receptor adapt at different rates - adaptation means that receptors respond to changes in stimulation one time - adaptation allows much greater sensitivity while avoiding saturation - saves the expense of unnecessary action potentials this highlights salient moments when something changes - there is great sensitivity without saturating.

Question 191

What is lateral inhibition?

Answer 191

When you touch skin, more than one afferent fires up to the brain stem. if the pressure against the skin is exactly the same they will all be activated to the sam extent, and each will damp down their firing rate. if there is any bit where the stimulation is stronger than elsewhere then the afferent will be different. the only one responding well will get stronger, and will be damped down in other location to get a really clean signal through

Question 192

Why do we have lateral inhibition?

Answer 192

- one of many forms of inhibition that 'sculpt' sensory signals - means that sensory systems respond to changes in stimulation from place to place - allows much greater sensitivity while avoiding saturation - saves the expense of unnecessarily APs allows receptors to encode a he range of stimulus contrasts between locations without the danger of saturation - it controls sensory systems and is one of the most important forms of inhibition.

Question 193

What is ADAPTATION?

Answer 193

damps down responses to homogenous temporal information highlighting times when stimulus strength changes

Question 194

What are examples of the brain getting perception very wrong?

Answer 194

- pain - phantom limbs - synaesthesia (auditory input forms colour processing) - epileptic activity

Question 195

What are nociceptors?

Answer 195

primary afferents with sensory nerve ending in the periphery. they are part of the somatosensory system. they differ from touch receptors as their axons terminate in the spinal cord and don't go to the brain stem

Question 196

What are the two classes of nociceptors?

Answer 196

- Adelta | - C

Question 197

What are Adelta nociceptors?

Answer 197

- reasonably fast - responds to a variety of things - primary mechanical trauma or noxious heat - synapse in spinal cord with secondary afferents - the stabbing pain you feel when you are first injured

Question 198

What are C nociceptors?

Answer 198

- this second class has C fibres which have think non-myelinated axons - they re very slow and don't send the warning signal - reporting on going situations - eg intese pressure, noxious cold or heat - wide rang elf inflammatory mediators - produce the throbbing, aching, long term pain that persists until the injury is healed

Question 199

How do nociceptors respond to inflammation?

Answer 199

- C fibres are pro inflammation - can release a variety of substances from their terminals, including substance P - destroyed cells release their contents into extracellular space, particularly potassium - this depolarises any near by nerve cells including C fibres - the potassium triggers inflammation via inflammatory mechanisms - in the process of this you see the release of histamine, bradykinin and prostaglandins - prostaglandins make the cells more responsive to the other substances - depolarisation spreads to the other terminals which will release pro inflammatory peptides such as substance P - this will depolarise overlapping C fibre territories also - the initial cut ends up being surrounded by an extended region with swelling, tenderness and redness - this is good because it means the initial injury is surrounded by a hypersensitive region, which prevents you using it, and exposing it to further injury, therefore it is protected

Question 200

How do nociceptors contribute to inflammation?

Answer 200

Note in particular increases in histamine release and prostaglandin production, as well as recruitment of immune cells, vasodilation and extravasation. nociceptors release chemicals that recruit immune cells and cause inflammation

Question 201

What is the difference between sensation and perception?

Answer 201

Sensation: awareness that an event has occurred Perception: what is it? where is it? what does it mean? what should i do? localisation and discrimination of pain

Question 202

What is referred pain?

Answer 202

- each organ has a characteristic pattern of referred pain - this is why the homunculus doesn't have viscera - pain dissent up to the cortex in referred pain e.g. heart attack - NOT sent down to the hand

Question 203

What are the types of subconscious signals that the CNS controls?

Answer 203

- control of movement - autonomic responses - emotional and behavioural responses

Question 204

What happens in medial pain pathways?

Answer 204

- control of attention, arousal and autonomic systems | - someone that is hurt will suddenly be very alert, fast heart rate, sweating etc

Question 205

In what ways is arousal affected in modulatory pathways?

Answer 205

- sleep and wakefulness - focussing attention - switching attention

Question 206

How does 'normal' pain result?

Answer 206

from tissue damage stimulating nociceptors

Question 207

What is sensitisation of pain?

Answer 207

nociceptive pain may be increased by sensitisation but this is only normal provided that it fades

Question 208

What is neurogenic pain from?

Answer 208

neurogenic pain may be triggered by injury, but becomes independent of tissue damage. we sometimes continue to feel pain long after the injury has gone away - his is neurogenic pain

Question 209

How could long term potentiation contribute to chronic pain states?

Answer 209

you can get this in adults. if you cut or injury a nerve it will start firing. High frequency activation - long term potentiation. Anticonvulsants ana be used as a treatment for chronic pain, and this is becomes some can reduce the effectiveness of potentiated synapses.

Question 210

What does it mean that aberrant activity can become self-sustaining?

Answer 210

aberrant activity in one location can generate aberrant activity elsewhere.

Question 211

Why is pathological pain associated with abnormal cerebral cortical activity?

Answer 211

- cortical responses to mildly painful stimuli can be detected via fMRI - activity levels correlate with reported pain - both are increased in pathological pain states

Question 212

What is the difference between nociceptive pain and neuropathic pain?

Answer 212

Nociceptive: tissue damage Neuropathic: brain/nerve damage

Question 213

What are some examples of major analgesic drugs?

Answer 213

- opioids - NSAIDS - tricyclic antidepressants - anti-convulsants (Na+ channel blockers) - Ca2+ channel blockers - cannabinoids

Question 214

What are opiates?

Answer 214

substance from poppy somniferum (sleep producing) e.g. morphine, codeine

Question 215

What are opioids?

Answer 215

endogenous/synthetic compounds that produce morphine-like effects

Question 216

Where do opioids act?

Answer 216

at G-protein-coupled-receptors - all linked to Gi/G0 subtypes: MOP, DOP and KOP

Question 217

About MOP receptors...

Answer 217

MOP receptors are often associated with actions of morphine. MOP receptor is most prominently linked to analgesia. Receptors can couple with each other (not just MOP) and with other GPCRs. They are very complex.

Question 218

What do opioids do?

Answer 218

opioids reduce synaptic transmission - very different to NSAIDS decreased VGCCs --> decreased NT release K+ efflux --> hyper polarisation decreased neural firing both mechanisms reduce nociceptive conduction

Question 219

What are euphoric effects of opioids?

Answer 219

euphoria - give a powerful sense of 'well-being' and relief of stress - this is a very important analgesic tool and patients are often anxious and distressed. This is thought to be due to increased dopamine neurotransmission. this is caused by disinhibition of GABAnergic interneurones in 'reward' areas

Question 220

What are respiratory effects of opioids?

Answer 220

Respiratory depression opioid receptors are found in respiratory areas of the brain: pre-botzinger complex, brain stem and medullary nuclei chemoreceptors this causes suppression of the respiratory pattern and the chemoreceptors are less sensitive to PCO2 arterial increase in PCO2 - normally would increase the ventilation rate but this cannot occur due to the presence of the opioid opioid-induced respiratory depression is not linked to CVS complication - so is better tolerated than other drugs that effect both respiration and CVS e.g. barbiturates --> respiratory failure is the commonest cause of death in opioid overdose

Question 221

What are other effects of opioids?

Answer 221

- cough - vomiting - pupillary constriction - GI increase in tone, constipation - histamine release from mast cells - tolerance/dependence

Question 222

What are examples of commonly encountered opioids?

Answer 222

- codeine - methadone - diamorphine (heroin) - --> morphine (morphine goes into morphine-3-glucuronide (inactive) and morphine-6-glucuronide (active)) which is then excreted by the kidneys

Question 223

What is naloxone?

Answer 223

blocks all opioid receptors, reverses morphine-induced symptoms, used to reverse overdose problems

Question 224

What is buprenorphine?

Answer 224

long duration of action, heroin on top induces little effects, treatment of heroin addiction.

Question 225

How can the primary motor cortex be identified on the brain?

Answer 225

- part of frontal lobe - inverted omega sign on superior surface of brain (river thames sign) - can find central sulcus just behind it in MRI/CT scans it is often easier to see on the left side, perhaps because most people are right handed and so their left side is dominant - backwards door knob

Question 226

How an you find the central sulcus on a midsagittal brain surface?

Answer 226

- follow cingulate sulcus posteriorly - when it deflect upwards forms eh corpus callous os the marginal part (pars marginalis) - central sulcus immediately infront, sloping down and back at right angles

Question 227

What is the prefrontal region?

Answer 227

- non-motor - includes entire orbital region - 3/4 of frontal cortex - 30% of total cortical surface area Broca's area is in this region eg Phineas Gage

Question 228

What is the prefrontal region responsible for?

Answer 228

- cognition - goal orientate behaviour - social interactions - intelligence - creativity eg Phileas Gage

Question 229

what are the two main regions of the prefrontal cortex?

Answer 229

DORSOLATERAL PREFRONTAL CORTEX ORBITOMEDIAL PREFRONTAL CORTEX

Question 230

What is the dosrsolateral prefrontal cortex?

Answer 230

- cognitive funcitons - "executive functions" - takes part in basal ganglia loops that pass through the caudate nucleus - regulation of normal thinking - abnormally active ein OCD patients Also contains frontal eye fields which control gaze and attention - which can be affected in frontal lobe damage.

Question 231

What is the orbitomedial prefrontal cortex?

Answer 231

- regulation of behaviour, personality and social conduct | - lesions: rude, disinhibited and inappropriate. Decision making and judgement severely impaired.

Question 232

What is the strutter of the parietal lobe?

Answer 232

- posterior to central sulcus, above lateral sulcus - lateral parietal region contains post central gyrus/primary somatosensory cortex (immediately behind the motor strip) - map of body corresponding to tactile sensitivity and discriminative touch - the res tis divided into superior and inferior parietal lobules by intraparietal sulcus

Question 233

What are the functional areas of the parietal lobe?

Answer 233

POSTCENTRAL GYRUS/SENSORY STRIP POSTERIOR PARIETAL CORTEX POSTERIOR PARIETAL REGION

Question 234

What is the postcentral gyrus/sensory strip?

Answer 234

- somatic sensation | - termination point for ascending somatic sensory pathways

Question 235

What is the posterior parietal cortex?

Answer 235

- behind sensory strip - somatosensory association cortex - visuospatial representation of objects in the extra personal space - localisation and movement - receives projections forms he visual pathway ("where" pathway) telling where objects are and how they're moving - also important for object interaction

Question 236

What is the posterior parietal region?

Answer 236

- in cooperation wit the frontal lobe - daily activities (walking, knife and fork, dressing) - damage affects these functions - identifies interesting objets in the environment - projection to frontal eye fields controlling visual attention and voluntary gaze - posterior parietal strokes and lesions can cause attentional problems including neglect of half of the world - some patients may be unaware f the problem and think they are fine - this is called ANOSOGNOSIA

Question 237

What are praxes?

Answer 237

semi-automatic motor sequences (e.g. scissors, shoelaces). these are stored in the prefrontal cortex and selected b the posterior parietal lobe. difficulty with this is called APRAXIA.

Question 238

What is Gerstmann Syndrome?

Answer 238

in posterior parietal region the left hemisphere is dominant/verbal it is involved in symbolic representation, concepts of number, maths and physical ability and reading and writing lesions cause problems with this and this is gerstmann syndrome

Question 239

What is the PRECUNEUS?

Answer 239

in te medial part of the parietal lobe between the paracentral lobule and the cuneus of the occipital lobe there is increased blood flow to this area during day dreaming, quiet contemplation, meditation, recalling personal (episodic) memory and visualising in the 'minds eye'

Question 240

What is the anatomy of the occipital lobe?

Answer 240

- posterior to the parieto-occipital sulcus and pre occipital notch - medial, lateral and inferior surfaces - concerned entirely with vision

Question 241

what is the medial occipital lobe?

Answer 241

- divided by the calcimine sulcus into wedge shapes cuneus and tone shaped lingual gyrus 0 primary visual cortex in calcimine sulcus - most of exposed surface consists of visual association cortex - visual information relating to forma dn colour passes inferiorly to the temporal lobe in the temporal love visual stream ("what" pathway) - informations integrated by lateral and inferior temporal cortex to identify and categorise objects --> failure to do so is AGNOSIA

Question 242

What is the temporal lobe?

Answer 242

- below lateral sulcus - posterior boundary is the pre occipital notch - composed of superior, middle and inferior temporal gyro, defined by superior and inferior temporal sulk - the superior surface is flat and hide in the lateral sulcus contains the primary auditory cortex which receives the central auditory pathways. the surrounding cortical territories the auditory association cortex which is responsible for recognition of speech sounds in the language dominant hemisphere. the lateral temporal region is involved in recognition of objects and in categorisation

Question 243

What are the two language areas?

Answer 243

Brocas area and Wernickes area surrounding areas in the inferior parietal lobe are involved in the understanding of written language/reading

Question 244

What is Broca's area?

Answer 244

- in the inferior frontal gyrus - "motor" language area - production of speech and language

Question 245

What is Wernicke's area?

Answer 245

- in the posterior third of the superior temporal gyrus - "sensory" language area - recognition of speech sounds and understanding spoken language

Question 246

What is the arcuate fasciculus?

Answer 246

- arc shape white matter bundle - connects anterior and posterior language areas- begins at the frontal lobe and passes posteriorly and sweeps down into the temporal lobe

Question 247

In general terms what is dysphasia?

Answer 247

an acquired disorder of spoken and written language

Question 248

What happens as a result of anterior hemispheric lesions in the region of broca's area?

Answer 248

- non-fluent dysphasia: slow, disjointed, hesitant speech - patient becomes frustrates - comprehension relatively preserved (multi-step task test)

Question 249

What happens as a result of posterior hemispheric lesions in the region of wernicke's area?

Answer 249

- fluent dysphasia: fast, flowing speech but nonsense - patient often unconcerned and unaware - comprehension severely affected

Question 250

What is conduction aphasia?

Answer 250

patient has normal expression and comprehension but a selective difficulty with repeating phrases. often due to a lesion in the arcuate fasciculus which is said to disconnect the sensory and motor language areas

Question 251

What is global dysphasia/aphasia?

Answer 251

both language areas are affected and there is a sever deficit in language expression and comprehension

Question 252

What is the homologue of Brocas area?

Answer 252

it is in the non-dominant hemisphere | important for non-verbal aspects of speech e.g. rate, rhythm, tone, gestures and facial expressions

Question 253

What is the homologue of Wernicke's area?

Answer 253

in the non-dominant hemisphere | important for understanding subtlety of tone e.g. recognising sarcasm

Question 254

What is the definition of hypertension?

Answer 254

sustained elevation of systolic and diastolic blood pressure >140/90 mmHG

Question 255

What are the causes of hypertension?

Answer 255

primary (idiopathic/essential): no identifiable cause secondary to: renal disease, adrenal tumours, aortic coarctation, steroid reaction

Question 256

What damage can hypertension do to blood vessels?

Answer 256

contribute to all aspects of hypertensive organ damage. blood vessels themselves undergo atheroma and aneurysm formation in large vessels, elastic reduplication in small vessels

Question 257

What damage can hypertension do to the heart?

Answer 257

left ventricular hypertrophy, left heart failure (LHF)

Question 258

What damage can hypertension do to the lungs?

Answer 258

pulmonary oedema due to LHF

Question 259

What damage can hypertension do to the kidneys?

Answer 259

nephrosclerosis, renal failure

Question 260

What damage can hypertension do to the eye?

Answer 260

retinal capillary damage, haemorrhages, exudates

Question 261

What damage can hypertension do to the brain?

Answer 261

micro aneurysms and stroke ischaemic cortical atrophy/dementia

Question 262

What is hypertensive heart disease?

Answer 262

increased load causes concentric left ventricular hpertrophy

Question 263

What is hypertensive nephropathy?

Answer 263

granular cortical atrophy due to nephrocsclerosis - loss of a glomerulus causes atrophy of the nephron

Question 264

What is hypertensive retinopathy?

Answer 264

can be mild, moderate or late chronic ('malignant' acute) MILD: nicking of retinal veins by overlying arterioles, normally they run alongside MODERATE: straightened, wider capillaries - flame shaped haemorrhages - 'cotton wool' spots - (later) 'hard' exudates around macula LATE CHRONIC: papilloedema, haemorrhage

Question 265

How are the blood vessels involved in hypertension?

Answer 265

BP controlled by the arterioles, especially the latter - they e resistance vessels which can constrict of relax to alter the peripheral resistance. change sin the luminal diameter of the arterioles are the most important component in regulating systemic arterial BP. the resistance of flow is equivalent to the fourth power of the diameter. therefore, a 50% decrease in the lumen results in a 16-fold increase in the pressure

Question 266

What changes occur to the blood vessel in hypertension?

Answer 266

- resistance arterials show elastic duplication - 'hyaline arteriosclerosis' damages arterioles as plasma exudes into the intimate and deeper layers of the wall, sometimes out of the smaller vessels - glassy pink appearance on histology - endothelium is subject to damage by shearing forces applied y the high pressure cardiac output: atheroma is likely to develop at sites of endothelial damage due to hypertension - atheroma tends to affect larger blood vessels, so does not increase peripheral resistance sufficiently to cause hypertension, however the two disease are often encountered together

Question 267

What is the blood pressure equation?

Answer 267

BP = CO x TPR

Question 268

What stimulates vasodilation or constriction in the blood vessels?

Answer 268

baroreceptors in the carotid sinus are sensitive to stretching of the artery and signal BP alterations to the brain stimulating vasoconstriction or dilation chemoreceptors in the carotid bodies and aortic bodies respond to decreased oxygen tension, increased CO2 and increased H+ ions in the renin-angiotensin-aldosterone system the kidney juxtaglomerular complex releases renin in response to low renal blood flow/low blood Na+/sympathetic NS stimulation

Question 269

What is the renin-angiotensin-aldosterone system?

Answer 269

renin cleaves angiotensinogen in the blood to angiotensin I. lung capillary cell enzyme ACE forms angiotensin II from I.

Question 270

How does angiotensin II increase BP?

Answer 270

- peripheral vasoconstriction of resistance vessels - stimulating aldosterone release by the adrenal cortex = increases water reabsorption by the kidney - stimulates ADH secretion by posterior pituitary = increases water reabsorption by the kidney - stimulated thirst = increased blood volume - stimulates cardiac hypertrophy - thanes sympathetic nervous system stimulation by increasing noradrenaline release and decreasing reuptake at sympathetic nerve endings - negative feedback is by NATRIURETIC PEPTIDES (ANP and BNP), released by the heart

Question 271

What is an aneurysm?

Answer 271

a bulge in the wall of a blood vessel

Question 272

What is a true aneurysm?

Answer 272

when the entire wall of the vessel bulges - sometimes part of the wall is cut or torn, usually by trauma and the inner layers urge through he tear - some people would term this a false aneurysm because not all the layers are affected

Question 273

What is a false aneurysm?

Answer 273

occur if the artery wall is punctured and blood tracks out int adjacent tissue, but it contained locally by scar tissue. this expands as further blood is pumped out of the vessel wall

Question 274

What are examples of types of aneurysm?

Answer 274

- berry (saccular) aneurysms - micro aneurysms - abdominal aortic aneurysms - stretched aortic ring

Question 275

What is a berry aneurysm?

Answer 275

typically occur at the bifuratons of the arteries in tech circle of willis. their rupture usually causes subarachnoid haemorrhage

Question 276

What are micro aneurysms?

Answer 276

typically occur in cerebral arteries in patients with hypertension. their rupture cause intracerebral haemorrhage

Question 277

What are abdominal aneurysms?

Answer 277

usually secondary to atheroma and may rupture casing intraperitoneal haemorrhage and death, or throw odd thromboembolic causing ischaemia and gangrene

Question 278

What is stretched aortic ring aneurysm?

Answer 278

can be due to aortic dissection ('dissecting aneurysm') or symphilitic aneurysm. both develop due to weakening of the media and may rupture, causing haemopericardium an cardiac tamponade

Question 279

Where do aneurysms often occur?

Answer 279

often occur at points of weakness - usually due to atheroma - sometimes due to inflammatory image - occasionally due to connective tissue abnormalities - sometimes follow trauma

Question 280

What do aneurysms look like?

Answer 280

- most are secondary to atheroma and are fusiform (spindle shaped) - saccular aneurysms often occur after focal damage to a vessel - berry aneurysms are saccular and are due to focal vessel wall weakness at the point of bifurcation

Question 281

What are possible complications of aneurysms?

Answer 281

- rupture - thrombosis - thromboembolism

Question 282

What is aortic dissection - 'dissecting aneurysm'?

Answer 282

typical of an elderly person with medial degeneration or marfan's syndrome - a congenitally weak media scenario: - tear in intimate,typically aortic root, allows blood to enter the aortic wall and form a parallel track - this may rupture back into the aortic or rupture through the adventitia, causing death by cardiac tamponade or exsanguination

Question 283

What is ischaemic stroke?

Answer 283

- 80% of stroke cases - thromboembolic: sources include thrombus over atheroma at carotid bifurcation; mural thrombus from heart - primary occlusion of intracerebral artery/arteriole - lacunar: occlusion of single penetrating artery ~1/4 of ischaemic strokes fall into this category. tiny lesions 0.2-15mm diameter, can be silent, associated with white matter lesions and 'vascular' dementia, or catastrophic e.g. brainstem

Question 284

What is haemorrhage stroke?

Answer 284

- 20% of cases | - most commonly due to rupture of cerebral micro aneurysm secondary to hypertension

Question 285

What is the ischaemic penumbra?

Answer 285

- the core of an infarct will undergo irretrievable and irreversible necrosis - the adjacent territory is only relatively ischaemic, as there may be a degree of compensation from nearby blood supplies - if arterial perfusion can be stored within 3 hours, much of the 'penumbra' territory may be salvaged. some benefit to treatment up to 6 hours later - ischaemic damage to endothelium may render newly perfused vessels leaky, so restoration of function may not be as good as hoped and bleeding may occur

Question 286

What do the clinical effects of a stroke depend on?

Answer 286

- site - size - speed of restoration of circulation/evacuation of blood clot

Question 287

What are the acute and chronic features of stroke?

Answer 287

ACUTE: headache/neurologicla deficit, confusion, coma, death CHRONIC: site dependent

Question 288

What is a space occupying lesion (SOL)?

Answer 288

A massive bleed acts as a SOL in the brain and can cause herniation of the brain and death due to coning - the squeezing of the brain and brainstem through the foramen magnum as a result of swelling. It may lead to a loss of basic cardiorespiratory function.

Question 289

What are the three main sites at which herniation of the brain can occur in response to a SOL in the brian?

Answer 289

- beneath the FALX CEREBRI - through the TENTORIUM CEREBELLI - through the FORAMEN MAGNUM

Question 290

What is liquification necrosis in the brain?

Answer 290

cerebral lesions due to strokes are soft due to liquification necrosis o the brain tissue, which i a type of necrosis which results in transformation of the tissue into a liquid viscous mass.. When this s cleared by macrophages, cystic spaces remain in the brain. Near by gloss is the brains equivalent to scarring.

Question 291

What are lacunar artefacts?

Answer 291

- typically seen in diabetes and or hypertension, usually with extensive small vessel atheroma - affect deep penetrating arterioles - typically to basal ganglia, brainstem, thalamus and deep white matter, small lesions 2-15mm - not space-occupying lesions - tiny cystic infarcts may be devastating e.g. if internal capsule is involved, a 2mm infarct mat cause a dense hemiplegia, if white matter can be clinically silent but contribute to vascular dementia - minimal additional symptoms due to small calibre vessels involved

Question 292

What is TIA?

Answer 292

Transient Ischaemic Attack - neurological deficit lasting 1 hour, diabetes - indication for immediate investigation and intervention

Question 293

What are methods of stroke management?

Answer 293

anti platelet therapy: aspirin, clopidogrel, dipyridamole thrombolysis (best within 3 hours may have functional benefit up to 6 hours later) evacuation of clot

Question 294

What are methods of stroke prevention?

Answer 294

- smoking cessation: tax++ on cigarettes - aspirin for those at risk - decrease salt intake - treat atrial fibrillation: warfarin, and new direct anticoagulants developed - fast recognition of TIA

Question 295

What is subarachnoid haemorrhage?

Answer 295

often considered together with occlusive or haemorrhage strokes. SAH is not a stroke on technical grounds, since is involves vessels which are external to the brain itself. however, SAH can induce spasm in cerebral arteries, on reason for the high mortality and morbidity in this condition.

Question 296

What are types of intracranial haemorrhage other than stroke?

Answer 296

- extradural haemorrhage - subdural haemorrhage - subarachnoid haemorrhage - cerebral contusions - multiple petechial haemorrhages

Question 297

What is extradural haemorrhage?

Answer 297

typically parietal due to rupture of middle meningeal artery, often acute. 'lucid interval' common after initial consciousness because tough dura takes time to stretch

Question 298

What is subdural haemorrhage?

Answer 298

eg rupture of wins crossing subdural space; may be acute (post trauma, similar to extradural) or chronic - typical in dementia as shrunken bean renders shearing injury more likely

Question 299

Why are cerebral contusions?

Answer 299

trauma - may be 'contra-coup' injury

Question 300

What are multiple petechial haemorrhages?

Answer 300

obstruction of small arterioles and capillaries e.g. falciparum malaria, DIC. Capillary obstruction causes multiple tiny infarcts but because the disease is not primarily of cerebral blood vessels and disseminated through the body, this is not a stroke

Question 301

What are the meninges?

Answer 301

dura mater: thick layer adherent to skull | pia-arachnoid: fused delicate membrane which follows the contours of the brain

Question 302

Subarachnoid vs subdural haemorrhage?

Answer 302

subarachnoid: often follows ruptured berry aneurysm, blood is confined beneath pia/arachnoid and follows the brain contours subdural: formation is the result of trauma, blood clot lies between the arachnoid and dural meninges

Question 303

Why are most infarcts pale and solid?

Answer 303

due to coagulation necrosis eg splenic or renal infarcts

Question 304

What are watershed zones?

Answer 304

regions of the body that receive dual blood supply from the most distal branches of two large arteries, such as the splenic flexure of the large intestine

Question 305

What is watershed zone infarction?

Answer 305

ischemia, or blood flow blockage, that is localized to the border zones between the territories of two major arteries in the brain

Question 306

Why does watershed zone infarction occur?

Answer 306

due to hypo perfusion at the boundaries of arterial territories: brain, colon, heart if BP suddenly drops profoundly, e.g. following profuse haemorrhage, tissue at the periphery of adjacent arterial territories mat be starved of oxygen and undergo infarction

Question 307

What are typical examples of watershed zone infarction?

Answer 307

the splice flexor of the colon and the watershed zones of the cerebral arteries making up the circle of willis

Question 308

What water shed zone infarction would affect the brain?

Answer 308

- anterior cerebral artery territory - middle cerebral artery territory - posterior cerebral artery territory leaves a watershed zone

Question 309

What special requirements does cerebral circulation have?

Answer 309

- neuronal cell bodies (grey matter) make up 40% of brain tissue and are intolerant of hypoxia - without O2 neuronal damage occurs in several minutes. Therefore the primary requirement of the brain is a constant O2 rich blood supply. - for proper function the brain has a very high O2 consumption, so constantly requires a high blood flow (100 ml/min/100g grey matter) - local functioning within the bran requires constant changes in local blood flow

Question 310

In what ways does the brain adapt for the special requirements of cerebral circulation?

Answer 310

- high O2 consumption/size - high proportion of cardiac output/size - high resting O2 extraction of 35% (body average is 25%)

Question 311

What structural special features does the brain have regarding cerebral circulation?

Answer 311

to achieve constant high flow of O2 rich blood to the brain, the circulation has developed the circle of willis. an anastomosis.. to achieve high O2 delivery/extraction to neurones, capillary density is very high (3000-4000 per mm^2) - ficks law: J= -DA ∆C/ Blood brain barrier: formed of very tight endothelial junctions

Question 312

What arteries are in the circle of willis?

Answer 312

- anterior cerebral artery - internal carotid artery - middle cerebral artery - posterior cerebral artery - posterior communicating artery - vertebral artery - basilar artery

Question 313

What are the functional special features of the brian in terms of cerebral circulation?

Answer 313

- the brain controls the CVS to safeguard its own blood supply by: carotid sits baroreceptors which monitor cerebral perfusion pressure (BP) and controlling heart/peripheral vasculature through reflexes - cerebral resistance vessels are spared from baroreceptor reflex-induced vasoconstriction - auto-regulation is extremely well developed (myogenic response) - local metabolic vasodilation is well developed - tight blood-brain barrier controls the access and outflow solutes

Question 314

What is the system of nervous control of cerebral arteries?

Answer 314

- cerebral arteries 'outside' the brain receive dense innervation from sympathetic nerves - cerebral arterioles 'within' the brain have little innervation - little involvement of cerebral vasculature in baroreceptor reflex - 5-HT (serotonin) is abundant in perivascular nerves around cerebral arteries - perivascular sensory fibres (nociceptors) mediate the pain of vascular headaches in strokes and the later phase of migraine

Question 315

What happens at the blood brain barrier?

Answer 315

There is a scanty vesicular transport system - continuous tight junctions - O2, CO2 and general anaesthetics can go across as they are all lipid soluble - carrier-mediated transport (facilitate diffusion) of glucose and amino acids

Question 316

What is the function of the BBB?

Answer 316

KEEP OUT: circulating neuro-active chemicals that would interfere with neuronal signalling e.g. catecholamines KEEP IN: neurotransmitters - otherwise they would be continuously washed out of brain due to the high blood flow

Question 317

In what areas is the BBB detective to allow access of signalling molecules?

Answer 317

- area postrema of brainstem: emetic molecules (vomiting centre), angiotensin II (sympathetic stimulation) - sub-fornicular organ of hypothalamus: angiotensin II (thirst sensation) - periventricular osmoreceptors (hypothalamus): plasma osmolarity (ADH secretion)

Question 318

What are special problems of the cerebral circulation?

Answer 318

1. postural hypotension 2. cerebral artery vasospasm 3. cerebrovascular accidents or 'strokes' 4. encasement in rigid cranium -- cerebral tumours or haemorrhage cause a SOL rain gin intracranial pressure = Cushings reflex (increased BP and reflex bradycardia)

Question 319

What is postural hypotension exacerbated by?

Answer 319

- warmth - bed rest - zero gravity

Question 320

What is vasospasm due to?

Answer 320

local vasoconstrictor agents - 5-HT from peripheral nerves - prodromal phase of migraine - neuropeptide Y from perivascular nerves - endothelin-1 from vascular endothelium - vasoconstriction - K+ ions from damaged cells - excitability of vascular tissue

Question 321

What is vasospasm reduced by?

Answer 321

- Ca2+ channel blockers (acting on vascular smooth muscle) | - Eta receptor blockers

Question 322

What is vasospasm?

Answer 322

sudden constriction of a blood vessel, reducing its diameter and flow rate.

Question 323

What types of cerebrovascular accidents (CVAs, 'strokes') are there?

Answer 323

OBSTRUCTION 80% - cerebral artery thrombosis/embolism - due to atheroma - small arterial emboli shed from atheromatous carotid artery/vertebral artery cause repeated 'transient ischaemic attacks' (TIA) which resolve in hours between episodes HAEMORRHAGE 20% - sub-arachnoid/intra-cerebral - rupture of berry aneurysm (younger adults) - neurological damage is due partly to the triggered vasospasm - not just lots of blood flow

Question 324

How does a SOL lead to Cushing's reflex?

Answer 324

- SOL - increased sympathetic vasoconstrictor activity - increased TPR - increased BP - baroreflex and bradycardia

Question 325

What does the neural retina do?

Answer 325

detects light and contains efferents which go out and form the optic nerve, carrying signals back to the thalamus

Question 326

What is the different role of rods and cones?

Answer 326

Cones: daylight ('photopic') vision Rods: night time ('scotopic') vision

Question 327

How does the retina send information to the brain?

Answer 327

we have afferents wit ganglion cells. axons run across the surface of the retina. the gap is bridged by interneurones in the inner nuclear layer. bipolar cells form bridges between photoreceptors and underlying ganglion cells. these are connected to overlying cones.

Question 328

What is the receptive field?

Answer 328

the bit of the visual image focussed onto the overlying cones

Question 329

Why is light scattered as it passes through the first few layers of the eye?

Answer 329

because they are translucent. this is a weakness in he design of the eye, as the light becomes 'blurred' as a result of this. this causes poor sampling so the light is sampled by cones which are scattered /separated by large numbers of rod photoreceptors.

Question 330

Why does resolution get poorer as you go further out of the visual field?

Answer 330

the input from these two ganglion cells is convergent and they all converge into a single ganglion cell. these get larger and larger the further out you go of the visual field, and so resolution gets poorer and poorer

Question 331

Why is the peripheral retina only capable of coarse vision?

Answer 331

- the visual image is optically blurred - the cone photoreceptors are large and widely spaced (separated by larger number of rods) - the signals from many cones converse onto single ganglion cells

Question 332

Where is the exception to the fovea having no overlying blood vessels?

Answer 332

the centre of the retina, and this is why we don't have really poor vision. round the very centre is the optic nerve had and this is what we mean when we talk about central vision.

Question 333

What is the macula lucida?

Answer 333

an area with yellow pigment near the centre of the retina - it is the blind spot

Question 334

What is the fovea?

Answer 334

a small, central pit composed of closely packed cones in the eye. It is located in the center of the macula lutea of the retina

Question 335

Why is there a foveal pitch?

Answer 335

there is a small region where the ganglion cell layer and interneurone later is pushed aside, leaving a pit which exposes the photoreceptors. light coming in through here doesn't have to pass through all the layers and this is the one part of your eye where the image is well focussed. the ganglion cells connecting here don't have convergence. the sampling isn't blurred by convergence. input form those cones kept separate all the way back to the primary visual cortex.

Question 336

How is the fovea specialised for high resolution?

Answer 336

- overlying layers and blood vessels are absent, so the image is well focussed - it contains only cone receptors - which are narrow and closely packed - the signals form the photoreceptors are kept separate

Question 337

Why do we not have colour vision on the outer edges of the retina?

Answer 337

the wiring between the rods and the ganglion cells isn't specific enough to pull out the individual differences. the further out of the periphery you go, the worse it gets.

Question 338

What are the various things that can happen to the light entering the eye?

Answer 338

- hit the transparent corey and pass straight through - stopped by the iris - pass through the pupil and be brought into focus on the retina by the optics of the eye

Question 339

What parts of the eye bend the light to bring it into focus?

Answer 339

the cornea does this most. we need the lens as well though which is weaker but is adjustable, whereas the cornea is fixed. the lens allows near and far focus and so it accommodates for different distances of vision.

Question 340

What does the pupil do?

Answer 340

the pupil allows light through. the visual system can adapt to a huge range of light levels and the pupil size change isn't predominantly responsible for this. the bigger the pupil, the more blue in the image because you get more light rays going through and so more bending. however, the pupil can never be a single pin prick in size because we need to allow enough light in for the image to be useful.

Question 341

What des the sphincter papillae do?

Answer 341

it is a ring muscle - when this muscle contracts the pupil gets smaller.

Question 342

What are the short ciliary nerves?

Answer 342

part of the sympathetic nervous system and use Ach, hence atropine will make the pupil engaged for examinations.

Question 343

What is the preganglionic pathway?

Answer 343

The preganglionic pathway is driven from the retina itself. CNIII with ciliary ganglion at the end of it, the ganglion cell in the retina is activated if the retina is illuminated. the signal is sent back to other places such as the brain stem to the nucleus. the pretectal nucleus activates the edinger westphal nucleus, which activates the ciliary ganglion. these reflex pathways allow the pupil to contract when light becomes brighter in that eye.

Question 344

What does the pretectal nucleus do?

Answer 344

- activates edinger westphal nucleus (which activates cilia ganglion) - feeds to both sides so both sides of retina are activated and so both pupils will contract at the same time - bilateral from front to back because of the afferents and efferents - both eyes will react in the same way at the same time

Question 345

What do we look for in pupil examinations and why?

Answer 345

We look for both pupils reacting in the same way at the same time. We want to see this because the pathways of the preganglionic fibres running through CNIII are very sensitive to raised intercranial pressure, which if raised stops them from functioning, and one will respond more slowing and then you know there is something badly wrong.

Question 346

What is the ciliary muscle?

Answer 346

- also ring shaped - ring controls the lens (NOT the iris) - when the muscle contracts the ring gets smaller and the ring of suspensory ligaments that connect the end to this ring of muscle becomes slack, allowing the lens to get fatter in shape - if it is pulled flat by the sensory ligaments, when it contracts and relaxes the ligaments, it becomes round - a round lens has stronger refractive power. this is how the lens accommodates to different distances of vision

Question 347

What is the dilator papillae?

Answer 347

- a radial muscle - when it contracts it pulls the pupil open - this is driven by the long ciliary nerves which are part of the sympathetic nervous system, releasing noradrenaline - when you see it suddenly dilate this is not always in response to light - it is due to a strong emotional drive - for example dear or love, and it is not controlled by light

Question 348

In what way are the optics of the normal eye matched to the length of the eyeball?

Answer 348

if you have perfect vision the length of the eye is perfectly matched to the strength of your optics. the light rays will enter the eye basically parallel and only need a little bit of extra power in the lens. When getting closer, you need more refractive power and fatten up the lens and it all works out and the image is in focus.

Question 349

What does it mean if the eye is myopic?

Answer 349

- if the optics are too strong for the length of the eye - if you are looking at something close the image will focus in front of the retina - this is short sighted - image is focussed by resetting the eye into distance vision, reducing the power of the eye and so we can get something close into focus - however this means we can't then see far away because we ant flatten the lens any further

Question 350

How do you fix a myopic eye?

Answer 350

- negative lens - diverges the light rays, weakening the power of the natural and artificial optics - the glass lens makes things smaller

Question 351

What does it mean if the eye is hypermetropic?

Answer 351

- long sighted - optics too weak for the eye - looking into the distance, the image will focus behind the retina - reset the eye for close vision and fatten the lens to bring image into focus - can't then look at something close up as the lens can't fatten anymore; run out of focal power

Question 352

How do you fix a hypermetropic eye?

Answer 352

- positive lens - increasing power of optics bringing image into focus - can see far at distance but need glasses for close work

Question 353

Why does the lens have very little regenerative capacity?

Answer 353

- because to be transparent needs to have very few organelles - by age 45 lens will have become fixed meaning it will have stopped being malleable and ti will have stopped responding to changes in ciliary muscle (if lucky it will fix at a useful distance and won't need varifocals)

Question 354

What is cataract?

Answer 354

when the proteins in the lens degenerate and the lens becomes opaque. this happens with age, and can only be fixed by removing the lens and replacing it with an artificial one

Question 355

What is the primary visual pathway?

Answer 355

- what we use to describe the eye - have a pathway associated with reflexes - all nuclei involved in this kind of movement of the eye are down in the brain stem, the biggest and most prominent is the superior colliculus - the ganglion cells in the eye that project back have branches that go down to the brain stem to drive these processes - these structures aren't involved directly in visual perception - these come form the lateral cells in the retina to the primary visual cortex which sits in the occipital cortex embedded in the calcimine tissue which has a deep sulcus in the inside of the cortex at that point

Question 356

What is meant by a retina topic map?

Answer 356

there is a sort of map laid out within the retina - neighbouring points within the retina project to neighbouring points within the cortex. on the LHS of the cortex there is a map of the right, and on the RHS there is a map of the left. the bits with many ganglion cells have a huge representation in the retina topic map. the macula of the retina takes up half of the visual cortex

Question 357

What is the rule that has to be learnt for the visual pathways?

Answer 357

- LHS is on the right side of the brain - the right visual world is on the LHS of the brain - the left eye will cross the nasal part of the retina and the temporal half will stay on the same side the same happen for the other half of the visual world - this can be worked out from the first principles

Question 358

What happens if you have damage infront of the optic chiasm?

Answer 358

- the damage will be independent in the two pathways - might have blind spots in both eye, but they will be different and won't match, as they will have occurred independently

Question 359

What will happen if you have damage behind the chiasm?

Answer 359

behind the chiasm, axons from a matching part of the 2 retinae lie close together, so any lesion will take out a matching part of the visual field that is being projected back from the 2 eyes. if it matches in both eyes then you know it is from behind the chiasm

Question 360

How do we map the visual field?

Answer 360

- vertical line on little cartoon = central axis of vision - area between 2 lines is the blind spot - nasal region always smaller than the temporal because the nose gets in the way - temporal region always about 90 degrees

Question 361

What are binocular visual fields?

Answer 361

- about the same - binocular vision - two eyes used together

Question 362

What could visual field defects be caused by?

Answer 362

- retinal injury - tumour - infection - metabolic disease

Question 363

What is the main target of the retinal output?

Answer 363

the dorsal lateral geniculate nucleus in the thalamus, which in turn projects to the primary visual cortex (area V1)

Question 364

What is the structure of the retina?

Answer 364

- layered structure that lines the back of the eye - outermost part is pigmented epithelium, single row of melanin containing cells providing vital support for adjacent photoreceptors and absorb stray light rays - other layers formed of neurones which aggregate into nuclear layers (cell bodies and nuclei) and plexiform layers (nerve cell processes and synapses) - outermost neural layer contains photoreceptors; small cells without axons which synapse with other retinal cells in the outer plexiform layer - innermost layer: retinal ganglion cells, they have axons and therefore fire APs - the axons stream across the virtual (inner) surface of the retina and exit to form the optic nerve - photoreceptors and ganglion cells linked by bipolar cells - bipolar cells span the vertical depth of the retina, indirectly linked via horizontal and amacrine cells, which extend horizontally to link neighbouring parts of the retina

Question 365

Why are retinotopic maps distorted?

Answer 365

because the central retina is specialised for high acuity vision and is therefore massively over-represented in comparison to the peripheral

Question 366

Where do the projections from each eye go to?

Answer 366

- temporal half of retina projects to ipsilateral side of brain - nasal half projects to contralateral side - the axons cross over the optic chiasm

Question 367

When is the normal pattern of connections to the visual cortex established?

Answer 367

during the 'critical period' in early development, as a result of competitive interactions between the 2 sets of afferents if the vision in one eye is seriously compromised during that period then its afferents will lose the competition for synaptic site the afferents from the normal eye take over more of the visual cortex than usual, leaving the compromised eye with little input to the cortical circuitry. even if the initial problem is cured at a later stage, the eye will remain 'amblyopic'

Question 368

What happens in the visual response of transduction?

Answer 368

- the stacked disks of membrane in the photoreceptor outer segment contain photopigment, a photosensitive molecule formed from a membrane-bound protein (ospin) an a derivative of vitamin A called 'retinal' - light causes photo-isomerisation of the retina from the 11-cis to the all-trans form, which in turn triggers a G-protein mediated outline above, hyper polarising the cell and reducing the release of transmitter. - conversely, decreasing illumination permits the channel to open again - the photoreceptors are exited by dark objects in the visual scene and inhibited by light.

Question 369

What are photoreceptors vulnerable to?

Answer 369

- mutations affecting the many proteins the visual cycle | - to conditions that compromise there oxygen supply

Question 370

How does the visual stymie identify colours?

Answer 370

- there are 3 types of cone photoreceptor that respond most effectively to long, medium and short (red, green and blue) wavelengths respectively - this is because they contain photopigments with different light absorbing characteristics - the visual system needs to compare the responses of one type of cone with another in order to identify colours, so people lacking one or more cone types have difficulty distinguishing some or all colours

Question 371

What are the ways of light adaptation in the eye?

Answer 371

- rods are exceptionally sensitive to light - a rod can produce a measurable response to a single photon - downside to this sensitivity is that their photopigments are totally 'bleached' by even dullest day - while cone photoreceptors need a lot of light to produce any response at all, they will continue to respond in even the brightest conditions - whereas each ganglion cell receives in put from one or very few cones, that same cell will receive input from many hundreds of rods the night vision pathway gains even greatest sensitivity, but at the expense of very poor resolution - thus people with defective cones can only see at all in very dim condition and even then they have very poor acuity

Question 372

What are large receptor voided sensitive to?

Answer 372

fiat or fast moving objects

Question 373

What does the fovea capture?

Answer 373

only cones (especially slender ones) there is no convergence - outside the fovea, the output of more than one cone converges onto each ganglion cell

Question 374

What range of frequency can humans hear?

Answer 374

20Hx - 20kHz

Question 375

What is the auditory part f the ear?

Answer 375

cochlea - contains a complex arrangement of membranes that are designed to vibrate in response to sound waves and by doing so activate sensory receptors ('hair cells')

Question 376

What do hair cells do?

Answer 376

in turn release glutamate onto the peripheral endings of primary afferent nerve cells, exciting them and generating a signal that is sent to the cochlear nucleus

Question 377

How is sound passed through the outer and inner ear?

Answer 377

- sound captured and amplified by trumpet like outer ear - channeled towards the 'tympanic membrane' - vibration of air causes membrane to vibrate - tympanic membrane is in contact with a chain of three middle ear bones (auditory ossicles), the last of which presses against a membrane-covered entrance (oval window) in the bone surrounding the inner ear - ossicles amplify the sound via a lever-like action, but they are primarily needed to ensure that the sound waves don't simple echo back off the air-water interface - in this way sound waves are converted into vibrations of the inner ear fluid

Question 378

What in the inner ear?

Answer 378

a system of tunnels and spaces channelled into the petrous portion of the temporal bone

Question 379

What does the inner ear/bony labyrinth include?

Answer 379

- cochlea (snail shaped auditory component) - central vestibule - semi-circular canals (3 looped tunnels extending out from the vestibule)

Question 380

What is perilymph?

Answer 380

an unexceptional sodium-rich extracellular fluid within the compartments of the inner ear

Question 381

What is the membranous labyrinth?

Answer 381

a smaller, membrane bound compartment within the inner ear/bony labyrinth which is filled with endolymph (a fluid low in sodium, rich in potassium) composed of the cochlear duct, auricle and saccule (linked pair of central chambers, both enclosed within bony vestibule) and three semi-circular ducts

Question 382

What happens at the stria vascularis in the ear?

Answer 382

chemical and electrical gradients between the endolymph and the surrounding tissue are generated by ion pumps in the stria vascularis

Question 383

What is the endolymphatic duct?

Answer 383

A thin tube that exits the petrous bone via the vestibular aqueduct and terminates in contact with the dura as the endolymphatic sac the duct and sac play a vital role in the control of endolymph volume

Question 384

Why does the volume of endolymph need to be carefully regulated?

Answer 384

Since an increase in pressure will create aberrant activity in the neural pathways and potential damage the receptors. This happens in Meniere's disease

Question 385

What is the structure of the cochlea?

Answer 385

- spiral shape containing three chambers separated by membranes - chambers extend in parallel along the length of the spiral, from the base to the apex - the upper and lower chambers (scala vestibule, scala tympani) are filled with perilymph, while the middle chamber (cochlear duct) is filled wth endolymph - cochlear duct and scala tympani are separated by the basilar membrane - running along the inner edge of this membrane is the spiral organ (organ of Corti) which also extends from the base to the apex of the cochlea - the sensory hair cells are part of this structure --> they sit with their apical surface facing into the endolymph-containing cochlear duct

Question 386

What are the auditory receptors like?

Answer 386

small, axones cells that have one distinguishing feature --> their apical surface carries a tuft of microvilli (stereo cilia), which are arranged in neat rows of increasing height. the tips of each row of stereo cilia are linked to their taller and smaller neighbours by fine-tip links formed of protein strands

Question 387

What are the hair cells arranged like?

Answer 387

The hair cells sit with their appeal surfaces in contact with the endolymph of the cochlear ducts. this has a very much higher electrical potential (more +ve ions) than hear cell intracellular fluid --> in the cochlea the endolymph is +80mV more positive than the rest of the extracellular fluid in the body

Question 388

How are the cation channels in the stereo cilia membrane opened?

Answer 388

when the stereo cilia are tilted in the direction of the tallest row, the tip-links are stretched puling the cartion channels open. Conversely, when the stereo cilia tilt away from the longest one, the channels close, allowing the hair cells to hyper polarise and reducing the release of the transmitter the key is to ensure that the hair cell stereo cilia tilt in response to sound

Question 389

What is the main cation in the endolymph?

Answer 389

K+ - therefore K+ ions are driven into the hair cell by the electrical potential gradient, depolarising the hair cells and increasing the release of transmitter from synaptic sites on their bases.

Question 390

How is it ensured that the hair cell stereo cilia tilt in response to sound?

Answer 390

by a clever arrangement of the fluid-filled passages and gelatinous membranes vibration of the inner ear fluid is transformed into the tilting of the stereo cilia, allowing K+ entry and thus causing a receptor potential

Question 391

What is the tectorial membrane?

Answer 391

a gelatinous flap overlying the organ of Corti and attached to the stereo cilia of the outermost hair cells the stereo cilia are trapped between the tectorial and basilar membranes and any vibration of these membranes will tilt them back and forth

Question 392

What does sound analysis and discrimination rely most heavily upon?

Answer 392

the single row of inner hair cells (IHC) given that a human cochlea contains only about 3500 of these, hearing is entirely dependent upon a very small number of cells (compared to the retina which contains millions of photoreceptors!) unfortunately hair cells are delicate. their numbers decline with age and they can be destroyed in many ways (ototoxic drugs, infections etc)

Question 393

Why do loud sounds lead to permanent hearing deficits?

Answer 393

the fierce vibrations can damage the fragile stereo cilia and lead to permanent hearing deficits - hair cells are not replaced when lost

Question 394

How can outer hair cells increase the strength of the inner hair cell responses?

Answer 394

they act as a cochlear amplifier when outer hair cells are depolarised by sound waves they shorten. when they shorten they pull on the basilar membrane in such a way that they boost the size of the basilar membrane vibrations - like a swing, if you push at the right moment it goes higher

Question 395

How does the auditory system determine the loudness of a sound?

Answer 395

- louder sounds cause a larger movement of the cochlear membranes and stereo cilia, leading to greater depolarisation of the hair cell and more transmitter release - thus, the louder the sound the more APs are fired by the afferent nerve bundle.

Question 396

How does the auditory system determine the pitch of sound?

Answer 396

- structure of basilar membrane and associated hair cells varies along the length of the cochlea so different points along the membrane have a natural tendency to oscillate at different frequencies - therefore high frequency sounds activate hair cells close to the base of the cochlea and low frequency sounds activate those close to the apex - the outer hair cells amplify the basilar membrane vibrations in such a way that they boost this selectivity - much of the auditory system is organised 'topotopically' i.e. the pathway from the cochlea terminate in an orderly fashion, so that cells at one end of a nucleus or cortical area receive input from the base of the cochlea and are tuned to high pitch sounds, while those as the other end receive input from the apex and are tunes to low pitch sounds - the brain can therefore determine the pitch of a sound from the location of the cells that respond to it

Question 397

How does the auditory system recognise the origin of sound?

Answer 397

- hair cells excited afferents that have their cell bodies in the spiral ganglion and axons that exit the bony labyrinth via the internal auditory canal - they join the afferents of the vestibular system to create the 8th nerve - the auditory afferents terminate in the brain stem, in the dorsal and ventral cochlea nuclei - the ventral nucleus project in turn to the superior olivary nuclei. Here cells can determine the source of a sound by detecting tiny differences between the loudness and the timing of sound waves reaching the 2 ears

Question 398

What do the schwann cells associated with the vestibular branch tend to do?

Answer 398

schwann cells associated with the vestibular branch tend to produce tumours within the confines of the canal, which cause compression damage to the 7th and 8th nerves. they typically affect hearing in the first instance, and are therefore commonly known as 'acoustic neurones'

Question 399

What does the dorsal cochlear nucleus project to?

Answer 399

projects to the central nucleus of the inferior colliculus which also receives input from the olivary nuclei. - the pathway then continues via the medial geniculate nucleus of the thalamus to the cortex - inputs form the 2 ears are kept separate within the cochlear nuclei but are combined thereafter to produce binaural responses - the complexity of the subcortical pathways and the fact that several different cortical areas receive geniculate input, means that cortical lesions rarely result in total deafness - however, they may destroy a patients ability to analyse complex sounds - in particular, lesions to Wernicke's area seriously impair the ability to interpret spoken language

Question 400

What are the 'subcortical motor controllers'?

Answer 400

The basal ganglia and the cerebellum - "regulate planning and execution of voluntary movement" - both receive cortical inputs, both project to motor cortex via thalamus - both needed for smooth movement and posture - lesions lead to positive and negative motor symptoms

Question 401

About the cerebellum generally...

Answer 401

- 10% of brain volume, but >50% of brain neurones - has expanded during evolution - has 40X more input axons than output, most outputs are projected to motor areas, but NOT to the spinal cord.

Question 402

What are the three types of symptoms in cerebellar lesions?

Answer 402

1. hypotonia: low muscle tone, uncoordinated muscle contraction 2. postural ataxia: can't keep stable posture, e.g. sway and fall, especially with eyes closed 3. intention tremor: overshoot, oscillation of voluntary movement

Question 403

What is the function of the cerebellum?

Answer 403

- improves performance in future: motor learning | - rapid on-line refinement of a rapid ("ballistic") movement

Question 404

How is the cerebellum a feedback comparator?

Answer 404

The CBM can programme motor commands. This is spaced over around 2 seconds, and may take place for example when picking up an object. This is too slow for a ballistic movement as it is not fast enough for the cerebellum. - ok for motor learning - too slow for on-line control

Question 405

How is the CBM a feed-forward comparator?

Answer 405

there is enough programming in the cerebellum in the adult so that one can tell how a movement will go. this involves much more rapid feedback on how that set of motor commands will do. we therefore only have to make very small adjustments and can make the adjustment before the movement has even started thanks to the cerebellum.

Question 406

What are the three anatomical functions/domains of the CBM?

Answer 406

SPINOCEREBELLUM: modulates descending motor systems in brainstem (via nuclear formation, vestibularnuclei) VESTIBULOCEREBELLUM: regulates balance and eye movements (via vestibular nucleI) CEREBROCEREBELLUM: high level planning of movement; regulates cortical motor programmes (via thalamus to cortex)

Question 407

What is the cerebra-cerebellar pathway?

Answer 407

from the primary motor cortex the motor commands descend to the spinal cord and the skeletal muscles and send a collateral copy of those commands to the cerebellum this occurs via the pons via the inferior olive into the cerebellar cortex. this means that the action potential has less far to travel. the thing to not is the loop: the command goes from the cerebral motor cortex to the cerebellum and back to the cortex, continually modifying the commands going out

Question 408

What does the motor planning loop do?

Answer 408

this helps to modulate the set of commands coming from the cortex

Question 409

What are the types of cells in the cerebellum?

Answer 409

``` cerebellar matrix (highly regular structure, basic circuit) purkinje cells (huge neurones) granule cells (very numerous, approx 10^11) ```

Question 410

What is the output of the CBM via?

Answer 410

purkinje cells (GABAergic, inhibitory) --> deep cerebellar nuclei (excitatory) --> thalamus --> hence cerebral cortex

Question 411

What causes a purkinje cell to fire?

Answer 411

There is a layer of dendrites. The climbing fibre comes form the inferior olive and wraps around a given purkinje cell and makes multiple synapses. When the climbing fibre finds and action potential, the purkinje cell fires.

Question 412

What are the two excitatory inputs into the purkinje cell?

Answer 412

CLIMBING FIBRES from the cerebral cortex --> inferior olive (there is one per P-cell and there are around 10 P-cells per C-fibre) Mossy fibres from pons/brianstem --> PARALLEL FIBRES from granule cells (there are around 1 million parallel fibres per P cell and many P-cells per parallel fibre)

Question 413

What are the local inhibitory neurones of purkinje fibres?

Answer 413

basket, stellate and golgi cells

Question 414

What happens when the purkinje cell fires at the same time as it makes a movement?

Answer 414

mean that you learn the movement was good and you can remember how to do it again

Question 415

What is involved in cerebellar learning?

Answer 415

- climbing fibres: very potent input to the P cell - produce long-term changes in responsiveness to parallel fibre input - modified synaptic strength in the circuit

Question 416

What is the difference between the CBM's role in motor learning and as a feed-forward comparator?

Answer 416

MOTOR LEARNING: when movement is repeated, CBM gives corrective feedback FEED-FORWARD COMPARATOR: CBM refines a rapid movement on-line

Question 417

What is the basal ganglia?

Answer 417

a collection of deep brain nuclei, comprised of the thalamus, thalamic nuclei, the globes pallid us and the putamen (lentiform nucleus).

Question 418

How does the basal ganglia lead to nice control of the motor cortex?

Answer 418

there are loops in the basal ganglia of inhibition balanced with stimulation which leads to the control of motor function.

Question 419

Where are the motor signals in the basal ganglia primarily coming from?

Answer 419

the primary motor cortex the motor signal is started in the supplementary motor areas, to the motor cortex and to the basal ganglia. There are lots of steps which ensure it is a smooth motor programme

Question 420

What happens when the basal ganglia malfunction?

Answer 420

abnormal movements: - chorea - dystonia - tics - myoclonus - tremor - hemiballisimus - bradyknesia psychiatric disturbances: - anxiety - OCD - depression - ADHD can have both types of symptoms

Question 421

What are the signs of parkinson disease?

Answer 421

- bradykinesia - rigidity - tremor - postural instability - reduced facial expressiveness - festinant gait - reduced arm swing

Question 422

What is the layout of nigral degeneration in PD?

Answer 422

presentation in PD is asymmetrical, so they present with the affected side being contralateral to where the substantial nigra is affected

Question 423

What are the causes of parkinson?

Answer 423

- genetic factors: LRRK2 20-30% all cases - environmental: - less common in smokers - well water - insecticides - is it infectious? neurologists get it a lot!

Question 424

What NT is involved a lot in PD?

Answer 424

dopamine!

Question 425

How is a DAT scan used in PD diagnosis?

Answer 425

by looking at levels of dopamine associated transport (DAT). it binds to the substantial nigra, then buries it forward into the caudate nucleus. the scan will show the substantial nigra lighting up very asymmetrically in patients with PD

Question 426

How are MPTP models used in PD?

Answer 426

dopamine is metabolised and this can be reconstructed in MPTP models. When MPTP is with MAOB it forms free radicals which cause cell death, which dopamine does too. We can use MAOB inhibitors.

Question 427

What is the difference between PD and MPTP treated common marmosets?

Answer 427

PD: - primary pathology in substantial nigra - loss of NA and 5-HT containing neurones - akinesia/bradykinesia, rigidity and tremor and postural abnormalities - lewy bodies - progressive - motor complications MPTP treated marmosets: - selective nigral toxicity - no loss of NA and 5-HT - akinesia/bradykinesia, rigidity and postural abnormalities but no resting tremor - no lewy bodies - non-progressive - motor complications

Question 428

What was discovered in the MPTP models?

Answer 428

the problem is that they aren't the same disease, but if the marmosets were given dopamine agonists they ended up not developing the motor complications. This was tried in clinical trial and those treated with dopamine agonists developed less motor complications

Question 429

What are the red flags of PD?

Answer 429

- wheelchair sign - non-response to L-DOPA - early falls in first year - symmetrical onset - vertical gaze palsy - autonomic failure - cerebellar/pyramidal signs

Question 430

What are the features of DLB (dementia with lewy bodies)?

Answer 430

- fluctuating confusion - hallucinations - poor visuospatial function - psychotic features e.g. delusions of infidelity - severe typical neuroleptic effect

Question 431

What can drugs do to increase the dopamine in PD patients?

Answer 431

dopamine is broken down by MAO, so if we give drugs to inhibit these pathways we can boost the dopamine in the brain.

Question 432

What may you choose as treatment for PD in early disease?

Answer 432

Neuroprotection: - antioxidants - rasagaline - selegiline - amantadine: glutamate agonist which blocks receptors - anti-muscarinics eg benzhexol Avoid L-DOPA because of possible complications if patient is young and PD is mild. These drugs don't always lead to a huge improvement so it is good to try and go for drugs that are less toxic in the long term.

Question 433

What do you aim to do in advanced disease of PD?

Answer 433

it is important to find the right combination of treatments for patients, because everyone is different in their response. you could use a combination of DOPA and agonists and there is a choice of DOPA regiments/preparations. Amantidine can be used for dyskinesias - it is a COMT inhibitor for end of dose deterioration atypical neuroleptics are used for psychosis/hallucinosis and acetyl-cholinesterase inhibitors can be used for dementia

Question 434

What is the nuclei accumbent involved in?

Answer 434

reward and addiction

Question 435

What part of PD treatment can lead to addiction problems?

Answer 435

dopamine agonists and dopamine itself can lead to impulse control disorders, 25% of male patients at high dose experience this. this is due to a structural change involved in reward and addiction - the dendrites around the neurones involved become shrunken and there is less filament expression within the neurones.

Question 436

What does the limbic system involve?

Answer 436

deep structures and it runs through the hippocampus, limbic cortex/cingulate, septal area in the basal forebrain, the hypothalamus and the amygdala.

Question 437

What occurs in dopamine dysregulation syndrome?

Answer 437

- addiction to dopaminergic stimulation - hyper sexuality - pathological gambling - punding this happens in PD patients taking L-DOPA and can also happen as a result of chocolate or coffee addiction!

Question 438

What is the dopamine see-saw?

Answer 438

suppress stimulate too little leads to parkinsonian signs, and too much leads to psychosis, dementia, dyskinesia etc

Question 439

What are future PD treatment possibilities?

Answer 439

DRUGS - dopaminergic and non dopaminergic - to treat symptoms/complcations - disease modifying e.g. isradipine, eventide, growth factors GENE THERAPIES - dopamine pathways, GFs, etc CELL BASED THERAPIES - stem cells (poss will be the main way)

Question 440

What are neuroleptic induced movement disorders?

Answer 440

ACUTE: - treatment: antimuscarinics - acute dystonia - oculogyric crisis - akathisia - neuroleptic malignant syndrome CHRONIC: - parkinsonian - tremor - tardive dyskinesia

Question 441

What is tourette syndrome?

Answer 441

another basal ganglia disorder which can involve motor or vocal tics

Question 442

What is Segawa's disease?

Answer 442

this is a disorder of dopamine metabolism, where not enough is produced. tetrahydrobiopterin deficiency due to GTP cyclehydrase deficiency.

Question 443

About essential tremor...

Answer 443

- 5% prevalence - familial - can be alcohol responsive - DRUGS: propranolol, some anticonvulsants (often ineffectivE) - thalamotomy/DBS up to 60% family history

Question 444

What are treatment methods for essential tremor?

Answer 444

- alcohol - propranolol - primidone - modern anti-epileptics - thalamotomy, deep brain stimulation

Question 445

Whats Wilson's disease?

Answer 445

autosomal recessive, copper overload, serum caeruloplasmin, copper, 24 hour urinary copper - chorea - dystonia - neurological - psychiatric - copper metabolism tissue - leads to cirrhosis and liver disease - disabling - have eye features if it is recognised early, it can be treated with copper collating agents and zinc.

Question 446

What is the vestibule-ocular reflex?

Answer 446

- head turns and eyes move equal extent opposite direction to preserve vision - vestibular afferents excite the vestibular nuclei at the pinto-medullary junction - the degree of excitation is modulated by the flocculi-nodular lobe of the CBM, with additional input from the fastigial nucleus - vestibular nuclei project axons in the medial longitudinal fascicles to the oculomotor, trochlear and abducens nuclei. These nuclei excite extra ocular muscles ---> the lateral rectus (abducens), the superior oblique (trochlear) and all the others (oculomotor)

Question 447

Why is the medial longitudinal fascicles susceptible to damage in multiple sclerosis?

Answer 447

it is heavily myelinated and is usually damaged between the VI and III nuclei the shorter path from the vestibular nuclei to the abducens nucleus often survives, so contralateral abduction occurs, but the longer path to the oculomotor nucleus is lost, so ipsilateral adduction is impaired. this results in a divergent squint (strabismus) and double vision (diplopia)

Question 448

What is the basic circuit of the vestibule-ocular reflex and why does it need to be modulated?

Answer 448

labyrinth --> through vestibulo-cochlear nerve --> to vestibular nuclei which excite the oculomotor, trochlear and abducens nuclei --? in turn exciting extra ocular muscles to produce compensatory eye movements by itself, this basic circuit over-compensates so the eye moves too much - a feed-forward inhibitory circuit reduces the compensation

Question 449

How is cerebellar modulation of the vestibule-ocular reflex achieved?

Answer 449

the vestibule-cochlear nerve and vestibular nuclei send mossy fibres to the granule cells in the CBM. Parallel fibres from the granule cells excite purkinje cells, which inhibit the vestibular nuclei, reducing the vestibule-ocular reflex this reduction is too great a third circuit corrects the over correction

Question 450

What is the third circuit correcting the initial modulation of the vestibule-ocular reflex?

Answer 450

retinal cells responding to movement of the optical image doe the retina project to the pretectal nuclei in the midbrain. pretectal nuclei excite neurones in the olive. climbing fibres form the olive project to purkinje cells. excitation of climbing fibres open calcium channels in the purkinje cells, activating kinases that phosphorylate open receptors to active purkinje fibres the phosphorylates receptors are depressed, reducing the excitation of the purkinje cells. this reduced cerebellar inhibition of the vestibular nuclei, allowing the vestibule-ocular reflex to regain some of its original amplitude.

Question 451

What is the medial vestibule-spinal tract?

Answer 451

- as well as projecting rostrally int he medial longitudinal fascicles, some vestibular axons project caudally into the cervical segments of the spinal cord - these axons, within the ventromedial descending pathways, project bilaterally to motor neurones involved in turning the head and in redirecting reaching movements made by the upper limb - turning the head supplements eye movements made by the vestibule-ocular reflex - redirection of reaching movements allows the upper limb to change direction to compensate for rotation of the body relative to a non-rotating target

Question 452

What is the vestibular systems role?

Answer 452

serves the sense of balance/equilibrium

Question 453

What two components if the vestibular system divided into?

Answer 453

- semi-circular canals - otolith organs the hair cells in the semi-circular canals respond to angular movement of the head, and those in the otolith organs respond to both linear movements of the head and the position of the head with respect to gravity this information is combined with the sensory input from muscles, joint and skin to create conscious awareness of the position of the body with respect to the outside world it also plays a vital role in the control of motor activity, by providing reflexive control of posture and eye position and feedback guidance of voluntary movements.

Question 454

How are the semi-circular canals arranged?

Answer 454

they are designed to sense angular acceleration (i.e. turning) of the head when the head it rotated in the plane of a canal, inertia causes the endolymph to lag behind the movement. this causes a displacement of the fluid relative to the canal itself

Question 455

What is the structure of the semi-circular canals like?

Answer 455

At the base of each canal is an expanded region called the ampulla, within which there is a ridge called the crust ampullaris the hair cells are located within the crust, arranged so that their stereo cilia stick out into the body of the ampulla. the stereo cilia bonding is enclosed within a gelatinous membrane called the scapula, that stretches across the duct and is sensitive to any displacement of the endolymph

Question 456

How are the hair cells arranged in the semi circular canals?

Answer 456

so that turning in one direction depolarises them, causing release of neurotransmitter and excitation of the afferent nerves, which turning in the other stops the release of NT eg in the horizontal canal, movement of the copular towards the utricle causes excitation and vice versa the canals are cunningly designed to ensure all possible planes and directions of angular movement are covered

Question 457

What is the arrangement of the ducts within the semi-circular canal?

Answer 457

- the three ducts are approximately perpendicular to one another - each is paired with one of the canals in the opposite side of the head - the anterior duct on one side is approximately parallel to and paired with the parallel duct on the other - the 2 horizontal ducts likewise both lie approximately in the same horizontal plane and form the 3rd pair - each pair responds optimally to movements in one pain, although most natural movements will cause a mixture of activation from more than one pair - any movement that causes an increase i output from one of a pair will decrease the output the other and vice versa

Question 458

How is the rate and direction of turn of the head signalled in the vestibule-ocular system?

Answer 458

signalled by the difference in activity of the 2 members of a pair of ducts - hence anything that causes different in activity will be interpreted as a head turn - this can happen if there is a pathological change in activity on one side and is the logic behind 'caloric testing'

Question 459

When are the left horizontal canal receptors maximally excited?

Answer 459

when the head it turned left - those in the horizontal canal system are simultaneously inhibited

Question 460

When are the left anterior canal receptors maximally excited?

Answer 460

by a combination of nodding the head forward and tilting it to the left - those in the right horizontal canal system are simultaneously inhibited

Question 461

When is the left posterior canal system maximally excited?

Answer 461

by a combination of tilting the head back and to the left - the right anterior is simultaneously inhibited

Question 462

What is meant by the endolymph 'catching up'?

Answer 462

if a turning movement continues at constant velocity for a several seconds then the endolymph will 'catch up' with the walls of the canal, at which point it will stop pressing on the cupula conversely, the endolymph continues to move for a few seconds after movement of the head has stopped, generating a signal in the opposite direction thus the semi-circular canal signal increases and decreases in the rate of movement (i.e. acceleration) rather than constant movement

Question 463

What tis the function of the otolith organs?

Answer 463

they are designed to respond to the linear movements of the head and the position of the head with respect to gravity

Question 464

What do the otolith organs consist of?

Answer 464

each consists of a patch of hair cells (the macula) on the inner wall of the membranous labyrinth overlying them is a gelatinous membrane weighted down with small calcium carbonate stones --> the hair cell stereo cilia are embedded in this membrane and may be tilted by movement of the membrane when the head moves in any direction, inertia causes the membrane to slip back in the opposite direction, tilting the stereo cilia hair cells where this is the direction of the kinocilium will be depolarised, and for those which it is the direction away from the kinocilium will be hyperpolarised

Question 465

How do the hair cells generate a signal that can give information about direction of movement and rate of linear acceleration?

Answer 465

depolarising or hyper polarising the hair cells will change the pattern of activity in their afferents, generating a signal that carries information about the direction of movement and the rate of linear acceleration

Question 466

What is the saccular otolith organ?

Answer 466

is on a vertical wall of the saccule, lying in the sagittal plane. it responds best to forwards-backwards and up-down movements. there is also evidence that this organ detects very low frequency sounds

Question 467

What is the utricular otolith organs?

Answer 467

lies mainlyint he horizontal plane and will respond best to a range of side to side as well as forwards backwards movements

Question 468

Why is the output of the otolith organs sensitive to changes in the direction of gravity?

Answer 468

the membranes sag downwards under the influence of gravity so the out put of the otolith organs is sensitive to changes in the direction of gravity