Neuroscience

Question 1

Define: brainstem

Answer 1

The part of the CNS (excluding cerebellum) that lies between the cerebrum and the SC

Question 2

Where does the brainstem lie?

Answer 2

Posterior cranial fossa

Question 3

What are the major divisions of the brainstem?

Answer 3

Medulla oblongata
Pons
Midbrain

Question 4

What are the numbers of the cranial nerves?

Answer 4

1 olfactory
2 optic
3 oculomotor
4 trochlea
5 trigeminal
6 abducens
7 facial
8 vestibulocochlear
9 glossopharyngeal
10 vagus
11 accessory
12 hypoglossal

Question 5

Which of the cranial nerves are sensory/motor/both?

Answer 5

SOME SAY MARRY MONEY BUT MY BROTHER SAYS BIG BOOBS MATTER MORE

1 sensory 
2 sensory
3 motor +para
4 motor
5 both
6 motor +para  
8 sensory
9 both +para
10 both +para
11 motor
12 motor

Question 6

CRANIAL NERVE 1 (name, fibres, structures innervated, functions)

Answer 6

Olfactory (sensory)

Structures innervated= Olfactory epithelium via olfactory bulb

Functions= Olfaction

Question 7

CRANIAL NERVE 2 (name, fibres, structures innervated, functions)

Answer 7

Optic (sensory)

Structures innervated= Retina

Functions= Vision

Question 8

CRANIAL NERVE 3 (name, fibres, structures innervated, functions)

Answer 8

Oculomotor (motor, parasympathetic)

Structures innervated= Superior, inferior and medial rectus
= Pupillary constrictor and ciliary muscle of the eyeball (via ciliary ganglion)

Function= Movement of the eyeball
= Pupillary constriction and accomodation

Question 9

CRANIAL NERVE 4 (name, fibres, structures innervated, functions)

Answer 9

Trochlear (motor)

Structures innervated= Superior oblique muscle

Function= Movement of the eyeball

Question 10

CRANIAL NERVE 5 (name, fibres, structures innervated, functions)

Answer 10

Trigeminal (motor and sensory)

Structures innervated= Face, scalp, cornea, nasal and oral cavities, cranial dura mater
= Muscles of mastication, tensor tympani muscle

Function= General sensation
= Opening closing the mouth, tension on tympanic membrane

Question 11

CRANIAL NERVE 6 (name, fibres, structures innervated, functions)

Answer 11

Abducens (motor)

Structures innervated= Lateral rectus muscle

Function= Movement of eyeball

Question 12

CRANIAL NERVE 7 (name, fibres, structures innervated, functions)

Answer 12

Facial (sensory, motor, para)

Structures innervated= Anterior 2/3 of tongue
= Muscles of facial expression, stapedius muscle
= Salivary and lacrimal glands via submandibular and pterygocalatine ganglia

Function= Taste
= Facial movement, tension on bones of middle ear
= Salivation and lacrimation

Question 13

CRANIAL NERVE 8 (name, fibres, structures innervated, functions)

Answer 13

Vestibulocochlear (sensory)

Structures innervated= Vestibular apparatus
= Cochlear

Function= Vestibular sensation (position of head)
= Hearing

Question 14

CRANIAL NERVE 9 (name, fibres, structures innervated, functions)

Answer 14

Glossopharyngeal (sensory, motor, para)

Structures innervated= Phaynx, posterior 1/3 of tongue
= Eustachian tube, middle ear
= Carotid body and sinus
= Stylopharyngeus muscle
= Parotic gland via otic ganglion

Function= General sensation and taste
= Chemo and baroreception
= Swallowing
= Salivation

Question 15

CRANIAL NERVE 10 (name, fibres, structures innervated, functions)

Answer 15

Vagus (sensory, motor, para)

Structures innervated= Pharynx, larynx, oesophagus, external ear
= Aortic bodies, aortic arch
= Thoracic and abdominal viscera
= Soft palate, pharynx, larynx, upper oesophagus
= Thoracic and abdominal viscera

Function= General sensation
= Chemo- and baroreception
= Visceral sensation
= Speech, swallowing, control of CVS, respiratory and GI tracts

Question 16

CRANIAL NERVE 11 (name, fibres, structures innervated, functions)

Answer 16

Accessory (motor)

Structures innervated= Stemocleidomastoid and trapezius

Function= Movement of head and shoulder

Question 17

CRANIAL NERVE 12 (name, fibres, structures innervated, functions)

Answer 17

Hypoglossal (motor)

Structures innervated= Intrinsic/extrinsic tongue muscles

Function= Movement of tongue

Question 18

Outline the functional classification of cranial nerves (NB. General/special afferent/efferent etc.)

Answer 18

General somatic afferent (GSA)
General visceral afferent (GVA)
General somatic efferent (GSE)
General visceral efferent (GVE)

Special somatic afferent
Special visceral afferent
Special visceral efferent

Question 19

What are GSA, GVA, GSE and GVE referring to?

Answer 19

GSA= sensation from skin and mucous membranes

GVA= sensation from GI tract, heart, vessels and lungs

GSE= muscles for eye and tongue movements

GVE= preganglionic parasympathetic

Question 20

What are the ‘special’ functional classifications referring to? (SSA, SVA, SVE)

Answer 20

Special somatic afferent= vision, hearing and equilibrium

Special visceral afferent= smell and taste

Special visceral afferent= muscles involved in chewing, facial expression, swallowing, vocal sounds and turning head

Question 21

Where is the Edinger Westphal nucleus?

Answer 21

Motor GVE

Midbrain

Question 22

Where are the oculomotor and trochlear nuclei?

Answer 22

Motor GSE

Midbrain

Question 23

Where is the abducens nuclei?

Answer 23

Motor GSE

Pons (middle of pons)

Question 24

Where are the trigeminal m and facial nuclei?

Answer 24

Motor SVE

Pons (trigeminal top, facial bottom)

Question 25

Where are the salivatory nuclei?

Answer 25

Motor GVE

Either side of pons-medulla junction

Question 26

Where is the vagus m nucleus?

Answer 26

Motor GVE

Medulla

Question 27

Where is the ambiguus nucleus?

Answer 27

Motor SVE

Medulla

Question 28

Where is the hypoglossal nucleus?

Answer 28

Motor GSE

Medulla

Question 29

Where is the accessory nucleus?

Answer 29

Motor SVE

Cervical spinal cord

Question 30

Where is the trigeminal s nuclei?

Answer 30

Sensory GSA

Midbrain, top of pons, down pons/medulla/SC

Question 31

Where is the vestibulocochlear nucleus?

Answer 31

Sensory SSA

Lower half of pons and top of medulla

Question 32

Where is the solitarius nucleus?

Answer 32

Sensory GVA/SVA

Medulla

Question 33

When substantia nigra is damaged, what happens?

Answer 33

Parkinson’s disease

Question 34

Where in the brainstem can the inferior colliculus, cerebral aqueduct, substantia nigra and cerebral peduncle be found?

Answer 34

Midbrain

Question 35

Where in the brainstem can the 4th ventricle, middle cerebellar peduncle and transverse fibres be found?

Answer 35

Pons

Question 36

Where in the brainstem can the 4th ventricle, inferior olivary nucleus and pyramids be found?

Answer 36

Medulla

Question 37

Where in the brainstem can dorsal columns, central canal and pyramidal decussation be found?

Answer 37

Lower medulla

Question 38

What causes lateral medullary syndrome?

Answer 38

Thrombosis of vertebral artery or PICA

Question 39

What is PICA?

Answer 39

Posterior inferior cerebellar artery

Question 40

What does thrombosis of vertebral artery or PICA cause?

Answer 40

Lateral medullary syndrome

Question 41

What are the symptoms of lateral medullary syndrome

Answer 41

Vertigo

Ipsilateral cerebellar ataxia

Ipsilateral loss of pain/thermal sense (face)

Horner’s syndrome

Hoarseness, difficulty in swallowing

Contralateral loss of pain/thermal sense (trunk and limbs)

Question 42

What does the lesion in lateral medullary syndrome disrupt? (3 nuclei, 2 tracts and 1 other area)

Answer 42

Vestibular nucleus
Spinal nucleus (trigeminal)
Nucleus ambiguus

Spinothalamic tract
Sympathetic tract

Inferior cerebellar peduncle

Question 43

What levels are the cervical plexus?

Answer 43

C1-C5

Question 44

What levels are the brachial plexus?

Answer 44

C5-T1

Question 45

What levels are the lumbar plexus?

Answer 45

L1-L4

Question 46

What levels are the sacral plexus?

Answer 46

L4-S4

Question 47

How many pairs of spinal nerves are in each group?

Answer 47

Cervical 8 pairs
Thoracic 12 pairs
Lumbar 5 pairs
Sacral 5 pairs
Coccygeal 1 pair

Question 48

Where is the lumbar enlargement?

Answer 48

Around T9-T10

Question 49

Where is the conus medularis?

Answer 49

Between T12 and L1

Question 50

What spinal segments are largest and smallest?

Answer 50

Around C5 (cervical enlargement)
Around L3 (lumbar enlargement) 

Smallest are sacral

Question 51

What spinal segment is the bone notch at the base of the neck?

Answer 51

C7

Question 52

What pathway goes from the primary somatosensory cortex to detect pain/crude touch?

Answer 52

Primary somatosensory cortex

Thalamus: ventral posterior lateral nucleus

(Secondary sensory neuron)

Anterolateral pathway (spinothalamic tract)

Spinal cord

(Primary sensory neuron via DRG)

Question 53

What is the purpose of spinothalamic tract?

Answer 53

To receive sensory info about pain, temperature, crude touch

Question 54

What are the major sensory pathways?

Answer 54

Posterior column-medial lemniscus pathway
Anterolateral (spinothalamic) pathways

SEE DIAGRAMS

Question 55

What are the major motor pathways?

Answer 55

The lateral corticospinal pathway
The anterior corticospinal pathway

SEE DIAGRAMS

Question 56

What are the divisions of autonomic pathways?

Answer 56

Sympathetic
Parasympathetic

SEE DIAGRAMS

Question 57

What is the cross-sectional structure of the spinal cord?

Answer 57

Central canal in the middle of the grey matter butterfly

White matter surrounds (contains nerve fibre tracts)

Sensory nerve root from top of grey matter (dorsal horn)-> sensory root ganglion-> spinal nerve

Motor nerve roots leave from the front of the SC

Question 58

What are the layers of the connective tissue that protect the SC?

Answer 58

Meninges

Pia mater
Arachnoid mater
Dura mater

Question 59

What kind of fibre tracts are found in the spinal cord?

Answer 59

Ascending tracts
Descending tracts
Bidirectional tracts

SEE DIAGRAMS FOR SPECIFICS

Question 60

What are the funiculi in white columns of the spinal cord?

Answer 60

Posterior funinculus
Anterior funinculus
Lateral funinculus

Question 61

What parts of the spinal cord cross-section is grey matter?

Answer 61

Posterior median sulcus
Grey commissure
Posterior (dorsal) horn
Anterior (ventral) horn
Lateral horn

Question 62

What receptors are part of the DRG system?

Answer 62

Nociceptors
Mechanoreceptors
Proprioceptors (also go to VH)

Question 63

How is locomotion controlled by the SC?

Answer 63

Sensory afferents, corticospinal, reticulospinal and CIN

Join V2a interneurons

Motor neuron

Question 64

What neurotransmitters and effector organs are involved in the somatic nervous system and autonomic nervous system?

Answer 64

SOMATIC
ACh
Skeletal muscle

ANS- SYMPATHETIC
ACh and NE
Smooth muscle, glands, cardiac muscle

ANS- PARASYMPATHETIC
ACh and ACh
Smooth muscle, glands, cardiac muscle

Question 65

What effect do the somatic and autonomic NSs have on their effectors? (stim or inhib?)

Answer 65

SNS= stimulatory

ANS= stimulatory or inhibitory depending on NT and Rs on effector organs

Question 66

What arteries are the blood supply to the spinal cord?

Answer 66

Anterior spinal artery
Vertebral artery
Subclavian artery
Radicular artery
Great vertebral radicular artery (artery of Adamkiewicz)
Lumbar radicular artery

Question 67

Percentage of body weight is made up by the brain

Answer 67

2%

Question 68

Percentage of cardiac output does the brain demand

Answer 68

10-20%

Question 69

Percentage of body O2 consumption does the brain demand

Answer 69

20%

Question 70

Percentage of liver glucose does the brain demand

Answer 70

66%

Question 71

What are the 2 sources of blood to the brain?

Answer 71

Internal carotid arteries

Vertebral arteries

Question 72

What do the internal carotid arteries branch to form?

Answer 72

2 major cerebral arteries

The anterior and middle cerebral arteries.

Question 73

What comes off the Circle of Willis?

Answer 73

Main venous arteries supplying brain

Question 74

Where is a build up of atherosclerotic plaques common and why?

Answer 74

Bifurcation in the common carotid artery

Blood gets here and suddenly becomes turbulent flow

Question 75

Biggest in the Circle of Willis

Answer 75

Middle cerebral artery

Question 76

What arteries are small and how does this affect blood supply in case of a vascular accident?

Answer 76

Blood supply can go to both sides if there is damage but posterior communicating arteries are often very small so compensatory flow can be difficult

Question 77

What is involved in venous drainage (4)?

Answer 77

Cerebral veins
Venous sinuses (folds in dura, most of drainage)
Dura mater
Internal jugular vein (all ends up here)

Question 78

Define: stroke

Answer 78

Rapidly developing focal disturbance of brain function of presumed vascular origin and of >24hours duration

Question 79

What percentage of strokes are infarctions and haemorrhages?

Answer 79

85% infarction

15% haemorrhage

Question 80

Define: transient ischaemic attack (TIA)

Answer 80

Rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours

Question 81

Define: infarction

Answer 81

Degenerative changes which occur in tissue following occlusion of an artery

Question 82

Define: cerebral ischaemia

Answer 82

Lack of sufficient blood supply to nervous tissue resulting in permanent damage if blood flow is not restored quickly

Question 83

Why is ischaemia different from anoxia/hypoxia?

Answer 83

Ischaemia relates to whole blood including oxygen, glucose, nutrients

Question 84

What causes occlusions?

Answer 84

Thrombosis

Embolism

Question 85

Define: thrombosis

Answer 85

Formation of a blood clot (thrombus)

Question 86

Define: embolism

Answer 86

Plugging of small vessel by material carried from larger vessel
E.g. thrombi from the heart or atherosclerotic debris from the internal carotid

Question 87

How can atherosclerosis be seen on imaging?

Answer 87

Yellow fat where it shouldn’t be

Question 88

Outline the epidemiology of strokes

Answer 88

3rd commonest cause of death

100,000 deaths in UK per annum

Question 89

What percentage of stroke survivors are permanently disabled or show an obvious neurological deficit?

Answer 89

50% of survivors are permanently disabled

70% show an obvious neurological deficit

Question 90

What are the main risk factors for strokes?

Answer 90

Age 
Hypertension
Cardiac disease
Smoking
Diabetes mellitus

Question 91

Where does the anterior cerebral artery supply?

Answer 91

Frontal area of brain

All the way back to parietal occipital fissure

Question 92

Where does the middle cerebral artery supply?

Answer 92

Most lateral area of temporal lobe

Question 93

Where does the posterior cerebral artery supply?

Answer 93

Around the occipital lobe area

Question 94

What happens if there is damage to the anterior cerebral artery?

Answer 94

Paralysis of contralateral leg (more than arm and face)
Disturbance of intellect, executive function and judgment
Loss of appropriate social behaviour

Question 95

What happens if there is damage to the middle cerebral artery?

Answer 95

“Classic stroke”
Contralateral hemiplegia (more of arm than leg)
Contralateral hemisensory deficits
Hemianopia
Aphasia (L sided lesion)

Question 96

What happens if there is damage to the posterior cerebral artery?

Answer 96

Visual deficits

• Homonymous hemianopia
• Visual agnosia

Question 97

What is a lacunar infarct?

Answer 97

Lacune is a small cavity
Deficit is dependent on anatomical location (appear in deep structures due to small vessel occlusion)
Hypertension

Question 98

What are the subtypes of haemorrhagic strokes?

Answer 98

Extradural
Subdural
Subarachnoid
Intracerebral

Question 99

What causes an extradural haemorrhagic stroke and what are the effects?

Answer 99

Trauma, immediate effects
Large blood clot outside dura
Requires urgent attention

Question 100

What causes a subdural haemorrhagic stroke and what are the effects?

Answer 100

Trauma, delayed effects

Question 101

What causes a subarachnoid haemorrhagic stroke?

Answer 101

Ruptured anaerysms

Vessels rupture and fill subarachnoid space with blood

Question 102

What causes an intracerebral haemorrhagic stroke?

Answer 102

Spontaneous hypertensive

Health of patient important e.g. age/risk factors

Question 103

Why should someone be admitted overnight after a stroke?

Answer 103

Subdural haematoma will feel ok after losing consciousness but need to be observed for 24h to check for delayed effects

Question 104

How much blood flows into the brain?

Answer 104

High

55ml/100g tissue/min

Question 105

What happens if blood flow to the brain is reduced by more than 50%?

Answer 105

Insufficient oxygen delivery

Function becomes significantly impaired

Question 106

How long does total cerebral blood flow (CBF) have to be interrupted to cause unconsciousness or irreversible damage?

Answer 106

4 seconds-> unconsciousness

Few minutes-> irreversible

Question 107

What is syncope?

Answer 107

Fainting

Common manifestation of reduced blood supply to the brain

Question 108

What causes syncope?

Answer 108

Low blood pressure
Postural changes
Vaso-vagal attack
Sudden pain
Emotional shock

(All result in a temporary interruption or reduction of blood flow to the brain)

Question 109

Approximate percentage of body glucose used by the brain

Answer 109

50-60%

Question 110

Why does the brain need glucose from the body?

Answer 110

Brain cannot store, synthesize or utilise any other source of energy

(In starvation, ketones can be metabolised)

Question 111

What happens when blood glucose drops below 2mM?

Answer 111

Unconsciousness
Coma
Ultimately death

Question 112

Normal fasting levels of glucose

Answer 112

4-6mM

Question 113

How is the brain’s constant need for oxygen and glucose regulated?

Answer 113

Mechanisms to maintain cerebral blood flow

Mechanisms which relate activity to requirement in specific brain regions to altered localised blood flow

Question 114

How is total cerebral blood flow regulated?

Answer 114

Autoregulation between MABP 60-160mmHg

Question 115

How do arteries respond to blood pressure to allow autoregulation of CBF?

Answer 115

Arteries and arterioles dilate/contract to maintain blood flow
Stretch-sensitive cerebral vascular smooth muscle contracts at high BP and relaxes at lower BP

Question 116

What happens below the autoregulatory pressure range of CBF?

Answer 116

Insufficient supply-> compromised brain function

Question 117

What happens above the autoregulatory pressure range of CBF?

Answer 117

Increased flow can lead to swelling of brain tissue (not accomodated by the closed cranium-> increased intracranial pressure-> danger

Question 118

What is local autoregulation?

Answer 118

Local brain activity determines the local 02 and glucose demands
Therefore local changes in blood supply are required

Neural and chemical control

Question 119

How is CBF controlled by neural factors?

Answer 119

Sympathetic nerve stimulation (to main cerebral arteries-> vasoconstriction)

Parasympathetic (facial nerve) stimulation (-> slight vasodilation)

Central cortical neurones (release vasoconstrictor NTs e.g. catecholamines)

Dopaminergic neurones (-> localized vasoconstriction)

Question 120

How do dopaminergic neurones have a local effect on CBF?

Answer 120

Innervate penetrating arterioles and pericytes around capillaries

May divert CBF to areas of high activity

DA may cause to contraction of pericytes via aminergic and serotoninergic receptors

Question 121

What is a pericyte?

Answer 121

Form of brain macrophages with diverse activities e.g. immune function, transport properties, contractile

Question 122

How are CNS tissues vascularised?

Answer 122

Arteries from pia penetrate into the brain parenchyma to form capillaries

Capillaries drain into venules and veins which drain into pial veins

Question 123

Is the CNS densely or sparsely vascularised?

Answer 123

Densely

No neurone >100um from a capillary

Question 124

How is CBF controlled by chemical factors?

Answer 124

Vasodilators:
CO2 (indirect)
pH (H+, lactic acid etc)
Nitric oxide 
K+
Adenosine
Anoxia
Other (kinins, prostaglandins, histamine endothelins)

Question 125

How does CO2 lead to cerebral arterial vasodilation?

Answer 125

CO2 crosses BBB from blood into smooth muscle cells

H+ crosses from neural tissue to smooth muscle cells

In smooth muscle CO2 binds with H2O bicarbonate and H+

SEE DIAGRAM

CO2 may also affect the production of NO (a potent relaxant of smooth muscle)

Question 126

How is brain activity mapped?

Answer 126

PET and fMRI

Studying local changes to cerebral blood flow

Question 127

Where is CSF produced?

Answer 127

By regions of choroid plexus in the cerebral ventricles

Question 128

What is the choroid plexus?

Answer 128

Ventricles, aqueducts and canals of the brain are lined with ependymal cells

Lining modified in some regions to form branched villus structures= choroid plexus

Question 129

How is CSF formed?

Answer 129

By choroid plexus
Capillaries leaky but adjacent ependymal cells have extensive tight junctions
Secrete CSF into ventricles

Question 130

What is the volume of CSF in circulation?

Answer 130

80-150ml

Question 131

How does CSF circulate?

Answer 131

Lateral ventricles

3rd ventricle via interventricular foramina

Down cerebral aqueduct into 4th ventricle

Into subarachnoid space via medial and lateral apertures)

Question 132

What is the function of CSF?

Answer 132

Protection (physical and chemical)
Nutrition of neurones
Transport of molecules

Question 133

Features of capillaries

Answer 133

Thin-walled
Abundant

Provide large s.a. for exchange

Question 134

List the different capillary types in order of leakiness

Answer 134

Moderately leaky= continuous
Leaky= fenestrated
Very leaky= sinusoid

Question 135

How much plasma leaks out of blood vessels per day?

Answer 135

8L (this means entire plasma volume must pass into the interstitial space and back into the blood circulation every 9 hours)

Question 136

What do endothelial cell-cell contacts of BBB capillaries have?

Answer 136

Extensive tight junctions

Question 137

What do tight junctions at the endothelial cell-cell contacts of BBB capillaries do?

Answer 137

Reduce solute and fluid leak across the capillary wall

Mainly applies to hydrophilic solutes e.g. glucose, AAs, toxins, and others

Question 138

What is the difference between a brain capillary and a cardiac muscle capillary?

Answer 138

Cardiac muscle capillary= continuous type, with transcellular vesicular transport

Brain capillary= continuous type, little transcellular vesicular transport

Question 139

What are IEJs?

Answer 139

Interendothelial junctions

Question 140

What are pericytes?

Answer 140

Pericytes are cells closely apposed to capillaries

Question 141

What do pericytes do and how are their associations important to maintain BBB properties?

Answer 141

Maintain capillary integrity and function

Peripheral vessels have sparse pericyte coverage, while BBB capillaries have dense pericyte coverage

In addition, BBB capillaries are covered on “end-feet” from astrocytes

Question 142

What prevents blood-borne infectious agents entering CNS tissue?

Answer 142

BBB

Question 143

What are CVOs?

Answer 143

Circumventricular organs

These are capillaries that lack BBB properties and are fenestrated (therefore leaky)

Need access to the blood

Question 144

Where are CVOs found?

Answer 144

Close to ventricles

Question 145

What are CVOs involved in?

Answer 145

Generally involved in secreting into the circulation or need to sample the plasma e.g. for toxins or electrolytes to regulate water intake

Need access to the blood

Question 146

What is secreted by the posterior pituitary and median eminence?

Answer 146

Hormones

CVOs

Question 147

What does the area postrema do?

Answer 147

Samples the plasma for toxins and will induce vomiting

CVOs

Question 148

Why do second-generation antihistamines not cause drowsiness?

Answer 148

They are polar so don’t cross the BBB

Old fashioned H1 blockers were hydrophobic so could cross the BBB and used as sedatives

Question 149

How does the BBB affect the treatment of Parkinson’s Disease?

Answer 149

Raise DA in brain
DA can’t pass through BBB so L-DOPA can cross the BBB and then get converted to DA in the brain
Without Carbidopa very little L-DOPA gets to the brain (stops L-DOPA being converted in the body, just the brain)

Question 150

Why is Carbidopa used with L-DOPA?

Answer 150

Administered with DOPA decarboxylase inhibitor (Carbidopa)

Carbidopa cannot cross the BBB so doesn’t affect conversion of L-DOPA in the brain but stops conversion in the body

Question 151

How is the thalamus organised?

Answer 151

Divided in two by third ventricle
Collection of individual nuclei with separate functions
Ipsilateral connections with forebrain
Nuclei are interconnected

Question 152

What is the function of the thalamus?

Answer 152

Relay centre between cerebral cortex and the rest of the CNS
Integrates info
Involved in virtually all functional systems

Question 153

How are the parts of thalamus described?

Answer 153

By their location

Question 154

Where does the reticular nucleus extend?

Answer 154

Over the whole lateral surface of the left thalamus

Question 155

What are the 4 main types of thalamic nuclei?

Answer 155

Specific - connected to primary cortical areas
Association - connected to association cortex
Intralaminar - connected to all cortical areas
Reticular – not connected to cortex

Question 156

What are the specific nuclei of the thalamus?

Answer 156

Connected to primary cortical areas

NUCLEUS -> CORTEX
Ventral lateral-> motor cortices (primary, ventral anterior premotor, supplementary)

Ventral anterior-> motor cortices (primary, ventral anterior premotor,supplementary)

Ventral posterolateral-> somatosensory (body)

Ventral posterolateral-> somatosensory (head)

Lateral geniculate-> visual

Medial geniculate-> auditory

Question 157

What are the association nuclei?

Answer 157

Connected to association cortex

NUCLEUS-> CORTEX
Anterior/lateral dorsal/dosromedial -> Mammillary bodies (ant), hypothalamus (lat dorsal), cingulate and prefrontal

Lateral posterior/pulvinar -> Parieto-temporo-occipital and prefrontal

Question 158

What thalamic nuclei are associated with RAS (reticular activating system)?

Answer 158

Intralaminar nuclei= diffuse cortical projections
Reticular nucleus= intrathalamic projections

Both receive inputs from reticular formation

Question 159

What is RAS (relates to thalamus)?

Answer 159

Reticular Activating System

Has intralaminar nuclei and reticular nucleus

Question 160

What causes thalamic syndrome and how does it present?

Answer 160

Posterior cerebral artery stroke
Sensation - reduced, exaggerated, altered
Pain
Emotional disturbance

Question 161

What is TBI?

Answer 161

Traumatic brain injury

Question 162

What does TBI cause even years after brain injury?

Answer 162

Neuroinflammation

Question 163

What is neuroinflammation and what can cause it?

Answer 163

Inflammation of the nervous tissue

It may be initiated in response to a variety of cues e.g. infection, traumatic brain injury, toxic metabolites, or autoimmunity

Question 164

What can cause neuroinflammation?

Answer 164

Infection, traumatic brain injury, toxic metabolites, or autoimmunity

Question 165

How does WM damage relate to amount of inflammation?

Answer 165

More severe WM damage-> more inflammation

Inflammation tracks along the axons (anterograde)

Question 166

How is the hypothalamus organised?

Answer 166

Divided in two by third ventricle
Collection of individual nuclei with separate functions
Largely ipsilateral connections with forebrain

Question 167

List the hypothalamic nuclei seen in the midline?

Answer 167

Fornix
Paraventricular nucleus
Anterior nucleus
Pre-optic nucleus
Suprachiasmatic nucleus
Supra-optic nucleus
Mammilary body
Posterior nucleus
Dorsomedial nucleus
Ventroedial nucleus
Infundibular nucleus

Question 168

What is the function of the hypothalamus?

Answer 168

Coordinates homeostatic mechanisms by the ANS, endocrine system and controlling behaviour

Question 169

What forebrain structures are associated with the hypothalamus?

Answer 169

Olfactory system

Limbic system- hippocampus, amygdala, cingulate cortex, septal nuclei

Question 170

What behaviours are controlled by the hypothalamus?

Answer 170

Eating and drinking
Expression of emotion
Sexual behaviour
Circadian rhythms
Memory

Question 171

How can the hypothalamus be damaged structurally?

Answer 171

Craniopharyngioma (and other tumours e.g. glioma, meningioma, dermoid, chordoma, hamartoma)
Sarcoidosis
Langerhans cell histiocytosis

Question 172

How might someone present with hypothalamic damage?

Answer 172

Anterior pituitary hormone substitution
Diabetes insipidus (polyuria, polydipsia)
Adipsia

Question 173

What are 3 main somatosensory receptor classes?

Answer 173

Mechanoreceptor
Thermoreceptor
Nociceptor

Question 174

What modalities do mechanoreceptors detect?

Answer 174

TOUCH
Light touch
Pressure
Vibration

PROPRIOCEPTION
Joint position
Muscle length
Muscle tension

Question 175

What are sensory receptors?

Answer 175

Transducers that convert energy (thermal/mechanical/light/chemical) from the environment into neuronal APs
Typically considered as the nerve ending

Question 176

What do sensory receptors need to trigger APs?

Answer 176

Adequate or threshold stimulus

Question 177

How is a sense organ formed?

Answer 177

Sensory receptor(s) surrounded by non-neural cells

Question 178

What do sense organs respond to?

Answer 178

Receptors in a specific sense organ respond to a specific stimulus at a much lower threshold than other receptors

Question 179

List examples of mechanoreceptors

Answer 179

Peritrichial ending
Plexuses (papillary, dermal, subcutaneous)
Pacinian corpuscle
End bulb
Merkel ending in epidermus
Meissner's corpuscle
Ruffini ending

Question 180

How are vibrations detected?

Answer 180

By rapidly adapting mechanoreceptors
Each fibre type has a different threshold
Receptors then generate cycles of APs
Thresholds overlap, therefore for certain vibrations different fibres may fire simultaneously

Question 181

Why might certain vibrations cause different fibres to fire simultaneously?

Answer 181

Thresholds overlap, therefore for certain vibrations different fibres may fire simultaneously

Question 182

What are Pacinian corpuscles and Meissner’s corpuscles most sensitive to?

Answer 182

Body most sensitive to 250 Hz
Pacinian corpuscles: 60-400 Hz (peak 250 Hz)
Meissner’s corpuscles: 5-300 Hz (peak 20-50 Hz)

Question 183

What does elevated vibratory threshold indicate?

Answer 183

Neurodegeneration (early sign)

Question 184

What’s the difference between an itch and a tickle?

Answer 184

TICKLE
Relatively mild stimulation
Something moving across skin
May be pleasurable
Areas of the body with naked unmyelinated afferent nerve fibres

ITCH (Pruritis)
Annoying
Local mechanical stimulation or chemical agents e.g. Histamine, Kinins
Relieved by scratching – stimulation of large nerve fibres overwhelms spinal transmission (closes the ‘Gate’)
Occurs in neuropathy, renal failure, dermatitis

Question 185

Why does scratching relieve an itch?

Answer 185

Stimulation of large nerve fibres overwhelms spinal transmission (closes the ‘Gate’)

Question 186

What are temperature gated channels?

Answer 186

Different receptor subtypes

Open and close at different ranges of temperature

Question 187

Where is temperature detection most sensitive?

Answer 187

Face and chest

Question 188

What do TRPV, TRPM8 and TRPV1 detect?

Answer 188

TRPV hot temperature and chillies
TRPM8 cold & menthol
TRPV1 hot but also cold (ice-burn)

Question 189

What are nociceptors?

Answer 189

Specialised peripheral cutaneous terminals

Respond to noxious or harmful stimuli

Question 190

How are nociceptors activated?

Answer 190

Typically high threshold required for activation
Direct activation of ion channel proteins e.g. Transient Receptor Potential (TRP) channels, Neurotrophin and G protein-coupled receptors

Question 191

Examples of nociceptors and their stimuli

Answer 191

Heat-> TRPV1 receptors
Cold-> TRPM8 receptors
pH <7-> Acid sensing ion channels (ASIC)
Intense pressure-> K+ channels

Question 192

How does depolarisation from nociception lead to the brain detecting pain?

Answer 192

Depolarisation-> AP in afferent nerve-> DH of SC-> brain

Question 193

What is the most common cutaneous nociceptor? What does it respond to?

Answer 193

Polymodal C fibre

Responds to pressure, temperature and chemical stimuli

Question 194

What is the most common skeletal nociceptor? What does it respond to?

Answer 194

Chemoreceptor (e.g. for lactic acid)

Question 195

What does loss of function mutation NaV1.7 cause?

Answer 195

Has protective physiological role

LoF means disabling self harm

Question 196

What substances can modulate nociception?

Answer 196

Prostaglandin
Substance P
Histamine
Serotonin
CGRP
Bradykinin
Potassium
Acetylcholine

Associated with inflammation (why inflam is painful)

Question 197

What is the stimulus threshold? How is this defined experimentally?

Answer 197

The weakest stimulus detectable
Adequate stimulus required to elicit a specific response or reflex
In experimental terms, the minimum stimulus that is detected >50% of the time
Varies in relation to anatomical location and between people

Question 198

How is info regarding somatosensory stimulus intensity conveyed?

Answer 198

Variation of frequency of APs generated
Number of separate receptors activated (recruitment)

Relationship between stimulus intensity and ultimate sensory discrimination may be linear or logarithmic

Question 199

What is a receptive field?

Answer 199

The area from which a stimulus elicits a neuronal response

Overlaps with others

Question 200

When there is increased stimulus intensity, what happens to the receptive field?

Answer 200

Recruitment of adjacent sensory receptors with increased stimulus intensity
The increased number of APs may be interpreted by the brain as increased intensity

Question 201

What is lateral inhibition?

Answer 201

Activation of one neural unit inhibits activation of other units
Mediated by interneurones within DH of SC

Question 202

How does lateral inhibition do?

Answer 202

Facilitates pinpoint accuracy in localisation of the stimulus
Facilitates enhanced sensory perception

Question 203

What is two-point discrimination?

Answer 203

Ability to detect that two stimuli are distinct from each other

Question 204

What is the two-point threshold?

Answer 204

Minimum distance required between two stimuli in order to perceive that they are two separate stimuli

Question 205

What does two-point discrimination depend on?

Answer 205

Peripheral mechanoreceptors
Spinal posterior column
Cortical function

Question 206

How does two-point discrimination vary in the body? Why?

Answer 206

65mm on the back
2mm on the fingers

Related to:
Density of innervation
Area of receptive field
Sensory homunculus

Question 207

What is neural adaptation?

Answer 207

A form of desensitisation
If a stimulus of constant strength is maintained for a period of time the frequency of action potentials diminishes (e.g. wearing clothes)

Question 208

Why is neural adaptation useful?

Answer 208

Facilitates ability to differentiate

meaningful from irrelevant information

Question 209

How do phasic and tonic receptors differ in neural adaptation?

Answer 209

Phasic receptors = Rapidly adaptive

Tonic receptors = Slowly adaptive

Question 210

What are the types of nerve fibre?

Answer 210

A alpha (proprioception, somatic motor), beta (touch, pressure), gamma (motor to muscle spindle), delta (pain, cold, touch)

B (postganglionic autonomics)

C dorsal root (pain, temperature, mechanoception), sympathetic (postganglionic sympathetic)

Question 211

How are cortical neurones involved in pain pathways?

Answer 211

Involved in the perception and interpretation of pain

Question 212

How are thalamic neurones involved in pain pathways?

Answer 212

Ventrobasal complex and Nucleus Reticularis have important reciprocal roles in modulation of nociceptive signals

Question 213

How are superficial DH neurones involved in pain pathways?

Answer 213

Crucial role in processing nociceptive signals

Question 214

Ascending pathway: touch and proprioception

Answer 214

Dorsal Column (Lemniscal system)
Decussation (crossing) in brainstem
Somatotopy throughout pathway
Lateral inhibition in dorsal column nuclei

Question 215

Ascending pathway: pain and temperature

Answer 215

Spinothalamic tract
Decussation in spinal cord via interneurones
Somatotopy throughout pathway

Important to consider in spinal cord injury

Question 216

What is Brown-Sequard Syndrome?

Answer 216

Hemisection of spinal cord

Question 217

How are spinal neurones modulated? What does this mean for the cortical response to peripheral input?

Answer 217

Spinal neurones respond to peripheral stimuli, but are modulated by interneurones and descending inhibitory controls
Therefore the cortical response may not always match the peripheral input (could be greater or lesser)

Question 218

What is the major excitatory synaptic transmitter? What does it activate

Answer 218

Glutamate

Activates multiple receptor classes: AMPA, NMDA, mGluR
Activates NMDAr by removing Mg2+ plug

Question 219

What does NMDAr activation cause?

Answer 219

NMDAr activation causes large Ca2+ influx-> multiple intracellular actions

Question 220

What may LTP of NMDAr cause?

Answer 220

LTP of NMDAr may occur-> hypersensitivity to pain

Question 221

What do NMDAr antagonists do?

Answer 221

Can relieve pain e.g. Ketamine

Question 222

What is the gate control theory? 3 examples

Answer 222

Non-painful stimulation can inhibit the transmission of pain from periphery to brain

E.g.
Rubbing elbow after banging it
Using a TENS machine
Spinal Cord Stimulation

Question 223

How can non-painful stimulation inhibit the transmission of pain from periphery to brain?

Answer 223

Gate theory

Small Aδ and C fibres transmit painful stimuli
Large Aβ fibres transmit non-noxious stimuli

Large Aβ fibres can prevent or reduce transmission of Aδ and C fibres within the dorsal horn of the spinal cord

‘Closing the Gate’
By activating inhibitory interneurones (GABAAR)

Question 224

What is a dorsal root ganglion?

Answer 224

Nerve rootlets from a central dorsal nerve root that forms the ganglion
Surrounded by dural sheath and minimal CSF

Question 225

What causes neuronal dysfunction in a DRG?

Answer 225

Associated with channelopathy (Ca2+, Na+) or second messengers may result in depolarisation in response to minor stimuli

Question 226

How can dorsal root ganglion dysfunction be treated?

Answer 226

X-Ray guided techniques including

• Transforaminal epidural
• Nerve root block
• Neuromodulation

Question 227

What is neuromodulation? How does it work?

Answer 227

Non-painful stimulation can inhibit the transmission of pain from periphery to brain
E.g. by stimulating SC or DRG

Large Aβ fibres can prevent or reduce transmission of Aδ and C fibres within the dorsal horn of the spinal cord
‘Closing the gate’ compensates for neuronal dysfunction
Useful in neuropathic pain

Question 228

What is descending modulation?

Answer 228

Descending pathways from brainstem structures can have inhibitory or excitatory influence on spinal nociceptive transmission
This monitoring system is always active

Question 229

What mediates descending modulation?

Answer 229

Mediated by spinal 5HT3, NA, GABAA and Glycine receptors

Question 230

What can loss of physiological inhibition result in?

Answer 230

Pathological hypersensitivity

Question 231

What are the 3 key somatosensory areas?

Answer 231

SI = Primary somatosensory cortex (in postcentral gryus)
SII = Secondary somatosensory cortex (in parietal operculum)
Posterior parietal cortex

Question 232

What is included in the association cortex?

Answer 232

Areas outside the primary areas
Essential for complex mental functions
Most developed part of the brain

Question 233

What parts of the brain are studied in an fMRI looking at the pain matrix?

Answer 233

Cortices (SI, SII, insular, anterior cingulate, prefrontal)
Brainstem
Amygdala
Cerebellum

Question 234

What is pain?

Answer 234

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

Pain is always subjective

Warns that something is wrong

Question 235

Why is pain important?

Answer 235

A warning that something is wrong
Associated with tissue damage
Has a protective function

Question 236

What pain fibres are fast and slow?

Answer 236

Fast (Aδ) and Slow (C fibres)

Question 237

What are the types of pain?

Answer 237

Nociceptive – tissue damage, typically Acute
Muscle – lactic acidosis, ischaemia
Superficial Somatic – well-localised
Visceral – deep, poorly localised
Referred – from an internal organ/structure e.g. Angina
Neuropathic – dysfunction of the nervous system

Question 238

How is pain detected?

Answer 238

Pathology-> nerve ending-> depolarisation-> AP in afferent nerve-> DH of SC-> brain

Question 239

What is pain called when it has no known pathological cause?

Answer 239

Malingering

Question 240

What drugs are in the WHO analgesic ladder?

Answer 240

1. Paracetamol & Aspirin (& Ibuprofen)
2. Codeine (& Tramadol)
3. Morphine

Question 241

What causes myalgia (muscle pain)?

Answer 241

Metabolic
Overuse
Stretching
Tension
Compression
Ischaemia
Tearing
Viral infection
Fibromyalgia
Angina

Question 242

What are the features of myalgia (muscle pain)?

Answer 242

Aching
Burning (lactic acidosis)
Cramping
Tightness
Crushing
Tenderness

Question 243

What is superficial/cutaneous somatic pain?

Answer 243

Related to the skin
Pressure
Too hot / cold
Inflammation
Injury
Infection
Burns

Question 244

What are the features of somatic pain?

Answer 244

Often well-localised
Sharp
Stinging
Aching
Burning 
Throbbing
Tightness
Sensitive

Question 245

What is visceral pain?

Answer 245

Pain arising from internal organs or viscera

Heart, oesophagus, stomach, duodenum, gallbladder, or pancreas, colon

Question 246

What is problematic about visceral pain?

Answer 246

Viscera have low density of sensory innervation
-> vague, diffuse, poorly localised pain

Not possible to reliably differentiate one organ’s pain from another

Pain may be referred

Question 247

Where is visceral pain often felt?

Answer 247

Characteristically midline pain at level of sternum/ epigastrium

Question 248

When does visceral hyperalgesia occur?

Answer 248

Neural sensitisation

IBS, dysmenorrhoea, refractory angina

Question 249

What are the features of referred pain?

Answer 249

At sites of body wall whose innervation enters spinal cord at the same level as the organ

Sharper, better localised then visceral pain

Question 250

What is the wind-up phenomenon of pain?

Answer 250

Short lasting synaptic plasticity

Repetitive stimulation of WDRs (wide dynamic range neurones) induces increased evoked response and post discharge with each stimulus

May precipitate long-term potentiation (LTP) i.e. long-lasting increase in efficacy of synaptic transmission

Wind-up and LTP related to neuropathic sensitisation

Question 251

What are WDRs? What do they do

Answer 251

Wide Dynamic Range neurones

Receive input from Aβ, Aδ and C fibres
Respond to full range of stimuli (touch, heat, chemical)
Fire APs in graded fashion
Exhibit ‘Wind-up’

Question 252

What is neuropathic pain?

Answer 252

Pain in an area of neurological dysfunction
Sharp, burning, electric shocks, squeezing

Can last after area has healed completely

Difficult to manage

Question 253

How does neuropathic pain respond to analgesic drugs?

Answer 253

Poor response
Delayed (1 month trial)
Medications generally safe

Question 254

Define: allodynia

Answer 254

Pain due to a stimulus that does not normally provoke pain

Question 255

Define: hyperalgesia

Answer 255

Increased pain from a stimulus that normally provokes pain

Question 256

Define: sensitization

Answer 256

Increased responsiveness of nociceptive neurons to their normal input

Question 257

Define: hypoalgesia

Answer 257

Diminished pain in response to a normally painful stimulus

Question 258

Define: hyperpathia

Answer 258

Painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold

Question 259

Define: parasthesia

Answer 259

Abnormal sensation, whether spontaneous or evoked

Question 260

Define: dysaethesia

Answer 260

Unpleasant abnormal sensation, whether spontaneous or evoked

Question 261

List examples of neuropathic pain

Answer 261

Complex Regional Pain Syndrome
Phantom limb pain
Chronic scar hypersensitivity/postsurgical pain
Post Herpetic Neuralgia
Central Post Stroke Pain
Radicular low back pain (sciatica)
Diabetic neuropathy
Chemotherapy induced neuropathy

Question 262

What is Complex Regional Pain Syndrome? Symptoms? How is it treated?

Answer 262

Severe form of neuropathic pain due to neurogenic inflammation and overexpression of nociceptive endings

Sensory: hyperaesthesia/allodynia
Vasomotor: temperature asymmetry/skin colour changes/asymmetry.
Sudomotor/oedema: oedema/sweating changes/asymmetry
Motor/trophic: decreased range of motion/motor dysfunction (weakness, tremor, dystonia)/trophic changes (hair, nail, skin)

Question 263

How can complex regional pain syndrome be treated?

Answer 263

MDT rehabilitation: Physio, OT, Psychology, PMP

Medications, Spinal Cord Stimulation, (nerve blocks)

Question 264

What is phantom limb pain?

Answer 264

Pain affecting amputeess or people with removed eyes, breasts and genitals
1/2 are painful neuropathic

Question 265

What causes phantom limb pain?

Answer 265

Remapping of the cortex (shown by fMRI studies)

Question 266

How is phantom limb pain treated?

Answer 266

Medication
Mirror therapy
Neuroma excision
8% capsaicin patches

Question 267

How can neuropathic pain be managed pharmacologically?

Answer 267

Antidepressants= Amitriptyline, Nortriptyline, Duloxetine

Anticonvulsants= Gabapentin, Pregabalin

Opioid trial= Tramadol, Buprenorphine, Methadone, Morphine

Hybrid= Tapentadol

Topical= 5% Lidocaine, Capsaicin 0.075% cream and 8% patches

Question 268

How is a response to neuropathic pain treatment defined?

Answer 268

30-50% less pain

Question 269

What does evidence suggest is the best treatment of chronic neuropathic pain?

Answer 269

1st line: TCA, SNRI, alpha-2-delta ligands (e.g. Gabapentin)

2nd line: Opioids and Tramadol

3rd line: Membrane stabilisers, NMDA antagonists, Capsaicin

Question 270

How do Qutenza 8% capsaicin patches work?

Answer 270

Applied to skin for a single 60min period (in hospital)
Binds to TRPV1 R on nerve endings (desensitises R directly and has direct toxicity to mitochondria)

HAIRCUT or PRUNING mechanism

Can be repeated after 3-4 months
Can get long benefit from single treatment (disease modification)
3rd line

Question 271

What patients is high strength capsaicin patch therapy useful for?

Answer 271

Patients with peripheral NP i.e. allodynia/hyperalgesia

Question 272

What is functional segregation of motor control?

Answer 272

Motor system is organised into different areas that control different aspects of movement

Question 273

What is hierarchical organisation of motor control?

Answer 273

High order areas of hierarchy are involved in more more complex tasks e.g. programme and decide movements, coord muscle activity

Low order areas perform lower level tasks e.g. execution of movement

Question 274

Which parts of the brain/SC are higher order/lower order?

Answer 274

Highest to lowest:
Association cortex
Motor cortex (primary motor cortex, premotor cortex, supplementary motor area)
Brain stem
Spinal cord 

NB. side loops through basal ganglia and cerebellum

Question 275

What is the basal ganglia comprised of?

Answer 275

Caudate nucleus
Putamen
Globus pallidus
Substantia nigra
Subthalamic nucleus

Question 276

What are the areas of the frontal lobe motor cortex? Broadmann’s area numbers>

Answer 276

Primary motor cortex or M1= Broadmann’s area 4

Premotor cortex= Broadmann’s area

Supplementary motor area= Broadmann’s area

Question 277

What is the location of M1 (Broadmann’s area 4)?

Answer 277

PRIMARY MOTOR CORTEX

Frontal lobe
Precentral gyrus
Anterior to central sulcus

Question 278

What is the function of M1 (Broadmann’s area 4)?

Answer 278

PRIMARY MOTOR CORTEX

Control fine, discrete, precise voluntary movements

Provide the descending signals to execute movements

Question 279

Where are Betz cells in the primary motor cortex?

Answer 279

Grey matter

Layer V

Question 280

What are descending cortical pathways? 2 egs.

Answer 280

Descending motor pathways
From cortex
Travel down to innervate abdomen, limbs and trunk

Question 281

Outline the path of the lateral corticospinal pathway?

Answer 281

PMC

UMN through midbrain (through cerebral peduncle)
Through pons
Through pyramid of medulla

DECUSSATION OF PYRAMIDS

Lateral corticospinal tract through SC

LMN through spinal nerve
To skeletal muscles in the distal parts of the limbs

Question 282

Outline the path of the anterior corticospinal pathway?

Answer 282

PMC

UMN through midbrain (through cerebral peduncle)
Through pons
Through pyramid of medulla

DECUSSATION OF SPINAL CORD

Anterior corticospinal tract through SC

LMN through spinal nerve
To skeletal muscles in the trunk and proximal parts of the limbs

Question 283

Where do the anterior and lateral corticospinal paths go to?

Answer 283

Anterior= skeletal muscles in trunk and proximal parts of the limbs

Lateral= skeletal muscles in distal parts of the limbs

Question 284

How are the tongue muscles innervated by descending muscle pathways?

Answer 284

CORTICOBULBAR TRACT

Head region motor cortex
Genu of internal capsule

DECUSSATES TO GO TO Hypoglossal nucleus

Hypoglossal nerve (through inferior olivary nucleus and pyramid)

Intrinsic tongue muscles, geniohyoid muscle, genioglossus muscle

Question 285

List 2 examples of pyramidal tracts?

Answer 285

Corticospinal tract

Cortibulbar tract

Question 286

What NTs are used between UMNs and LMNs and between LMNS and muscles?

Answer 286

Glutamate: from upper to lower motor neurons

Acetylcholine: from lower motor neurons to muscles

Question 287

What side of the body does the left cerebral surface control?

Answer 287

R side

Question 288

Who discovered the motor homunculus?

Answer 288

Penfield

Question 289

How can the organisation of the primary motor cortex be described?

Answer 289

Somatotopical organization
Penfield’s motor homunculus
Can change e.g. singer has greater area of vocalisation

Question 290

What is the location of the premotor cortex (Broadmann’s area 6)?

Answer 290

Frontal lobe, anterior to PMC

Question 291

What is the function of the premotor cortex (Broadmann’s area 6)?

Answer 291

Involved in planning movements

Regulates externally cued movements (e.g. reaching out for an apple that you see)

Question 292

What is the location of the supplementary motor cortex (Broadmann’s area 6)?

Answer 292

Frontal lobe

Anterior to PMC medially

Question 293

What is the function of the supplementary motor cortex (Broadmann’s area 6)?

Answer 293

Planning complex movements and programming sequencing of movements

Regulates internally driven movements (e.g. speech)

SMA becomes active when thinking about a movement before executing that movement

Question 294

What is the association cortex?

Answer 294

Not strictly motor area as activity doesn’t correlate with motor output/act

Posterior parietal cortex
Prefrontal cortex

Question 295

How is the posterior parietal cortex involved in motor function?

Answer 295

In association cortex

Ensures movements are targeted accurately to objects in external space

Question 296

How is the prefrontal cortex involved in motor function?

Answer 296

In association cortex

Involved in selection of appropriate movements for a particular course of action

Question 297

What are negative and positive signs of lesions?

Answer 297

Negative= loss of function
Positive= increased abnormal motor function (due to loss of inhibitory descending inputs)

Question 298

What are the negative and positive signs of an upper motor neuron lesion?

Answer 298

NEGATIVE SIGNS
Paresis: graded weakness of movements
Paralysis (plegia): complete loss of muscle activity

POSITIVE SIGNS
Spasticity: increased muscle tone
Hyperreflexia: exaggerated reflexes 
Clonus: abnormal oscillatory muscle contraction
Babinski’s sign

SYMPTOMS ON OTHER SIDE

Question 299

What is apraxia? What are the symptoms?

Answer 299

Upper motor neuron disorder of skilled movement (due to lesion of inferior parietal lobe or frontal lobe (PMC, SMA)

Progressive and neurodegenerative

Not caused by weakness, abnormal tone or posture or movement disorders (tremors or chorea)

Patients aren’t paretic but have lost info about how to perform skilled movements

Question 300

What are the most common causes of apraxia?

Answer 300

Stroke and dementia

Question 301

What are the main symptoms of lower motor neuron lesions?

Answer 301

Weakness
Hypotonia (reduced muscle tone)
Hyporeflexia (reduced reflexes) 
Muscle atrophy
Fasciculations
Fibrillations

Question 302

What are fasciculations? (LMN lesions)

Answer 302

Damaged motor units produce spontaneous APs resulting in a visible twitch

Question 303

What are fibrillations? (LMN lesions)

Answer 303

Spontaneous twitching of individual muscle fibres, recorded during needle electromyography examination

Question 304

What are the main signs in UMN disease?

Answer 304

Increased muscle tone (spasticity of limbs and tongue)
Brisk limbs and jaw reflexes
Babinski’s sign
Loss of dexterity
Dysarthria
Dysphagia

Question 305

What are the main signs in LMN disease?

Answer 305

Weakness
Muscle wasting
Tongue fasciculations and wasting
Nasal speech
Dysphagia

Question 306

What is included in the basal ganglia striatum?

Answer 306

Caudate and putamen

Question 307

What are the functions of the basal ganglia?

Answer 307

Elaborating associated movements e.g. swinging arms when walking
Moderating and coordinating movement (suppressing unwanted moves)
Performing movements in order

Question 308

What segments are the globus pallidus divided into?

Answer 308

Internal and external

Question 309

What pathways are in the circuit of the basal ganglia? Where do they project and what are there overall effects?

Answer 309

Direct pathway (no projection to STN)= overall excitatory effect on motor cortex
Indirect pathway (projection to STN)= overall inhibitory effect on motor cortex

Balance between these-> normal functioning of the basal ganglia

Question 310

What are the main neurotransmitters in the basal ganglia circuit?

Answer 310

Dopamine (+)
Glutamate (+)
GABA (-)

Question 311

Is basal ganglia control ipsilateral or contralateral?

Answer 311

It is uncrossed (unlike corticospinal tract): basal ganglia mediate function of the ispsilateral cortex

Question 312

What are the 2 classes of basal ganglia syndromes?

Answer 312

Hypokinetic: decreased movement (Parkinson’s Disease)

Hyperkinetic: increased movement (Huntington’s Disease)

Question 313

Is Parkinson’s disease hypo or hyperkinetic?

Answer 313

Hypo

Question 314

Is Huntington’s disease hypo or hyperkinetic?

Answer 314

Hyper

Question 315

What part of the basal ganglia is most affected in PD? What neurones does this affect?

Answer 315

Neuronal degeneration of substantia nigra pars compacta

Loss of >80% dopaminergic cells (nigro-striatal dopaminergic axons)

Question 316

What does degeneration of dopamine neurons in the SNc cause?

Answer 316

Loss of nigro-striatal dopaminergic axons in caudate and putamen
Disruption of the fine balance of excitation and inhibition
Reduction of the excitation of motor cortex

Question 317

What are the major signs of PD?

Answer 317

Bradykinesia
Hypomimic face
Akinesia
Rigidity
Tremor at rest
Parkinson's gait (shuffling)
Stooped posture

Question 318

Define: bradykinesia

Answer 318

Slowness of (small) movements e.g. doing up buttons, handling a knife

Question 319

Define: hypomimic face

Answer 319

Expressionless, mask-like e.g. absence of movements that normally animate the face

Question 320

Define: akinesia

Answer 320

Difficulty in the initiatIon of movements becausecannot initiate movements internally

Question 321

Define: rigidity

Answer 321

Muscle tone increase, causing resistance to externally imposed joint movements

Question 322

Define: tremor at rest

Answer 322

4-7Hz starts in one hand (pill-rolling tremor)

With time spreads to other parts of the body

Question 323

Define: Parkinsonian’s gait

Answer 323

Walking slow, small steps, shuffling feet, reduced arm swing

Question 324

What is Huntington’s disease caused by?

Answer 324

Neurodegenerative genetic disorder
Abnormality in chromosome 4, autosomic dominant
Degeneration of GABAergic neurones in striatium (caudate first, then putamen later)

Question 325

What does degeneration of GABAergic neurons in the striatum cause?

Answer 325

Disruption of the fine balance between inhibition and excitation
Motor cortex gets excessive excitatory input
Motor cortex continuously sends involuntary commands for movement sequences to the muscles

Question 326

What are the main signs of Huntington’s Disease?

Answer 326

Choreic movements (speech impairment, difficulty swallowing, unsteady gait)
Later= cognitive decline and dementia

Question 327

What is chorea? Egs?

Answer 327

Type of movement (in HD)
Rapid jerky involuntary movements of the body (hands and face affected first, then legs and rest of body)

Speech impairment
Difficulty swallowing
Unsteady gait

Question 328

What are the 3 lobes of the cerebellum (horizontal division)?

Answer 328

Anterior
Posterior
Flocculonodular

Question 329

What are the 3 zones of the cerebellum divided sagittally?

Answer 329

Vermis
Intermediate hemisphere
Lateral hermisphere

Question 330

The connections of the cerebellum are with the …… .. and the …… cerebral hemisphere?

Answer 330

The connections of the cerebellum are with the same side of the body and with the opposite cerebral hemisphere

Question 331

What are the main neurotransmitters in the cerebellum?

Answer 331

Glutamate (+)

GABA (-)

Question 332

What is the flocculonodular lobe connected with?

Answer 332

The vestibular system

‘Vestibulocerebellum”

Question 333

What is the function of the vestibulocerebellum (flocculonodular lobe)?

Answer 333

Regulation of gait, posture and equilibrium

Coordination of head movements with eye movements

Question 334

What is the function of the spinocerebellum (vermis and intermediate hemisphere)?

Answer 334

Coordination of speech
Adjustment of muscle tone
Coordination of limb movements

Question 335

What parts of the cerebellum is the spinocerebellum?

Answer 335

Vermis

Intermediate hemisphere

Question 336

What projects to the vermis?

Answer 336

Spinal afferents from axial portions of the body, trigeminal, visual and auditory inputs

Question 337

What projects to the intermediate hemisphere?

Answer 337

Spinal afferents from the limbs

Question 338

What part of the cerebellum is the cerebrocerebellum?

Answer 338

Lateral hemisphere

Question 339

What is the function of the cerebrocerebellum (lateral hemisphere)?

Answer 339

Coordination of skilled movements
Cognitive function, attention, processing of language
Emotional control

Question 340

What are the main functions of the cerebellum?

Answer 340

Maintenance of balance and posture
Coordination of voluntary movements (timing and force-> smooth moves)
Motor learning (adapting and fine-tuning, via trial and error)
Cognitive functions (language)

Question 341

What is vestibulocerebellar syndrome (flocculonodular syndrome)?

Answer 341

Damage (tumour) causes syndrome similar to vestibular disease

Causes gait ataxia and tendency to fall (even when patient sitting and eyes open

Question 342

What is spinocerebellar syndrome?

Answer 342

Damage (degeneration and atrophy associated with chronic alcoholism)

Affects mainly legs, causes abnormal gait and stance (wide-based)

Question 343

What is cerebrocerebellar syndrome (lateral cerebellar syndrome)?

Answer 343

Damage affects mainly arms/skilled coordinated movements (tremor) and speech

Question 344

What are the main symptoms of cerebellar disorders?

Answer 344

Ataxia
Disturbances of posture or gait (staggering/drunken) 
Dysmetria
Intention tremor
Dysdiadochokinesia
Scanning speech

Question 345

What are 2 of the more common cerebellar disorders?

Answer 345

Hereditary Friedrich's Ataxia
Multiple Sclerosis (acquired)

Question 346

Define: ataxia

Answer 346

General impairments in movement coordination and accuracy

Question 347

Define: dysmetria

Answer 347

Inappropriate force and distance for target-directed movement (knocking over a class not grabbing it)

Question 348

Define: intention tumour

Answer 348

Increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)

Question 349

Define: scanning speech

Answer 349

Staccato, due to impaired coordination of speech muscles

Question 350

Define: dysdiadochokinesia

Answer 350

Inability to perform rapidly altering movements (rapidly pronating and supinating hands and forearms)

Question 351

What is a synapse?

Answer 351

Contact or junction between presynaptic axon and postsynaptic axon
Allows for contact from neurone to muscle or from neurone to neurone

Question 352

What is the synaptic contact ratio for muscles and the CNS?

Answer 352

1: 1 for muscle
10000: 1 in the CNS

Question 353

What size is a typical synaptic cleft?

Answer 353

10-50nm

Question 354

How is the membrane potential of the postsynaptic neurone altered?

Answer 354

Altered in two direction by inputs
Can be made less negative (i.e. brought closer to threshold for firing- EPSP)
Can be made more negative (i.e. brought further away from threshold for firing- IPSP)

Graded effects= summation
- IPSPs and EPSPs summate

Question 355

What does the degree of summation (of IPSPs and EPSPs) determine?

Answer 355

How readily a neuron can reach threshold to produce an AP

Question 356

What is a NMJ?

Answer 356

Specialised synapse between the motor neuron and the motor end plate, the muscle fibre cell membrane

Question 357

What happens when an AP arrives at an NMJ?

Answer 357

Ca2+ influx causes ACh release
ACH binds to Rs on motor end plate
Ion channel opens- Na+ influx-> AP in muscle fibre

Question 358

What happens at rest to ACh release?

Answer 358

Individual vesicles release ACh at a very low rate

Cause miniature end-plate potentials (mEPP)

Question 359

What is an alpha motor neuron? What do they innervate?

Answer 359

Lower motor neurons of the brainstem and the spinal cord

Innervate the extrafusal muscle fibres of the skeletal muscles

Question 360

What does alpha motor neuron activation cause?

Answer 360

Muscle contraction

Question 361

What does the motor neuron pool contain?

Answer 361

All alpha motor neurons innervating a single muscle

Question 362

What is a motor unit?

Answer 362

Single motor neuron together with all the muscle fibres that it innervates
Samllest functional unit with which to produce force

Question 363

How many motor neurons do humans have?

Answer 363

Approx 420,000

Question 364

How many skeletal muscle fibres do humans have?

Answer 364

250 million skeletal muscle fibres

Question 365

How many muscle fibres are typically supplied by each motor neuron?

Answer 365

600 muscle fibres

Question 366

What does stimulation of one motor unit cause?

Answer 366

Contraction of all muscle fibres in that unit

Question 367

How many different motor unit types are there? How are they classified?

Answer 367

3 (I, IIa and IIIb)

Classified by the amount of tension generated. speed of contraction and fatiguability of the motor unit

Question 368

What two mechanisms allow the brain to regulate the force a single muscle can produce?

Answer 368

Recruitment

Rate coding

Question 369

How does recruitment allow the brain to regulate the force that a single muscle can produce? What does this allow?

Answer 369

Motor units are not randomly recruited= ordered
Governed by the “Size Principle”
Smaller units are recruited first (these are generally the slow twitch units)

More force required-> more units recruited

This allows fine control (e.g. when writing), under which low force levels are required

Question 370

How does rate coding allow the brain to regulate the force that a single muscle can produce?

Answer 370

A motor unit can fire at a range of frequencies

Slow units fire at a lower frequency

As the firing rate increases, the force produced by the unit increases

Summation occurs when units fire at frequency too fast to allow the muscle to relax between arriving action potentials.

Question 371

What relative frequency do fast and slow units fire at?

Answer 371

Fast units fire at higher frequency

Slow units fire at a lower frequency

Question 372

What are neurotrophic factors?

Answer 372

Type of growth factor
Prevents neuronal death
Promote growth of neurons after injury

Question 373

If a fast twitch muscle and a slow muscle are cross innervated, what happens to the FDL and soleus?

Answer 373

FDL= becomes slow
Soleus= becomes fast

Question 374

How can muscle fibre types change properties? Which fibre types in particular?

Answer 374

Under different conditions-> plasticity
IIB to IIA most common following training
I to II in cases of severe deconditioning or spinal cord injury

Question 375

Why does ageing lead to slower muscle contraction times?

Answer 375

Ageing associated with loss of type I and type II fibres (preferential loss of type II-> larger proportion of type I fibres in aged muscle-> slower contraction times)

Question 376

What does microgravity during spaceflight do to muscle fibres?

Answer 376

Shift from slow to fast muscle fibre types

Question 377

What motor and descending (efferent) pathways are pyramidal and extrapyramidal?

Answer 377

1. Pyramidal
   1a. Lateral corticospinal tract
   1b. Anterior corticospinal tract
2. Extrapyramidal
   2a. Rubrospinal tract
   2b. Reticulospinal tract
   2c. Vestibulospinal tract
   2d. Olivospinal tract

Question 378

What does 2c (vestibulospinal motor tract) do?

Answer 378

Regulates posture to maintain balance, and facilitates mainly α motoneurones of the postural, anti-gravity (extensor) muscles

Question 379

What does 2b (reticulospinal motor tract) do?

Answer 379

Coordinate automated movements of locomotion and posture (e.g. to painful stimuli)

Question 380

What does 2a (rubrospinal motor tract) do?

Answer 380

Automatic movements of arm in response to posture/balance changes

Question 381

What do 1b (lateral corticospinal motor tract) and the sacral region do?

Answer 381

Control voluntary movements

Question 382

What is a reflex?

Answer 382

An automatic and often inborn response to a stimulus that involves a nerve impulse passing inward from a receptor to a nerve centre and then outward to an effector (as a muscle or gland) without reaching the level of consciousness

Involuntary coordinated pattern of muscle contraction and relaxation elicited by peripheral stimuli

Question 383

How does the reflex relate to force? Use eg of bicep being tapped

Answer 383

If the biceps is tapped, the reflex occurs quickly and is related in size to how hard the biceps was hit

Question 384

Outline a reflex arc

Answer 384

Sensory receptor 
Sensory neuron
Integrating centre
Motor neuron
Effector

Question 385

What happens to a reflex in the dorsal roots are cut?

Answer 385

Decreased force

Reflex needs afferents

Question 386

Outline the monosynaptic stretch reflex

Answer 386

E.g. hit knee-> kick out foot

Stretching stimulates sensory R (muscle spindle)
Sensory neuron excited
Within integrating centre (SC)= sensory neuron activates motor neuron
Motor neuron excited
effector (same muscle) contracts and relieves the stretching
*antagonistic muscles relax

Question 387

What motor neuron does the Hoffman (H-) reflex involve?

Answer 387

Orthodromic motor

Question 388

Outline the polysynaptic reflexes (flexion withdrawal)

Answer 388

E.g. stepping on tack

Sensory receptor (dendrites of pain-sensitive neuron on bottom of foot)
Sensory neuron excited
Within integrating centre (SC)= sensory neuron activates interneurons in several SC segments
Motor neuronS excited
Effectors (flexor muscles) contract and withdraw leg

Question 389

Outline the flexion withdrawal and crossed extensor reflexs

Answer 389

E.g. stepping on tack with RIGHT FOOT

Sensory receptor (dendrites of pain-sensitive neuron on bottom of foot)
Sensory neuron excited
Within integrating centre (SC)= sensory neuron activates interneurons in several SC segments
Motor neuronS excited

Effectors:
Flexor muscles contract and withdraw RIGHT leg
Extensor muscles contract and extend LEFT leg

Question 390

What is the Jendrassik manoeuvre?

Answer 390

Patient makes a fist of clenches teeth when having patellar tendon tapped

Larger reflex response will be observed when the patient is occupied with the manoeuvre, as the manoeuvre may prevent the patient from consciously inhibiting or influencing his or her response to the hammer

Relates to supraspinal control of reflex

Question 391

What does the supraspinal control of reflexes do? How is this studied?

Answer 391

Higher centres of the CNS exert inhibitory and excitatory regulation upon the stretch reflex

Inhibitory control dominates in normal conditions

Studied with decerebration which reveals the excitatory control from supraspinal areas

Rigidity and spasticity can result from brain damage giving over-active or tonic stretch reflex

Question 392

How can higher centres influence reflexes?

Answer 392

Supraspinal control of reflexes

Activating alpha motor neurons
Activating inhibitory interneurons
Activating propriospinal neurons
Activating gamma motor neurons
Activating terminals of afferent fibres

Question 393

What higher centres and pathways are involved in supraspinal control of reflexes?

Answer 393

Cortex= corticospinal (fine control of limb movements, body adjustments)
Red nucleus= rubrospinal (automatic movements of arm in response to posture/balance changes)
Vestibular nuclei= vestibulospinal (altering posture to maintain balance)
Tectum= tectospinal (head movements in response to visual information)

Question 394

What does the gamma reflex loop do?

Answer 394

Involves gamma motor neurons

CNS can influence the stretch reflex via the gamma motoneurons

Gamma motoneuronsregulate how sensitive the stretch reflex is by tightening or relaxing the fibres within the spindle

Question 395

What is hyper-reflexia?

Answer 395

Loss of descending inhibition

Eg.g due to a stroke-? Clonus sign, Babinski sign

Question 396

What is the clonus sign?

Answer 396

Hyper-reflexia

Clonusat the ankle is tested by rapidly flexing the foot into dorsiflexion (upward), inducing a stretch to the gastrocnemius muscle

Subsequent beating of the foot will result, however only a sustainedclonus(5 beats or more) is considered abnormal

Question 397

What is the Babinski sign?

Answer 397

Hyper-reflexia

The Babinski reflex occurs after the sole of the foot has been firmly stroked

The big toe then moves upward or toward the top surface of the foot-> other toes fan out

This reflex is normal in children up to 2 years old

Question 398

What is hypo-reflexia?

Answer 398

Below normal or absent reflexes

Mostly associated with lower motor neuron diseases

Question 399

How is sound transmitted in the outer ear?

Answer 399

Air transmitted sound waves are directed toward the delicate hearing mechanisms

Pinna gently funnels sound waves into ear canal

Question 400

What is the role of the outer ear?

Answer 400

Focuses sound on the tympanic membrane

Boosts sound pressure

Question 401

How is sound transmitted by the inner ear?

Answer 401

Air movement strikes the tympanic membrane and vibrations-> oval window (smaller surface area means increased pressure)

Energy generated transferred from AIR medium to SOLID medium in middle ear

Ossicular chain of the middle ear connects to the eardrum via the malleus

Question 402

How are the ossicles connected to the eardrum?

Answer 402

The malleus

Question 403

What protects the inner ear from loud noises?

Answer 403

Stapedius muscle contracts

Protects ossicles and inner ear

Question 404

Describe the joint between the incus and stapes

Answer 404

Flexible

Ossicles use leverage to increase the force on the oval window

Question 405

What are the 3 ossicles?

Answer 405

Stapes
Incus
Malleus

Question 406

What is the function of the inner ear?

Answer 406

Transduce vibrations into nervous impulses

Also, produces frequency (or pitch) and intensity (or loudness) analysis of sound

Question 407

How is pressure of vibrations increased in the middle ear?

Answer 407

Change in surface area (tympanic membrane to oval window)-> increased pressure

Question 408

What are the 3 compartments of the inner ear and what do they contain?

Answer 408

Scala vestibuli (perilymph)
Scala media (endolymph)
Scala tympani (perilymph)

Question 409

Which inner ear compartment is closest to the basilar membrane?

Answer 409

Scala tympani

Question 410

The round window and oval window are found by which compartments of the inner ear?

Answer 410

Oval= scala vestibuli
Round= scala tympani

Question 411

What is the function of the perilymph?

Answer 411

Cushioning agent for the delicate structures of the centre chamber
Connected to CSF

Question 412

How is sound transduced in the inner ear?

Answer 412

Ossicular chain transfers energy from a solid medium to a fluid medium (of inner ear via stapes)

Stapes connects to oval window which moves when sound is transferred

Movement of oval window-> motion in cochlear fluid and along basilar membrane

Basilar membrane excites frequency specific areas of organ of Corti-> stimulates nerve endings

Question 413

How is the basilar membrane arranged?

Answer 413

Like a xylophone

BM is sensitive to different frequencies at different points along its length

Question 414

How many inner and outer hair cells are there in a normal adult?

Answer 414

20,000 OHCs

3,500 IHCs

Question 415

What do hair cells in the inner ear do?

Answer 415

Adjust sensitivity of nerve signal from sound stimulus

Question 416

What happens to hair cells due to higher amplitude (louder) sounds?

Answer 416

Greater deflection of sterocilia and K channel opening

Movement-> depolarisation

Question 417

What causes the hair cell to depolarise?

Answer 417

Upward movement of the basilar membrane displaces stereocilia away from modiolus-> K+ channels open-> K+ enters from endolymph-> hair cell depolarises

Question 418

What causes the hair cell to hyperpolarise?

Answer 418

Downward movement of the basilar membrane displaces stereocilia towards modiolus -> K+ channels close-> hair cell hyperpolarises

Question 419

What cranial nerve is involved in the central auditory pathway?

Answer 419

Vestibular nerve (VIII)

Question 420

Outline the central auditory pathways. (Note ipsilateral/bilateral parts)

Answer 420

Spiral ganglions from each cochlea project via auditory vestibular nerve (VIII) to the ipsilateral cochlear nuclei (monoaural neurons)

After this point all connections are bilateral

Question 421

Why is deafness in one ear due to central causes rare?

Answer 421

Must only be affecting the cochlear nucleus or VIII nerve

Because after cochlear nuclei, all connections are bilateral

Question 422

How is hearing organised in the brain?

Answer 422

Tonotopically organised
Based on sound frequency
In primary auditory cortex (which is surrounded by secondary auditory cortex)

Question 423

What are the main characteristics of sound?

Answer 423

Compressed and rarefied air
Frequency/pitch (Hz)
Amplitude/loudness (dB)

Question 424

What frequency is heard by humans?

Answer 424

20-20,000Hz

Question 425

How is the decibel scale organised?

Answer 425

Log scale because of the range of sensitivity (very large)

Question 426

How is hearing loss affected with age?

Answer 426

Hearing loss increases with age (from about 20y)

Particularly higher frequencies associated with human speech (2-5Hz)

Question 427

What is the main clinical condition associated with the outer ear?

Answer 427

The cartilage of the ear can become inflamed

Causes swelling, redness and pain of the outer ear= perichondritis

Question 428

How can the ear be evaluated?

Answer 428

Otoscopy (to study tympanic membrane)
Tuning fork (to differentiate between conductive and sensorineural hearing loss)

Question 429

What features of the tympanic membrane are being looked for?

Answer 429

Light reflection
Differentiation of its part
Mobility

Question 430

How is the tympanic membrane divided for description in clinic?

Answer 430

Posterior superior
Anterior superior
Posterior inferior
Anterior inferior

Question 431

Where are the pars flaccida, handle of malleus, umbo and a cone of light found?

Answer 431

Tympanic membrane

Question 432

What tuning forks are typically used and how does their size affect their frequency?

Answer 432

256Hz, 512 Hz and 1024 Hz are used

Larger forks vibrate at slower frequency

Question 433

How are tuning fork tests carried out?

Answer 433

Activated by striking examiner’s elbow or heal

Placed 2cm away from EAC for air conduction and on mastoid for bone conduction

Question 434

How is air conduction studied with a tuning fork?

Answer 434

Vibrating tuning fork is placed vertically in the meatus about 2 cm away from the EAC opening

Question 435

How is bone conduction studied with a tuning fork?

Answer 435

Foot plate of vibrating tuning fork is placed on the mastoid bone
Cochlea is stimulated directly by the vibrations conducted through the skull

Question 436

What are the two main types of tuning fork tests? What’s their difference?

Answer 436

Rinne and Weber tests

Rinne= evaluates hearing loss by comparing air conduction to bone conduction

Weber= evaluates conductive and sensorineural hearing losses

Question 437

How is the Weber test carried out?

Answer 437

Ask where they can hear the tuning fork when its placed in middle above head (normal= middle, if stronger in one hear that means there is a problem)

Question 438

How is hearing assessed?

Answer 438

Audiometry= speech audiometry or pure tone audiometry

Tympanometry

Otoacoustic emission

To check if hearing is normal, degree of hearing loss and type of hearing loss

Question 439

What is an audiometer?

Answer 439

Device used to produce sound of varying intensity and frequency in an audiometry test

Question 440

Audiometer results: what do the following mean?

• Air conduction hearing level lower than bone conduction
• Air conduction hearing level the same as bone conduction
• Air conduction hearing level higher than bone conduction

Answer 440

Air conduction hearing level lower than bone conduction= conductive hearing loss

Air conduction hearing level the same as bone conduction= sensorineural hearing loss

Air conduction hearing level higher than bone conduction= mixed hearing loss

Question 441

What does tynpanometry show?

Answer 441

The condition of the middle ear and mobility of the eardrum (tympanic membrane) and the conduction bones by creating variations of air pressure in the ear canal

SEE GRAPH- What is meant

Question 442

What does spontaneous otoacoustic emission show?

Answer 442

Measures OAEs

Often part of a newborn hearing screening program

Question 443

What are OAEs?

Answer 443

Otoacoustic emissions
Produced by cochlea along with sound
Cochlear OHCs as they expand and contract

Question 444

What are the main types of hearing loss?

Answer 444

Conductive hearing loss (outer or middle)
Sensorineural hearing loss (inner)
Mixed hearing loss

Question 445

What dB represents different kinds of hearing loss?

Answer 445

Normal hearing= 0-20
Mild hearing loss= 20-40
Moderate hearing loss= 40-70
Severe hearing loss= 70-90
Profound hearing loss= 90+

Question 446

What are the main outer ear causes of conductive hearing loss?

Answer 446

Congenital malformations
Impacted wax 
Foreign bodies
External otitis
Exostosis

Question 447

What congenital malformations can cause outer ear conductive hearing loss?

Answer 447

Congenital atresia= collapse or closure of air canal

Typically associated with congenital malformations of the middle ear

Question 448

How does impacted wax lead to mild hearing loss?

Answer 448

Blockage

Can be removed

Question 449

How can foreign bodies causing conductive hearing loss be removed?

Answer 449

Alcohol/oily solution or lidocaine (in case of insects)

More common in children (may need removal under GA)

Question 450

What is external otitis?

Answer 450

Swelling and redness EAC
Otorrhoea
Pain on mobilization of the ear and tragus

Systematic symptoms in severe cases

May be fungal infection

Question 451

What is exostosis?

Answer 451

Benign bone growth, usually in people with a history of exposure to repeated cold water
Usually multiple, bilateral (possible extension to the middle ear)
Hearing loss, external repeat ear infections, accumulation of ear wax

Question 452

What are the main middle ear causes of conductive hearing loss?

Answer 452

Acute otitis media
Otitis media with effusion
Chronic otitis media
Otosclerosis

Question 453

What is acute otitis media?

Answer 453

Inflammation of the middle ear

Common health problem in children

Question 454

What is otitis media with effusion?

Answer 454

Otitis media characterized by the accumulation of fluid
Common with history offlu
Hearing loss,ear fullness,autophonia

Question 455

What causes chronic otitis media?

Answer 455

Cholesteatomatous
- Congenitally acquired (primary, secondary)

OR

No cholesteatomatous

• Without perforation (OME, retraction TM)
• With perforation (inactive, active)

Question 456

What is a cholesteatoma?

Answer 456

Destructive and expanding growth consisting of keratinizing squamous epithelium in the middle ear and/or mastoid process
Serious but treatable ear condition

Question 457

What are the 2 main types of TM retraction?

Answer 457

Pars tensa

Pars flaccida

Question 458

What are the 2 main types of TM active?

Answer 458

Inactive

Active

Question 459

What is otosclerosis? How is it treated?

Answer 459

Begins as soft, spongy growth of new bone (normally near oval window but can be anywhere in middle ear)
90% people have no symptoms
10% have growth causing mobility of stapes to be reduced-> conductive hearing loss

Stapedectomy (removal and replacement with an artificial stapes)

Question 460

What are the sensorineural causes of hearing loss?

Answer 460

Presbyacusis
Sudden hearing loss
Ototoxic drugs
Infections
Noise-induced hearing loss

Question 461

What is presbyacusis?

Answer 461

Presbycusis is the loss of hearing that gradually occurs in most individuals as they grow older

Gradual and symmetric
Affects frequencies of speech

Begins in adolescence

Often associated with tinnitis

Question 462

Why is presbyacusis increasing?

Answer 462

Ageing european population
Decreased fertility, increased average life expectancy

Men 2x more affected (earlier and more significant)

Question 463

What is sudden sensorineural hearing loss?

Answer 463

SSHL (sudden deafness)
Unexplained, rapid loss of hearing usually in one ear
>30dB hearing reduction over at least 3 continuous frequencies, occurring over <72h

Question 464

What are ototoxic drugs?

Answer 464

Certain drugs that can cause sensorineural hearing loss
Mild and temporary to severe and permanent

E.g. 
Antibiotics: aminoglycosides, tetracyclines
Chemotherapeutic agents: cisplatin, 5-flurocilo
Acetylsalicylic acid
Diuretics
Beta Blockers
Tricyclic antidepressants
Antimalarials: quinine, chloroquine

Question 465

What infections can cause sensorineural hearing loss and/or disruptions of vestibular function?

Answer 465

Bacterial or viral infections that invade the inner ear

Other infectious diseases: Mumps, measles, meningitis, encephalitis, chicken pox, influenza, and syphilis can also invade the inner ear

Question 466

What is noise-induced hearing loss? (2 types)

Answer 466

ACOUSTIC TRAUMA
Injury due to brief exposure to very intense sounds such as gun shots, artillery fire, explosions, etc.
Hearing loss may be severe and permanent, but substantial recovery is common

LONG-TERM NOISE EXPOSURE
Damage results from long-term exposure to high levels of noise
Common in some occupational settings – heavy manufacturing and agriculture being the most common

Question 467

What is the dizziness triad?

Answer 467

Anxiety
Cardio-vascular disease/autonomic dysfunction
Spatial disorientation syndrome (especially vestibular disease)

Question 468

What can lead to spatial disorientation syndrome?

Answer 468

Migraine and epilepsy
Hyperventilation (due to anxiety)
CV disease/autonomic dysfunction

Question 469

How are spatial disorientation syndrome and CV disease/autonomic dysfunction related?

Answer 469

Motion sickness control of orthostatic tension

CV disease/autonomic dysfunction can lead to spatial disorientation syndrome

Question 470

What parts of the ear are most related to the vestibular system?

Answer 470

Semi-circular canals

Otolith organs

Question 471

What are semi circular canals stimulated by and what does this signal?

Answer 471

Stimulated by angular acceleration

Give approx signal of angular velocity

Question 472

What are otolith organs stimulated by and what does this signal?

Answer 472

Stimulated by linear acceleration and gravito-intertial force
Give signal of head acceleration and tily

Question 473

What are the signals from the semi-circular canals and otolith organs used for?

Answer 473

Control balance reactions

Provide spatial reference for other sensory motor co-ordinations

Provide compensatory reflexes (VOR)

Tune CV function for re-orientations

Serve perception of motion in space

Question 474

What is the different between self motion and world motion?

Answer 474

Self motion is when you feel as though you’re moving

World motion is when you see moving (e.g. on train)

Question 475

What are the main dysfunctions of the vestibular system? What functions do they affect?

Answer 475

ATAXIA
Problems of controlling balance reactions and spatial referencing

OSCILLOPSIA
Total loss of compensatory ocular reflexes (VOR)

NYSTAGMUS
Unilateral loss of compensatory ocular reflexes (VOR)

HYPOTENSION
Problems of tuning CV function for re-orientations

DIZZINESS
Problems of perception of motion in space

MOTION SICKNESS
Unusual stimulation of balance organs

Question 476

What kinds of vestibular disorders are there?

Answer 476

Structural
Functional
Both

Question 477

What are structural and functional vestibular disorders?

Answer 477

Structural
= destructive or irritative disease

Functional
= misinterpretation of sensory input
= maladaption
= loss of rules of correspondence between senses over awareness/magnification of sensory input

Both
= structural disorder provoking chronic dysfunction

ALL TREATED THE SAME WAY

Question 478

What is the vestibular system?

Answer 478

The sensory system that provides the leading contribution about movement and sense of balance

Together with the cochlea it constitutes the labyrinth of the inner ear in most mammals, situated in the vestibulum in the inner ear

Created to deduce orientation and motion in space (self and external entities)

Question 479

What are the labyrinths in the vestibular system?

Answer 479

Bony labyrinth= bound by petrous bone filled with perilymph

Membraneous labyrinth= 2 membranous sacs filled with endolymph: utricle and saccule (the otolith organs)

Question 480

What does the saccule give rise to?

Answer 480

Cochlear duct

Question 481

What does the utricle give rise to?

Answer 481

Semi-circular canals

Question 482

How long can vertigo last?

Answer 482

Seconds, minutes (most common), hours, days

Can also be fluctuating/continuous or silent

Question 483

What are the common causes of vertigo that lasts seconds?

Answer 483

Benign positional vertigo BPPV
Debris in canals-> intense vertigo and nausea

Paroxysmia (ephaptic) responds to Tegretol

Question 484

What are the common causes of vertigo that lasts minutes?

Answer 484

Vertebrobasilar insufficiency?

Migraine can lead to brief mild vertigo (possibly strong vertigo)

Question 485

What are the common causes of vertigo that lasts hours?

Answer 485

Meniere’s syndrome-> intense vertigo and nausea, hearing disturbance, pressure in repeated attacks

Question 486

What are the common causes of vertigo that lasts days?

Answer 486

Vestibular neuritis-> intense vertigo and nausea, hearing disturbance in an isolated attack

Herpes (Scarpa’s ganglion)?
Infarction of labyrinth?

Question 487

What are the common causes of vertigo that has a fluctuating duration or is continuous?

Answer 487

Uncompensated vestibular lesion-> mild vertigo and nausea

Functional midl vertigo and disproportionate disability

Question 488

What are the common causes of vertigo is silent?

Answer 488

Acoustic neuroma-> mild imbalance, tinnitis, hearing loss

Question 489

What is the vestibular ocular reflex? What does it do?

Answer 489

A reflex where activation of the vestibular system causes eye movement

Stabilises images on the retina during head movement by producing an eye movement in the opposite direction to head -> preserves image on centre of visual field

Controlled by canal

Question 490

When the head is stationary, what happens to the canals?

Answer 490

Equal resting tonus on canals

Question 491

What happens if a person sees a stimulation on the left?

Answer 491

Stimulation on L
Canal drives eyes L
Head turning leading canal is stimulated
Head turning trailing canal is turned off
Stimulated canal drives eyes R

Question 492

What is the head rotation test? What are the positive and negative results?

Answer 492

Rapid head rotation separately to R and L whilst patient views examiner’s eye

POSITIVE
During rotation towards the intact labyrinth the patient maintains fixation

NEGATIVE
During rotation towards the lesioned labyrinth the patient looses fixation
Eyes go with the head and after the movement the patient makes REFIXATION SACCADES back to the fixation point

Question 493

What does the abnormal head-thrust test test?

Answer 493

Detects unilateral hypofunction of the peripheral vestibular system caused mainly by acute vestibulopathy

Normally= functional vestibular system will ID any movement of head position and rapidly correct eye movement

Looking for presence/ absence of any corrective movement

Question 494

What is the vestibulo-ocular pathways?

Answer 494

Superior and medial vestibular neurons project to motor nuclei supplying extraocular muscles

Axons ascend in the MLF and excite the ipsilateral oculomotor (III) nucleus and the contralateral abducens (VI) nucleus

Question 495

What happens to the canals and nerve firing when the head accelerates to the R?

Answer 495

When the head accelerates to the R, the right canals are stimulated by increased firing on right vestibular nerve (firing decreases on left nerve)

(Opposite with L side)

Question 496

If the head is stationary, what happens to the L and R vestibular nerves?

Answer 496

Support a tonic resting discharge

Firing on l and r is equal and opposite they cancel each other out

Question 497

What happens if there is a vestibular lesion on one side (LEFT)?

Answer 497

Vestibular lesion on left side

Resting discharge on right side signals to the brain as if the head is moving towards the right

Patient feels like they are spinning to the right and has a nystagmus

Then right canal signals drive the eyes in a slow phase movement to the left (lesioned side)

Periodically, the brainstem generates fast phases (saccades) which drive the eyes back to the centre

This creates a VESTIBULAR NYSTAGMUS

(Right beating vestibular nystagmus in this case)

Question 498

What are the parameters when measuring the rotational response?

Answer 498

Peak velocity
VN/VS the ‘high frequency gain of the response
End point in time
Long ‘time constant’ of decay of nystagmus (roughly 1/4 end point time)

Compare parameters for 2 R and 2 L accelerations

Question 499

What is the caloric reflex test? How does it work?

Answer 499

Tests vestibulo-ocular reflex by irrigating cold then warm water into the external auditory canal (alternately)

Stimulates individual horizontal canals of the labyrinth

44 degrees C= canal excitation- eyes driven contralateral
30 degrees C= canal inhibition- tonus of opposite canal drives eyes ipsilateral

COWS= cold opposite, warm same

Assessment of the caloric response: nystagmus duration, peak velocity, subjective sensation

4 measurements: R + L, hot + cold

Question 500

What are the assessments that can be made by the caloric reflex test?

Answer 500

Normal= 40s irrigation normal response lasts for 1.5-2.5 minutes

Small amplitude short duration response to both hot and cold on one side-> canal paresis

Bilateral small short responses-> bilateral hypofunction

Asymmetry of hot/cold responses (a directional preponderance) is of little significant

Question 501

What are the symptoms, signs, course and treatments of typical vestibular neuritis?

Answer 501

Symptoms= vertigo, ocillopsia, imbalance, nausea, vomiting, abrupt onset

Sign= nystagmus, pallor obvious ataxia

Course= intense 1-2 days, recovery over week or so

Treatment= steroids and anti-viral (cyclovirs) and anti-emetic

Question 502

What are the signs of acute vestibular lesion?

Answer 502

Ipsilateral tilt
Attempted compensation
Ipsilateral head tilt and skew upwards

Question 503

What are the vestibulospinal pathways?

Answer 503

Lateral vestibulospinal tract

Medial vestibulospinal tract

Question 504

Outline the lateral vestibulospinal tract

Answer 504

Descends ipsilaterally in ventral funiculus of spinal cord

Axons terminate in lateral part of ventral horn and influence motor neurons to limb (especially extensor antigravity) muscles

Question 505

Outline the medial vestibulospinal tract

Answer 505

Descends bilaterally in medial longitudinal fasciculus (MLF) to cervical and upper thoracic spinal cord

Axons terminate in medial part of ventral horn and influence motor neurons to neck and back muscles

Question 506

How can vestibular disorder be treated?b

Answer 506

Reassurance that patient is understood

Pharmaco-treatment: steroids, anti-viral (-cyclovirs), anti-emetic. (tegretol for vestibular ‘paroxysmia’)

Treat associated anxiety, depression

Cognitive behaviour therapy with desensitisation and physiotherapy

Behavioural anxiolytic tactics

Minimise risk factors

Question 507

In benign positional vertigo (BPPV) how are people tested?

Answer 507

Placed on specific chair apparatus
Asked what they feel

Can study:

• Compensatory eye movement for tilt
• Compensatory eye movement for motion

Question 508

What are the symptoms of motion sickness?

Answer 508

PRIMARY
Signs of pallor and sweating
Nausea and vomiting

ASSOCIATED
Headache including triggering migraine attacks
Dizziness possibly with nystagmus
Instability and in-coordination
Postural discomfort and restlessness (provoking further motion sickness)
Drowsiness (sopite syndrome)
Feeling of eye strain

Question 509

How can motion sickness be treated?

Answer 509

Non-pharmacologically:

• Cognitive behavioural therapy with desensitisation (repeated small doses, no prolongs immersion)
• Behavioural anti-emetic and anxiolytic exercises (controlled breathing posture relaxation)

Question 510

What is the bony orbit?

Answer 510

Socket where the eye sits
Made up of different bones and holes
SEE DIAGRAM

Question 511

What is the opening of the eyelid called?

Answer 511

Palpebral fissure

Question 512

What are the lateral and medial canthi?

Answer 512

Canthus (pl. canthi) is either corner of the eye where the upper and lower eyelids meet

At medial and lateral ends/angles of the palpebral fissure

Question 513

Where is the lacrimal gland?

Answer 513

Located within the orbit

Latero-superior to the globe

Question 514

What is the difference between basal tears and reflex tears?

Answer 514

Basal tears= produced at constant level (in absence of irritation or stimulation)

Reflex tear= increased tear production in response to ocular irritation

Question 515

What is the tear reflex pathway?

Answer 515

Afferent pathway, CNS, efferent pathway, lacrimal gland

Question 516

How does a tear go from the lacrimal gland to exit the tear sac?

Answer 516

Tear produced by the Lacrimal Gland
Tear drains through the two puncta, opening on medial lid margin
Tear flows through the superior and the inferior canaliculi
Tear gathers in the Tear Sac
Tear exits the Tear Sac through the tear duct into the nose cavity

Question 517

What is the purpose of the tear film?

Answer 517

Coves a healthy cornea with
a thin layer of fluid
Lubricates eye

Question 518

What are the layers of the tear film? What does each layer do?

Answer 518

Superficial oily layer= lipid layer protects tear film from rapid evaporation (produced by a row of Meibomian Glands along the lid margins)

Aqueous tear film (tear gland)= forms bulk of tear film, delivers O2 and nutrients to surrounding tissue and protects from bacteria

Mucinous layer= on the Corneal Surface to maintain surface lubrication

Question 519

How do mucin molecules in the tear film act?

Answer 519

Bind water molecules

to the hydrophobic corneal epithelial cell surface

Question 520

What is the conjunctiva?

Answer 520

Thin, transparent tissue that covers the outer surface of the eye
Nourished by ting blood vessels that are nearly invisible to the naked eye

Question 521

Where is the conjunctiva found?

Answer 521

Begins at outer edge of cornea, covers visible part of the eye and lines the inside of the eyelids

Question 522

How big is the eye?

Answer 522

Anterior-posterior= 24mm in adults

Question 523

What are the 3 layers of the coat of the eye? What are the main features and functions of them?

Answer 523

Sclera= hard and opaque with high water content (white of the eye), for protecting eye and maintaining shape of eye

Choroid= pigmented and vascular, for providing circulation to the eye and shielding out unwanted scattered light

Retina= neurosensory tissue, for converting light into neurological impulses (to go to brain via optic nerve)

Question 524

What is the cornea?

Answer 524

Front-most part of anterior segment
Continuous with the scleral layer
Transparent

5 layers

Question 525

What does the cornea do?

Answer 525

Refraction – 2/3 of light focusing power
Physical barrier
Infection barrier

Question 526

Why is the cornea involved in refraction?

Answer 526

Refraction – 2/3 of power
Convex curvature
Higher refractive index than air
-> light focusing power

Question 527

Why does prolonged contact lens wearing compromise corneal tissue health?

Answer 527

Reduces oxygen supply to the cornea

Very prolonged-> increased risk of serious corneal eye infection

Question 528

What are the 5 layers of the cornea?

Answer 528

1- Epithelium 
2- Bowman’s Membrane
3- Stroma (thickest layer)
4- Descemet’s Membrane
5- Endothelium

Question 529

What does the stroma of the cornea do?

Answer 529

Regularity contributes towards transparency
Corneal nerve endings provides sensation and nutrients for healthy tissue
No blood vessels in normal cornea

Question 530

What does the endothelium of the cornea do?

Answer 530

Pumps fluid out of corneal and prevents corneal oedema

Only 1 layer of endothelial cell
No regeneration power
Endothelial cell density decreases with age
Endothelial cell dysfunction may result in corneal oedema and corneal cloudiness

Question 531

Where does the cornea get its nutrients and oxygen supply?

Answer 531

Tear film and aqueous fluid

Question 532

What is the UVEA? Where is it?

Answer 532

The vascular coat of the eyeball
Between the sclera and the retina
3 parts- iris, ciliary body, choroid

Question 533

What is the uvea composed of?

Answer 533

3 parts- iris, ciliary body, choroid

These are intimately connected (allows disease to spread)

Question 534

What are the anterior and posterior segments of the eye?

Answer 534

Anterior segment refers to the anatomical structures of the eye, in front of the lens

Posterior segment refers to the anatomical structures of the eye, behind the lens

Question 535

What are the two anatomical chambers within the eye?

Answer 535

Anterior chamber (smaller)
Posterior chamber

Question 536

Where is the anterior chamber and what does it do?

Answer 536

Between cornea and lens
Filled with clear aqueous fluid
Supplies nutrients to surrounding tissue

Question 537

Where is the posterior chamber and what does it do?

Answer 537

Between Lens and the Retina
Filled with a jelly substance= vitreous humour
Provides mechanical support

Question 538

What is the vitreous humour composed of?

Answer 538

98-99% water trapped in jelly matrix (collagen and glycosaminoglycan gel)

Question 539

Where is the choroid of the eye and what does it do?

Answer 539

Lies between the retina and sclera

Composed of layers of blood vessels that nourish the back of the eye

Question 540

What is the iris?

Answer 540

Coloured part of the eye
Controls light levels inside the eye similar to the aperture on a camera
Round opening in the centre of the iris called the pupil
Iris is embedded with tiny muscles that dilate (widen) and constrict (narrow) the pupil size

Question 541

What is the structure of the lens?

Answer 541

Outer acellular capsule
Regular inner elongated cell fibres (NB. important for transparency)
May loose transparency with age-> Cataracts

Question 542

What is the function of the lens?

Answer 542

Transparency (regular structure)
Refractive power (1/3 power)
Accommodation (elasticity)

Question 543

What is the lens zonules?

Answer 543

Fibrous ring which has the lens suspended in it
Consists of passive connective tissue
Tension along the stretched lesn zonules-> holds surface of the lens flat and tort

Question 544

What is the retina? What is the function of it?

Answer 544

Very thin layer of tissue that lines the inner part of the eye

Responsible for capturing the light rays that enter the eye
Light impulses then sent to brain for processing via optic nerve

Question 545

What is the structure of the retina? What do the layers do?

Answer 545

Outer thin layer of retinal pigment epithelium (nutrient support to retina, removes metabolic debris from photoreceptors)

Right behind is the choroid (Blood supply to the outer 1/3 retina (photoreceptors), pigment reduces light scattering)

Then an inner thicker layer (neuroretina made of photoreceptors and neurons, has outer, middle and inner layer)

Question 546

What are the layers of the neuroretina?

Answer 546

Outer layer- photoreceptors (1st order neuron)= detection of Light

Middle layer- bipolar cells (2nd order neurons)= local signal processing to improve contrast sensitivity, regulate sensitivity

Inner layer- retinal ganglion cells (3rd order neurons)= signal transmission from the eye to brain

Question 547

What does the optic nerve do?

Answer 547

Optic nerve transmits electrical impulses from the retina to the brain
Connects to the back of the eye near the macula

Question 548

What is the optic disc?

Answer 548

The visible portion of the optic nerve

Question 549

What is the macula?

Answer 549

Macula lutea (yellow patch)= pigmented region at the centre of the retina of about 6 mm in diameter
Small and highly sensitive
Fovea in the centre

Question 550

What is the fovea?

Answer 550

Fovea= at the centre of the macula

Characterized by an anatomical dip (foveal pit) due to the absence of the overlying ganglion cell layer

Has the highest concentration of photo-receptors required for fine vision

High concentration of cones, but low concentration of rods

Question 551

How can the macula and fovea be clinically assessed?

Answer 551

With an OCT scan (Optical Coherence Tomography)

Question 552

What is the ciliary body?

Answer 552

Ring-shaped tissue surrounding the lens (between anterior and posterior segment)
Behind the iris

Question 553

What is the iris?

Answer 553

Fat and ring-shaped tissue that
regulates the amount of light entering into the eye
Immediately in front of the ciliary body and lens

Question 554

What are the 2 layers are the iris?

Answer 554

Thin posterior pigmented epithelial layer

Thick anterior layer,
composed of stromal tissue and smooth muscles

Question 555

How do you treat raised intraocular pressure using the uvea-sclera pathway?

Answer 555

Prostaglandin analgoues (reduce pressure 20%, works on uvea-sclera pathway)

Question 556

Retina gives rise anteriorly to….

Answer 556

Ciliary body epithelium

Posterior (epithelial) layer of iris

Question 557

Choroid gives rise anteriorly to…

Answer 557

Ciliary body stroma

Anterior (stromal) layer of iris

Question 558

How is the ciliary body involved in nutrient supply?

Answer 558

Secretes aqueous fluid in the eye (into anterior chamber)

Aqueous fluid supplies nutrients

Question 559

Where does intraocular aqueous fluid flow?

Answer 559

Anteriorly into the anterior chamber

Question 560

What does the trabecular meshwork of the eye do?

Answer 560

Drains fluid out the eye

Question 561

What is normal intraocular pressure?

Answer 561

12-21mmHg

Question 562

Outline what the aqueous flow includes

Answer 562

80-90% TM Canal of Schlemm

Rest= uveal-scleral outflow

Question 563

What is glaucoma?

Answer 563

Eye condition characterized by sustained high intraocular pressure

Retinal ganglion cell death and enlarged optic disc cupping

Leads to gradual and cumulative damage to the optic nerve tissue in the posterior segment of the eye
If untreated-> loss of peripheral vision progressively, eventual blindness

Question 564

What are the main types of glaucoma? How do they present?

Answer 564

Primary open angle glaucoma= commonest, normally asymptomatic until advanced stages of the disease

Closed angle glaucoma= can be acute or chronic, can be sudden painful red eye and drop in vision

Question 565

What causes primary open angle glaucoma?

Answer 565

Trabecular meshwork dysfunction (functional blockage)

Question 566

What causes closed angle glaucoma?

Answer 566

Forward displacement of iris,
narrowing the trabecular meshwork drainage angle

Occurs commonly in patients with hypermetropia, or long-sightedness

Question 567

Which organ produces aqueous fluid in the eye?
Iris
Ciliary body
Trabecular meshwork
Choroid

Answer 567

Ciliary body

Question 568

Which type of cells in the eye are primarily affect in glaucoma?
Photoreceptors
Retinal pigment epithelial cells
Bipolar cells 
Retinal ganglion cells

Answer 568

Retinal ganglion cells

Question 569

Where is the blind spot?

Answer 569

Where the optic nerve meets the retina

There are no light sensitive cells

Question 570

What is the corresponding anatomic landmark for the physiological blind spot?
Macula
Fovea
Optic disc
Ora serrata

Answer 570

Optic disc

Question 571

What can be seen by central and peripheral vision?

Answer 571

CENTRAL (foveal, focus)
Detail day vision, colour vision
Reading, facial recognition
Central fine vision

PERIPHERAL (motion)
Shape, movement, night vision
Navigation vision

Question 572

How are central and peripheral vision assessed?

Answer 572

Central= visual acuity assessment (loss of foveal vision-> poor visual acuity)

Peripheral= visual field assessment (extensive loss of visual field-> severe loss of peripheral vision)

Question 573

What happens if a patient loses central vision?

Answer 573

Problems with reading,

and recognizing faces

Question 574

What are the main classes of photoreceptors?

Answer 574

Rods and cones

Question 575

Wha is the difference between rod and cone photoreceptors?

Answer 575

ROD
Longer outer segment with photo-sensitive pigment
100 times more sensitive to light than cones
Slow response to light
Responsible for night vision (Scotopic Vision)
120 million rods

CONE
Less sensitive to light, but faster response
Responsible for day light fine vision and colour vision (Photopic Vision)
6 million cones

Question 576

How are photopigments synthesized in photoreceptors?

Answer 576

Photopigments are synthesized in the inner segment and transported to the outer segment disks

Distal disks are shed from the tips and absorbed by retinal pigment epithelium cells by phagocytosis

Question 577

What photopigment is found in rods? How does it lead to an AP?

Answer 577

Rhodopsin (reacts maximally to one single light frequency,
namely at 498 nano-meters in humans)

Opsin= transmembrane Protein
Cofactor= 11 cis-Retinal (Vitamin A derived)

Cofactor reacts to photon

• > Conformal changes to Rhodopsin
• > G-protein pathway
• > Closure of ion channels and hyperpolarization
• > Action potential

Question 578

What photopigment is found in cone photopigments?

Answer 578

3 subtypes of photopsin

React to 3 light frequencies

Question 579

Describe the photoreceptor distribution

Answer 579

Cone photoreceptors are distributed only within the macula

Rod photo-receptors are widely distributed all over the retina, with the highest density just outside the macula
The density of rod photo-ceptors gently tails off towards the periphery
Completely absent within the macula

SEE DIAGRAM

Question 580

What is scotopic vision?

Answer 580

Night vision

Question 581

What is photopic vision?

Answer 581

Day vision

Question 582

Where is the highest concentration of rod photoreceptors in the retina?
Optic disc
Fovea
10-20 degrees away from fovea
20-40 degrees away from fovea

Answer 582

20-40 degrees away from fovea

Question 583

How is colour vision determines by frequency spectrum?

Answer 583

Rod photopigment – 498nm (blue-green)

Cone photopigments (in human)
S-Cone 420-440nm (blue)
M-Cone 534-545nm (green)
L-Cone 564-580nm (red)

M (green) and L (red) peaks are much closer to each other

Question 584

What is the most common form of colour deficiency?

Answer 584

Commonest form of colour vision deficiency – M Cone peak shifted to L Cone peak resulting in red-green confusion (Deuteranomaly)

Question 585

What cones does yellow light stimulate?

Answer 585

Yellow light has a wavelength between the peak sensitivity wavelengths of M-Cones and L-Cones

Yellow light stimulates both M-cones and L-cones equally

Biologically, we experience yellow light as a combination of green and red light

Question 586

What percentage of congenital colour deficiencies affect males and females?

Answer 586

8% male

0.5% females

Question 587

What is the ishihara test?

Answer 587

Colour perception test
Ishihara isochromatic plates can test for red-green deficiencies only

Patients with colour vision deficiencies will not recognize any pattern or recognize the wrong pattern

Question 588

What is dark adaptation and how does it occur?

Answer 588

Increase in light sensitivity in dark

Biphasic Process

• Cone adaptation 7 minutes
• Rod adaptation 30 minutes (need regeneration of rhodopsin)

Question 589

What is light adaptation and how does it occur?

Answer 589

Adaptation from dark to light

Occurs over 5 minutes
Bleaching of photo-pigments
Neuro-adaptation
Inhibition of Rod/Cone function

Question 590

Which is the commonest form of colour vision deficiency in humans?

Answer 590

Red-green confusion

Question 591

What are the landmarks in a digital image of the retina with a fundus camera?

Answer 591

Optic disc

Ganglion cells exit via optic nerve, physiological blind spot

Macula (and macula lutea yellow patch)

Superio-temporal retinal artery and vein (vein darker and thicker)

Superio-nasal retina artery and vein

Question 592

What do retinal arteries do?

Answer 592

Retinal arteries provide circulation to the inner 2/3 of the retina

Question 593

What happens in an ageing vitreous?

Answer 593

Liquifies and collapses with age resulting in posterior vitreous detachment

Vitreous separates from retina

Patient experiences vitreous detachment as seeing “floaters”

May be occasionally associated with retina tear

Patients are advised to see an ophthalmologist for retina examination to exclude retinal tear

Question 594

What is refraction?

Answer 594

Light passing through one medium to another, strikes a boundary at some angle of incidence (measured from normal line) -> changes speed due to change in material density

Leads to sensation of ‘bending’ of light- light doesn’t travel in straight line through multiple mediums

More dense= slower movement of light

Use indices of refraction

Question 595

What is the index of refraction?

Answer 595

The index of refraction is defined as the speed of light in vacuum divided by the speed of light in the medium

Denominator will always be smaller so index will be equal to or greater than 1

Index regards to the new medium

Question 596

What happens to light when it reaches a new medium?

Answer 596

Some light reflects off the boundary (angle of incidence)

Some light refracts to the boundary (angle of refraction)

Angle of i being bigger or smaller (NOT THE SAME) as angle of r depends on angle of light

Question 597

What are the 2 basic types of lenses?

Answer 597

Convex (takes light rays and converges them on to a point)

Concave (takes light rays and diverges them outwards)

Question 598

How is the eye like a camera?

Answer 598

LIGHT REFRACTION
It focuses the incoming light ray from a distance
onto the retina to form a clear image

REGULATION OF LIGHT ENTRY INTO THE EYE
Pupil, pigmented uvea

MAINTENANCE OF THE SHAPE OF EYE
Scleral coat
Maintenance of intraocular pressure- ciliary body, trabecular meshwork

VISUAL INFO PROCESSING
Retina, optic nerve
The retina converts image into nerve impulses,
to be transmitted to the brain via the optic nerve

Question 599

What is emmetropia?

Answer 599

When the cornea and the lens have just the right refractive power,
to focus a clear image from distance onto the retina

Parrallel rays converge exactly on the fovea (retinal surface)-> clear image formed-> SEE CLEARLY AT A DISTANCE

NB. Cornea contributes 2/3 of refractive power
Lens contributes 1/3 of refractive power

Question 600

What is ametropia? List examples

Answer 600

Refractive error
Mismatch between axial length and refractive power
Parallel light rays don’t fall on the retina (no accomodation)
e.g. myopia, hyperopia, astigmatism, presbyopia

Question 601

What is myopia?

Answer 601

Short-sightedness

Question 602

What causes myopia?

Answer 602

In myopia (short sightedness), light ray from distance objects focuses IN FRONT OF the retinal surface

Globe too long or high corneal curvature

Image from near object converges on the retinal surface

Patient see near objects clearly without glasses but need concave lenses to see clearly at distance

Question 603

What is hypermetropia?

Answer 603

Long-sightedness

Question 604

What causes hypermetropia/hyperopia?

Answer 604

In hypermetropia (long sightedness), parallel rays (distant image) focus BEHIND the retinal surface

Caused by short globe or flat corneal surface

Probably inherited

Blurred vision without optical correction (glasses)

Can be corrected with convex lens to provide additional converging power

Blurred vision exacerbated by near vision

Question 605

What are the symptoms of hyperopia?

Answer 605

Visual acuity at near tends to blur relatively early
Blurred vision is more noticeable if person is tired or weak lighting

Asthenopic symptoms= eyepain, headache in frontal region, burning sensation in eyes, blepharoconjunctivitis

Amblyopia= lazy eye from uncorrected hyperopia

Question 606

What is astigmatism? What happens without correction?

Answer 606

In astigmatism, the cornea is oval rather than spherical-shaped (hereditary)

Parallel rays come to focus in 2 focal lines rather than a single focal point

The refractive power varies along different meridians, or planes so see distant objects as blurred ellipses

Without correction,
patients see round objects as blurred ellipses, instead of blurred discs.

Question 607

What are the symptoms of astigmatism?

Answer 607

Asthenopic symptoms
Blurred vision
Distortion of vision
Head tilting and turning

Question 608

How is astigmatism treated?

Answer 608

Patient requires special astigmatic glasses correction, with variable correction for every meridian

Regular= cylinder lenses with or without spherical lenses
Irregular astigmatism= rigid CL, surgery

Question 609

What is the near response triad?

Answer 609

Adaptation for near vision

TRIAD:

1) Pupillary miosis (sphincter pupillae) to increase depth of field
2) Convergence (medial recti from both eyes) to align both eyes towards a near object
3) Accommodation (circular ciliary muscle) to increase the refractive power of lens for near vision

Question 610

What is presbyopia?

Answer 610

Naturally occurring loss of accommodation (focus for near objects)
Onset from age 40 years
Distant vision intact

Question 611

How can presbyopia be treated?

Answer 611

Corrected by reading glasses (convex lenses) to increase refractive power of the eye

Some people may need bifocal/trifocal glasses or progressive power glasses (all with convex lenses in near vision)

Question 612

What is the mechanism of accommodation?

Answer 612

Contraction of the circular ciliary muscle inside the ciliary body

This relaxes the zonules that are normally stretched between the ciliary body attachment and the lens capsule attachment

NB. Zonules= passive elastic bands with no active contractile muscle

Without zonular tension, the lens returns to its natural convex shape due to its innate elasticity
-> increased refractive power of the lens

Mediated by the efferent CNIII

Question 613

What are the disadvantages and complications of contact lenses?

Answer 613

DISADVANTAGES= careful daily cleaning and disinfection, expense

COMPLICATION= infectious keratitis, giant papillary conjunctivitis, corneal vascularization, severe chronic conjunctivitis

Question 614

What are intraocular lenses?

Answer 614

Replacement of cataract crystalline lens
Give best optical correction for aphakia
Avoid significant magnification and distortion caused by spectacle lenses

Question 615

What surgical options are available for myopia?

Answer 615

Keratorefractive srugery 
Intraocular surgery (clear lens extraction)

Question 616

Which statement is false for myopia?

1. May be associated with large globe
2. Light ray converges behind the retina
3. May be associated with increased corneal curvature
4. Unable to see objected clearly at distance without glasses or other optical correction

Answer 616

Light ray converges behind the retina

Question 617

In accommodation, which of the following events doesn’t take place?

1. Relaxation of circular ciliary muscle
2. Relaxation of zonules
3. Thickening of lens
4. Increase of lens refractive power

Answer 617

Relaxation of circular ciliary muscle

Question 618

Outline the visual pathway anatomy

Answer 618

Eye

Optic nerve- ganglion nerve fibres

Optic chiasm- half of the nerve fibres cross here

Optic tract- ganglion nerve fibres exit as optic tract

Lateral geniculate nucleus- ganglion nerve fibres synapse at LGN

Optic radiation- 4th order neuron

Primary visual cortex or striate cortex- within the occipital lobe

Extrastriate cortex

Question 619

What does the visual pathway do?

Answer 619

Transmits signal from eye to the visual cortex

Question 620

What are the first, second and third order neurons in the visual pathway?

Answer 620

1st= rod and cone retinal photoreceptors
2nd= retinal bipolar cells
3rd= retinal ganglion cells

Question 621

What cranial nerve is involved in the visual pathway?

Answer 621

Optic nerve (CN II)

Question 622

How many fibres cross the midline at the optic chiasma?

Answer 622

53%

Partial decussation

Question 623

How is visual signal modulated?

Answer 623

2nd and 3rd order neurons within the retina modulate visual signal, before transmitting the signal to the brain

Involves receptive fields

Question 624

What is the receptive field of a neuron in vision?

Answer 624

Retinal space within which incoming light can alter the firing pattern of a neuron

Question 625

What is the difference between the receptive field of photoreceptors and ganglion cells?

Answer 625

The receptive field of ganglion cells covers a much larger area than that of a single photo-receptor

Photo-receptor receptive fields synapse upon the ganglion cells indirectly via bipolar cells

SEE DIAGRAM

Question 626

What is difference in convergence on the receptive field of rods and cones? What does this mean?

Answer 626

In general, fewer number of cone photo-receptors synapse upon the same ganglion cell than rod photo-receptors

Cone system has lower convergence

This means that ganglion cells in the cone system have a smaller receptive field than ganglion cells in the rod system

Question 627

How does convergence of rod systems differ by location?

Answer 627

Rod system near macula has lower convergence than the rod system at the peripheral retina

Question 628

Do ganglion cells in the cone or rod system have a larger receptive field?

Answer 628

Rods

Question 629

What does a small receptive field (eye) mean?

Answer 629

Low convergence
Fine visual acuity
Low light sensitivity

Question 630

What does a large receptive field (eye) mean?

Answer 630

High convergence
Coarse visual acuity
Higher light sensitivity

Question 631

What can retinal ganglion cells be divided into?

Answer 631

On-centre

Off-centre

Question 632

What stimulates/inhibits on-centre ganglion?

Answer 632

Stimulated by light at the centre of the receptive field

Inhibited by light on the edge of the receptive field

Question 633

What stimulates/inhibits off-centre ganglion?

Answer 633

Inhibited by light at the centre of the receptive field

Stimulated by light on the edge of the receptive field

Question 634

Why are on-centre and off-centre ganglion cells important?

Answer 634

Contrast sensitivity

Enhanced edge sensitivity

Question 635

Outline the route of crossed fibres and uncrossed fibres through the optic chiasma

Answer 635

Crossed fibres- originating from nasal retina, responsible for temporal visual field

Uncrossed fibres- originating from temporal retina, responsible for nasal visual field

Question 636

What happens if there is a lesion anterior to the optic chiasma?

Answer 636

Affect visual field in one eye only

Question 637

What happens if there is a lesion posterior to the optic chiasma?

Answer 637

Affect visual field in both eyes
Right sided lesion-> left homonymous hemianopias in both eyes
Left sided lesion-> right homonymous hemianopias in both eyes

Question 638

What happens if there is a lesion at the optic chiasma?

Answer 638

Damages crossed ganglion fibres from nasal retina in both eyes
Leads to temporal field deficit in both eyes- bitemporal hemianopia

Question 639

What are the most common types of damage to a patient’s visual field? (6)

Answer 639

Monocular blindness
Bitemporal hemianopia
Right/left nasal hemianopia
Homonymous hemianopia
Quadrant anopia
Macular sparing

Question 640

What is bitemporal hemianopia usually caused by?

Answer 640

Enlargement of pituitary gland tumour (presses on optic chiasma from below)

Question 641

What is homonymous hemianopia usually caused by?

Answer 641

Stroke or cerebrovascular accident in the brain

Question 642

Where is the primary visual cortex (striate cortex)?

Answer 642

Situated along calcarine sulcus

DIstinct stripe in the optic radiation myelinated fibres projecting into the visual cortex

Question 643

What is the primary visual cortex representation?

Answer 643

Disproportionately large area representing the macular central vision within the PVC

Above calcarine fissure= inferior visual field
Below calcarine fissure= superior visual field

Left PVC= right hemifield from both eyes
Right PVC= left hemifield from both eyes

Question 644

What does the primary visual cortex specialise in?

Answer 644

Processing visual information of static and moving objects

Question 645

What are the columns in the primary visual cortex sensitive to?

Answer 645

Columns with unique sensitivity to visual stimulus of a particular orientation

Right eye and left dominant columns intersperse each other

Question 646

What is macular sparing? Why does it happen?

Answer 646

Homonymous hemianopia of contralateral side to lesion (e.g. from stroke)

Macula area spared

Area within PVC representing the macula is well protected because dual blood supply (R and L posterior cerebral arteries)

Question 647

What is the extrastriate cortex?

Answer 647

Area around the PVC within the occipital lobe

Converts basic visual information such as position and orientation,
into complex human precepts like motion and object representation

Question 648

What are the extrastriate dorsal and ventral pathways? What does damage cause?

Answer 648

Dorsal= how pathway= PVC to posterior parietal lobe (deals with motion detection)
- Damage-> motion blindness

Ventral= what pathway= PVC to temporal visual cortex (deals with object representation and face recognition)
- Damage-> cerebral achromatopsia

Question 649

What is the pupillary function?

Answer 649

Regulates amount of light entering into the eye

Question 650

What happens to the pupil in light?

Answer 650

Pupil constriction

Decreases spherical aberrations and glare

Increases depth of field

Reduces bleaching of photo-pigments

Pupillary constriction mediated by parasymapthetic nerve (within CN III)

Question 651

What happens to the pupil in dark?

Answer 651

Pupil dilatation

Increases light sensitivity in the dark by allowing more light into the eye

Pupillary dilatation mediated by sympathetic nerve

Question 652

Outline the AFFERENT pupillary reflex pathway

Answer 652

Rod and cone photoreceptors synapse on bipolar cells which synapse on retinal ganglion cells

Pupil-specific ganglion cells exits at posterior third of optic tract before entering the lateral geniculate nucleus
(synapse at pretectal nucleus in brain stem)

Afferent pathway from each eye synapses on Edinger-Westphal nuclei on both sides in the brainstem

Question 653

Outline the EFFERENT pupillary reflex pathway

Answer 653

Edinger-Westphal nucleus

• > oculomotor nerve efferent
• > synapses at ciliary ganglion
• > short posterior ciliary nerve
• > pupillary sphincter

Question 654

What is the direct pupillary reflex?

Answer 654

Constriction of pupil of the light in stimulated eye

Question 655

What is the consensual pupillary reflex?

Answer 655

Constriction of pupil of other eye (not the stimulated one)

Question 656

What is the neurological basis of the direct and consensual reflex?

Answer 656

Afferent pathway on either side alone will stimulate efferent (outgoing) pathway on both sides

Question 657

What is the right afferent defect (pupil)?

Answer 657

E.g. damage to optic nerve
No pupil constriction in both eyes when right eye is stimulated with light
Normal pupil constriction in both eyes when left eye is stimulated with light

Question 658

What is the right efferent defect (pupil constriction)?

Answer 658

E.g. Damage to right 3rd nerve
No right pupil constriction whether right or left eye is stimulated with light
Left pupil constricts whether right or left eye is stimulated with light

Question 659

What is the unilateral afferent defect (pupil)?

Answer 659

Different response pending on which eye is stimulated

Question 660

What is the unilateral efferent defect (pupil)?

Answer 660

Same unequal response between left and right eye irrespective which eye is stimulated

Question 661

What does the swinging torch test study?

Answer 661

Relative afferent pupillary defect

Partial pupillary response still present when the damaged eye is stimulated
Elicited by the swinging torch test- alternating stimulation of right and left eye with light
Both pupils constrict when light swings to left undamaged side
Both pupils paradoxically dilate when light swings to the right damaged side

Question 662

Why is eye movement necessary?

Answer 662

Voluntary or involuntary of movement of eyes

Necessary for acquiring and tracking visual stimuli

Question 663

How is eye movement facilitated?

Answer 663

6 extraocular muscles (innervated by 3, 4, 6 CNs)

Question 664

What is eye duction?

Answer 664

Eye movement in one eye

Question 665

What is eye version?

Answer 665

Simultaneous movement of both eyes in same direction

Question 666

What is eye vergence?

Answer 666

Simultaneous movement of both eyes in opposite direction

Question 667

What is eye convergence?

Answer 667

Simultaneous adduction (inward) movement in both eyes when viewing a near object

Question 668

How can looking up be described?

Answer 668

Elevation

Supraduction- one eye
Supraversion- both eyes

Question 669

How can looking down be described?

Answer 669

Depression

Infraduction- one eye
Infraversion- both eyes

Question 670

How can looking right be described?

Answer 670

Dextroversion

Right abduction
Left adduction

Question 671

How can looking left be described?

Answer 671

Levoversion

Right adduction
Left abduction

Question 672

What is torsion of the eye?

Answer 672

Rotation of eye around the anterior-posterior axis of the eye

Question 673

What is a saccade? (e.g.s)

Answer 673

Short fast burst of eye movement (up to 900deg/sec)

Voluntary or involuntary

Reflexive saccade to external stimuli
Scanning saccade
Predictive saccade to track objects
Memory-guided saccade

Question 674

What is slow pursuit (eye movement)? (e.g.s)

Answer 674

Smooth pursuit- sustained slow movement

Involuntary

Slow movement – up to 60°/s
Driven by motion of a moving target across the retina

Question 675

What is nystagmus?

Answer 675

Oscillatory eye movement

Question 676

What is optokinetic nystagmus?

Answer 676

Smooth pursuit and fast phase reset saccade

Question 677

Why is the optokinetic nystagmus reflex useful?

Answer 677

To test visual acuity in pre-verbal children by observing the presence of nystagmus movement in response to moving grating patterns of various spatial frequencies

Presence of optokinetic nystagmus in response to moving grating signifies that the subject has sufficient visual acuity to perceive the grating pattern

Question 678

What are the 6 extraocular muscles responsible for eye movements? Where do they originate from?

Answer 678

Superior rectus, medial rectus, inferior rectus, lateral rectus- originating from orbit apex and attached to the anterior globe and pull backwards
* rectus= straight muscles

Inferior oblique, superior oblique- attached to the posterior globe and pull forwards

Question 679

What do the lateral and medial recti do?

Answer 679

Lateral (external) rectus= abduction (attached to temporal side of eye, moves eye towards outside of head)

Medial (internal) rectus= adduction (attached on nasal side of eye, moves eye towards nose)

Question 680

What do the superior and inferior recti do?

Answer 680

Superior rectus= maximal elevation when eye is in abducted position

Inferior rectus= maximal depression eye is in abducted position

Question 681

What do the superior and inferior oblique muscles do?

Answer 681

Superior oblique= maximal depression when eye is in adducted position (attached high on temporal side of eye, passes under superior rectus, travels through trochlea)-> DOWN AND IN

Inferior oblique= maximal elevation when eye is in adducted position (attached low on nasal side of eye, passes over inferior rectus)-> UP AND OUT

Question 682

What extraocular muscles are controlled by CN 3, 4 and 6?

Answer 682

THREE (occulomotor)
Superior rectus 
Inferior rectus
Medial rectus
Inferior oblique

FOUR (trochlear)
Superior oblique

SIX (abducens)
Lateral rectus

Question 683

What CN is lesioned if one eye goes out and down?

Answer 683

Third

Question 684

What CN is lesioned if one eye goes in?

Answer 684

Sixth

Question 685

How does the muscle of the vertical rectus act?

Answer 685

When the eye is adducted, the anterior-posterior axis of the eye is no longer aligned with the vertical rectus muscle action

Torsion motion is produced instead of vertical movement

–

When the eye is abducted, the anterior-posterior axis of the eye is aligned with the vertical rectus muscles

Superior rectus- elevation
Inferior rectus- depression

Question 686

How do oblique muscles act?

Answer 686

Attach behind globe equator
Pull forwards and nasally

When the eye is abducted, the anterior-posterior axis of the eye is no longer aligned with the action of the oblique muscles as in the diagram

Torsion motion is produced instead of vertical movement

When the eye is adducted, the anterior-posterior axis of the eye is aligned with the vertical rectus muscles

Superior rectus- depression
Inferior rectus- elevation

Question 687

How do different parts of the third cranial nerve innervate the extraocular muscles?

Answer 687

SUPERIOR BRANCH
Superior rectus= elevates eye
Lid levator= raises eyelid

INFERIOR
Inferior rectus= depresses eye
Medial rectus= adducts eye
Inferior oblique= elevates eye
Parasympathetic nerve= constricts pupil

Question 688

How is the fourth cranial nerve involved in innervation of the extraocular muscles?

Answer 688

Superior oblique= depresses eye

Question 689

How is the fourth cranial nerve involved in innervation of the extraocular muscles?

Answer 689

Lateral rectus= abducts eye

Question 690

What happens in complete third nerve palsy?

Answer 690

Affected eye down and out
Droopy eyelid

Unopposed superior oblique innervated by fourth nerve (down)
Unopposed lateral rectus action innervated by sixth nerve (out)

Question 691

What happens in sixth nerve palsy?

Answer 691

Affected eye unable to abduct and deviates inwards

Double vision worsen on gazing to the side of the affected eye

Question 692

How can you test the function of the 6 extra-ocular muscles?

Answer 692

Need to isolate the action of each of them by maximising the action of the muscle to be tested and minimizing the action of other muscles

Lateral rectus muscle action is best tested in the abducted position

Medial rectus muscle action is best tested in the adducted position

Superior rectus muscle action is best tested in the elevated and abducted position

Inferior rectus muscle action is best tested in the depressed and abducted position

Inferior oblique is best tested in the elevated and adducted position

Superior oblique is best tested in the depressed and adducted position

Question 693

What does Hering’s Law of Equal innervation state?

Answer 693

There is equal innate innervation to both muscles from both eyes,
involved in conjugate or paired eye movements

E.g. in dextroversion, or right gaze, there is simultaneous right eye abduction and left eye adduction

Question 694

What is the Medial Longitudinal Fasciculus (MLF) in the midbrain for?

Answer 694

Responsible for coordinating eye movements in both eyes during R and L gaze

Question 695

What is internuclear ophthalmoplegia?

Answer 695

Damage to medial longitudinal fasciculus (MLF) e.g. due to MS

Right eye abduction not accompanied by left eye adduction
Accompanied by nystagmus on right gaze

Violates Herring’s Law of Equal Innervation

Question 696

What is Sherrington’s Law of Reciprocal Innervation

Answer 696

Agonist muscles contract while antagonist muscles relax

E.g. in dextroversion (R gaze), right eye lateral rectus and left eye medial rectus contract,
while right eye medial rectus and left lateral rectus relax

Violated in Duane’s Syndrome

Question 697

What is vertigo?

Answer 697

Illusion of movement

Usually rotational or ‘true vertigo’

Question 698

What are the most common types of spinning felt by vertigo patients?

Answer 698

Spinning world

Head spinning

Question 699

What are symptoms of disorders of balance?

Answer 699

Vertigo
Dizziness/giddiness
Unsteadiness

Question 700

How many people experience dizziness at some time?

Answer 700

1/4 people experience dizziness

80% severe enough to see doctor

Question 701

What are the main types of vestibular disorders? (E.g.s)

Answer 701

Peripheral e.g. labyrinth and VIII nerve
Vestibular neuritis, BPPV, Meniere’s disease

Central e.g. CNS (brainstem/cerebellum)
Stroke, MS, tumours

Question 702

For peripheral vestibular disorders:
Onset of vertigo
Severity of vertigo
Paroxysmal/continuous
Relation with head/body position/movement
Nausea/vomiting
Type of nystagmus
Intensity of nystagmus affected by fixation
Nystagmus fatigability
Hearing loss
CNS symptoms/signs
Catch up saccade

Answer 702

Onset of vertigo= sudden/gradual

Severity of vertigo= intense

Paroxysmal/continuous= paroxysmal

Relation with head/body position/movement= yes

Nausea/vomiting= frequent, prominent

Type of nystagmus= horixontal or torsional (NEVER VERTICAL)

Intensity of nystagmus affected by fixation= intensity decreased

Nystagmus fatigability- decreases or disappears with repeated testing

Hearing loss= may be present

CNS symptoms/signs= absent

Catch up saccade= one side will have

Question 703

For central vestibular disorders:
Onset of vertigo
Severity of vertigo
Paroxysmal/continuous
Relation with head/body position/movement
Nausea/vomiting
Type of nystagmus
Intensity of nystagmus affected by fixation
Nystagmus fatigability
Hearing loss
CNS symptoms/signs
Catch up saccade

Answer 703

Onset of vertigo= sudden/gradual

Severity of vertigo= less intense

Paroxysmal/continuous= constant

Relation with head/body position/movement= no

Nausea/vomiting= infrequent, less severe

Type of nystagmus= horizontal, torsional, VERTICAL

Intensity of nystagmus affected by fixation= unaffected

Nystagmus fatigability= remains prominent on repeated testing

Hearing loss= frequent

CNS symptoms/signs= very frequent

Catch up saccade= no

Question 704

How can vestibular disorders be classified by duration/recurrence? (E.g.s)

Answer 704

Acute
Intermittent (starts and stops e.g. within day)
Recurrent (comes back maybe 6 months later)
Progressive

ACUTE

INTERMITTENT (starts and stops e.g. within day):

RECURRENT (comes back maybe 6 months later:

Question 705

List 2 examples of vestibular disorders that are acute

Answer 705

Vestibular Neuritis (‘labyrinthitis’)
Labyrinthine concussion

Question 706

List 1 example of a vestibular disorder that is intermittent

Answer 706

Benign Paroxysmal Positional Vertigo (bppv)

Question 707

List 2 examples of vestibular disorders that are recurrent

Answer 707

Meniere’s Disease - rare

Migraine - common

Question 708

List 1 example of vestibular disorders that is progressive

Answer 708

Acoustic neuroma (8th nerve)

Question 709

What does an acute unilateral vestibular lesion cause?

Answer 709

Syndrome

Many ethiologies

Question 710

What part of the vestibulo-ocular reflex is involved in angular acceleration?

Answer 710

3 semi-circular canals

Question 711

What part of the vestibulo-ocular reflex is involved in linear acceleration?

Answer 711

2 otolith organs

Question 712

What vestibular projection lesions cause nystagmus?

Answer 712

Vestibuo-ocular

Question 713

What vestibular projection lesions cause unsteadiness?

Answer 713

Vestibulo-spinal

Question 714

What vestibular projection lesions cause nausea?

Answer 714

Vestibulo-autonomic

Question 715

What vestibular projection lesions cause vertigo?

Answer 715

Vestibulo-cortical

Question 716

What physiology of the vestibulo-ocular reflex is affected in vestibular disorders?

Answer 716

Vestibular tone
Lesion induced asymmetry
Visual suppression of nystagmus
VOR suppression
Vestibular compensation

Question 717

Outline the symptoms of vestibular neuritis (vest neuronitis/viral labyrinthitis)

Answer 717

Sudden, unilateral vestibular loss

Vertigo, nausea, unsteadiness, nystagmus

Hearing spared
No CNS symptoms or findings

Viral ‘flavour’ (after URTI- mini-epidemics)

Days to weeks

Question 718

Outline the symptoms of BPPV?

Answer 718

Benign paroxysmal position vertigo

Onset sudden (notice when they wake up and sit up)

Actual attack = 10secs (autonomic features-> feel like 2-3 mins)

Dizziness
Vertigo
Loss of balance or unsteadinesss
Nausea
Vomiting

Question 719

What test is used clinically for BPPV? How does it show BPPV?

Answer 719

Dix-Hallpike manoeuvre
Patient rapidly moved from sitting to supine (head 45 degrees turned to right)
After 20-30s-> patient returned to sitting position CHECK FOR NYSTAGMUS

Pathognomonic= classic rotatory nystagmus with latency and limited duration

Negative test only means active canalithiasis not present at that moment

Question 720

What is Meniere’s disease caused by and what are the symptoms?

Answer 720

Build up of endolymphatic pressure (‘hydrops’) causes rupture of membrane

This-> perilymph and endolymph mix-> violent sensation of pressure-> vertigo attack

Hearing impaired  (Meniere’s triad: vertigo, tinnitus and deafness)
Low frequency hearing loss

Question 721

How is Meniere’s disease treated?

Answer 721

Eventually disease burns itself out (takes 15-20 years) but can’t wait so:

Reduce salt intake
Medication- antihistamine (betahistine) 
Inject gentamicin (destroys balance part of the inner ear)

Question 722

What are symptoms of recurrent vesibular disorder migraine?

Answer 722

History of migraine
Migraine symptoms during vertigo attack
Hearing usually spared
Response to treatment

Question 723

What causes chronic vestibular disorder? Why is it chronic?

Answer 723

Dizzy patient- can have many aetiologies
Anxiety= confounding factor

Reasons for chronicity:
Lack of full vestibular compensation
Inadequate testing
Idiosyncratic reactions

Question 724

What can cause central vestibular disorders?

Answer 724

Acute brainstem or cerebellar lesion e.g. MS or vascular

Chronic/progressive= cerebellar degeneration

Question 725

What are possible causes of dizziness that are not vestibular?

Answer 725

Heart disorders
Presyncopal episodes
Orthostatic hypotension
Anaemia
Hypoglicemia
Psychological
Gait disorders

Cause unsteadiness rather than true vertigo

Question 726

How many different odours are there?

Answer 726

2000-4000

Question 727

What kind of cells are found in the olfactory epithelium?

Answer 727

Bipolar olfactory neurons
Sustentacular cells
Basal cells

Question 728

What happens to cells in the olfactory epithelium over time?

Answer 728

Progressive loss with age

Question 729

What is found in the cribriform plate?

Answer 729

Olfactory receptor cells

Extend upwards to glomeruli in olfactory bulb

Question 730

What happens to olfactory receptor cells that enter the olfactory bulb?

Answer 730

Form glomerulus

Second-order olfactory neuron extends away from cribriform plate to form olfactory tract

Question 731

Outline the olfactory system from olfactory bulb to the cortex

Answer 731

Olfactory bulb (mitral cells)
Olfactory tract (splits into mediate and lateral striate) -> Olfactory stria
Piriform and orbitofrontal cortex

Question 732

How are autonomic responses to smell promoted?

Answer 732

Connects from the cortex to the brainstem

Question 733

What is anosmia?

Answer 733

Inability to smell

Commonly due to face trauma

Question 734

What are prodromal auras? What are they caused by?

Answer 734

Many epilepsy patients have focal area in temporal lobe

Before seizure piriform area-> sensation of a smell

Question 735

What can loss of smell be indicative of?

Answer 735

Normal ageing or sign of degenerative disease

Question 736

What/where is the limbic system?

Answer 736

Structurally and functionally interrelated areas considered as a single functional complex

Rim or limbus of cortex adjacent to corpus callosum to diencephalon

Question 737

What are the functions of the limbic system?

Answer 737

Maintenance of homeostasis (via activation of visceral effector mechanisms, modulation of pituitary hormone release and initiation of feeding and drinking)

Agonist (defence and attack) behaviour

Sexual and reproductive behaviour

Memory

Question 738

Where is the hippocampus?

Answer 738

Sits in floor of ventricle

Posterior to amygdala

Question 739

What kind of axons are in the amygdala?

Answer 739

GM- unmyelinated (sits in WM)

Question 740

What does the Papez circuit show?

Answer 740

Neural circuit for the control of emotional expression= basis of emotional experiences

Question 741

What are the components of the Papez circuit?

Answer 741

He-Man ate a cat

Hippocampus (limbi system) 
VIA FORNIX 
Mamillary body (hypothalamus)
VIA MTT
Anterior thalamic nucleus (thalamus)
Cingulate cortex (limbic system)
VIA CINGULUM BUNDLE
Back to hippocampus

NB. Also neocortex contributed to cingulate cortex

Question 742

What part of the Papez circuit….?
Emotional colouring
Emotional experience
Emotional expression

Answer 742

Emotional colouring= neocortex
Emotional experience= cingulate cortex
Emotional expression= hypothalamus

Question 743

What are the main connects of the hippocampus?

Answer 743

Afferent= perforant pathway to entorhinal cortex
Efferent= fimbria/fornix

Question 744

What is the entorhinal cortex

Answer 744

Main interface b/w hippocampus and neocortex

Lays down new memories

Question 745

What are the functions of the hippocampus?

Answer 745

Memory and learning

Question 746

What conditions are caused if the hippocampus is damaged?

Answer 746

Alzheimer’s disease

Epilepsy

Question 747

What is tau immunostaining?

Answer 747

A histologic technique in which multiple sections of brain tissue from a postmortem examination of a patient with dementia of unknown aetiology are stained with anti-tau protein antibodies to see the type of dementia

Question 748

What plaques are involved in AD?

Answer 748

Amyloid beta plaque aggregation in parenchyma

Affects hippocampus early and hard

Question 749

Outline the anatomical progression of AD and the symptoms they cause

Answer 749

EARLY
Hippocampus and entorhinal cortex
Short-term memory problems

MODERATE
Parietal lobe
Dressing apraxia

LATE
Frontal lobe
Loss of executive skills

Question 750

What are the main connections of the amygdala?

Answer 750

Afferent= Olfactory cortex, septum, temporal neocortex, hippocampus, brainstem
Efferent= Stria terminalis

Question 751

What are the functions of the amygdala?

Answer 751

Fear and anxiety

Fight or flight

Question 752

What is Klüver-Bucy syndrome?

Answer 752

Syndromeresulting from bilateral lesions of the medial temporal lobe (including amygdaloid nucleus)

Symptoms= 
Hypersexuality
Hyperorality
Visual agnosia
Docility

Question 753

What structures of the brain are associated with aggression?

Answer 753

Hypothalamus
Brainstem (periaqueductal grey)
Amygdala
Raphe nuclei (5-HT)

Question 754

What are the main connections of the septum?

Answer 754

Afferent= amygdala, olfactory tract, hippocampus, brainstem
Efferent= stria medularis thalami, hippocampus, hypothalamus

NB. some output via fornix

Question 755

What is the pathway involved in drug dependence?

Answer 755

Mesolimbic pathway (dopamine)

Midbrain (A10)-> MFB-> cortex/nucleus accumbens/amygdala

Question 756

What do opioids, nicotine, amphetamines, ethanol and cocaine do to the limbic system?

Answer 756

Increase DA release in nucleus accumbens

Stimulate midbrain neurons, promote DA release or inhibit DA reuptake

Question 757

What is consciousness?

Answer 757

Consciousness is the brain state that enable us to experience the world around us and within one-self
Distinct from automatic behaviours that occur in a rather unconscious manner
Consciousness is not the same as being alert or attentive

Question 758

How are levels and contents of consciousness different?

Answer 758

Levels reflect the level of alerting
Contents= QUALIA experience/subjectivity and impression of visual world

Alertness vs subjective experience and metacognition

Question 759

What is metacognition?

Answer 759

Awareness and understanding of one’s own thought process

‘Cognition about cognition’

Question 760

Is an alert/attentive state sufficient for consiousness?

Answer 760

No

Question 761

What is the reticular activity system in the midbrain responsible for?

Answer 761

Reticular formation (RF) regulates many vital functions

In consciousness- neurotransmitters alert the cortex
Degree of activity in reticular system is associated with alertness/levels of consciousness

Question 762

Where/how does the reticular formation project?

Answer 762

Thalamus and cortex
Allows sensory signals to reach cortical sites of conscious awareness e.g. frontoparietal cortex

Projects from locus coeruleus with noradrenergic neurones (to cortex)
From ventral tegmental area (to cortex) with dopaminergic neurones
Also have cholinergic neurons (to thalamus)

Involves mesolimbic, nigrostriatal, mesocortical and tuberoinfundibular tracts

Question 763

What do cholinergic neurons in the reticular formation do?

Answer 763

Boost the level of activity in cerebral cortex via the thalamus

Question 764

What can electroencephalography (EEG) be used to measure when studying consciousness?

Answer 764

Monitor level of arousal

Question 765

What Hz are delta, theta, alpha and beta waves?

Answer 765

Delta= up to 4Hz
Theta= 4-8 Hz
Alpha= 8-13 Hz
Beta= 13-30Hz

Question 766

What do higher frequency neural oscillations (gamma range approx 40Hz indicate)?

Answer 766

40 Hz associated with the
creation of conscious contents in the focus of the mind’s eye, via thalamocortical
feedback loops

Question 767

What wave predominates in sleep?

Answer 767

Delta

Question 768

What wave predominates in drowiness?

Answer 768

Theta

Question 769

What wave predominates when relaxed/eyes closed?

Answer 769

Alpha

Question 770

What wave predominates during waking consciousness?

Answer 770

Beta

Question 771

What happens if there is damage to the RF/thalamus or a massive bilateral cortical insult (-> coma)?

Answer 771

State of unconsciousness
Persistent vegetative state (due to disconnection of cortex from brainstem or widespread cortical damage)
Brain death (due to brainstem death)

Question 772

What can cause a coma?

Answer 772

Persistent vegetative state 
Brain death (due to brainstem death)
Metabolic (e.g. hypoxia, hypoglycaemia, intoxication)

Question 773

What are the categories in the Glasgow coma scale? What scores can be given?

Answer 773

Eyes open (1-4)
Verbal responses (1-5)
Motor responses (1-6)

Question 774

What do scores in the GCS tell you?

Answer 774

Score of 3= lowest possible, severe brain injury and brain death

Higher the score, the better

Question 775

What are the GCS requirements for eyes open?

Answer 775

1-4
none 
in response to pain 
in response to speech 
spontaneous

Question 776

What are the GCS requirements for verbal responses?

Answer 776

1-5
none 
incomprehensible sounds 
inappropriate words
disoriented speech 
oriented speech

Question 777

What are the GCS requirements for motor responses?

Answer 777

1-6
none 
extensor response to pain
flexor response to pain 
withdrawal to pain 
localisation of pain 
obeys commands

Question 778

What kinds of brain injuries can lead to altered states of consciousness?

Answer 778

Contusion
Concussion
Diffuse axonal injury

Question 779

What is a brain contusion?

Answer 779

A region of injured tissue or skin in which blood capillaries have been ruptured; a bruise

Cerebral contusion can be associated with multiple microhaemorrhages, small blood vessel leaks into brain tissue

Question 780

What is a diffuse axonal injury?

Answer 780

Diffuse axonal injury (DAI) is a brain injury in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area.

Question 781

What is a concussion?

Answer 781

Concussion is the sudden but short-lived loss of mental function that occurs after a blow or other injury to the head

It is the most common but least serious type of brain injury

Question 782

Is attention necessary for conscious awareness?

Answer 782

Yes but not sufficient

Being alert and aware not sufficient for conscious processes

Question 783

What is a persistent vegetative state?

Answer 783

Irreversible coma due to disconnection of cortex from brainstem or widespread cortical damage
Brainstem still functioning so reflexes, postural movements and sleep-wake cycle may be present
In coma, can be aroused THIS IS DIFFERENT but both groups are unconsciouss

Question 784

What is brain death?

Answer 784

Irreversible coma due to brainstem death
Body kept alive artificially
Decision to cease treatment depends on demo of absence of brainstem reflexes and response to hypercapnia
Spinal reflexes and some postural movements may be present

Question 785

What brain lesion causes achromatopsia?

Answer 785

Eliminate awareness of colour

Lesion in extrastriate cortex

Question 786

What brain lesion leads to lack of awareness for stimuli in contralateral visual field?

Answer 786

Parietal lesion

Question 787

What causes left visual neglect?

Answer 787

Breakdown of conscious awareness after right parietal damage (40-60% patients= due to right hemisphere stroke)

Patients remain unconscious of info from left visual field despite PVC in occipital lobe being intact (ignore L side)
Info doesn’t reach awareness (RF is disrupted)

Question 788

How can visual neglect bet investigated?

Answer 788

Star cancelation test (patients cancel fewer stars)
Visual exploration (patient will not cross midline to look left)

Question 789

Does visual neglect syndrome result from damage to occipital region?

Answer 789

No- primary visual cortex is intact

RF is disrupted

Question 790

Why can fMRI be used to study consciousness?

Answer 790

Pictures of brain as patients complete tasks (holding certain info in their mind which activates certain areas)
Active areas picked up by scanner
Networks which are important for different tasks can be seen

Question 791

What is blindisght?

Answer 791

Brain-damaged (occipital visual cortez) patients who are perceptyally blind of their visual field but can demonstrate some responses to visual stimuli
I.e. they display aspects of consciousness e.g. manually interacting with unseen objects and avoiding unseen obstacles

Question 792

How can you detect awareness in the vegetative state? Coma, ‘vigil’

Answer 792

Still studying neural correlate of consciousness (recently use MRIs to detect level of consciousness in vegetative state)

No single brain region for consciousness
Feed-forward processing
(subliminal or non-conscious)
Top-down recurrent processing
(conscious access)

Question 793

What is feed-forward processing?

Answer 793

Subliminal or non-conscious

Question 794

What is top-down recurrent processing?

Answer 794

Conscious access

Question 795

Brain activation for unconconsious info in patietns with visual neglect (Rees et al, 1993) showed…

Answer 795

Patients performed a face/house detection task inside the MRI scanner and indicated when they could see objects
Study showed activation in the brain (striate and extrastriate) for info which could be received but not processed therefore patient can’t ‘see’ the objects

Question 796

What are the behavioural criteria of sleep?

Answer 796

Stereotypic or species-specific posture
Minimal movement
Reduced responsiveness to external stimuli
Reversible with stimulation – unlike coma, anaesthesia or death

Question 797

How is the physiological criteria of sleep recorded?

Answer 797

Brain activity with EEG (electroencephalogramm)
Eye movements with EOG (electrooculogramm)
Muscle movements (tone)with EMG (electromyogramm)

Question 798

What are the stages of sleep?

Answer 798

Awake
Stage 1 & 2= NREM
Stage 3 & 4= NREM
Stage 5= REM

Question 799

What do the EEG, EOG and EMG show in an awake patient?

Answer 799

EEG= Fast activity (beta)
EOG= Some eye movements 
EMG= Strong muscle tone

Question 800

What do the EEG, EOG and EMG show in a patient in stage 1 & 2 of sleep?

Answer 800

EEG= Slowing of brain activity (theta) 
EOG= None
EMG= Reduced muscle tone

Question 801

What do the EEG, EOG and EMG show in a patient in stage 3 & 4 of sleep?

Answer 801

EEG= Even slower brain activity (delta)
EOG= None
EMG= Further reduced muscle tone

Question 802

What do the EEG, EOG and EMG show in a patient in stage 5 of sleep (REM)?

Answer 802

EEG= Speeding up of brain activity (similar to beta in awake person)
EOG= Rapid and wide
EMG= Minimal tone (almost none)

Question 803

What is NREM sleep?

Answer 803

Non-REM

Slow wave sleep

Question 804

How long does each sleep stage last in an average cycle?

Answer 804

1 hour and half overall (70 mins excluding REM)

12 min= awake
13 min= stage 1
13 min= stage 2
12 min= stage 3
10 min= stage 4
10-20 min= REM sleep

Very quickly into REM sleep

Question 805

What controls the sleep/wave cycle?

Answer 805

Lateral hypothalamus (LH) promotes wakefulness (stimulates RAS)

Ventrolateral preoptic (VLP) nucleus promotes sleep (inhibits RAS)

Suprachiasmatic nucleus synchronises sleep with falling night level (affects VLP, LH and pineal)
Pineal-> melatonin

Question 806

What system in the brain maintains arousal?

Answer 806

Reticular activating system
Controls consciousness
Modulate activity of cerebral cortex directly or through thalamus

Question 807

What controls the circadian synchronisation of sleep/wake cycle?

Answer 807

Suprachiasmatic nucleus

Synchronises sleep with falling night level

As light level falls, input from retina activates suprachiasmatic nucleus and has relationships with nuclei controlling sleep/wake cycle

Affects VLP, LH and pineal

Pineal-> melatonin secretion (main function- on pituitary)

Question 808

How do we know sleep is necessary?

Answer 808

Most/all animals sleep
Sleep deprivation is detrimental
Sleep is regulated accurately

Question 809

What are the effects of sleep deprivation? What happens in rats and humans?

Answer 809

Sleepiness, irritability
Performance decrements/ increased risk of errors and accidents
Concentration/learning difficulties
Glucose intolerance
Reduced leptin/increased appetite
Hallucinations (after long sleep deprivation)
Death- rats (14-40 days), humans (fatal familial insomnia)

Question 810

What does sleep loss do to ability brain activation when performing mathematical tasks?

Answer 810

Reduced ability

Lower brain activation

Question 811

After sleep loss what happens to regulate sleep?

Answer 811

Reduced latency to sleep onset
Increase of slow wave sleep (NREM)
Increase of REM sleep (after selective REM sleep deprivation)

Question 812

What are the functions of sleep? Why can these be argued against?

Answer 812

Restoration and recovery- but active individuals do not sleep more
Energy conservation- 10% drop in BMR (but lying still is just as effective)
Predator avoidance
Specific brain functions

Question 813

When do dreams occur?

Answer 813

Can occur in REM and NREM sleep
Most frequent in REM sleep
More easily recalled in REM sleep
Contents of dreams are more emotional than ‘real life’

Question 814

Where is brain activity high during dreams?

Answer 814

Brain activity in limbic system higher than in frontal lobe during dreams

Question 815

What are the functions of dreams?

Answer 815

Safety valve for antisocial emotions
Disposal of unwanted memories
Memory consolidation

NREM sleep: declarative memory
REM sleep: procedural memory

Question 816

What memory consolidation happens in NREM and REM?

Answer 816

NREM sleep: declarative memory

REM sleep: procedural memory

Question 817

List sleep disorders

Answer 817

Insomnia

Narcolepsy

Question 818

What is insomnia?

Answer 818

High prevalence
Most cases transient

Causes of chronic cases:

• Physiological e.g. sleep apnea, chronic pain
• Brain dysfunction e.g. depression, fatal familial insomnia, night working

Treatment: most hypnotics enhance GABAergic circuits

Question 819

What is narcolepsy?

Answer 819

Falling asleep repeatedly during the day and disturbed sleep during the night
Cataplexy = suddenly all muscles in body lose their tone -> fall

Dysfunction of control of REM sleep

Orexin deficiency –genetic or autoimmune?

Question 820

What effect does shift work have on sleep?

Answer 820

Night working causes physiological processes to become desynchronised

This can lead to sleep disorders, fatigue and an increased risk for some conditions such as obesity, diabetes and cancer

Question 821

What is found in the cerebral cortex?

Answer 821

Grey matter structure
White matter association fibres
Grey matter function
Testing grey matter function
Hemispheric specialisation

Question 822

What is in the GM of the brain?

Answer 822

Neuronal cell bodies, dendrites, synaptic connections, glial cells

50 billion neurons and x10 glial cells

Only 30% surface easily visible as 70% hidden within sulci

Question 823

What is in the WM of the brain?

Answer 823

Myelinated neuronal axons forming white matter tracks

Question 824

How many cortical layers are there?

Answer 824

6
Roman numerals (with letters for laminar subdivisons)

Question 825

True or false: each of the cortical laminae in the neocortex (which covers the bulk of the cerebral hemispheres and is defined by six layers) has characteristic functional and anatomical features

Answer 825

True

Question 826

Where are smaller pyramidal neurons found in the cortical layers? What kind of connections predominate?

Answer 826

Layers II and III

Primarily corticocortical connections

Question 827

What kind of connections predominate in Layer I

Answer 827

Neuropil

Question 828

Which cortical layer has the most stellate neurons?

Answer 828

Layer IV is typically rich in stellate neurons with locally ramifying axons

Question 829

Where do the neurons in layer IV of the cortex receive input from?

Answer 829

In the primary sensory cortices, these neurons receive input from the thalamus, the major sensory relay from the periphery

Question 830

What layer are pyramidal neurons whose axons typically leave the cortex found?

Answer 830

Layer V, and to a lesser degree layer VI, contain pyramidal neurons whose axons typically leave the cortex

Question 831

How many distinct cortical regions or cytoarchitectonic did Brodmann describe?

Answer 831

About 50

Histological map of brain

Question 832

Which cortical layers receive input and which give output?

Answer 832

Layer 4 receives input
Layers 1- 3 send output to cortex
Layers 5 and 6 send output to non-cortex

Question 833

Which layer of the cortex is closer to the dorsal surface?

Answer 833

Layer I

Layer VI closest to ventral layer

Question 834

What cortical layer has the primary visual cortex?

Answer 834

Layer IV

Question 835

What is the relationship between cortical columns?

Answer 835

Columns stacked next to each other are connected (but looser than within each column)

Some are functionally connected

Question 836

Outline the role of the occipital lobe (and how lesions may affect this)

Answer 836

Visual association cortex analyses different attributes of visual image in different places

Form and colour analyzed along ventral pathway; spatial relationships & movement along dorsal pathway

Lesions affect specific aspects of visual perception

Question 837

Outline the role of the parietal lobe (and how lesions may affect this)

Answer 837

Posterior parietal association cortex creates spatial map of body in surroundings, from multi-modality information

Injury may cause disorientation, inability to read map or understand spatial relationships, apraxia, hemispatial neglect (primarily associated with right hemisphere)

Question 838

Outline the role of the temporal lobe (and how lesions may affect this)

Answer 838

Language, object recognition, memory, emotion

Injury leads to agnosia, receptive aphasia

Question 839

Outline the role of the frontal lobe (and how lesions may affect this)

Answer 839

Judgement, foresight, personality, appreciation of self in relation to world

Injury leads to deficits in planning and inappropriate behaviour

Question 840

What are association fibres?

Answer 840

Connect areas within the same hemisphere

Question 841

What are commissural fibres?

Answer 841

Connect left hemisphere to righ hemisphere

Question 842

What are projection fibres?

Answer 842

Connect cortex with lower brain structures e.g. thalamus, brainstem and SC

Question 843

What is another name for short association fibres?

Answer 843

U fibres

Connecting neighbouring gyra usually

Question 844

What are 4 examples of long association fibres and what do they connect?

Answer 844

Superior Longitudinal Fasciculus (connects frontal and occipital lobes)

Arcuate Fasciculus (connects frontal and temporal lobes)

Inferior Longitudinal Fasciculus (connects temporal and occipital lobes)

Uncinate Fasciculus (connects anterior frontal and temporal lobes)

Question 845

What does the superior longitudinal fasciculus connect?

Answer 845

Frontal and occipital lobes

Question 846

What does the arcuate fasciculus connect?

Answer 846

Frontal and temporal lobes

Question 847

What does the inferior longitudinal fasciculus connect?

Answer 847

Temporal and occipital lobes

Question 848

What does the uncinate fasciculus connect?

Answer 848

Anterior frontal and temporal lobes

Question 849

What kind of fibres is the corpus callosum?

Answer 849

Commissural

Question 850

What kind of fibres is the anterior commissure?

Answer 850

Commissural

Question 851

What are the functions of the frontal lobe GM?

Answer 851

PRODUCTION OF VOLUNTARY SKELETAL MUSCLE MOVEMENTS
Primary motor cortex, BA 4 (precentral gyrus)
Premotor cortex, BA6
(Motor association area)

COORDINATES INFO FROM OTHER ASSOCIATION AREAS
Prefrontal association area

Question 852

What are the functions of the parietal lobe GM?

Answer 852

RECOGNITION AND INTERPRETATION OF SENSORY INFO FROM SKIN, MUSCLES, TASTE BUDS
Sensory association area
Primary somatosensory cortex (postcentral gyrus)

Question 853

What are the functions of the occipital lobe GM?

Answer 853

VISION
Visual association area
Primary visual cortex

Question 854

What are the functions of the temporal lobe GM?

Answer 854

HEARING
Auditory association area
Primary auditory cortex

Question 855

What does a lesion in the primary motor cortex cause?

Answer 855

Paralysis (full or partial loss of fine voluntary movements in the contralateral side

Paresis (muscular weakness)

Question 856

What does a lesion in the motor association area cause?

Answer 856

Apraxia (difficulty with motor planning to perform voluntary movements and tasks)

Question 857

What happened to Phineas Gage?

Answer 857

Damage to prefrontal association area

Question 858

What happens when the prefrontal association area is damaged? (e.g. Phineas Gage)

Answer 858

Changes to:
Personality 
Self-control
Attention
Planning
Emotions
Motivation
Decision making
Reasoning
Judgment

Question 859

What is Broca’s motor aphasia?

Answer 859

Prefrontal lesion

Impaired speech production but preserved comprehension

Question 860

What happens if there is a lesion in the primary somatosensory cortex?

Answer 860

Sensory deficits (in PERCEPTION of basic sensory information)

Question 861

What happens if there is a lesion in sensory association areas?

Answer 861

Sensory deficits (in INTERPRETATION of sensory information)

Question 862

What is spatial neglect? What can it affect?

Answer 862

Unawareness of the contralateral side

Affects:
Tactile recognition
Flavour recognition
Spatial orientation
Ability to read maps 
Reading (alexia)
Writing (agraphia)
Calculations (acalculia)

Question 863

What happens if there is a lesion in the primary visual cortex?

Answer 863

Blindness in the corresponding part of the visual field (deficit in perception of basic visual information)

Question 864

What happens if there is a lesion in the visual association area?

Answer 864

Visual deficits (in interpretation of visual information)

Question 865

What is prosopagnosia?

Answer 865

Inability to recognise familiar faces or learn new faces (aka face blindness)

Usually due to lesion of the visual posterior association area

Question 866

What happens if there is a lesion of the primary auditory cortex?

Answer 866

Deafness (deficit in perception of basic auditory information); unilateral lesions cause partial deafness in both ears

Question 867

What happens if there is a lesion of the auditory association areas?

Answer 867

Visual deficits (in interpretation of auditory information)

Question 868

What is Wernicke’s receptive aphasia?

Answer 868

Impaired comprehension but preserved speech production

Question 869

What happened to HM?

Answer 869

Amnesic patient
Most of hippocampus and adjacent tissues in medial temporal lobe were removed
Lead to anterograde amnesia

Question 870

What is anterograde amnesia?

Answer 870

Inability to form new memories

Question 871

What is the difference between primary and association cortices?

Answer 871

PRIMARY
Function predictable
Organised topographically
Left-right symmetry

ASSOCIATION
Function less predictable
Not organised topographically
Left-right symmetry weak or absent

Question 872

What does TMS measure?

Answer 872

Transcranial magnetic stimulation

Measures effects of interference with normal info processing due to electro-magnetic stimulation of neurons

Question 873

What are the advantages of TMS over lesion/patient studies?

Answer 873

The effects of stimulation are generally more spatially precise than naturally occurring lesions, which are often large and vary greatly across patients (i.e., better spatial resolution);

Healthy participants can be used as their own controls (within-subject design), thereby avoiding the issue of potential differences in pre-morbid abilities between patients and controls;

There is insufficient time for functional reorganization to take place during TMS, meaning that recovery processes are unlikely to confound the results;

Allows to investigate temporal dynamics of on-line neuronal processing

Question 874

What does PET study in the brain?

Answer 874

Measures changes in amount of blood flow directly to a brain region

Uses radioactive tracer attached to a molecule to locate brain areas where that particular molecule is being absorbed in the brain

Question 875

What does fMRI study in the brain?

Answer 875

Measures changes in amount of blood oxygen in a brain region

Question 876

What does electroencephalography measure?

Answer 876

Electric signal generated by the brain

Electrophysiological monitoring method to record electrical activity of teh brain

Question 877

What does magnetoencephalography measure?

Answer 877

Measures magnetic field generated by the electric currents in the brain

Functional neuroimaging technique for mapping brain activity

Question 878

What does hemispheric specialisation mean?

Answer 878

LEFT
Verbal and analytic functions
Language dominant

RIGHT
Non-verbal and creative functions
Spatial processing

Question 879

What is tractography?

Answer 879

Diffusion tensor imaging

Measure the effect of lesions in white matter or how these lesions might disconnect different brain areas

Movement of water molecules in the brain can be used to infer the underlying structure of white matter